PARIS – Most diarrhea that leads patients to seek medical advice is actually a false alarm, said gastroenterologist Nassim Hammoudi, MD, PhD, of the Lariboisière Hospital in Paris, during France’s annual general medicine conference (JNMG 2023). He said that doctors need to understand the characteristics of chronic diarrhea and adapt its management accordingly. In his presentation, Dr. Hammoudi highlighted the clinical signs that should be considered.

Mechanisms of chronic diarrhea

Chronic diarrhea can result from different mechanisms, such as motility disorders related to accelerated intestinal transit, malabsorption, osmotic diarrhea, and secretory diarrhea, which are often interlinked. When an endoscopy is performed, it is recommended to conduct multilevel biopsies to detect microscopic colitis, which Dr. Hammoudi believes is “probably underdiagnosed.”

Diarrhea is defined as the passage of frequent stools (more than three a day), soft to liquid in consistency, and a daily weight exceeding 300 g. It is considered chronic when it persists for more than a month.
 

Identifying false diarrhea

Practitioners must first distinguish between genuine and false diarrhea, with the latter presenting in most consultations. “Thorough questioning is fundamental,” Dr. Hammoudi emphasized. It is essential to determine the daily stool count, the presence of nocturnal stools, and stool consistency. “A soft stool passed once a day is not diarrhea,” he said.

The most challenging form of false diarrhea to identify is what he called “constipated person’s diarrhea.” These patients, who are typically elderly, reside in care homes, and are bed-bound and taking morphine, have daily liquid stools but are actually constipated. “Taking antidiarrheal medications makes the situation worse,” said Dr. Hammoudi.

Another type of false diarrhea is tenesmus, in which patients feel like they have a full rectum, even though it is physiologically empty. The recurring urge to defecate results in mucus discharges that resemble diarrhea. Inflammatory rectal involvement could be the cause, necessitating a gastroenterology consultation.

Anal incontinence can also cause false diarrhea. It is more common in elderly people residing in care homes and in women in the postpartum period. This condition is difficult to manage and requires referral to a gastroenterologist.
 

Chronic diarrhea: Could cancer be the culprit?

After ruling out false diarrhea, clinicians should be vigilant for warning signs. The first question to consider, said Dr. Hammoudi, is whether the chronic diarrhea is associated with a lesion. Several criteria should prompt a colonoscopy, especially to search for colorectal cancer lesions:

• Age greater than 50 years
• Personal or family history of colorectal cancer
• Recent changes in bowel habits
• Rectal bleeding
• Nighttime stools
• Unexplained weight loss
• Iron-deficiency anemia

Obvious causes of chronic diarrhea should be prioritized in the management plan. Medications top the list, with more than 500 treatments – for example, ACE inhibitors, proton pump inhibitors (PPIs), antidiabetic drugs, colchicine, magnesium, laxatives – known to have diarrhea as a side effect.

Certain dietary habits can also exacerbate diarrhea, such as milk consumption in cases of lactose intolerance, or excessive sugar intake, which can lead to osmotic diarrhea.
 

IBS is often at play

Once these causes have been ruled out, several etiological pathways should be investigated. The first relates to motility issues, which are the most common diarrhea-related problem, said Dr. Hammoudi.

This type of diarrhea is linked to rapid intestinal transit time and is characterized by postprandial bowel movements (occurring shortly after a meal). Here, patients experience urgency and notice identifiable food debris in their stools. It tends to stop when fasting and can be treated effectively with antidiarrheals.

Irritable bowel syndrome (IBS) is the main cause of rapid intestinal transit diarrhea. It is defined as recurrent abdominal pain (at least 1 day/week) over a period of 3 months, associated with two of the following criteria: pain eases or worsens on passing feces, change in frequency of bowel movements, change in the consistency of stools.

Symptoms may come on suddenly, sometimes after taking antibiotics, and may result in misdiagnosis.

IBS medications treat the symptoms. Antispasmodics, such as trimebutine, phloroglucinol (Spasfon), or pinaverium bromide (Dicetel) are recommended, even there can be a placebo effect. The antidiarrheal medication loperamide (Imodium) can also be used. Probiotics may be beneficial, as an imbalanced intestinal microbiota is often implicated.

Dietary changes can also have a positive impact. Encouraging a diet rich in fruit and vegetables to enhance fiber intake is advised. A low FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet, targeting short-chain carbohydrates, can also be tried to identify foods to avoid, although it may be challenging to stick to.

Postinfectious IBS is a frequent cause of rapid intestinal transit diarrhea. It generally follows an episode of acute infectious diarrhea. “Symptoms may come on suddenly, sometimes after taking antibiotics, and may result in misdiagnosis,” said Dr. Hammoudi. This type of IBS often resolves spontaneously within 6 months.
 

Consider the possibility of SIBO

Another cause of rapid intestinal transit diarrhea is small intestinal bacterial overgrowth (SIBO). It is difficult to distinguish between IBS and SIBO. Often, affected patients are diabetic, overweight, or have had bowel surgery.

The only way to diagnose SIBO is by conducting a breath test to measure the production of hydrogen and methane by the microbiota after ingesting sugar. However, the test is difficult to access and not fully covered by social security plans in France, said Dr. Hammoudi.

In cases of suspected SIBO and severe symptoms, a 7- to 10-day course of antibiotics can be attempted to provide relief, although a diagnosis should be confirmed before considering this option, Dr. Hammoudi said.
 

Malabsorption diarrhea

Another major cause of chronic diarrhea is malabsorption, characterized by large, fatty stools that are difficult to flush. Despite a normal diet, this type of diarrhea is associated with weight loss and nutritional deficiencies.

Its diagnosis involves measuring fat in the stools (steatorrhea) and possibly testing fecal elastase, an enzyme produced by the pancreas that is involved in digestion.

The most important causes of malabsorption diarrhea are pancreatic insufficiency, celiac disease, and Crohn’s disease. Generally, any lesion in the small intestine can lead to malabsorption-related diarrhea.

Celiac disease, or gluten intolerance, is an autoimmune condition triggered by a reaction to gluten proteins. Several antibodies can be produced in the presence of gluten proteins. Diagnosis is confirmed by positive antitransglutaminase antibodies and a duodenal biopsy through esophagogastroduodenoscopy.

The only treatment for celiac disease is a lifelong gluten-free diet. Celiac disease is increasingly diagnosed in adults, said Dr. Hammoudi, and should be considered as a possibility. This condition must be distinguished from gluten sensitivity, which can cause digestive issues, possibly leading to rapid intestinal transit diarrhea. “The only treatment for celiac disease is a lifelong gluten-free diet,” Dr. Hammoudi added.

Crohn’s disease, a type of inflammatory bowel disease, affects the entire digestive tract, particularly the terminal small intestine, which promotes malabsorption. In ulcerative colitis, another IBD affecting the rectum, any associated rectal syndrome can result in false diarrhea with stools containing blood and mucus.

Osmotic diarrhea, on the other hand, is linked to the presence of highly osmotic agents in the digestive tract. This type of diarrhea is watery and short-lived, stopping once the agents are no longer absorbed. The main culprits are lactose (in cases of lactose intolerance) and laxatives.
 

Drug-induced microscopic colitis

Secretory diarrhea is characterized by excessive secretions by the digestive tract, leading to significant potassium loss. This type of diarrhea is not related to food intake and is resistant to fasting.

Major causes of secretory diarrhea include microscopic colitis, parasitic infections, and endocrine tumors. Between 10% and 15% of patients with chronic diarrhea and apparently normal colonoscopy have microscopic colitis.

Dr. Hammoudi advised specialists seeking to determine the cause of chronic diarrhea to routinely collect multilevel bowel biopsies during colonoscopies from macroscopically normal mucosa to rule out microscopic colitis.

Microscopic colitis is mainly linked to the use of medications like PPIs and NSAIDs. These drugs can induce malabsorption-related diarrhea by damaging the intestinal wall.

In addition to discontinuing the implicated medication, the treatment for microscopic colitis includes low-dose budesonide (multiple brands). Biologics used in IBD may also be considered in cases of recurrent colitis.

Finally, exudative enteropathy can be a distinct cause of chronic diarrhea. It is characterized by albumin leakage (Waldmann’s disease) and manifests with edema, malnutrition, and significant hypoalbuminemia.

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

PARIS – Most diarrhea that leads patients to seek medical advice is actually a false alarm, said gastroenterologist Nassim Hammoudi, MD, PhD, of the Lariboisière Hospital in Paris, during France’s annual general medicine conference (JNMG 2023). He said that doctors need to understand the characteristics of chronic diarrhea and adapt its management accordingly. In his presentation, Dr. Hammoudi highlighted the clinical signs that should be considered.

Mechanisms of chronic diarrhea

Chronic diarrhea can result from different mechanisms, such as motility disorders related to accelerated intestinal transit, malabsorption, osmotic diarrhea, and secretory diarrhea, which are often interlinked. When an endoscopy is performed, it is recommended to conduct multilevel biopsies to detect microscopic colitis, which Dr. Hammoudi believes is “probably underdiagnosed.”

Diarrhea is defined as the passage of frequent stools (more than three a day), soft to liquid in consistency, and a daily weight exceeding 300 g. It is considered chronic when it persists for more than a month.
 

Identifying false diarrhea

Practitioners must first distinguish between genuine and false diarrhea, with the latter presenting in most consultations. “Thorough questioning is fundamental,” Dr. Hammoudi emphasized. It is essential to determine the daily stool count, the presence of nocturnal stools, and stool consistency. “A soft stool passed once a day is not diarrhea,” he said.

The most challenging form of false diarrhea to identify is what he called “constipated person’s diarrhea.” These patients, who are typically elderly, reside in care homes, and are bed-bound and taking morphine, have daily liquid stools but are actually constipated. “Taking antidiarrheal medications makes the situation worse,” said Dr. Hammoudi.

Another type of false diarrhea is tenesmus, in which patients feel like they have a full rectum, even though it is physiologically empty. The recurring urge to defecate results in mucus discharges that resemble diarrhea. Inflammatory rectal involvement could be the cause, necessitating a gastroenterology consultation.

Anal incontinence can also cause false diarrhea. It is more common in elderly people residing in care homes and in women in the postpartum period. This condition is difficult to manage and requires referral to a gastroenterologist.
 

Chronic diarrhea: Could cancer be the culprit?

After ruling out false diarrhea, clinicians should be vigilant for warning signs. The first question to consider, said Dr. Hammoudi, is whether the chronic diarrhea is associated with a lesion. Several criteria should prompt a colonoscopy, especially to search for colorectal cancer lesions:

• Age greater than 50 years
• Personal or family history of colorectal cancer
• Recent changes in bowel habits
• Rectal bleeding
• Nighttime stools
• Unexplained weight loss
• Iron-deficiency anemia

Obvious causes of chronic diarrhea should be prioritized in the management plan. Medications top the list, with more than 500 treatments – for example, ACE inhibitors, proton pump inhibitors (PPIs), antidiabetic drugs, colchicine, magnesium, laxatives – known to have diarrhea as a side effect.

Certain dietary habits can also exacerbate diarrhea, such as milk consumption in cases of lactose intolerance, or excessive sugar intake, which can lead to osmotic diarrhea.
 

IBS is often at play

Once these causes have been ruled out, several etiological pathways should be investigated. The first relates to motility issues, which are the most common diarrhea-related problem, said Dr. Hammoudi.

This type of diarrhea is linked to rapid intestinal transit time and is characterized by postprandial bowel movements (occurring shortly after a meal). Here, patients experience urgency and notice identifiable food debris in their stools. It tends to stop when fasting and can be treated effectively with antidiarrheals.

Irritable bowel syndrome (IBS) is the main cause of rapid intestinal transit diarrhea. It is defined as recurrent abdominal pain (at least 1 day/week) over a period of 3 months, associated with two of the following criteria: pain eases or worsens on passing feces, change in frequency of bowel movements, change in the consistency of stools.

Symptoms may come on suddenly, sometimes after taking antibiotics, and may result in misdiagnosis.

IBS medications treat the symptoms. Antispasmodics, such as trimebutine, phloroglucinol (Spasfon), or pinaverium bromide (Dicetel) are recommended, even there can be a placebo effect. The antidiarrheal medication loperamide (Imodium) can also be used. Probiotics may be beneficial, as an imbalanced intestinal microbiota is often implicated.

Dietary changes can also have a positive impact. Encouraging a diet rich in fruit and vegetables to enhance fiber intake is advised. A low FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet, targeting short-chain carbohydrates, can also be tried to identify foods to avoid, although it may be challenging to stick to.

Postinfectious IBS is a frequent cause of rapid intestinal transit diarrhea. It generally follows an episode of acute infectious diarrhea. “Symptoms may come on suddenly, sometimes after taking antibiotics, and may result in misdiagnosis,” said Dr. Hammoudi. This type of IBS often resolves spontaneously within 6 months.
 

Consider the possibility of SIBO

Another cause of rapid intestinal transit diarrhea is small intestinal bacterial overgrowth (SIBO). It is difficult to distinguish between IBS and SIBO. Often, affected patients are diabetic, overweight, or have had bowel surgery.

The only way to diagnose SIBO is by conducting a breath test to measure the production of hydrogen and methane by the microbiota after ingesting sugar. However, the test is difficult to access and not fully covered by social security plans in France, said Dr. Hammoudi.

In cases of suspected SIBO and severe symptoms, a 7- to 10-day course of antibiotics can be attempted to provide relief, although a diagnosis should be confirmed before considering this option, Dr. Hammoudi said.
 

Malabsorption diarrhea

Another major cause of chronic diarrhea is malabsorption, characterized by large, fatty stools that are difficult to flush. Despite a normal diet, this type of diarrhea is associated with weight loss and nutritional deficiencies.

Its diagnosis involves measuring fat in the stools (steatorrhea) and possibly testing fecal elastase, an enzyme produced by the pancreas that is involved in digestion.

The most important causes of malabsorption diarrhea are pancreatic insufficiency, celiac disease, and Crohn’s disease. Generally, any lesion in the small intestine can lead to malabsorption-related diarrhea.

Celiac disease, or gluten intolerance, is an autoimmune condition triggered by a reaction to gluten proteins. Several antibodies can be produced in the presence of gluten proteins. Diagnosis is confirmed by positive antitransglutaminase antibodies and a duodenal biopsy through esophagogastroduodenoscopy.

