HIV-infected women with cervical cancer have significantly lower survival rates than women with cervical cancer who are not infected, investigators found.

A study of 348 women with invasive cervical cancer in Botswana, a nation with robust and wide-reaching HIV prevention and antiretroviral therapy (ART) programs, showed that women who had HIV infections had a twofold greater risk for death within 3 years than women without HIV, reported Scott Dryden-Peterson, MD, from the Brigham and Women’s Hospital and Harvard TH Chan School of Public Health in Boston, and his colleagues.

“Even in the context of good access to and use of ART, HIV infection more than doubled the risk of death among women who received curative guideline-concordant therapy. Competing mortality from HIV-associated infections seemed to contribute minimally to the excess risk of death; rather, earlier oncologic progression among women with HIV seemed to account for the excess mortality,” they wrote (J Clin Oncol. 2016 Aug 29. doi: 10.1200/JCO.2016.67.9613).

It is well known that HIV infection significantly increases the risk of cervical cancer, with HIV-infected women having a sixfold greater risk for the malignancy than women in the general population, the investigators stated.

Whether HIV has a detrimental effect on cervical cancer–specific survival was unclear, however, prompting them to investigate the question in a cohort of 348 women, 231 of whom were infected with HIV, 96 of whom were free of infection, and 21 of whom had unknown HIV status.

Of the women with HIV, 189 (81.8%) had started on ART before their cancers were diagnosed, and had been on therapy for a median of 4.8 years. Most of the HIV-infected women had CD4 cell counts that fell in the moderate or mildly immunosuppressed range (median 397 cells per microliter). Of this group, only 24 had CD4 counts below 200, the threshold for a diagnosis of AIDS.

After a median follow-up of 19.7 months, 157 participants had died, including 117 women with HIV infections and 40 without infections.

Three-year survival, the primary outcome, was 35% for women with HIV, compared with 48% for uninfected women.

In an analysis adjusted for age, cancer stage, CD4 cell counts, duration of ART, radiation dose received and treatment intent (curative or palliative), the hazard ratio for death among women with HIV was 1.95 (P = .007).

In an analysis restricted to women who received therapy with curative intent, the HR was 2.35 (P = .002), and an analysis restricted to women who received therapy with curative intent that adhered to clinical guidelines showed that the HR for death among HIV-infected women was 2.65 (P = .037).

Of note, the detrimental effect of HIV on survival was highest among women with stage I (HR, 4.03) and stage II (HR, 2.44) cancers, compared with stages III or IV (P = .035).

Among women with CD4 cell counts below 250, the HR for death was 2.75. This risk diminished with increasing cell counts, but remained significantly higher among women with near-normal counts (350 to 500 cells/microliter; HR, 1.87; significant according to confidence intervals).

“Advanced stage and poor treatment completion contributed to high mortality overall,” the investigators wrote.

HIV-infected women with cervical cancer have significantly lower survival rates than women with cervical cancer who are not infected, investigators found.

A study of 348 women with invasive cervical cancer in Botswana, a nation with robust and wide-reaching HIV prevention and antiretroviral therapy (ART) programs, showed that women who had HIV infections had a twofold greater risk for death within 3 years than women without HIV, reported Scott Dryden-Peterson, MD, from the Brigham and Women’s Hospital and Harvard TH Chan School of Public Health in Boston, and his colleagues.

“Even in the context of good access to and use of ART, HIV infection more than doubled the risk of death among women who received curative guideline-concordant therapy. Competing mortality from HIV-associated infections seemed to contribute minimally to the excess risk of death; rather, earlier oncologic progression among women with HIV seemed to account for the excess mortality,” they wrote (J Clin Oncol. 2016 Aug 29. doi: 10.1200/JCO.2016.67.9613).

It is well known that HIV infection significantly increases the risk of cervical cancer, with HIV-infected women having a sixfold greater risk for the malignancy than women in the general population, the investigators stated.

Whether HIV has a detrimental effect on cervical cancer–specific survival was unclear, however, prompting them to investigate the question in a cohort of 348 women, 231 of whom were infected with HIV, 96 of whom were free of infection, and 21 of whom had unknown HIV status.