The only treatment for celiac disease is a lifelong gluten-free diet. Celiac disease is increasingly diagnosed in adults, said Dr. Hammoudi, and should be considered as a possibility. This condition must be distinguished from gluten sensitivity, which can cause digestive issues, possibly leading to rapid intestinal transit diarrhea. “The only treatment for celiac disease is a lifelong gluten-free diet,” Dr. Hammoudi added.

Crohn’s disease, a type of inflammatory bowel disease, affects the entire digestive tract, particularly the terminal small intestine, which promotes malabsorption. In ulcerative colitis, another IBD affecting the rectum, any associated rectal syndrome can result in false diarrhea with stools containing blood and mucus.

Osmotic diarrhea, on the other hand, is linked to the presence of highly osmotic agents in the digestive tract. This type of diarrhea is watery and short-lived, stopping once the agents are no longer absorbed. The main culprits are lactose (in cases of lactose intolerance) and laxatives.
 

Drug-induced microscopic colitis

Secretory diarrhea is characterized by excessive secretions by the digestive tract, leading to significant potassium loss. This type of diarrhea is not related to food intake and is resistant to fasting.

Major causes of secretory diarrhea include microscopic colitis, parasitic infections, and endocrine tumors. Between 10% and 15% of patients with chronic diarrhea and apparently normal colonoscopy have microscopic colitis.

Dr. Hammoudi advised specialists seeking to determine the cause of chronic diarrhea to routinely collect multilevel bowel biopsies during colonoscopies from macroscopically normal mucosa to rule out microscopic colitis.

Microscopic colitis is mainly linked to the use of medications like PPIs and NSAIDs. These drugs can induce malabsorption-related diarrhea by damaging the intestinal wall.

In addition to discontinuing the implicated medication, the treatment for microscopic colitis includes low-dose budesonide (multiple brands). Biologics used in IBD may also be considered in cases of recurrent colitis.

Finally, exudative enteropathy can be a distinct cause of chronic diarrhea. It is characterized by albumin leakage (Waldmann’s disease) and manifests with edema, malnutrition, and significant hypoalbuminemia.

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

PARIS – Most diarrhea that leads patients to seek medical advice is actually a false alarm, said gastroenterologist Nassim Hammoudi, MD, PhD, of the Lariboisière Hospital in Paris, during France’s annual general medicine conference (JNMG 2023). He said that doctors need to understand the characteristics of chronic diarrhea and adapt its management accordingly. In his presentation, Dr. Hammoudi highlighted the clinical signs that should be considered.

Mechanisms of chronic diarrhea

Chronic diarrhea can result from different mechanisms, such as motility disorders related to accelerated intestinal transit, malabsorption, osmotic diarrhea, and secretory diarrhea, which are often interlinked. When an endoscopy is performed, it is recommended to conduct multilevel biopsies to detect microscopic colitis, which Dr. Hammoudi believes is “probably underdiagnosed.”

Diarrhea is defined as the passage of frequent stools (more than three a day), soft to liquid in consistency, and a daily weight exceeding 300 g. It is considered chronic when it persists for more than a month.
 

Identifying false diarrhea

Practitioners must first distinguish between genuine and false diarrhea, with the latter presenting in most consultations. “Thorough questioning is fundamental,” Dr. Hammoudi emphasized. It is essential to determine the daily stool count, the presence of nocturnal stools, and stool consistency. “A soft stool passed once a day is not diarrhea,” he said.

The most challenging form of false diarrhea to identify is what he called “constipated person’s diarrhea.” These patients, who are typically elderly, reside in care homes, and are bed-bound and taking morphine, have daily liquid stools but are actually constipated. “Taking antidiarrheal medications makes the situation worse,” said Dr. Hammoudi.

Another type of false diarrhea is tenesmus, in which patients feel like they have a full rectum, even though it is physiologically empty. The recurring urge to defecate results in mucus discharges that resemble diarrhea. Inflammatory rectal involvement could be the cause, necessitating a gastroenterology consultation.

Anal incontinence can also cause false diarrhea. It is more common in elderly people residing in care homes and in women in the postpartum period. This condition is difficult to manage and requires referral to a gastroenterologist.
 

Chronic diarrhea: Could cancer be the culprit?

After ruling out false diarrhea, clinicians should be vigilant for warning signs. The first question to consider, said Dr. Hammoudi, is whether the chronic diarrhea is associated with a lesion. Several criteria should prompt a colonoscopy, especially to search for colorectal cancer lesions:

• Age greater than 50 years
• Personal or family history of colorectal cancer
• Recent changes in bowel habits
• Rectal bleeding
• Nighttime stools
• Unexplained weight loss
• Iron-deficiency anemia

Obvious causes of chronic diarrhea should be prioritized in the management plan. Medications top the list, with more than 500 treatments – for example, ACE inhibitors, proton pump inhibitors (PPIs), antidiabetic drugs, colchicine, magnesium, laxatives – known to have diarrhea as a side effect.

Certain dietary habits can also exacerbate diarrhea, such as milk consumption in cases of lactose intolerance, or excessive sugar intake, which can lead to osmotic diarrhea.
 

IBS is often at play

Once these causes have been ruled out, several etiological pathways should be investigated. The first relates to motility issues, which are the most common diarrhea-related problem, said Dr. Hammoudi.

This type of diarrhea is linked to rapid intestinal transit time and is characterized by postprandial bowel movements (occurring shortly after a meal). Here, patients experience urgency and notice identifiable food debris in their stools. It tends to stop when fasting and can be treated effectively with antidiarrheals.

Irritable bowel syndrome (IBS) is the main cause of rapid intestinal transit diarrhea. It is defined as recurrent abdominal pain (at least 1 day/week) over a period of 3 months, associated with two of the following criteria: pain eases or worsens on passing feces, change in frequency of bowel movements, change in the consistency of stools.

Symptoms may come on suddenly, sometimes after taking antibiotics, and may result in misdiagnosis.

IBS medications treat the symptoms. Antispasmodics, such as trimebutine, phloroglucinol (Spasfon), or pinaverium bromide (Dicetel) are recommended, even there can be a placebo effect. The antidiarrheal medication loperamide (Imodium) can also be used. Probiotics may be beneficial, as an imbalanced intestinal microbiota is often implicated.

Dietary changes can also have a positive impact. Encouraging a diet rich in fruit and vegetables to enhance fiber intake is advised. A low FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diet, targeting short-chain carbohydrates, can also be tried to identify foods to avoid, although it may be challenging to stick to.

Postinfectious IBS is a frequent cause of rapid intestinal transit diarrhea. It generally follows an episode of acute infectious diarrhea. “Symptoms may come on suddenly, sometimes after taking antibiotics, and may result in misdiagnosis,” said Dr. Hammoudi. This type of IBS often resolves spontaneously within 6 months.
 

Consider the possibility of SIBO

Another cause of rapid intestinal transit diarrhea is small intestinal bacterial overgrowth (SIBO). It is difficult to distinguish between IBS and SIBO. Often, affected patients are diabetic, overweight, or have had bowel surgery.

The only way to diagnose SIBO is by conducting a breath test to measure the production of hydrogen and methane by the microbiota after ingesting sugar. However, the test is difficult to access and not fully covered by social security plans in France, said Dr. Hammoudi.

In cases of suspected SIBO and severe symptoms, a 7- to 10-day course of antibiotics can be attempted to provide relief, although a diagnosis should be confirmed before considering this option, Dr. Hammoudi said.
 

Malabsorption diarrhea

Another major cause of chronic diarrhea is malabsorption, characterized by large, fatty stools that are difficult to flush. Despite a normal diet, this type of diarrhea is associated with weight loss and nutritional deficiencies.

Its diagnosis involves measuring fat in the stools (steatorrhea) and possibly testing fecal elastase, an enzyme produced by the pancreas that is involved in digestion.

The most important causes of malabsorption diarrhea are pancreatic insufficiency, celiac disease, and Crohn’s disease. Generally, any lesion in the small intestine can lead to malabsorption-related diarrhea.

Celiac disease, or gluten intolerance, is an autoimmune condition triggered by a reaction to gluten proteins. Several antibodies can be produced in the presence of gluten proteins. Diagnosis is confirmed by positive antitransglutaminase antibodies and a duodenal biopsy through esophagogastroduodenoscopy.

The only treatment for celiac disease is a lifelong gluten-free diet. Celiac disease is increasingly diagnosed in adults, said Dr. Hammoudi, and should be considered as a possibility. This condition must be distinguished from gluten sensitivity, which can cause digestive issues, possibly leading to rapid intestinal transit diarrhea. “The only treatment for celiac disease is a lifelong gluten-free diet,” Dr. Hammoudi added.

Crohn’s disease, a type of inflammatory bowel disease, affects the entire digestive tract, particularly the terminal small intestine, which promotes malabsorption. In ulcerative colitis, another IBD affecting the rectum, any associated rectal syndrome can result in false diarrhea with stools containing blood and mucus.

Osmotic diarrhea, on the other hand, is linked to the presence of highly osmotic agents in the digestive tract. This type of diarrhea is watery and short-lived, stopping once the agents are no longer absorbed. The main culprits are lactose (in cases of lactose intolerance) and laxatives.
 

Drug-induced microscopic colitis

Secretory diarrhea is characterized by excessive secretions by the digestive tract, leading to significant potassium loss. This type of diarrhea is not related to food intake and is resistant to fasting.

Major causes of secretory diarrhea include microscopic colitis, parasitic infections, and endocrine tumors. Between 10% and 15% of patients with chronic diarrhea and apparently normal colonoscopy have microscopic colitis.

Dr. Hammoudi advised specialists seeking to determine the cause of chronic diarrhea to routinely collect multilevel bowel biopsies during colonoscopies from macroscopically normal mucosa to rule out microscopic colitis.

Microscopic colitis is mainly linked to the use of medications like PPIs and NSAIDs. These drugs can induce malabsorption-related diarrhea by damaging the intestinal wall.

In addition to discontinuing the implicated medication, the treatment for microscopic colitis includes low-dose budesonide (multiple brands). Biologics used in IBD may also be considered in cases of recurrent colitis.

Finally, exudative enteropathy can be a distinct cause of chronic diarrhea. It is characterized by albumin leakage (Waldmann’s disease) and manifests with edema, malnutrition, and significant hypoalbuminemia.

This article was translated from the Medscape French edition. A version of this article appeared on Medscape.com.

BOSTON – With the current demand for type 2 diabetes drugs that both improve glycemic control and help patients shed large amounts of weight, liver specialists have speculated that the metabolic benefits could also extend to the liver.

Spoiler alert: they do.

In a retrospective study of patients with metabolic-associated fatty liver disease (MAFLD) and type 2 diabetes mellitus (T2DM) who received either a sodium-glucose cotransporter 2 (SGLT-2) inhibitor or glucagon-like peptide-1 (GLP-1) agonist, 87% of those who lost at least 3% of body weight within 8 weeks eventually experienced normalization of alanine aminotransferase (ALT) levels, reported Takamasa Ohki, MD, PhD, and colleagues from the department of gastroenterology at Mitsui Memorial Hospital in Tokyo.

“Body weight reduction within 8 weeks after administration of these agents was an independent factor [that] contributed to rapid improvement of ALT. Maintenance of body weight and T2DM after normalization of ALT was also very important,” they wrote in a scientific poster presented at the annual meeting of the American Association for the Study of Liver Diseases.
 

The biggest losers benefit most

Dr. Ohki and colleagues evaluated the effectiveness of SGLT-2 inhibitors and GLP-1 agonists as treatment of MAFLD for patients with T2DM.

They conducted a retrospective study of 233 patients who had both conditions and who received either of the drug classes at their institution from June 2010 through December 2021; the most recent follow-up was in December 2022. The primary endpoint of the study was normalization of ALT values.

A total of 54 patients had a 3% or greater reduction in body weight within 8 weeks of beginning treatment with their respective drugs. The researchers found that for 47 of these patients (87%), ALT values normalized; the 12-, 24-, and 36-month cumulative normalization rates were 61%, 73%, and 80%, respectively.

In contrast, among the 179 patients who did not lose weight as robustly or rapidly, 137 (76.5%) demonstrated normalization of ALT, with cumulative normalization rates of 41%, 59% and 69%, respectively (P < .01).

In multivariate analysis that controlled for age, sex, smoking, hypertension, dyslipidemia, weight reduction, and antidiabetes drug use, body weight reduction of at least 3% within 8 weeks of beginning treatment with either an SLT-2 or GLP-1 agent was associated independently with normalization of ALT, with a hazard ratio (HR) of 0.67 (P = .028).

Improvement of T2DM was an independent predictor for ALT normalization (HR, 0.64; P = .015).

Other factors contributing to ALT normalization included use of sulfonylurea (HR, 0.63; P < .01) and insulin (HR, 0.54; P < .01).

In all, 103 of the 184 patients with initial normalization of ALT values experienced a recurrence of ALT elevation during follow-up. In multivariate analysis, body weight gain and exacerbation of T2DM were independent factors for ALT reexacerbation (HR, 0.52 and 0.48, respectively; P < .01 for both comparisons).
 

Duration of effect uncertain

Philip A. Newsome, PhD, FRCPE, professor of experimental hepatology and honorary consultant hepatologist at the University of Birmingham, England, who was not involved in the study, has conducted research into the metabolic effects of SGLT-2 inhibitors and GLP-1 agonists. In an interview, he said that both drug classes are likely to have positive near-term effects on metabolic dysfunction–associated steatohepatitis (MASH, formerly NASH) through their effects on glucose control and reduction in associated comorbidities.

“The unknown question,” he added, is what will happen in the long term. “I think there are some uncertainties around what proportion of patients will essentially be downstaged or downgraded such that they don’t develop any other problem; I suspect that will be the case in very many patients. However, I suspect there will also be a large proportion that end up requiring additional therapy above and beyond weight loss,” said Dr. Newsome.

The investigators did not report a funding source for the study. Dr. Ohki and colleagues have disclosed no relevant financial relationships. Dr. Newsome has consulted on behalf of his institution with Novo Nordisk, BMS, Gilead, Pfizer, Poxel, and Intercept and has received a grant from Pharmaxis and Boehringer Ingelheim.
 

A version of this article appeared on Medscape.com.

BOSTON – With the current demand for type 2 diabetes drugs that both improve glycemic control and help patients shed large amounts of weight, liver specialists have speculated that the metabolic benefits could also extend to the liver.

Spoiler alert: they do.

In a retrospective study of patients with metabolic-associated fatty liver disease (MAFLD) and type 2 diabetes mellitus (T2DM) who received either a sodium-glucose cotransporter 2 (SGLT-2) inhibitor or glucagon-like peptide-1 (GLP-1) agonist, 87% of those who lost at least 3% of body weight within 8 weeks eventually experienced normalization of alanine aminotransferase (ALT) levels, reported Takamasa Ohki, MD, PhD, and colleagues from the department of gastroenterology at Mitsui Memorial Hospital in Tokyo.

“Body weight reduction within 8 weeks after administration of these agents was an independent factor [that] contributed to rapid improvement of ALT. Maintenance of body weight and T2DM after normalization of ALT was also very important,” they wrote in a scientific poster presented at the annual meeting of the American Association for the Study of Liver Diseases.
 

The biggest losers benefit most

Dr. Ohki and colleagues evaluated the effectiveness of SGLT-2 inhibitors and GLP-1 agonists as treatment of MAFLD for patients with T2DM.

They conducted a retrospective study of 233 patients who had both conditions and who received either of the drug classes at their institution from June 2010 through December 2021; the most recent follow-up was in December 2022. The primary endpoint of the study was normalization of ALT values.

A total of 54 patients had a 3% or greater reduction in body weight within 8 weeks of beginning treatment with their respective drugs. The researchers found that for 47 of these patients (87%), ALT values normalized; the 12-, 24-, and 36-month cumulative normalization rates were 61%, 73%, and 80%, respectively.

In contrast, among the 179 patients who did not lose weight as robustly or rapidly, 137 (76.5%) demonstrated normalization of ALT, with cumulative normalization rates of 41%, 59% and 69%, respectively (P < .01).

In multivariate analysis that controlled for age, sex, smoking, hypertension, dyslipidemia, weight reduction, and antidiabetes drug use, body weight reduction of at least 3% within 8 weeks of beginning treatment with either an SLT-2 or GLP-1 agent was associated independently with normalization of ALT, with a hazard ratio (HR) of 0.67 (P = .028).

Improvement of T2DM was an independent predictor for ALT normalization (HR, 0.64; P = .015).

Other factors contributing to ALT normalization included use of sulfonylurea (HR, 0.63; P < .01) and insulin (HR, 0.54; P < .01).

In all, 103 of the 184 patients with initial normalization of ALT values experienced a recurrence of ALT elevation during follow-up. In multivariate analysis, body weight gain and exacerbation of T2DM were independent factors for ALT reexacerbation (HR, 0.52 and 0.48, respectively; P < .01 for both comparisons).
 

Duration of effect uncertain

Philip A. Newsome, PhD, FRCPE, professor of experimental hepatology and honorary consultant hepatologist at the University of Birmingham, England, who was not involved in the study, has conducted research into the metabolic effects of SGLT-2 inhibitors and GLP-1 agonists. In an interview, he said that both drug classes are likely to have positive near-term effects on metabolic dysfunction–associated steatohepatitis (MASH, formerly NASH) through their effects on glucose control and reduction in associated comorbidities.

“The unknown question,” he added, is what will happen in the long term. “I think there are some uncertainties around what proportion of patients will essentially be downstaged or downgraded such that they don’t develop any other problem; I suspect that will be the case in very many patients. However, I suspect there will also be a large proportion that end up requiring additional therapy above and beyond weight loss,” said Dr. Newsome.

The investigators did not report a funding source for the study. Dr. Ohki and colleagues have disclosed no relevant financial relationships. Dr. Newsome has consulted on behalf of his institution with Novo Nordisk, BMS, Gilead, Pfizer, Poxel, and Intercept and has received a grant from Pharmaxis and Boehringer Ingelheim.
 

A version of this article appeared on Medscape.com.

BOSTON – With the current demand for type 2 diabetes drugs that both improve glycemic control and help patients shed large amounts of weight, liver specialists have speculated that the metabolic benefits could also extend to the liver.

Spoiler alert: they do.

In a retrospective study of patients with metabolic-associated fatty liver disease (MAFLD) and type 2 diabetes mellitus (T2DM) who received either a sodium-glucose cotransporter 2 (SGLT-2) inhibitor or glucagon-like peptide-1 (GLP-1) agonist, 87% of those who lost at least 3% of body weight within 8 weeks eventually experienced normalization of alanine aminotransferase (ALT) levels, reported Takamasa Ohki, MD, PhD, and colleagues from the department of gastroenterology at Mitsui Memorial Hospital in Tokyo.

“Body weight reduction within 8 weeks after administration of these agents was an independent factor [that] contributed to rapid improvement of ALT. Maintenance of body weight and T2DM after normalization of ALT was also very important,” they wrote in a scientific poster presented at the annual meeting of the American Association for the Study of Liver Diseases.
 

The biggest losers benefit most

Dr. Ohki and colleagues evaluated the effectiveness of SGLT-2 inhibitors and GLP-1 agonists as treatment of MAFLD for patients with T2DM.

They conducted a retrospective study of 233 patients who had both conditions and who received either of the drug classes at their institution from June 2010 through December 2021; the most recent follow-up was in December 2022. The primary endpoint of the study was normalization of ALT values.

A total of 54 patients had a 3% or greater reduction in body weight within 8 weeks of beginning treatment with their respective drugs. The researchers found that for 47 of these patients (87%), ALT values normalized; the 12-, 24-, and 36-month cumulative normalization rates were 61%, 73%, and 80%, respectively.

In contrast, among the 179 patients who did not lose weight as robustly or rapidly, 137 (76.5%) demonstrated normalization of ALT, with cumulative normalization rates of 41%, 59% and 69%, respectively (P < .01).

In multivariate analysis that controlled for age, sex, smoking, hypertension, dyslipidemia, weight reduction, and antidiabetes drug use, body weight reduction of at least 3% within 8 weeks of beginning treatment with either an SLT-2 or GLP-1 agent was associated independently with normalization of ALT, with a hazard ratio (HR) of 0.67 (P = .028).

Improvement of T2DM was an independent predictor for ALT normalization (HR, 0.64; P = .015).

Other factors contributing to ALT normalization included use of sulfonylurea (HR, 0.63; P < .01) and insulin (HR, 0.54; P < .01).

In all, 103 of the 184 patients with initial normalization of ALT values experienced a recurrence of ALT elevation during follow-up. In multivariate analysis, body weight gain and exacerbation of T2DM were independent factors for ALT reexacerbation (HR, 0.52 and 0.48, respectively; P < .01 for both comparisons).
 

Duration of effect uncertain

Philip A. Newsome, PhD, FRCPE, professor of experimental hepatology and honorary consultant hepatologist at the University of Birmingham, England, who was not involved in the study, has conducted research into the metabolic effects of SGLT-2 inhibitors and GLP-1 agonists. In an interview, he said that both drug classes are likely to have positive near-term effects on metabolic dysfunction–associated steatohepatitis (MASH, formerly NASH) through their effects on glucose control and reduction in associated comorbidities.

“The unknown question,” he added, is what will happen in the long term. “I think there are some uncertainties around what proportion of patients will essentially be downstaged or downgraded such that they don’t develop any other problem; I suspect that will be the case in very many patients. However, I suspect there will also be a large proportion that end up requiring additional therapy above and beyond weight loss,” said Dr. Newsome.

The investigators did not report a funding source for the study. Dr. Ohki and colleagues have disclosed no relevant financial relationships. Dr. Newsome has consulted on behalf of his institution with Novo Nordisk, BMS, Gilead, Pfizer, Poxel, and Intercept and has received a grant from Pharmaxis and Boehringer Ingelheim.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Lower-extremity (LE) lymphedema increases the risk for all types of skin cancer on the lower extremities.

METHODOLOGY:

• In the retrospective cohort study, researchers reviewed reports at Mayo Clinic for all patients who had LE lymphedema, limiting the review to those who had an ICD code for lymphedema.
• 4,437 patients with the ICD code from 2000 to 2020 were compared with 4,437 matched controls.
• The records of patients with skin cancer diagnoses were reviewed manually to determine whether the skin cancer, its management, or both were a cause of lymphedema; cancers that caused secondary lymphedema were excluded.
• This is the first large-scale study evaluating the association between LE lymphedema and LE skin cancer.

TAKEAWAY:

• 211 patients (4.6%) in the LE lymphedema group had any ICD code for LE skin cancer, compared with 89 (2%) in the control group.
• Among those with LE lymphedema, the risk for skin cancer was 1.98 times greater compared with those without lymphedema (95% confidence interval, 1.43-2.74; P < .001). Cases included all types of skin cancer.
• Nineteen of 24 patients with unilateral LE lymphedema had a history of immunosuppression.
• In the group of 24 patients with unilateral LE lymphedema, the lymphedematous LE was more likely to have one or more skin cancers than were the unaffected LE (87.5% vs. 33.3%; P < .05), and skin cancer was 2.65 times more likely to develop on the affected LE than in the unaffected LE (95% CI, 1.17-5.99; P = .02).

IN PRACTICE:

“Our findings suggest the need for a relatively high degree of suspicion of skin cancer at sites with lymphedema,” senior author, Afsaneh Alavi, MD, professor of dermatology at the Mayo Clinic, said in a Mayo Clinic press release reporting the results.

SOURCE:

The study was conducted by researchers at the Mayo Clinic and Meharry Medical College, Nashville. It was published in the November 2023 Mayo Clinic Proceedings.

LIMITATIONS:

This was a single-center retrospective study, and patients with LE lymphedema may be overdiagnosed with LE skin cancer because they have a greater number of examinations.

DISCLOSURES:

Dr. Alavi reports having been a consultant for AbbVie, Boehringer Ingelheim, InflaRx, Novartis, and UCB SA and an investigator for Processa Pharmaceuticals and Boehringer Ingelheim. The other authors had no disclosures.

A version of this article first appeared on Medscape.com.

TOPLINE:

Lower-extremity (LE) lymphedema increases the risk for all types of skin cancer on the lower extremities.

METHODOLOGY:

• In the retrospective cohort study, researchers reviewed reports at Mayo Clinic for all patients who had LE lymphedema, limiting the review to those who had an ICD code for lymphedema.
• 4,437 patients with the ICD code from 2000 to 2020 were compared with 4,437 matched controls.
• The records of patients with skin cancer diagnoses were reviewed manually to determine whether the skin cancer, its management, or both were a cause of lymphedema; cancers that caused secondary lymphedema were excluded.
• This is the first large-scale study evaluating the association between LE lymphedema and LE skin cancer.

TAKEAWAY:

• 211 patients (4.6%) in the LE lymphedema group had any ICD code for LE skin cancer, compared with 89 (2%) in the control group.
• Among those with LE lymphedema, the risk for skin cancer was 1.98 times greater compared with those without lymphedema (95% confidence interval, 1.43-2.74; P < .001). Cases included all types of skin cancer.
• Nineteen of 24 patients with unilateral LE lymphedema had a history of immunosuppression.
• In the group of 24 patients with unilateral LE lymphedema, the lymphedematous LE was more likely to have one or more skin cancers than were the unaffected LE (87.5% vs. 33.3%; P < .05), and skin cancer was 2.65 times more likely to develop on the affected LE than in the unaffected LE (95% CI, 1.17-5.99; P = .02).

IN PRACTICE:

“Our findings suggest the need for a relatively high degree of suspicion of skin cancer at sites with lymphedema,” senior author, Afsaneh Alavi, MD, professor of dermatology at the Mayo Clinic, said in a Mayo Clinic press release reporting the results.

SOURCE:

The study was conducted by researchers at the Mayo Clinic and Meharry Medical College, Nashville. It was published in the November 2023 Mayo Clinic Proceedings.

LIMITATIONS:

This was a single-center retrospective study, and patients with LE lymphedema may be overdiagnosed with LE skin cancer because they have a greater number of examinations.

DISCLOSURES:

Dr. Alavi reports having been a consultant for AbbVie, Boehringer Ingelheim, InflaRx, Novartis, and UCB SA and an investigator for Processa Pharmaceuticals and Boehringer Ingelheim. The other authors had no disclosures.

A version of this article first appeared on Medscape.com.

TOPLINE:

Lower-extremity (LE) lymphedema increases the risk for all types of skin cancer on the lower extremities.

METHODOLOGY:

• In the retrospective cohort study, researchers reviewed reports at Mayo Clinic for all patients who had LE lymphedema, limiting the review to those who had an ICD code for lymphedema.
• 4,437 patients with the ICD code from 2000 to 2020 were compared with 4,437 matched controls.
• The records of patients with skin cancer diagnoses were reviewed manually to determine whether the skin cancer, its management, or both were a cause of lymphedema; cancers that caused secondary lymphedema were excluded.
• This is the first large-scale study evaluating the association between LE lymphedema and LE skin cancer.

TAKEAWAY:

• 211 patients (4.6%) in the LE lymphedema group had any ICD code for LE skin cancer, compared with 89 (2%) in the control group.
• Among those with LE lymphedema, the risk for skin cancer was 1.98 times greater compared with those without lymphedema (95% confidence interval, 1.43-2.74; P < .001). Cases included all types of skin cancer.
• Nineteen of 24 patients with unilateral LE lymphedema had a history of immunosuppression.
• In the group of 24 patients with unilateral LE lymphedema, the lymphedematous LE was more likely to have one or more skin cancers than were the unaffected LE (87.5% vs. 33.3%; P < .05), and skin cancer was 2.65 times more likely to develop on the affected LE than in the unaffected LE (95% CI, 1.17-5.99; P = .02).

IN PRACTICE:

“Our findings suggest the need for a relatively high degree of suspicion of skin cancer at sites with lymphedema,” senior author, Afsaneh Alavi, MD, professor of dermatology at the Mayo Clinic, said in a Mayo Clinic press release reporting the results.

SOURCE:

The study was conducted by researchers at the Mayo Clinic and Meharry Medical College, Nashville. It was published in the November 2023 Mayo Clinic Proceedings.

LIMITATIONS:

This was a single-center retrospective study, and patients with LE lymphedema may be overdiagnosed with LE skin cancer because they have a greater number of examinations.