Of the women with HIV, 189 (81.8%) had started on ART before their cancers were diagnosed, and had been on therapy for a median of 4.8 years. Most of the HIV-infected women had CD4 cell counts that fell in the moderate or mildly immunosuppressed range (median 397 cells per microliter). Of this group, only 24 had CD4 counts below 200, the threshold for a diagnosis of AIDS.

After a median follow-up of 19.7 months, 157 participants had died, including 117 women with HIV infections and 40 without infections.

Three-year survival, the primary outcome, was 35% for women with HIV, compared with 48% for uninfected women.

In an analysis adjusted for age, cancer stage, CD4 cell counts, duration of ART, radiation dose received and treatment intent (curative or palliative), the hazard ratio for death among women with HIV was 1.95 (P = .007).

In an analysis restricted to women who received therapy with curative intent, the HR was 2.35 (P = .002), and an analysis restricted to women who received therapy with curative intent that adhered to clinical guidelines showed that the HR for death among HIV-infected women was 2.65 (P = .037).

Of note, the detrimental effect of HIV on survival was highest among women with stage I (HR, 4.03) and stage II (HR, 2.44) cancers, compared with stages III or IV (P = .035).

Among women with CD4 cell counts below 250, the HR for death was 2.75. This risk diminished with increasing cell counts, but remained significantly higher among women with near-normal counts (350 to 500 cells/microliter; HR, 1.87; significant according to confidence intervals).

“Advanced stage and poor treatment completion contributed to high mortality overall,” the investigators wrote.

HIV-infected women with cervical cancer have significantly lower survival rates than women with cervical cancer who are not infected, investigators found.

A study of 348 women with invasive cervical cancer in Botswana, a nation with robust and wide-reaching HIV prevention and antiretroviral therapy (ART) programs, showed that women who had HIV infections had a twofold greater risk for death within 3 years than women without HIV, reported Scott Dryden-Peterson, MD, from the Brigham and Women’s Hospital and Harvard TH Chan School of Public Health in Boston, and his colleagues.

“Even in the context of good access to and use of ART, HIV infection more than doubled the risk of death among women who received curative guideline-concordant therapy. Competing mortality from HIV-associated infections seemed to contribute minimally to the excess risk of death; rather, earlier oncologic progression among women with HIV seemed to account for the excess mortality,” they wrote (J Clin Oncol. 2016 Aug 29. doi: 10.1200/JCO.2016.67.9613).

It is well known that HIV infection significantly increases the risk of cervical cancer, with HIV-infected women having a sixfold greater risk for the malignancy than women in the general population, the investigators stated.

Whether HIV has a detrimental effect on cervical cancer–specific survival was unclear, however, prompting them to investigate the question in a cohort of 348 women, 231 of whom were infected with HIV, 96 of whom were free of infection, and 21 of whom had unknown HIV status.

Of the women with HIV, 189 (81.8%) had started on ART before their cancers were diagnosed, and had been on therapy for a median of 4.8 years. Most of the HIV-infected women had CD4 cell counts that fell in the moderate or mildly immunosuppressed range (median 397 cells per microliter). Of this group, only 24 had CD4 counts below 200, the threshold for a diagnosis of AIDS.

After a median follow-up of 19.7 months, 157 participants had died, including 117 women with HIV infections and 40 without infections.

Three-year survival, the primary outcome, was 35% for women with HIV, compared with 48% for uninfected women.

In an analysis adjusted for age, cancer stage, CD4 cell counts, duration of ART, radiation dose received and treatment intent (curative or palliative), the hazard ratio for death among women with HIV was 1.95 (P = .007).

In an analysis restricted to women who received therapy with curative intent, the HR was 2.35 (P = .002), and an analysis restricted to women who received therapy with curative intent that adhered to clinical guidelines showed that the HR for death among HIV-infected women was 2.65 (P = .037).

Of note, the detrimental effect of HIV on survival was highest among women with stage I (HR, 4.03) and stage II (HR, 2.44) cancers, compared with stages III or IV (P = .035).

Among women with CD4 cell counts below 250, the HR for death was 2.75. This risk diminished with increasing cell counts, but remained significantly higher among women with near-normal counts (350 to 500 cells/microliter; HR, 1.87; significant according to confidence intervals).

“Advanced stage and poor treatment completion contributed to high mortality overall,” the investigators wrote.

Extramedullary disease is common in newly diagnosed acute myeloid leukemia, and frequently occurs in at least two sites, but is not an independent prognostic factor for overall survival, according to an analysis of 11 clinical trials.

“Importantly, the presence of extramedullary disease should not affect the choice of post-remission therapy,” concluded Dr. Chezi Ganzel of Shaare Zedek Medical Center, Jerusalem, Israel, together with his associates on behalf of the ECOG-ACRIN Cancer Research Group.

Extramedullary disease was found in anywhere from 2% to 30% of AML patients in past studies, and its prognostic impact was “unfavorable in some reports, but not in others,” the investigators noted. To help clarify the issue, they studied patients aged 15 years and up with newly diagnosed AML from 11 clinical trials conducted between 1980 and 2008. The initial study population included 3,522 patients, of which 282 were excluded for having promyelocytic leukemia (168 patients), leukemia that was not AML (29 patieints), no baseline assessment of extramedullary disease (41 patients), no survival data (20 patients), or no eligibility for retrospective central review (24 patients). That left 3,240 patients, of whom 769 (24%) had extramedullary disease. The most commonly involved sites included the lymph nodes (about 12% of patients), spleen (7%), liver (5%), skin (5%), and gingiva (4%). Only 1% of patients had detectable central nervous system involvement. Most (65%) of patients had one site of extramedullary disease, while 21% had two sites, and the rest had more extensive involvement (J Clin Oncol. 2016 Aug 29. doi: 10.1200/JCO.2016.67.1305).

Rates of complete remission were 59.7% overall, 59% among patients with extramedullary disease, and 60% among patients without extramedullary disease, the investigators said. Just as the presence of extramedullary disease did not significantly affect the likelihood of complete remission, nor did any specific site of extramedullary disease, although there was a non-significant trend toward lower rates of complete remission among patients with splenic or gingival involvement.

The median overall survival for the cohort was 1 year. Univariate analyses linked the presence of any extramedullary disease (P = .005) and involvement of the skin (P = .002), spleen (P less than .001), and liver (P less than .001) with shorter overall survival. However, none of these relationships held up in a multivariable analysis that accounted for other significant prognostic factors, including earlier year of registration, older age, high white blood cell count, low platelet count, poor performance status, high cytogenetic risk status, and not achieving a complete remission, said the researchers.“It is possible that individual sites of extramedullary disease are, in fact, associated with poorer prognosis [but that] these patients also have other unfavorable prognostic factors, such as high white blood cell count and unfavorable cytogenetics,” the researchers commented.

Based on this large study, treatment decisions “should be made on the basis of recognized AML prognostic factors, irrespective of the presence of extramedullary disease,” they concluded.

The National Institutes of Health supported the work. Dr. Ganzel had no disclosures.

Extramedullary disease is common in newly diagnosed acute myeloid leukemia, and frequently occurs in at least two sites, but is not an independent prognostic factor for overall survival, according to an analysis of 11 clinical trials.

“Importantly, the presence of extramedullary disease should not affect the choice of post-remission therapy,” concluded Dr. Chezi Ganzel of Shaare Zedek Medical Center, Jerusalem, Israel, together with his associates on behalf of the ECOG-ACRIN Cancer Research Group.

Extramedullary disease was found in anywhere from 2% to 30% of AML patients in past studies, and its prognostic impact was “unfavorable in some reports, but not in others,” the investigators noted. To help clarify the issue, they studied patients aged 15 years and up with newly diagnosed AML from 11 clinical trials conducted between 1980 and 2008. The initial study population included 3,522 patients, of which 282 were excluded for having promyelocytic leukemia (168 patients), leukemia that was not AML (29 patieints), no baseline assessment of extramedullary disease (41 patients), no survival data (20 patients), or no eligibility for retrospective central review (24 patients). That left 3,240 patients, of whom 769 (24%) had extramedullary disease. The most commonly involved sites included the lymph nodes (about 12% of patients), spleen (7%), liver (5%), skin (5%), and gingiva (4%). Only 1% of patients had detectable central nervous system involvement. Most (65%) of patients had one site of extramedullary disease, while 21% had two sites, and the rest had more extensive involvement (J Clin Oncol. 2016 Aug 29. doi: 10.1200/JCO.2016.67.1305).