DISCLOSURES:

Dr. Alavi reports having been a consultant for AbbVie, Boehringer Ingelheim, InflaRx, Novartis, and UCB SA and an investigator for Processa Pharmaceuticals and Boehringer Ingelheim. The other authors had no disclosures.

A version of this article first appeared on Medscape.com.

Here is how old I am: When I graduated from medical school in 1977, marketing was prohibited. It was the legal profession that challenged the ban on advertising by professionals, leading to a landmark Supreme Court decision (Bates v State Bar of Arizona, 1977), which opened the door to marketing in the legal and medical professions.

Since then, marketing has become a critical component of growing, sustaining, and supporting private medical practices. Strategies range from the basic Internet website through postings on the major social media sites, and occasionally to larger-budget campaigns involving local radio, television, or billboard advertising.

All these methods are effective, to varying degrees; but nothing provides as much benefit – relative to its comparatively low cost – as the original marketing tool, word-of-mouth patient referrals. According to one survey, a clear majority of Americans still consider word-of-mouth recommendations to be the most influential element driving purchase decisions. Of course, some of your new patients already come from such referrals; but you can get a lot more by actively encouraging your existing patients to sing your praises, rather than waiting for them to do it on their own.

Soliciting current patients for referrals does take a little planning, structure, and a basic understanding of exactly how patient referral programs work. When executed correctly, a patient referral program can add substantial growth to your practice at minimal cost.

Your first step, as with any new project, should be to identify your goals: Clearly define what kind of patients you are looking to attract. Do you want more patients for cosmetic procedures, medical treatment, skin cancer screenings, a specific diagnosis (such as psoriasis), or a general mix? Design your announcements, brochures, and other literature (more on that in a minute) with those goals in mind.

Next, identify any applicable federal or state laws that dictate what you can and cannot legally do to encourage such referrals. It might be tempting, for example, to offer discounts on future services for successful referrals; but some medical groups frown on it, some states prohibit it, and the Federal Anti-Kickback Statute makes it illegal to pay anyone to refer Medicare or Medicaid patients to you if you file a claim for your services. In my experience, most patients are happy to recommend someone whom they believe provides excellent care to a friend or relative without any sort of monetary incentive; but if you plan to offer a material reward of any kind, run it by your attorney first.

Once your legal ducks are in order, make patients aware that you are accepting new patients and would welcome referrals by posting notices to that effect around your office and on your website and social media pages. Outline exactly what sort of patients (based on your goals, above) you are looking for, how to refer someone, whom to contact, and what kind of information is needed. Make it clear why existing patients should refer someone to your practice. Remind them of your specialized training, advanced technology, and patient-focused approach to health care. Highlight the benefits of the program and encourage your patients to participate.

Before implementation, you will need to educate your employees about the referral program and its benefits. All staff members should understand the program and be able to answer basic questions about it from patients or referring professionals. Encourage staffers to actively promote the program during patient interactions.

Then, start making some decisions. How, specifically, will you be requesting referrals in the office? Many physicians are not comfortable asking patients themselves. If you are going to let your assistants or receptionists do it, you will need to write a script for them to follow. An example of a basic script might be, “If you are happy with the care you are receiving here, we would love for you to tell your friends and family about us.” Your staff can then hand out cards, brochures, or both to reinforce the message, and perhaps send a follow-up email to remind them.

A referral system isn’t worth the effort if you don’t know whether it is working. Establish a system to track and monitor referrals. This could be as simple as a spreadsheet or purchasing a more sophisticated software program. Ensure that you can accurately identify and credit the referring patients for their referrals.

Make sure to thank referring patients with a thank-you note or email. Expressing gratitude will encourage continued participation in the program.

A successful referral program does not happen overnight. It relies on providing exceptional patient care and building strong relationships with your existing patients. By implementing such a program, you can leverage the satisfaction and loyalty of your patients to attract new patients and grow your private practice.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Here is how old I am: When I graduated from medical school in 1977, marketing was prohibited. It was the legal profession that challenged the ban on advertising by professionals, leading to a landmark Supreme Court decision (Bates v State Bar of Arizona, 1977), which opened the door to marketing in the legal and medical professions.

Since then, marketing has become a critical component of growing, sustaining, and supporting private medical practices. Strategies range from the basic Internet website through postings on the major social media sites, and occasionally to larger-budget campaigns involving local radio, television, or billboard advertising.

All these methods are effective, to varying degrees; but nothing provides as much benefit – relative to its comparatively low cost – as the original marketing tool, word-of-mouth patient referrals. According to one survey, a clear majority of Americans still consider word-of-mouth recommendations to be the most influential element driving purchase decisions. Of course, some of your new patients already come from such referrals; but you can get a lot more by actively encouraging your existing patients to sing your praises, rather than waiting for them to do it on their own.

Soliciting current patients for referrals does take a little planning, structure, and a basic understanding of exactly how patient referral programs work. When executed correctly, a patient referral program can add substantial growth to your practice at minimal cost.

Your first step, as with any new project, should be to identify your goals: Clearly define what kind of patients you are looking to attract. Do you want more patients for cosmetic procedures, medical treatment, skin cancer screenings, a specific diagnosis (such as psoriasis), or a general mix? Design your announcements, brochures, and other literature (more on that in a minute) with those goals in mind.

Next, identify any applicable federal or state laws that dictate what you can and cannot legally do to encourage such referrals. It might be tempting, for example, to offer discounts on future services for successful referrals; but some medical groups frown on it, some states prohibit it, and the Federal Anti-Kickback Statute makes it illegal to pay anyone to refer Medicare or Medicaid patients to you if you file a claim for your services. In my experience, most patients are happy to recommend someone whom they believe provides excellent care to a friend or relative without any sort of monetary incentive; but if you plan to offer a material reward of any kind, run it by your attorney first.

Once your legal ducks are in order, make patients aware that you are accepting new patients and would welcome referrals by posting notices to that effect around your office and on your website and social media pages. Outline exactly what sort of patients (based on your goals, above) you are looking for, how to refer someone, whom to contact, and what kind of information is needed. Make it clear why existing patients should refer someone to your practice. Remind them of your specialized training, advanced technology, and patient-focused approach to health care. Highlight the benefits of the program and encourage your patients to participate.

Before implementation, you will need to educate your employees about the referral program and its benefits. All staff members should understand the program and be able to answer basic questions about it from patients or referring professionals. Encourage staffers to actively promote the program during patient interactions.

Then, start making some decisions. How, specifically, will you be requesting referrals in the office? Many physicians are not comfortable asking patients themselves. If you are going to let your assistants or receptionists do it, you will need to write a script for them to follow. An example of a basic script might be, “If you are happy with the care you are receiving here, we would love for you to tell your friends and family about us.” Your staff can then hand out cards, brochures, or both to reinforce the message, and perhaps send a follow-up email to remind them.

A referral system isn’t worth the effort if you don’t know whether it is working. Establish a system to track and monitor referrals. This could be as simple as a spreadsheet or purchasing a more sophisticated software program. Ensure that you can accurately identify and credit the referring patients for their referrals.

Make sure to thank referring patients with a thank-you note or email. Expressing gratitude will encourage continued participation in the program.

A successful referral program does not happen overnight. It relies on providing exceptional patient care and building strong relationships with your existing patients. By implementing such a program, you can leverage the satisfaction and loyalty of your patients to attract new patients and grow your private practice.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

Here is how old I am: When I graduated from medical school in 1977, marketing was prohibited. It was the legal profession that challenged the ban on advertising by professionals, leading to a landmark Supreme Court decision (Bates v State Bar of Arizona, 1977), which opened the door to marketing in the legal and medical professions.

Since then, marketing has become a critical component of growing, sustaining, and supporting private medical practices. Strategies range from the basic Internet website through postings on the major social media sites, and occasionally to larger-budget campaigns involving local radio, television, or billboard advertising.

All these methods are effective, to varying degrees; but nothing provides as much benefit – relative to its comparatively low cost – as the original marketing tool, word-of-mouth patient referrals. According to one survey, a clear majority of Americans still consider word-of-mouth recommendations to be the most influential element driving purchase decisions. Of course, some of your new patients already come from such referrals; but you can get a lot more by actively encouraging your existing patients to sing your praises, rather than waiting for them to do it on their own.

Soliciting current patients for referrals does take a little planning, structure, and a basic understanding of exactly how patient referral programs work. When executed correctly, a patient referral program can add substantial growth to your practice at minimal cost.

Your first step, as with any new project, should be to identify your goals: Clearly define what kind of patients you are looking to attract. Do you want more patients for cosmetic procedures, medical treatment, skin cancer screenings, a specific diagnosis (such as psoriasis), or a general mix? Design your announcements, brochures, and other literature (more on that in a minute) with those goals in mind.

Next, identify any applicable federal or state laws that dictate what you can and cannot legally do to encourage such referrals. It might be tempting, for example, to offer discounts on future services for successful referrals; but some medical groups frown on it, some states prohibit it, and the Federal Anti-Kickback Statute makes it illegal to pay anyone to refer Medicare or Medicaid patients to you if you file a claim for your services. In my experience, most patients are happy to recommend someone whom they believe provides excellent care to a friend or relative without any sort of monetary incentive; but if you plan to offer a material reward of any kind, run it by your attorney first.

Once your legal ducks are in order, make patients aware that you are accepting new patients and would welcome referrals by posting notices to that effect around your office and on your website and social media pages. Outline exactly what sort of patients (based on your goals, above) you are looking for, how to refer someone, whom to contact, and what kind of information is needed. Make it clear why existing patients should refer someone to your practice. Remind them of your specialized training, advanced technology, and patient-focused approach to health care. Highlight the benefits of the program and encourage your patients to participate.

Before implementation, you will need to educate your employees about the referral program and its benefits. All staff members should understand the program and be able to answer basic questions about it from patients or referring professionals. Encourage staffers to actively promote the program during patient interactions.

Then, start making some decisions. How, specifically, will you be requesting referrals in the office? Many physicians are not comfortable asking patients themselves. If you are going to let your assistants or receptionists do it, you will need to write a script for them to follow. An example of a basic script might be, “If you are happy with the care you are receiving here, we would love for you to tell your friends and family about us.” Your staff can then hand out cards, brochures, or both to reinforce the message, and perhaps send a follow-up email to remind them.

A referral system isn’t worth the effort if you don’t know whether it is working. Establish a system to track and monitor referrals. This could be as simple as a spreadsheet or purchasing a more sophisticated software program. Ensure that you can accurately identify and credit the referring patients for their referrals.

Make sure to thank referring patients with a thank-you note or email. Expressing gratitude will encourage continued participation in the program.

A successful referral program does not happen overnight. It relies on providing exceptional patient care and building strong relationships with your existing patients. By implementing such a program, you can leverage the satisfaction and loyalty of your patients to attract new patients and grow your private practice.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

PHOENIX – Early responders to zilucoplan, the newly approved medication for myasthenia gravis, have sustained benefit for up to 60 weeks, a new analyses show.

“The information [in the studies] is valuable in making clinical decisions in managing myasthenia gravis, which is a chronic autoimmune condition that requires long-term use of immunosuppressives,” said Xinli Du, MD, PhD, an assistant professor in the department of neurology at Virginia Commonwealth University in Richmond, who was not involved in the research.

“Compared with conventional immunosuppressants, which take 3-9 months to know if the patient will respond, this is definitely a game-changer,” she said.

The research was presented at the 2023 annual meeting of the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM).
 

FDA approval

Approved by the U.S. Food and Drug Administration in October, the targeted peptide inhibitor of complement component 5 represents the only once-daily self-administered subcutaneous injection for adult patients with acetylcholine receptor autoantibody–positive (AChR+) generalized myasthenia gravis.

The multicenter, phase 3, placebo-controlled RAISE trial demonstrated that zilucoplan was associated with significant improvement in myasthenia gravis–specific outcomes in adult patients with mild to severe AChR+ generalized myasthenia gravis.

Of note, approximately 40% of patients in the zilucoplan phase 2 and 3 clinical trials have a significant response as early as the first week of treatment. For the current post hoc analysis, first author Miriam Freimer, MD, and colleagues took a closer look at the longer-term outcomes in these patients in the ongoing RAISE-XT open-label extension study.

In these two double-blind studies, patients were randomly assigned to receive either daily subcutaneous injections of 0.3 mg/kg zilucoplan or placebo.

Among 93 patients receiving zilucoplan in the two studies, 40 (43%) were identified as early responders based on having at least a 3-point reduction from baseline on the Myasthenia Gravis Activities of Daily Living scale (MG-ADL) within 1 week of treatment, and 31 (33%) qualified based on having at least 5-point reductions in Quantitative Myasthenia Gravis (QMG), at week 1.

Of these early responders, more than 80% meeting the MG-ADL and 85% meeting QMG criteria continued to show a treatment response at each assessment through week 60 in the open-label RAISE-XT trial.

Furthermore, week 1 responders maintained their response for 88.1% of their total treatment time in the MG-ADL group and 88.8% of their total treatment time on treatment in the QMG group, representing a median zilucoplan treatment duration of 450 days.

Of note, the week 1 early responders had no significant differences, compared with the study’s overall population. Participants had a mean age of 49.6 years versus 52.9 years in the overall population. Approximately 40% of patients in both studies were men, and 60%-64% were disease class III as assessed by the Myasthenia Gravis Foundation of America criteria.

“It is very exciting to see such a high response of rapid responders. This means that some patients may be able to avoid steroids or be able to taper them faster than with other accepted treatments for myasthenia gravis,” said Dr. Freimer, director of the division of neuromuscular disorders and the codirector of the Myasthenia Gravis Clinic at the Ohio State University in Columbus.
 

Impact on fatigue

In a separate post hoc analysis of patients who entered RAISE-XT, the researchers evaluated long-term effects of zilucoplan on fatigue.

Improvements in fatigue were already apparent at the end of the RAISE trial, with the least squares mean (LSM) change from baseline in fatigue assessed after 12 weeks with the Neuro-QOL T-score being –6.26 for zilucoplan (n = 86) compared with an increase of 2.65 for placebo (n = 88; LSM difference, –3.61; nominal P = .0060).

Patients who received placebo in the RAISE trial were able to switch to zilucoplan in the RAISE-XT open-label trail, and among those who did, fatigue, as measured in the T-scores, improved significantly within 1 week of switching.