Rates of complete remission were 59.7% overall, 59% among patients with extramedullary disease, and 60% among patients without extramedullary disease, the investigators said. Just as the presence of extramedullary disease did not significantly affect the likelihood of complete remission, nor did any specific site of extramedullary disease, although there was a non-significant trend toward lower rates of complete remission among patients with splenic or gingival involvement.

The median overall survival for the cohort was 1 year. Univariate analyses linked the presence of any extramedullary disease (P = .005) and involvement of the skin (P = .002), spleen (P less than .001), and liver (P less than .001) with shorter overall survival. However, none of these relationships held up in a multivariable analysis that accounted for other significant prognostic factors, including earlier year of registration, older age, high white blood cell count, low platelet count, poor performance status, high cytogenetic risk status, and not achieving a complete remission, said the researchers.“It is possible that individual sites of extramedullary disease are, in fact, associated with poorer prognosis [but that] these patients also have other unfavorable prognostic factors, such as high white blood cell count and unfavorable cytogenetics,” the researchers commented.

Based on this large study, treatment decisions “should be made on the basis of recognized AML prognostic factors, irrespective of the presence of extramedullary disease,” they concluded.

The National Institutes of Health supported the work. Dr. Ganzel had no disclosures.

Extramedullary disease is common in newly diagnosed acute myeloid leukemia, and frequently occurs in at least two sites, but is not an independent prognostic factor for overall survival, according to an analysis of 11 clinical trials.

“Importantly, the presence of extramedullary disease should not affect the choice of post-remission therapy,” concluded Dr. Chezi Ganzel of Shaare Zedek Medical Center, Jerusalem, Israel, together with his associates on behalf of the ECOG-ACRIN Cancer Research Group.

Extramedullary disease was found in anywhere from 2% to 30% of AML patients in past studies, and its prognostic impact was “unfavorable in some reports, but not in others,” the investigators noted. To help clarify the issue, they studied patients aged 15 years and up with newly diagnosed AML from 11 clinical trials conducted between 1980 and 2008. The initial study population included 3,522 patients, of which 282 were excluded for having promyelocytic leukemia (168 patients), leukemia that was not AML (29 patieints), no baseline assessment of extramedullary disease (41 patients), no survival data (20 patients), or no eligibility for retrospective central review (24 patients). That left 3,240 patients, of whom 769 (24%) had extramedullary disease. The most commonly involved sites included the lymph nodes (about 12% of patients), spleen (7%), liver (5%), skin (5%), and gingiva (4%). Only 1% of patients had detectable central nervous system involvement. Most (65%) of patients had one site of extramedullary disease, while 21% had two sites, and the rest had more extensive involvement (J Clin Oncol. 2016 Aug 29. doi: 10.1200/JCO.2016.67.1305).

Rates of complete remission were 59.7% overall, 59% among patients with extramedullary disease, and 60% among patients without extramedullary disease, the investigators said. Just as the presence of extramedullary disease did not significantly affect the likelihood of complete remission, nor did any specific site of extramedullary disease, although there was a non-significant trend toward lower rates of complete remission among patients with splenic or gingival involvement.

The median overall survival for the cohort was 1 year. Univariate analyses linked the presence of any extramedullary disease (P = .005) and involvement of the skin (P = .002), spleen (P less than .001), and liver (P less than .001) with shorter overall survival. However, none of these relationships held up in a multivariable analysis that accounted for other significant prognostic factors, including earlier year of registration, older age, high white blood cell count, low platelet count, poor performance status, high cytogenetic risk status, and not achieving a complete remission, said the researchers.“It is possible that individual sites of extramedullary disease are, in fact, associated with poorer prognosis [but that] these patients also have other unfavorable prognostic factors, such as high white blood cell count and unfavorable cytogenetics,” the researchers commented.

Based on this large study, treatment decisions “should be made on the basis of recognized AML prognostic factors, irrespective of the presence of extramedullary disease,” they concluded.

The National Institutes of Health supported the work. Dr. Ganzel had no disclosures.

The presence or absence of minimal residual disease predicted progression-free and, to a lesser degree, overall survival among chronic lymphocytic leukemia (CLL) patients who achieved complete or partial remission with six courses of chemoimmunotherapy, based on two randomized phase III trials.

These findings underscore the value of measuring minimal residual disease (MRD) in patients who respond to a defined period of CLL therapy, Dr. Gabor Kovacs of the University of Cologne (Germany) and his associates wrote Aug. 29 in the Journal of Clinical Oncology.

The investigators examined the predictive value of measuring MRD in peripheral blood by using four-color flow cytometry at a threshold of 10^-4 by analyzing data from 554 adult CLL patients who achieved complete or partial remission during two phase III trials – one (CLL8) comparing fludarabine and cyclophosphamide with fludarabine, cyclophosphamide, and rituximab (FCR) and a second (CLL10) comparing FCR with bendamustine plus rituximab (J Clin Oncol. 2016 Aug 29. doi:10.1200/JCO.2016.67.1305).

The median progression-free survival (PFS) after the end of treatment was 61 months for the 34% (186 patients) who attained MRD-negative complete remission (CR), 54 months for the 29% of patients who attained MRD-negative partial remission (PR), 35 months for the 7% of patients who attained MRD-positive CR, and 21 months for the 30% of patients who attained MRD-positive PR. Progression-free survival did not differ significantly between MRD-negative CR and MRD-negative PR patients, but was significantly longer for MRD-negative PR patients than for MRD-positive CR patients (P = .048).

Progression-free survival was even more distinct for MRD-positive CR patients, compared with those who attained MRD-positive PR (P = .002). Overall survival was significantly shorter only when patients had MRD-positive PR rather than MRD-negative CR (72 months vs. not reached, P = .001).

Among the MRD-negative PR patients, 16% had only residual lymphadenopathy, 11% had only bone marrow involvement, 48% had only splenomegaly, and 25% had more than one organ system affected, the researchers noted. Importantly, PFS for MRD-negative PR with residual splenomegaly (63 months) was similar to that for MRD-negative CR (61 months, P = .354).

In contrast, patients with MRD-negative PR and residual lymphadenopathy had shorter PFS than did MRD-negative CR patients (31 months, P = .001). “We hypothesize that residual splenomegaly after chemoimmunotherapy often represents tissue that does not contribute to a subsequent clinical progression,” the researchers commented.

They also noted an important caveat – their findings are only valid for patients who received a defined period of CLL treatment followed by observation (without maintenance), not for patients who are treated indefinitely until progression.

The CLL8 and CLL10 trials were funded by Roche, Mundipharma, and the German Federal Ministry of Education and Research. Dr. Kavocs disclosed support for travel, accommodations, and expenses from Roche and Celgene.

The presence or absence of minimal residual disease predicted progression-free and, to a lesser degree, overall survival among chronic lymphocytic leukemia (CLL) patients who achieved complete or partial remission with six courses of chemoimmunotherapy, based on two randomized phase III trials.

These findings underscore the value of measuring minimal residual disease (MRD) in patients who respond to a defined period of CLL therapy, Dr. Gabor Kovacs of the University of Cologne (Germany) and his associates wrote Aug. 29 in the Journal of Clinical Oncology.

The investigators examined the predictive value of measuring MRD in peripheral blood by using four-color flow cytometry at a threshold of 10^-4 by analyzing data from 554 adult CLL patients who achieved complete or partial remission during two phase III trials – one (CLL8) comparing fludarabine and cyclophosphamide with fludarabine, cyclophosphamide, and rituximab (FCR) and a second (CLL10) comparing FCR with bendamustine plus rituximab (J Clin Oncol. 2016 Aug 29. doi:10.1200/JCO.2016.67.1305).

The median progression-free survival (PFS) after the end of treatment was 61 months for the 34% (186 patients) who attained MRD-negative complete remission (CR), 54 months for the 29% of patients who attained MRD-negative partial remission (PR), 35 months for the 7% of patients who attained MRD-positive CR, and 21 months for the 30% of patients who attained MRD-positive PR. Progression-free survival did not differ significantly between MRD-negative CR and MRD-negative PR patients, but was significantly longer for MRD-negative PR patients than for MRD-positive CR patients (P = .048).

Progression-free survival was even more distinct for MRD-positive CR patients, compared with those who attained MRD-positive PR (P = .002). Overall survival was significantly shorter only when patients had MRD-positive PR rather than MRD-negative CR (72 months vs. not reached, P = .001).