Fatigue further improved out to week 16 in terms of T-scores for the placebo-switch as well as zilucoplan groups, and the improvements in the scores were sustained through week 60 (mean change from RAISE baseline, –10.71 [n = 42] and –9.15 [n = 42], respectively).

“Fatigue is a challenge for patients with [generalized myasthenia gravis]. Zilucoplan significantly and clinically meaningfully improved myasthenic fatigue versus placebo during RAISE,” the investigators report.

“Further improvements were observed during RAISE-XT and were sustained up to 60 weeks of treatment,” they added.
 

Favorable safety profile

Zilucoplan continued to show a favorable safety profile in the RAISE-XT trial and was well tolerated in the long term.

The most common adverse reactions (10% or more) in patients with generalized myasthenia gravis were injection-site reactions, upper respiratory tract infection, and diarrhea.

Though additional therapies have also recently entered the market for generalized myasthenia gravis, they are either intravenous or subcutaneous infusions requiring a health care professional to administer them.

“This self-administered medication allows patients to be more independent and can even travel since it is not dependent on an infusion center,” Dr. Freimer noted.

However, similar to the other complement inhibitors, zilucoplan carries a risk for infection, particularly meningitis, Dr. Du noted. “Complement meningitis vaccination protocol and close monitoring for signs of infection are required,” she said.

However, she added, “the rapid action benefits shown as early as week 1 are impressive, and potentially open the door to use as adjunctive therapy in myasthenia gravis crisis.”

“I think zilucoplan definitely adds more excitement to the already active field of myasthenia gravis management,” she said.

The study was funded by UCB Pharma. Dr. Freimer has reports she has served as a paid consultant for argenx, UCB Pharma, and Alexion Pharmaceuticals and reports research support from the National Institutes of Health, UCB Pharma, Jansen Pharmaceuticals, Alnylam, Avidity, and Fulcrum. Dr. Du reports no disclosures.

A version of this article appeared on Medscape.com.

PHOENIX – Early responders to zilucoplan, the newly approved medication for myasthenia gravis, have sustained benefit for up to 60 weeks, a new analyses show.

“The information [in the studies] is valuable in making clinical decisions in managing myasthenia gravis, which is a chronic autoimmune condition that requires long-term use of immunosuppressives,” said Xinli Du, MD, PhD, an assistant professor in the department of neurology at Virginia Commonwealth University in Richmond, who was not involved in the research.

“Compared with conventional immunosuppressants, which take 3-9 months to know if the patient will respond, this is definitely a game-changer,” she said.

The research was presented at the 2023 annual meeting of the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM).
 

FDA approval

Approved by the U.S. Food and Drug Administration in October, the targeted peptide inhibitor of complement component 5 represents the only once-daily self-administered subcutaneous injection for adult patients with acetylcholine receptor autoantibody–positive (AChR+) generalized myasthenia gravis.

The multicenter, phase 3, placebo-controlled RAISE trial demonstrated that zilucoplan was associated with significant improvement in myasthenia gravis–specific outcomes in adult patients with mild to severe AChR+ generalized myasthenia gravis.

Of note, approximately 40% of patients in the zilucoplan phase 2 and 3 clinical trials have a significant response as early as the first week of treatment. For the current post hoc analysis, first author Miriam Freimer, MD, and colleagues took a closer look at the longer-term outcomes in these patients in the ongoing RAISE-XT open-label extension study.

In these two double-blind studies, patients were randomly assigned to receive either daily subcutaneous injections of 0.3 mg/kg zilucoplan or placebo.

Among 93 patients receiving zilucoplan in the two studies, 40 (43%) were identified as early responders based on having at least a 3-point reduction from baseline on the Myasthenia Gravis Activities of Daily Living scale (MG-ADL) within 1 week of treatment, and 31 (33%) qualified based on having at least 5-point reductions in Quantitative Myasthenia Gravis (QMG), at week 1.

Of these early responders, more than 80% meeting the MG-ADL and 85% meeting QMG criteria continued to show a treatment response at each assessment through week 60 in the open-label RAISE-XT trial.

Furthermore, week 1 responders maintained their response for 88.1% of their total treatment time in the MG-ADL group and 88.8% of their total treatment time on treatment in the QMG group, representing a median zilucoplan treatment duration of 450 days.

Of note, the week 1 early responders had no significant differences, compared with the study’s overall population. Participants had a mean age of 49.6 years versus 52.9 years in the overall population. Approximately 40% of patients in both studies were men, and 60%-64% were disease class III as assessed by the Myasthenia Gravis Foundation of America criteria.

“It is very exciting to see such a high response of rapid responders. This means that some patients may be able to avoid steroids or be able to taper them faster than with other accepted treatments for myasthenia gravis,” said Dr. Freimer, director of the division of neuromuscular disorders and the codirector of the Myasthenia Gravis Clinic at the Ohio State University in Columbus.
 

Impact on fatigue

In a separate post hoc analysis of patients who entered RAISE-XT, the researchers evaluated long-term effects of zilucoplan on fatigue.

Improvements in fatigue were already apparent at the end of the RAISE trial, with the least squares mean (LSM) change from baseline in fatigue assessed after 12 weeks with the Neuro-QOL T-score being –6.26 for zilucoplan (n = 86) compared with an increase of 2.65 for placebo (n = 88; LSM difference, –3.61; nominal P = .0060).

Patients who received placebo in the RAISE trial were able to switch to zilucoplan in the RAISE-XT open-label trail, and among those who did, fatigue, as measured in the T-scores, improved significantly within 1 week of switching.

Fatigue further improved out to week 16 in terms of T-scores for the placebo-switch as well as zilucoplan groups, and the improvements in the scores were sustained through week 60 (mean change from RAISE baseline, –10.71 [n = 42] and –9.15 [n = 42], respectively).

“Fatigue is a challenge for patients with [generalized myasthenia gravis]. Zilucoplan significantly and clinically meaningfully improved myasthenic fatigue versus placebo during RAISE,” the investigators report.

“Further improvements were observed during RAISE-XT and were sustained up to 60 weeks of treatment,” they added.
 

Favorable safety profile

Zilucoplan continued to show a favorable safety profile in the RAISE-XT trial and was well tolerated in the long term.

The most common adverse reactions (10% or more) in patients with generalized myasthenia gravis were injection-site reactions, upper respiratory tract infection, and diarrhea.

Though additional therapies have also recently entered the market for generalized myasthenia gravis, they are either intravenous or subcutaneous infusions requiring a health care professional to administer them.

“This self-administered medication allows patients to be more independent and can even travel since it is not dependent on an infusion center,” Dr. Freimer noted.

However, similar to the other complement inhibitors, zilucoplan carries a risk for infection, particularly meningitis, Dr. Du noted. “Complement meningitis vaccination protocol and close monitoring for signs of infection are required,” she said.

However, she added, “the rapid action benefits shown as early as week 1 are impressive, and potentially open the door to use as adjunctive therapy in myasthenia gravis crisis.”

“I think zilucoplan definitely adds more excitement to the already active field of myasthenia gravis management,” she said.

The study was funded by UCB Pharma. Dr. Freimer has reports she has served as a paid consultant for argenx, UCB Pharma, and Alexion Pharmaceuticals and reports research support from the National Institutes of Health, UCB Pharma, Jansen Pharmaceuticals, Alnylam, Avidity, and Fulcrum. Dr. Du reports no disclosures.

A version of this article appeared on Medscape.com.

PHOENIX – Early responders to zilucoplan, the newly approved medication for myasthenia gravis, have sustained benefit for up to 60 weeks, a new analyses show.

“The information [in the studies] is valuable in making clinical decisions in managing myasthenia gravis, which is a chronic autoimmune condition that requires long-term use of immunosuppressives,” said Xinli Du, MD, PhD, an assistant professor in the department of neurology at Virginia Commonwealth University in Richmond, who was not involved in the research.

“Compared with conventional immunosuppressants, which take 3-9 months to know if the patient will respond, this is definitely a game-changer,” she said.

The research was presented at the 2023 annual meeting of the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM).
 

FDA approval

Approved by the U.S. Food and Drug Administration in October, the targeted peptide inhibitor of complement component 5 represents the only once-daily self-administered subcutaneous injection for adult patients with acetylcholine receptor autoantibody–positive (AChR+) generalized myasthenia gravis.

The multicenter, phase 3, placebo-controlled RAISE trial demonstrated that zilucoplan was associated with significant improvement in myasthenia gravis–specific outcomes in adult patients with mild to severe AChR+ generalized myasthenia gravis.

Of note, approximately 40% of patients in the zilucoplan phase 2 and 3 clinical trials have a significant response as early as the first week of treatment. For the current post hoc analysis, first author Miriam Freimer, MD, and colleagues took a closer look at the longer-term outcomes in these patients in the ongoing RAISE-XT open-label extension study.

In these two double-blind studies, patients were randomly assigned to receive either daily subcutaneous injections of 0.3 mg/kg zilucoplan or placebo.

Among 93 patients receiving zilucoplan in the two studies, 40 (43%) were identified as early responders based on having at least a 3-point reduction from baseline on the Myasthenia Gravis Activities of Daily Living scale (MG-ADL) within 1 week of treatment, and 31 (33%) qualified based on having at least 5-point reductions in Quantitative Myasthenia Gravis (QMG), at week 1.

Of these early responders, more than 80% meeting the MG-ADL and 85% meeting QMG criteria continued to show a treatment response at each assessment through week 60 in the open-label RAISE-XT trial.

Furthermore, week 1 responders maintained their response for 88.1% of their total treatment time in the MG-ADL group and 88.8% of their total treatment time on treatment in the QMG group, representing a median zilucoplan treatment duration of 450 days.

Of note, the week 1 early responders had no significant differences, compared with the study’s overall population. Participants had a mean age of 49.6 years versus 52.9 years in the overall population. Approximately 40% of patients in both studies were men, and 60%-64% were disease class III as assessed by the Myasthenia Gravis Foundation of America criteria.

“It is very exciting to see such a high response of rapid responders. This means that some patients may be able to avoid steroids or be able to taper them faster than with other accepted treatments for myasthenia gravis,” said Dr. Freimer, director of the division of neuromuscular disorders and the codirector of the Myasthenia Gravis Clinic at the Ohio State University in Columbus.
 

Impact on fatigue

In a separate post hoc analysis of patients who entered RAISE-XT, the researchers evaluated long-term effects of zilucoplan on fatigue.

Improvements in fatigue were already apparent at the end of the RAISE trial, with the least squares mean (LSM) change from baseline in fatigue assessed after 12 weeks with the Neuro-QOL T-score being –6.26 for zilucoplan (n = 86) compared with an increase of 2.65 for placebo (n = 88; LSM difference, –3.61; nominal P = .0060).

Patients who received placebo in the RAISE trial were able to switch to zilucoplan in the RAISE-XT open-label trail, and among those who did, fatigue, as measured in the T-scores, improved significantly within 1 week of switching.

Fatigue further improved out to week 16 in terms of T-scores for the placebo-switch as well as zilucoplan groups, and the improvements in the scores were sustained through week 60 (mean change from RAISE baseline, –10.71 [n = 42] and –9.15 [n = 42], respectively).

“Fatigue is a challenge for patients with [generalized myasthenia gravis]. Zilucoplan significantly and clinically meaningfully improved myasthenic fatigue versus placebo during RAISE,” the investigators report.

“Further improvements were observed during RAISE-XT and were sustained up to 60 weeks of treatment,” they added.
 

Favorable safety profile

Zilucoplan continued to show a favorable safety profile in the RAISE-XT trial and was well tolerated in the long term.

The most common adverse reactions (10% or more) in patients with generalized myasthenia gravis were injection-site reactions, upper respiratory tract infection, and diarrhea.

Though additional therapies have also recently entered the market for generalized myasthenia gravis, they are either intravenous or subcutaneous infusions requiring a health care professional to administer them.

“This self-administered medication allows patients to be more independent and can even travel since it is not dependent on an infusion center,” Dr. Freimer noted.

However, similar to the other complement inhibitors, zilucoplan carries a risk for infection, particularly meningitis, Dr. Du noted. “Complement meningitis vaccination protocol and close monitoring for signs of infection are required,” she said.

However, she added, “the rapid action benefits shown as early as week 1 are impressive, and potentially open the door to use as adjunctive therapy in myasthenia gravis crisis.”

“I think zilucoplan definitely adds more excitement to the already active field of myasthenia gravis management,” she said.

The study was funded by UCB Pharma. Dr. Freimer has reports she has served as a paid consultant for argenx, UCB Pharma, and Alexion Pharmaceuticals and reports research support from the National Institutes of Health, UCB Pharma, Jansen Pharmaceuticals, Alnylam, Avidity, and Fulcrum. Dr. Du reports no disclosures.

A version of this article appeared on Medscape.com.

Artificial intelligence can distinguish overlapping inflammatory conditions with total accuracy, according to a new study presented at the annual meeting of the American College of Rheumatology.

Texas pediatricians faced a conundrum during the pandemic. Endemic typhus, a flea-borne tropical infection common to the region, is nearly indistinguishable from multisystem inflammatory syndrome in children (MIS-C), a rare condition set in motion by SARS-CoV-2 infection. Children with either ailment had seemingly identical symptoms: fever, rash, gastrointestinal issues, and in need of swift treatment. A diagnosis of endemic typhus can take 4-6 days to confirm.

Tiphanie Vogel, MD, PhD, a pediatric rheumatologist at Texas Children’s Hospital, Houston, and colleagues sought to create a tool to hasten diagnosis and, ideally, treatment. To do so, they incorporated machine learning and clinical factors available within the first 6 hours of the onset of symptoms.

The team analyzed 49 demographic, clinical, and laboratory measures from the medical records of 133 children with MIS-C and 87 with endemic typhus. Using deep learning, they narrowed the model to 30 essential features that became the backbone of AI-MET, a two-phase clinical-decision support system.

Phase 1 uses 17 clinical factors and can be performed on paper. If a patient’s score in phase 1 is not determinative, clinicians proceed to phase 2, which uses an additional 13 weighted factors and machine learning.

In testing, the two-part tool classified each of the 220 test patients perfectly. And it diagnosed a second group of 111 patients with MIS-C with 99% (110/111) accuracy.

Of note, “that first step classifies [a patient] correctly half of the time,” Dr. Vogel said, so the second, AI phase of the tool was necessary for only half of cases. Dr. Vogel said that’s a good sign; it means that the tool is useful in settings where AI may not always be feasible, like in a busy ED.

Melissa Mizesko, MD, a pediatric rheumatologist at Driscoll Children’s Hospital in Corpus Christi, Tex., said that the new tool could help clinicians streamline care. When cases of MIS-C peaked in Texas, clinicians often would start sick children on doxycycline and treat for MIS-C at the same time, then wait to see whether the antibiotic brought the fever down.

“This [new tool] is helpful if you live in a part of the country that has typhus,” said Jane Burns, MD, director of the Kawasaki Disease Research Center at the University of California, San Diego, who helped develop a similar AI-based tool to distinguish MIS-C from Kawasaki disease. But she encouraged the researchers to expand their testing to include other conditions. Although the AI model Dr. Vogel’s group developed can pinpoint MIS-C or endemic typhus, what if a child has neither condition? “It’s not often you’re dealing with a diagnosis between just two specific diseases,” Dr. Burns said.

Dr. Vogel is also interested in making AI-MET more efficient. “This go-round we prioritized perfect accuracy,” she said. But 30 clinical factors, with 17 of them recorded and calculated by hand, is a lot. “Could we still get this to be very accurate, maybe not perfect, with less inputs?”

In addition to refining AI-MET, which Texas Children’s eventually hopes to make available to other institutions, Dr. Vogel and associates are also considering other use cases for AI. Lupus is one option. “Maybe with machine learning we could identify clues at diagnosis that would help recommend targeted treatment,” she said

Dr. Vogel disclosed potential conflicts of interest with Moderna, Novartis, Pfizer, and SOBI. Dr. Burns and Dr. Mizesko disclosed no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Artificial intelligence can distinguish overlapping inflammatory conditions with total accuracy, according to a new study presented at the annual meeting of the American College of Rheumatology.

Texas pediatricians faced a conundrum during the pandemic. Endemic typhus, a flea-borne tropical infection common to the region, is nearly indistinguishable from multisystem inflammatory syndrome in children (MIS-C), a rare condition set in motion by SARS-CoV-2 infection. Children with either ailment had seemingly identical symptoms: fever, rash, gastrointestinal issues, and in need of swift treatment. A diagnosis of endemic typhus can take 4-6 days to confirm.

Tiphanie Vogel, MD, PhD, a pediatric rheumatologist at Texas Children’s Hospital, Houston, and colleagues sought to create a tool to hasten diagnosis and, ideally, treatment. To do so, they incorporated machine learning and clinical factors available within the first 6 hours of the onset of symptoms.

The team analyzed 49 demographic, clinical, and laboratory measures from the medical records of 133 children with MIS-C and 87 with endemic typhus. Using deep learning, they narrowed the model to 30 essential features that became the backbone of AI-MET, a two-phase clinical-decision support system.

Phase 1 uses 17 clinical factors and can be performed on paper. If a patient’s score in phase 1 is not determinative, clinicians proceed to phase 2, which uses an additional 13 weighted factors and machine learning.

In testing, the two-part tool classified each of the 220 test patients perfectly. And it diagnosed a second group of 111 patients with MIS-C with 99% (110/111) accuracy.

Of note, “that first step classifies [a patient] correctly half of the time,” Dr. Vogel said, so the second, AI phase of the tool was necessary for only half of cases. Dr. Vogel said that’s a good sign; it means that the tool is useful in settings where AI may not always be feasible, like in a busy ED.

Melissa Mizesko, MD, a pediatric rheumatologist at Driscoll Children’s Hospital in Corpus Christi, Tex., said that the new tool could help clinicians streamline care. When cases of MIS-C peaked in Texas, clinicians often would start sick children on doxycycline and treat for MIS-C at the same time, then wait to see whether the antibiotic brought the fever down.

“This [new tool] is helpful if you live in a part of the country that has typhus,” said Jane Burns, MD, director of the Kawasaki Disease Research Center at the University of California, San Diego, who helped develop a similar AI-based tool to distinguish MIS-C from Kawasaki disease. But she encouraged the researchers to expand their testing to include other conditions. Although the AI model Dr. Vogel’s group developed can pinpoint MIS-C or endemic typhus, what if a child has neither condition? “It’s not often you’re dealing with a diagnosis between just two specific diseases,” Dr. Burns said.

Dr. Vogel is also interested in making AI-MET more efficient. “This go-round we prioritized perfect accuracy,” she said. But 30 clinical factors, with 17 of them recorded and calculated by hand, is a lot. “Could we still get this to be very accurate, maybe not perfect, with less inputs?”

In addition to refining AI-MET, which Texas Children’s eventually hopes to make available to other institutions, Dr. Vogel and associates are also considering other use cases for AI. Lupus is one option. “Maybe with machine learning we could identify clues at diagnosis that would help recommend targeted treatment,” she said

Dr. Vogel disclosed potential conflicts of interest with Moderna, Novartis, Pfizer, and SOBI. Dr. Burns and Dr. Mizesko disclosed no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Artificial intelligence can distinguish overlapping inflammatory conditions with total accuracy, according to a new study presented at the annual meeting of the American College of Rheumatology.

Texas pediatricians faced a conundrum during the pandemic. Endemic typhus, a flea-borne tropical infection common to the region, is nearly indistinguishable from multisystem inflammatory syndrome in children (MIS-C), a rare condition set in motion by SARS-CoV-2 infection. Children with either ailment had seemingly identical symptoms: fever, rash, gastrointestinal issues, and in need of swift treatment. A diagnosis of endemic typhus can take 4-6 days to confirm.

Tiphanie Vogel, MD, PhD, a pediatric rheumatologist at Texas Children’s Hospital, Houston, and colleagues sought to create a tool to hasten diagnosis and, ideally, treatment. To do so, they incorporated machine learning and clinical factors available within the first 6 hours of the onset of symptoms.

The team analyzed 49 demographic, clinical, and laboratory measures from the medical records of 133 children with MIS-C and 87 with endemic typhus. Using deep learning, they narrowed the model to 30 essential features that became the backbone of AI-MET, a two-phase clinical-decision support system.

Phase 1 uses 17 clinical factors and can be performed on paper. If a patient’s score in phase 1 is not determinative, clinicians proceed to phase 2, which uses an additional 13 weighted factors and machine learning.

In testing, the two-part tool classified each of the 220 test patients perfectly. And it diagnosed a second group of 111 patients with MIS-C with 99% (110/111) accuracy.

Of note, “that first step classifies [a patient] correctly half of the time,” Dr. Vogel said, so the second, AI phase of the tool was necessary for only half of cases. Dr. Vogel said that’s a good sign; it means that the tool is useful in settings where AI may not always be feasible, like in a busy ED.

Melissa Mizesko, MD, a pediatric rheumatologist at Driscoll Children’s Hospital in Corpus Christi, Tex., said that the new tool could help clinicians streamline care. When cases of MIS-C peaked in Texas, clinicians often would start sick children on doxycycline and treat for MIS-C at the same time, then wait to see whether the antibiotic brought the fever down.

“This [new tool] is helpful if you live in a part of the country that has typhus,” said Jane Burns, MD, director of the Kawasaki Disease Research Center at the University of California, San Diego, who helped develop a similar AI-based tool to distinguish MIS-C from Kawasaki disease. But she encouraged the researchers to expand their testing to include other conditions. Although the AI model Dr. Vogel’s group developed can pinpoint MIS-C or endemic typhus, what if a child has neither condition? “It’s not often you’re dealing with a diagnosis between just two specific diseases,” Dr. Burns said.

Dr. Vogel is also interested in making AI-MET more efficient. “This go-round we prioritized perfect accuracy,” she said. But 30 clinical factors, with 17 of them recorded and calculated by hand, is a lot. “Could we still get this to be very accurate, maybe not perfect, with less inputs?”

In addition to refining AI-MET, which Texas Children’s eventually hopes to make available to other institutions, Dr. Vogel and associates are also considering other use cases for AI. Lupus is one option. “Maybe with machine learning we could identify clues at diagnosis that would help recommend targeted treatment,” she said

Dr. Vogel disclosed potential conflicts of interest with Moderna, Novartis, Pfizer, and SOBI. Dr. Burns and Dr. Mizesko disclosed no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

SAN DIEGO – Patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD) who start a tumor necrosis factor inhibitor (TNFi) appear to have rates of survival and respiratory-related hospitalization similar to those initiating a non-TNFi biologic disease-modifying antirheumatic drug (bDMARD) or Janus kinase inhibitor (JAKi), results from a large pharmacoepidemiologic study show.

“These results challenge some of the findings in prior literature that perhaps TNFi should be avoided in RA-ILD,” lead study investigator Bryant R. England, MD, PhD,  said in an interview. The findings were presented during a plenary session at the American College of Rheumatology annual meeting.

Dr. England, associate professor of rheumatology and immunology at the University of Nebraska Medical Center, Omaha, said that while RA-ILD carries a poor prognosis, a paucity of evidence exists on the effectiveness and safety of disease-modifying therapies in this population.

It’s a pleasant surprise “to see that the investigators were unable to demonstrate a significant difference in the risk of respiratory hospitalization or death between people with RA-ILD initiating non-TNFi/JAKi versus TNFi. Here is a unique situation where a so called ‘negative’ study contributes important information. This study provides needed safety data, as they were unable to show that TNFi results in worsening of severe RA-ILD outcomes,” Sindhu R. Johnson, MD, PhD, professor of medicine at the University of Toronto, said when asked for comment on the study.

University of Toronto

“While this study does not address the use of these medications for the treatment of RA-ILD, these data suggest that TNFi may remain a treatment option for articular disease in people with RA-ILD,” said Dr. Johnson, who was not involved with the study.

For the study, Dr. England and colleagues drew from Veterans Health Administration data between 2006 and 2018 to identify patients with RA-ILD initiating TNFi or non-TNFi biologic/JAKi for the first time. Those who received ILD-focused therapies such as mycophenolate and antifibrotics were excluded from the analysis.

The researchers used validated administrative algorithms requiring multiple RA and ILD diagnostic codes to identify RA-ILD and used 1:1 propensity score matching to compare TNFi and non-TNFi biologic/JAKi factors such as health care use, comorbidities, and several RA-ILD factors, such as pretreatment forced vital capacity, obtained from electronic health records and administrative data. The primary outcome was a composite of time to respiratory-related hospitalization or death using Cox regression models.

Dr. England reported findings from 237 TNFi initiators and 237 non-TNFi/JAKi initiators. Their mean age was 68 years and 92% were male. After matching, the mean standardized differences of variables in the propensity score model improved, but a few variables remained slightly imbalanced, such as two markers of inflammation, inhaled corticosteroid use, and body mass index. The most frequently prescribed TNFi drugs were adalimumab (51%) and etanercept (37%), and the most frequently prescribed non-TNFi/JAKi drugs were rituximab (53%) and abatacept (28%).

The researchers observed no significant difference in the primary outcome between non-TNFi/JAKi and TNFi initiators (adjusted hazard ratio [aHR], 1.22; 95% confidence interval [CI], 0.92-1.60). They also observed no significant differences in respiratory hospitalization, all-cause mortality, or respiratory-related death at 1 and 3 years. In sensitivity analyses with modified cohort eligibility requirements, no significant differences in outcomes were observed between non-TNFi/JAKi and TNFi initiators.

During his presentation at the meeting, Dr. England posed the question: Are TNFi drugs safe to be used in RA-ILD?

“The answer is: It’s complex,” he said. “Our findings don’t suggest that we should be systematically avoiding TNFis with every single person with RA-ILD. But that’s different than whether there are specific subpopulations of RA-ILD for which the choice of these therapies may differ. Unfortunately, we could not address that in this study. We also could not address whether TNFis have efficacy at stopping, slowing, or reversing progression of the ILD itself. This calls for us as a field to gather together and pursue clinical trials to try to generate robust evidence that can guide these important clinical decisions that we’re making with our patients.”

He acknowledged certain limitations of the analysis, including its observational design. “So, despite best efforts to minimize bias with pharmacoepidemiologic designs and approaches, there could still be confounding and selection,” he said. “Additionally, RA-ILD is a heterogeneous disease characterized by different patterns and trajectories. While we did account for several RA- and ILD-related factors, we could not account for all heterogeneity in RA-ILD.”

When asked for comment on the study, session moderator Janet Pope, MD, MPH, professor of medicine in the division of rheumatology at the University of Western Ontario, London, said that the study findings surprised her.

“Sometimes RA patients on TNFis were thought to have more new or worsening ILD vs. [those on] non-TNFi bDMARDs, but most [data were] from older studies where TNFis were used as initial bDMARD in sicker patients,” she told this news organization. “So, data were confounded previously. Even in this study, there may have been channeling bias as it was not a randomized controlled trial. We need a definitive randomized controlled trial to answer this question of what the most optimal therapy for RA-ILD is.”

Dr. England reports receiving consulting fees and research support from Boehringer Ingelheim, and several coauthors reported financial relationships from various pharmaceutical companies and medical publishers. Dr. Johnson reports no relevant financial relationships. Dr. Pope reports being a consultant for several pharmaceutical companies. She has received grant/research support from AbbVie/Abbott and Eli Lilly and is an adviser for Boehringer Ingelheim.

A version of this article appeared on Medscape.com.

SAN DIEGO – Patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD) who start a tumor necrosis factor inhibitor (TNFi) appear to have rates of survival and respiratory-related hospitalization similar to those initiating a non-TNFi biologic disease-modifying antirheumatic drug (bDMARD) or Janus kinase inhibitor (JAKi), results from a large pharmacoepidemiologic study show.

“These results challenge some of the findings in prior literature that perhaps TNFi should be avoided in RA-ILD,” lead study investigator Bryant R. England, MD, PhD,  said in an interview. The findings were presented during a plenary session at the American College of Rheumatology annual meeting.

Dr. England, associate professor of rheumatology and immunology at the University of Nebraska Medical Center, Omaha, said that while RA-ILD carries a poor prognosis, a paucity of evidence exists on the effectiveness and safety of disease-modifying therapies in this population.