Among the MRD-negative PR patients, 16% had only residual lymphadenopathy, 11% had only bone marrow involvement, 48% had only splenomegaly, and 25% had more than one organ system affected, the researchers noted. Importantly, PFS for MRD-negative PR with residual splenomegaly (63 months) was similar to that for MRD-negative CR (61 months, P = .354).

In contrast, patients with MRD-negative PR and residual lymphadenopathy had shorter PFS than did MRD-negative CR patients (31 months, P = .001). “We hypothesize that residual splenomegaly after chemoimmunotherapy often represents tissue that does not contribute to a subsequent clinical progression,” the researchers commented.

They also noted an important caveat – their findings are only valid for patients who received a defined period of CLL treatment followed by observation (without maintenance), not for patients who are treated indefinitely until progression.

The CLL8 and CLL10 trials were funded by Roche, Mundipharma, and the German Federal Ministry of Education and Research. Dr. Kavocs disclosed support for travel, accommodations, and expenses from Roche and Celgene.

The presence or absence of minimal residual disease predicted progression-free and, to a lesser degree, overall survival among chronic lymphocytic leukemia (CLL) patients who achieved complete or partial remission with six courses of chemoimmunotherapy, based on two randomized phase III trials.

These findings underscore the value of measuring minimal residual disease (MRD) in patients who respond to a defined period of CLL therapy, Dr. Gabor Kovacs of the University of Cologne (Germany) and his associates wrote Aug. 29 in the Journal of Clinical Oncology.

The investigators examined the predictive value of measuring MRD in peripheral blood by using four-color flow cytometry at a threshold of 10^-4 by analyzing data from 554 adult CLL patients who achieved complete or partial remission during two phase III trials – one (CLL8) comparing fludarabine and cyclophosphamide with fludarabine, cyclophosphamide, and rituximab (FCR) and a second (CLL10) comparing FCR with bendamustine plus rituximab (J Clin Oncol. 2016 Aug 29. doi:10.1200/JCO.2016.67.1305).

The median progression-free survival (PFS) after the end of treatment was 61 months for the 34% (186 patients) who attained MRD-negative complete remission (CR), 54 months for the 29% of patients who attained MRD-negative partial remission (PR), 35 months for the 7% of patients who attained MRD-positive CR, and 21 months for the 30% of patients who attained MRD-positive PR. Progression-free survival did not differ significantly between MRD-negative CR and MRD-negative PR patients, but was significantly longer for MRD-negative PR patients than for MRD-positive CR patients (P = .048).

Progression-free survival was even more distinct for MRD-positive CR patients, compared with those who attained MRD-positive PR (P = .002). Overall survival was significantly shorter only when patients had MRD-positive PR rather than MRD-negative CR (72 months vs. not reached, P = .001).

Among the MRD-negative PR patients, 16% had only residual lymphadenopathy, 11% had only bone marrow involvement, 48% had only splenomegaly, and 25% had more than one organ system affected, the researchers noted. Importantly, PFS for MRD-negative PR with residual splenomegaly (63 months) was similar to that for MRD-negative CR (61 months, P = .354).

In contrast, patients with MRD-negative PR and residual lymphadenopathy had shorter PFS than did MRD-negative CR patients (31 months, P = .001). “We hypothesize that residual splenomegaly after chemoimmunotherapy often represents tissue that does not contribute to a subsequent clinical progression,” the researchers commented.

They also noted an important caveat – their findings are only valid for patients who received a defined period of CLL treatment followed by observation (without maintenance), not for patients who are treated indefinitely until progression.

The CLL8 and CLL10 trials were funded by Roche, Mundipharma, and the German Federal Ministry of Education and Research. Dr. Kavocs disclosed support for travel, accommodations, and expenses from Roche and Celgene.

TORONTO – A scratch-and-sniff test that asks subjects to identify 40 odors and ranks olfaction is almost as powerful a predictor of Alzheimer’s disease as is a positive test for amyloid.

Low scores on the University of Pennsylvania Smell Identification Test (UPSIT) are linked to a thinning of the entorhinal cortex – the brain region where amyloid plaques are thought to first appear as Alzheimer’s disease takes hold, Seonjoo Lee, PhD, reported at the Alzheimer’s Association International Conference.