It’s a pleasant surprise “to see that the investigators were unable to demonstrate a significant difference in the risk of respiratory hospitalization or death between people with RA-ILD initiating non-TNFi/JAKi versus TNFi. Here is a unique situation where a so called ‘negative’ study contributes important information. This study provides needed safety data, as they were unable to show that TNFi results in worsening of severe RA-ILD outcomes,” Sindhu R. Johnson, MD, PhD, professor of medicine at the University of Toronto, said when asked for comment on the study.

University of Toronto

“While this study does not address the use of these medications for the treatment of RA-ILD, these data suggest that TNFi may remain a treatment option for articular disease in people with RA-ILD,” said Dr. Johnson, who was not involved with the study.

For the study, Dr. England and colleagues drew from Veterans Health Administration data between 2006 and 2018 to identify patients with RA-ILD initiating TNFi or non-TNFi biologic/JAKi for the first time. Those who received ILD-focused therapies such as mycophenolate and antifibrotics were excluded from the analysis.

The researchers used validated administrative algorithms requiring multiple RA and ILD diagnostic codes to identify RA-ILD and used 1:1 propensity score matching to compare TNFi and non-TNFi biologic/JAKi factors such as health care use, comorbidities, and several RA-ILD factors, such as pretreatment forced vital capacity, obtained from electronic health records and administrative data. The primary outcome was a composite of time to respiratory-related hospitalization or death using Cox regression models.

Dr. England reported findings from 237 TNFi initiators and 237 non-TNFi/JAKi initiators. Their mean age was 68 years and 92% were male. After matching, the mean standardized differences of variables in the propensity score model improved, but a few variables remained slightly imbalanced, such as two markers of inflammation, inhaled corticosteroid use, and body mass index. The most frequently prescribed TNFi drugs were adalimumab (51%) and etanercept (37%), and the most frequently prescribed non-TNFi/JAKi drugs were rituximab (53%) and abatacept (28%).

The researchers observed no significant difference in the primary outcome between non-TNFi/JAKi and TNFi initiators (adjusted hazard ratio [aHR], 1.22; 95% confidence interval [CI], 0.92-1.60). They also observed no significant differences in respiratory hospitalization, all-cause mortality, or respiratory-related death at 1 and 3 years. In sensitivity analyses with modified cohort eligibility requirements, no significant differences in outcomes were observed between non-TNFi/JAKi and TNFi initiators.

During his presentation at the meeting, Dr. England posed the question: Are TNFi drugs safe to be used in RA-ILD?

“The answer is: It’s complex,” he said. “Our findings don’t suggest that we should be systematically avoiding TNFis with every single person with RA-ILD. But that’s different than whether there are specific subpopulations of RA-ILD for which the choice of these therapies may differ. Unfortunately, we could not address that in this study. We also could not address whether TNFis have efficacy at stopping, slowing, or reversing progression of the ILD itself. This calls for us as a field to gather together and pursue clinical trials to try to generate robust evidence that can guide these important clinical decisions that we’re making with our patients.”

He acknowledged certain limitations of the analysis, including its observational design. “So, despite best efforts to minimize bias with pharmacoepidemiologic designs and approaches, there could still be confounding and selection,” he said. “Additionally, RA-ILD is a heterogeneous disease characterized by different patterns and trajectories. While we did account for several RA- and ILD-related factors, we could not account for all heterogeneity in RA-ILD.”

When asked for comment on the study, session moderator Janet Pope, MD, MPH, professor of medicine in the division of rheumatology at the University of Western Ontario, London, said that the study findings surprised her.

“Sometimes RA patients on TNFis were thought to have more new or worsening ILD vs. [those on] non-TNFi bDMARDs, but most [data were] from older studies where TNFis were used as initial bDMARD in sicker patients,” she told this news organization. “So, data were confounded previously. Even in this study, there may have been channeling bias as it was not a randomized controlled trial. We need a definitive randomized controlled trial to answer this question of what the most optimal therapy for RA-ILD is.”

Dr. England reports receiving consulting fees and research support from Boehringer Ingelheim, and several coauthors reported financial relationships from various pharmaceutical companies and medical publishers. Dr. Johnson reports no relevant financial relationships. Dr. Pope reports being a consultant for several pharmaceutical companies. She has received grant/research support from AbbVie/Abbott and Eli Lilly and is an adviser for Boehringer Ingelheim.

A version of this article appeared on Medscape.com.

SAN DIEGO – Patients with rheumatoid arthritis-associated interstitial lung disease (RA-ILD) who start a tumor necrosis factor inhibitor (TNFi) appear to have rates of survival and respiratory-related hospitalization similar to those initiating a non-TNFi biologic disease-modifying antirheumatic drug (bDMARD) or Janus kinase inhibitor (JAKi), results from a large pharmacoepidemiologic study show.

“These results challenge some of the findings in prior literature that perhaps TNFi should be avoided in RA-ILD,” lead study investigator Bryant R. England, MD, PhD,  said in an interview. The findings were presented during a plenary session at the American College of Rheumatology annual meeting.

Dr. England, associate professor of rheumatology and immunology at the University of Nebraska Medical Center, Omaha, said that while RA-ILD carries a poor prognosis, a paucity of evidence exists on the effectiveness and safety of disease-modifying therapies in this population.

It’s a pleasant surprise “to see that the investigators were unable to demonstrate a significant difference in the risk of respiratory hospitalization or death between people with RA-ILD initiating non-TNFi/JAKi versus TNFi. Here is a unique situation where a so called ‘negative’ study contributes important information. This study provides needed safety data, as they were unable to show that TNFi results in worsening of severe RA-ILD outcomes,” Sindhu R. Johnson, MD, PhD, professor of medicine at the University of Toronto, said when asked for comment on the study.

University of Toronto

“While this study does not address the use of these medications for the treatment of RA-ILD, these data suggest that TNFi may remain a treatment option for articular disease in people with RA-ILD,” said Dr. Johnson, who was not involved with the study.

For the study, Dr. England and colleagues drew from Veterans Health Administration data between 2006 and 2018 to identify patients with RA-ILD initiating TNFi or non-TNFi biologic/JAKi for the first time. Those who received ILD-focused therapies such as mycophenolate and antifibrotics were excluded from the analysis.

The researchers used validated administrative algorithms requiring multiple RA and ILD diagnostic codes to identify RA-ILD and used 1:1 propensity score matching to compare TNFi and non-TNFi biologic/JAKi factors such as health care use, comorbidities, and several RA-ILD factors, such as pretreatment forced vital capacity, obtained from electronic health records and administrative data. The primary outcome was a composite of time to respiratory-related hospitalization or death using Cox regression models.

Dr. England reported findings from 237 TNFi initiators and 237 non-TNFi/JAKi initiators. Their mean age was 68 years and 92% were male. After matching, the mean standardized differences of variables in the propensity score model improved, but a few variables remained slightly imbalanced, such as two markers of inflammation, inhaled corticosteroid use, and body mass index. The most frequently prescribed TNFi drugs were adalimumab (51%) and etanercept (37%), and the most frequently prescribed non-TNFi/JAKi drugs were rituximab (53%) and abatacept (28%).

The researchers observed no significant difference in the primary outcome between non-TNFi/JAKi and TNFi initiators (adjusted hazard ratio [aHR], 1.22; 95% confidence interval [CI], 0.92-1.60). They also observed no significant differences in respiratory hospitalization, all-cause mortality, or respiratory-related death at 1 and 3 years. In sensitivity analyses with modified cohort eligibility requirements, no significant differences in outcomes were observed between non-TNFi/JAKi and TNFi initiators.

During his presentation at the meeting, Dr. England posed the question: Are TNFi drugs safe to be used in RA-ILD?

“The answer is: It’s complex,” he said. “Our findings don’t suggest that we should be systematically avoiding TNFis with every single person with RA-ILD. But that’s different than whether there are specific subpopulations of RA-ILD for which the choice of these therapies may differ. Unfortunately, we could not address that in this study. We also could not address whether TNFis have efficacy at stopping, slowing, or reversing progression of the ILD itself. This calls for us as a field to gather together and pursue clinical trials to try to generate robust evidence that can guide these important clinical decisions that we’re making with our patients.”

He acknowledged certain limitations of the analysis, including its observational design. “So, despite best efforts to minimize bias with pharmacoepidemiologic designs and approaches, there could still be confounding and selection,” he said. “Additionally, RA-ILD is a heterogeneous disease characterized by different patterns and trajectories. While we did account for several RA- and ILD-related factors, we could not account for all heterogeneity in RA-ILD.”

When asked for comment on the study, session moderator Janet Pope, MD, MPH, professor of medicine in the division of rheumatology at the University of Western Ontario, London, said that the study findings surprised her.

“Sometimes RA patients on TNFis were thought to have more new or worsening ILD vs. [those on] non-TNFi bDMARDs, but most [data were] from older studies where TNFis were used as initial bDMARD in sicker patients,” she told this news organization. “So, data were confounded previously. Even in this study, there may have been channeling bias as it was not a randomized controlled trial. We need a definitive randomized controlled trial to answer this question of what the most optimal therapy for RA-ILD is.”

Dr. England reports receiving consulting fees and research support from Boehringer Ingelheim, and several coauthors reported financial relationships from various pharmaceutical companies and medical publishers. Dr. Johnson reports no relevant financial relationships. Dr. Pope reports being a consultant for several pharmaceutical companies. She has received grant/research support from AbbVie/Abbott and Eli Lilly and is an adviser for Boehringer Ingelheim.

A version of this article appeared on Medscape.com.

SAN DIEGO – Pregnancy in patients with vasculitis had a higher risk for preterm delivery and preeclampsia/eclampsia – especially those with small-vessel vasculitis – compared with the general obstetric population, in a large analysis of administrative claims data presented at the American College of Rheumatology annual meeting.

“We suspect that there is a relationship between the increased risk of these serious hypertensive disorders and preterm delivery, given the higher risk of medically indicated preterm delivery,” one the of the study authors, Audra Horomanski, MD, said in an interview prior to her presentation in a plenary session at the meeting.

Limited data exist on the risks of pregnancy in patients with systemic vasculitis, according to Dr. Horomanski, a rheumatologist who directs the Stanford Vasculitis Clinic at Stanford (Calif.) University. “The majority of what we do know comes from relatively small cohort studies,” she said. “This is the first U.S., nationwide database study looking at the risk of preterm delivery and other adverse pregnancy outcomes.”

Steve Fisch Photography

Hospital for Special Surgery

A version of this article appeared on Medscape.com.

SAN DIEGO – Pregnancy in patients with vasculitis had a higher risk for preterm delivery and preeclampsia/eclampsia – especially those with small-vessel vasculitis – compared with the general obstetric population, in a large analysis of administrative claims data presented at the American College of Rheumatology annual meeting.

“We suspect that there is a relationship between the increased risk of these serious hypertensive disorders and preterm delivery, given the higher risk of medically indicated preterm delivery,” one the of the study authors, Audra Horomanski, MD, said in an interview prior to her presentation in a plenary session at the meeting.

Limited data exist on the risks of pregnancy in patients with systemic vasculitis, according to Dr. Horomanski, a rheumatologist who directs the Stanford Vasculitis Clinic at Stanford (Calif.) University. “The majority of what we do know comes from relatively small cohort studies,” she said. “This is the first U.S., nationwide database study looking at the risk of preterm delivery and other adverse pregnancy outcomes.”

Steve Fisch Photography

Hospital for Special Surgery

A version of this article appeared on Medscape.com.

SAN DIEGO – Pregnancy in patients with vasculitis had a higher risk for preterm delivery and preeclampsia/eclampsia – especially those with small-vessel vasculitis – compared with the general obstetric population, in a large analysis of administrative claims data presented at the American College of Rheumatology annual meeting.

“We suspect that there is a relationship between the increased risk of these serious hypertensive disorders and preterm delivery, given the higher risk of medically indicated preterm delivery,” one the of the study authors, Audra Horomanski, MD, said in an interview prior to her presentation in a plenary session at the meeting.

Limited data exist on the risks of pregnancy in patients with systemic vasculitis, according to Dr. Horomanski, a rheumatologist who directs the Stanford Vasculitis Clinic at Stanford (Calif.) University. “The majority of what we do know comes from relatively small cohort studies,” she said. “This is the first U.S., nationwide database study looking at the risk of preterm delivery and other adverse pregnancy outcomes.”

Steve Fisch Photography

Hospital for Special Surgery

A version of this article appeared on Medscape.com.

The Centers for Disease Control and Prevention said 3% of children starting kindergarten in the 2022-2023 school year received an exemption from one of the four key vaccines – the highest exemption rate ever reported in the United States.

Of the 3% of children who got exemptions, 0.2% were for medical reasons and 2.8% for nonmedical reasons, the CDC report said. The overall exemption rate was 2.6% for the previous school year. 

Though more children received exemptions, the overall national vaccination rate remained steady at 93% for children entering kindergarten for the 2022-2023 school year. Before the COVID-19 pandemic, the overall rate was 95%, the CDC said.

“The bad news is that it’s gone down since the pandemic and still hasn’t rebounded,” Sean O’Leary, MD, a University of Colorado pediatric infectious diseases specialist, told The Associated Press. “The good news is that the vast majority of parents are still vaccinating their kids according to the recommended schedule.”

The CDC report did not offer a specific reason for higher vaccine exemptions. But it did note that the increase could be caused by the COVID-19 pandemic and COVID vaccine hesitancy. 

“There is a rising distrust in the health care system,” Amna Husain, MD, a pediatrician in private practice in North Carolina and a spokesperson for the American Academy of Pediatrics, told NBC News. Vaccine exemptions “have unfortunately trended upward with it.”

Exemption rates varied across the nation. The CDC said 40 states reported a rise in exemptions and that the exemption rate went over 5% in 10 states: Alaska, Arizona, Hawaii, Idaho, Michigan, Nevada, North Dakota, Oregon, Utah, and Wisconsin. Idaho had the highest exemption rate in 2022 with 12%.

While requirements vary from state to state, most states require students entering kindergarten to receive four vaccines: MMR, DTaP, polio, and chickenpox.

A version of this article first appeared on WebMD.com.

The Centers for Disease Control and Prevention said 3% of children starting kindergarten in the 2022-2023 school year received an exemption from one of the four key vaccines – the highest exemption rate ever reported in the United States.