“The findings indirectly suggest that impairment in odor identification may precede thinning in the entorhinal cortex in the early clinical stage of AD,” she concluded.

According to William Kriesl, MD, poor UPSIT sores are also related to brain levels of amyloid beta and are almost as predictive of cognitive decline.

These sensory changes appear to be one of the earliest manifestations of Alzheimer’s disease, the researchers said at the Alzheimer’s Association International Conference. Their studies also suggest that the test has a place in the clinic as an easy and inexpensive screening tool for patients with memory complaints, Dr. Kreisl said at the Alzheimer’s Association International Conference.

The amyloid biomarker tests currently available are not suitable for wide dissemination. Amyloid brain scans are currently investigative; they are also invasive, expensive, and not covered by Medicare or any private insurance. Lumbar punctures are also invasive and expensive, and almost universally disliked by patients. Additionally, there is little consensus on how to interpret CSF amyloid levels.

“We need easy, noninvasive biomarkers that can be deployed in the clinic for patients who are concerned about their risk of memory decline,” said Dr. Kreisl of Columbia University Medical Center, New York. “Odor identification testing may provide to be a useful tool in helping physicians counsel patients who are concerned about this.”

His study concluded that the UPSIT predicted Alzheimer’s disease almost as well as invasive amyloid biomarkers. The scratch-and-sniff test asks subjects to identify 40 odors and ranks olfaction as normal, or mildly, moderately or severely impaired.

Dr. Kreisl examined the relationship between UPSIT and brain amyloid beta in 84 subjects, 58 of whom had mild cognitive impairment (MCI) at baseline. All of these subjects had either an amyloid brain scan or a lumbar puncture to measure amyloid in cerebrospinal fluid. They were followed for at least 6 months.

At follow-up, 67% of the group of participants showed cognitive decline. After correcting for age, gender, and education, patients who were amyloid-positive on imaging or in CSF were more than 7 times as likely to have experienced cognitive decline [Odds Ratio (OR) 7.3]. Overall, UPSIT score alone didn’t predict cognitive decline, Dr. Kreisl said. However, when it was imputed as a continuous variable, patients with a score of less than 35 on the 40-item test were four times more likely to show cognitive decline than those with a score of 35 or higher (OR 4).

In fact, these low UPSIT scores were much more common among amyloid-positive patients. Of the 38 patients who were positive for amyloid beta on either diagnostic test, 32 had an UPSIT score of less than 35 while six had a score of 35 or higher. Among the 46 amyloid-negative patients, 28 had low UPSIT scores and 18 had normal UPSIT scores.

Combining amyloid status and UPSIT in a single predictive model didn’t increase accuracy above that of either variable alone, which suggests olfactory dysfunction is not being completely driven by amyloid brain pathology.

“This makes sense because other factors like neurofibrillary tangle burden and other neurodegeneration are also involved in influencing how the UPSIT score predicts memory decline,” he said.

In a separate study, Dr. Lee examined the relationship of UPSIT performance to entorhinal cortical thickness in 397 cognitively normal subjects who were involved in the Washington Heights-Inwood Columbia Aging Project. These subjects took the UPSIT and had magnetic resonance brain imaging both at baseline and at 4 years’ follow-up. Over that time, 50 transitioned to dementia, and 49 of them were diagnosed with Alzheimer’s disease. Another 79 subjects experienced cognitive decline, which was defined as a decline of at least one standard deviation in the average of the three cognitive composite scores of memory, language and visuospatial domains.

In comparing the groups with and without dementia, Dr. Lee found significant differences in the follow-up UPSIT score (23 vs. 27) and entorhinal cortical thickness (2.9 vs. 3.1 mm).

One standard deviation in performance on the UPSIT score was associated with a significant 47% increase in the risk of dementia, while one standard deviation in entorhinal cortical thickness was associated with a 22% increase in the risk. However, Dr. Lee said, the interaction of entorhinal thickness and UPSIT score was only significant in the group of subjects who transitioned to dementia.

Dr. Richard Caselli, professor of neurology at the Mayo Clinic, Scottsdale, Ariz., commented on the limited clinical utility of the UPSIT in a video interview.

Neither Dr. Lee nor Dr. Kreisl had any financial declarations.