Of the 3% of children who got exemptions, 0.2% were for medical reasons and 2.8% for nonmedical reasons, the CDC report said. The overall exemption rate was 2.6% for the previous school year. 

Though more children received exemptions, the overall national vaccination rate remained steady at 93% for children entering kindergarten for the 2022-2023 school year. Before the COVID-19 pandemic, the overall rate was 95%, the CDC said.

“The bad news is that it’s gone down since the pandemic and still hasn’t rebounded,” Sean O’Leary, MD, a University of Colorado pediatric infectious diseases specialist, told The Associated Press. “The good news is that the vast majority of parents are still vaccinating their kids according to the recommended schedule.”

The CDC report did not offer a specific reason for higher vaccine exemptions. But it did note that the increase could be caused by the COVID-19 pandemic and COVID vaccine hesitancy. 

“There is a rising distrust in the health care system,” Amna Husain, MD, a pediatrician in private practice in North Carolina and a spokesperson for the American Academy of Pediatrics, told NBC News. Vaccine exemptions “have unfortunately trended upward with it.”

Exemption rates varied across the nation. The CDC said 40 states reported a rise in exemptions and that the exemption rate went over 5% in 10 states: Alaska, Arizona, Hawaii, Idaho, Michigan, Nevada, North Dakota, Oregon, Utah, and Wisconsin. Idaho had the highest exemption rate in 2022 with 12%.

While requirements vary from state to state, most states require students entering kindergarten to receive four vaccines: MMR, DTaP, polio, and chickenpox.

A version of this article first appeared on WebMD.com.

The Centers for Disease Control and Prevention said 3% of children starting kindergarten in the 2022-2023 school year received an exemption from one of the four key vaccines – the highest exemption rate ever reported in the United States.

Of the 3% of children who got exemptions, 0.2% were for medical reasons and 2.8% for nonmedical reasons, the CDC report said. The overall exemption rate was 2.6% for the previous school year. 

Though more children received exemptions, the overall national vaccination rate remained steady at 93% for children entering kindergarten for the 2022-2023 school year. Before the COVID-19 pandemic, the overall rate was 95%, the CDC said.

“The bad news is that it’s gone down since the pandemic and still hasn’t rebounded,” Sean O’Leary, MD, a University of Colorado pediatric infectious diseases specialist, told The Associated Press. “The good news is that the vast majority of parents are still vaccinating their kids according to the recommended schedule.”

The CDC report did not offer a specific reason for higher vaccine exemptions. But it did note that the increase could be caused by the COVID-19 pandemic and COVID vaccine hesitancy. 

“There is a rising distrust in the health care system,” Amna Husain, MD, a pediatrician in private practice in North Carolina and a spokesperson for the American Academy of Pediatrics, told NBC News. Vaccine exemptions “have unfortunately trended upward with it.”

Exemption rates varied across the nation. The CDC said 40 states reported a rise in exemptions and that the exemption rate went over 5% in 10 states: Alaska, Arizona, Hawaii, Idaho, Michigan, Nevada, North Dakota, Oregon, Utah, and Wisconsin. Idaho had the highest exemption rate in 2022 with 12%.

While requirements vary from state to state, most states require students entering kindergarten to receive four vaccines: MMR, DTaP, polio, and chickenpox.

A version of this article first appeared on WebMD.com.

Can green tea lower your risk of colorectal cancer? It depends on who – and what research – you believe. 

Evidence that links green tea and a lower risk of colorectal cancer goes both ways. Some researchers have found little or no significant risk from drinking the popular tea, while others point to a potential benefit. Now add two more studies – one that found no reduced risk and another that seems to strengthen the link between green tea and a lower risk of colon cancer. 

Randomized controlled trials – where some people get randomly assigned to drink green tea and others do not – are considered the gold standard of medical research. Combine the findings from several of these trials, the thinking goes, and the findings get even stronger. 

Combining random trials so far shows no advantage from green tea. But there may still be a benefit, said lead researcher Vishal Chandel, MD, who is affiliated with Suburban Community Hospital in Norristown, Pa. It could be that there are just not enough randomized controlled trials yet to show green tea has a protective effect.

“Many, many factors contribute to colorectal cancer, and one of them is diet. One thing which struck me was tea, because tea is something that people consume all over the world, and it has shown some stronger effects in Japan and in China,” said Dr. Chandel. 
 

Comparing hundreds of people 

Dr. Chandel and colleagues found three randomized controlled trials that looked at the link between green tea and colorectal cancer risk. Combined, the data included 451 people with colorectal cancer and 460 others without cancer who made up a control, or comparison, group. 

They found green tea consumption did not reduce the risk of colorectal cancer in a statically significant way. 

“There are only three randomized controlled trials from anywhere concerning green tea and colon cancer,” Dr. Chandel said. “We really need more. If we had 7, 8, or 10 … I’m very positive we will have a much stronger association to say that green tea can have a positive effect.”
 

Comparing thousands of people 

Dr. Chandel and colleagues also performed another study where they looked at less rigorous evidence – 10 cohort studies and 15 prospective case-control studies. These studies included 198,488 cancer cases and 581,556 controls. This time, they found a stronger link between green tea and a reduced risk of colorectal cancer. 

The “meta-analysis results indicate a lower tendency to develop colorectal cancer with green tea consumption, with reduced risk of colorectal cancer more pronounced in Asia than America or Europe,” the authors note. “Although there is insufficient epidemiological data to conclude at present that green tea can have protective effects in human beings.”

Dr. Chandel presented the findings of both studies in Vancouver at the American College of Gastroenterology annual scientific meeting.
 

Why green tea?

Dr. Chandel said he studied colorectal cancer because it is the third most diagnosed cancer worldwide, accounting for about 10% of all new cancer cases in 2020, according to the World Health Organization’s Global Cancer Observatory data. It is also a common cause of cancer death globally, second only to lung cancer. 

Green tea contains high level of polyphenols known as catechins. The main catechin in green tea believed to provide cancer protective effects is epigallocatechin-3 gallate (EGCG). EGCG “has been shown in some studies to inhibit or prevent colon cancer,” Dr. Chandel said. 

EGCG is present in higher amounts in green tea, compared with black or oolong tea, because green tea is made from unfermented, unoxidized tea leaves.
 

Difficult to read the tea leaves

These studies “add to the literature, which remains undefined regarding the role of green tea in reducing the risk of colorectal cancer,” Catherine Eng, MD, a spokesperson for the American Society of Clinical Oncology, said when asked to comment.

Although combining three trials did not reveal a significant benefit, looking at a greater number of studies did in some populations, said Dr. Eng, codirector of gastrointestinal oncology and chair of surgical and medical oncology at Vanderbilt-Ingram Cancer Center in Nashville. 

“Potential benefit for green tea in reducing the risk of colorectal cancer was noted in the Asian cases but was not found to be statistically significant in the European or U.S. studies,” she said. “Currently, the role of dietary consumption of green tea on reducing the risk of colorectal cancer is not well established and requires further investigation.”

A version of this article appeared on WebMD.com.

Can green tea lower your risk of colorectal cancer? It depends on who – and what research – you believe. 

Evidence that links green tea and a lower risk of colorectal cancer goes both ways. Some researchers have found little or no significant risk from drinking the popular tea, while others point to a potential benefit. Now add two more studies – one that found no reduced risk and another that seems to strengthen the link between green tea and a lower risk of colon cancer. 

Randomized controlled trials – where some people get randomly assigned to drink green tea and others do not – are considered the gold standard of medical research. Combine the findings from several of these trials, the thinking goes, and the findings get even stronger. 

Combining random trials so far shows no advantage from green tea. But there may still be a benefit, said lead researcher Vishal Chandel, MD, who is affiliated with Suburban Community Hospital in Norristown, Pa. It could be that there are just not enough randomized controlled trials yet to show green tea has a protective effect.

“Many, many factors contribute to colorectal cancer, and one of them is diet. One thing which struck me was tea, because tea is something that people consume all over the world, and it has shown some stronger effects in Japan and in China,” said Dr. Chandel. 
 

Comparing hundreds of people 

Dr. Chandel and colleagues found three randomized controlled trials that looked at the link between green tea and colorectal cancer risk. Combined, the data included 451 people with colorectal cancer and 460 others without cancer who made up a control, or comparison, group. 

They found green tea consumption did not reduce the risk of colorectal cancer in a statically significant way. 

“There are only three randomized controlled trials from anywhere concerning green tea and colon cancer,” Dr. Chandel said. “We really need more. If we had 7, 8, or 10 … I’m very positive we will have a much stronger association to say that green tea can have a positive effect.”
 

Comparing thousands of people 

Dr. Chandel and colleagues also performed another study where they looked at less rigorous evidence – 10 cohort studies and 15 prospective case-control studies. These studies included 198,488 cancer cases and 581,556 controls. This time, they found a stronger link between green tea and a reduced risk of colorectal cancer. 

The “meta-analysis results indicate a lower tendency to develop colorectal cancer with green tea consumption, with reduced risk of colorectal cancer more pronounced in Asia than America or Europe,” the authors note. “Although there is insufficient epidemiological data to conclude at present that green tea can have protective effects in human beings.”

Dr. Chandel presented the findings of both studies in Vancouver at the American College of Gastroenterology annual scientific meeting.
 

Why green tea?

Dr. Chandel said he studied colorectal cancer because it is the third most diagnosed cancer worldwide, accounting for about 10% of all new cancer cases in 2020, according to the World Health Organization’s Global Cancer Observatory data. It is also a common cause of cancer death globally, second only to lung cancer. 

Green tea contains high level of polyphenols known as catechins. The main catechin in green tea believed to provide cancer protective effects is epigallocatechin-3 gallate (EGCG). EGCG “has been shown in some studies to inhibit or prevent colon cancer,” Dr. Chandel said. 

EGCG is present in higher amounts in green tea, compared with black or oolong tea, because green tea is made from unfermented, unoxidized tea leaves.
 

Difficult to read the tea leaves

These studies “add to the literature, which remains undefined regarding the role of green tea in reducing the risk of colorectal cancer,” Catherine Eng, MD, a spokesperson for the American Society of Clinical Oncology, said when asked to comment.

Although combining three trials did not reveal a significant benefit, looking at a greater number of studies did in some populations, said Dr. Eng, codirector of gastrointestinal oncology and chair of surgical and medical oncology at Vanderbilt-Ingram Cancer Center in Nashville. 

“Potential benefit for green tea in reducing the risk of colorectal cancer was noted in the Asian cases but was not found to be statistically significant in the European or U.S. studies,” she said. “Currently, the role of dietary consumption of green tea on reducing the risk of colorectal cancer is not well established and requires further investigation.”

A version of this article appeared on WebMD.com.

Can green tea lower your risk of colorectal cancer? It depends on who – and what research – you believe. 

Evidence that links green tea and a lower risk of colorectal cancer goes both ways. Some researchers have found little or no significant risk from drinking the popular tea, while others point to a potential benefit. Now add two more studies – one that found no reduced risk and another that seems to strengthen the link between green tea and a lower risk of colon cancer. 

Randomized controlled trials – where some people get randomly assigned to drink green tea and others do not – are considered the gold standard of medical research. Combine the findings from several of these trials, the thinking goes, and the findings get even stronger. 

Combining random trials so far shows no advantage from green tea. But there may still be a benefit, said lead researcher Vishal Chandel, MD, who is affiliated with Suburban Community Hospital in Norristown, Pa. It could be that there are just not enough randomized controlled trials yet to show green tea has a protective effect.

“Many, many factors contribute to colorectal cancer, and one of them is diet. One thing which struck me was tea, because tea is something that people consume all over the world, and it has shown some stronger effects in Japan and in China,” said Dr. Chandel. 
 

Comparing hundreds of people 

Dr. Chandel and colleagues found three randomized controlled trials that looked at the link between green tea and colorectal cancer risk. Combined, the data included 451 people with colorectal cancer and 460 others without cancer who made up a control, or comparison, group. 

They found green tea consumption did not reduce the risk of colorectal cancer in a statically significant way. 

“There are only three randomized controlled trials from anywhere concerning green tea and colon cancer,” Dr. Chandel said. “We really need more. If we had 7, 8, or 10 … I’m very positive we will have a much stronger association to say that green tea can have a positive effect.”
 

Comparing thousands of people 

Dr. Chandel and colleagues also performed another study where they looked at less rigorous evidence – 10 cohort studies and 15 prospective case-control studies. These studies included 198,488 cancer cases and 581,556 controls. This time, they found a stronger link between green tea and a reduced risk of colorectal cancer. 

The “meta-analysis results indicate a lower tendency to develop colorectal cancer with green tea consumption, with reduced risk of colorectal cancer more pronounced in Asia than America or Europe,” the authors note. “Although there is insufficient epidemiological data to conclude at present that green tea can have protective effects in human beings.”

Dr. Chandel presented the findings of both studies in Vancouver at the American College of Gastroenterology annual scientific meeting.
 

Why green tea?

Dr. Chandel said he studied colorectal cancer because it is the third most diagnosed cancer worldwide, accounting for about 10% of all new cancer cases in 2020, according to the World Health Organization’s Global Cancer Observatory data. It is also a common cause of cancer death globally, second only to lung cancer. 

Green tea contains high level of polyphenols known as catechins. The main catechin in green tea believed to provide cancer protective effects is epigallocatechin-3 gallate (EGCG). EGCG “has been shown in some studies to inhibit or prevent colon cancer,” Dr. Chandel said. 

EGCG is present in higher amounts in green tea, compared with black or oolong tea, because green tea is made from unfermented, unoxidized tea leaves.
 

Difficult to read the tea leaves

These studies “add to the literature, which remains undefined regarding the role of green tea in reducing the risk of colorectal cancer,” Catherine Eng, MD, a spokesperson for the American Society of Clinical Oncology, said when asked to comment.

Although combining three trials did not reveal a significant benefit, looking at a greater number of studies did in some populations, said Dr. Eng, codirector of gastrointestinal oncology and chair of surgical and medical oncology at Vanderbilt-Ingram Cancer Center in Nashville. 

“Potential benefit for green tea in reducing the risk of colorectal cancer was noted in the Asian cases but was not found to be statistically significant in the European or U.S. studies,” she said. “Currently, the role of dietary consumption of green tea on reducing the risk of colorectal cancer is not well established and requires further investigation.”

A version of this article appeared on WebMD.com.