[email protected]

On Twitter @alz_gal

TORONTO – A scratch-and-sniff test that asks subjects to identify 40 odors and ranks olfaction is almost as powerful a predictor of Alzheimer’s disease as is a positive test for amyloid.

Low scores on the University of Pennsylvania Smell Identification Test (UPSIT) are linked to a thinning of the entorhinal cortex – the brain region where amyloid plaques are thought to first appear as Alzheimer’s disease takes hold, Seonjoo Lee, PhD, reported at the Alzheimer’s Association International Conference.

“The findings indirectly suggest that impairment in odor identification may precede thinning in the entorhinal cortex in the early clinical stage of AD,” she concluded.

According to William Kriesl, MD, poor UPSIT sores are also related to brain levels of amyloid beta and are almost as predictive of cognitive decline.

These sensory changes appear to be one of the earliest manifestations of Alzheimer’s disease, the researchers said at the Alzheimer’s Association International Conference. Their studies also suggest that the test has a place in the clinic as an easy and inexpensive screening tool for patients with memory complaints, Dr. Kreisl said at the Alzheimer’s Association International Conference.

The amyloid biomarker tests currently available are not suitable for wide dissemination. Amyloid brain scans are currently investigative; they are also invasive, expensive, and not covered by Medicare or any private insurance. Lumbar punctures are also invasive and expensive, and almost universally disliked by patients. Additionally, there is little consensus on how to interpret CSF amyloid levels.

“We need easy, noninvasive biomarkers that can be deployed in the clinic for patients who are concerned about their risk of memory decline,” said Dr. Kreisl of Columbia University Medical Center, New York. “Odor identification testing may provide to be a useful tool in helping physicians counsel patients who are concerned about this.”

His study concluded that the UPSIT predicted Alzheimer’s disease almost as well as invasive amyloid biomarkers. The scratch-and-sniff test asks subjects to identify 40 odors and ranks olfaction as normal, or mildly, moderately or severely impaired.

Dr. Kreisl examined the relationship between UPSIT and brain amyloid beta in 84 subjects, 58 of whom had mild cognitive impairment (MCI) at baseline. All of these subjects had either an amyloid brain scan or a lumbar puncture to measure amyloid in cerebrospinal fluid. They were followed for at least 6 months.

At follow-up, 67% of the group of participants showed cognitive decline. After correcting for age, gender, and education, patients who were amyloid-positive on imaging or in CSF were more than 7 times as likely to have experienced cognitive decline [Odds Ratio (OR) 7.3]. Overall, UPSIT score alone didn’t predict cognitive decline, Dr. Kreisl said. However, when it was imputed as a continuous variable, patients with a score of less than 35 on the 40-item test were four times more likely to show cognitive decline than those with a score of 35 or higher (OR 4).

In fact, these low UPSIT scores were much more common among amyloid-positive patients. Of the 38 patients who were positive for amyloid beta on either diagnostic test, 32 had an UPSIT score of less than 35 while six had a score of 35 or higher. Among the 46 amyloid-negative patients, 28 had low UPSIT scores and 18 had normal UPSIT scores.

Combining amyloid status and UPSIT in a single predictive model didn’t increase accuracy above that of either variable alone, which suggests olfactory dysfunction is not being completely driven by amyloid brain pathology.

“This makes sense because other factors like neurofibrillary tangle burden and other neurodegeneration are also involved in influencing how the UPSIT score predicts memory decline,” he said.

In a separate study, Dr. Lee examined the relationship of UPSIT performance to entorhinal cortical thickness in 397 cognitively normal subjects who were involved in the Washington Heights-Inwood Columbia Aging Project. These subjects took the UPSIT and had magnetic resonance brain imaging both at baseline and at 4 years’ follow-up. Over that time, 50 transitioned to dementia, and 49 of them were diagnosed with Alzheimer’s disease. Another 79 subjects experienced cognitive decline, which was defined as a decline of at least one standard deviation in the average of the three cognitive composite scores of memory, language and visuospatial domains.

In comparing the groups with and without dementia, Dr. Lee found significant differences in the follow-up UPSIT score (23 vs. 27) and entorhinal cortical thickness (2.9 vs. 3.1 mm).

One standard deviation in performance on the UPSIT score was associated with a significant 47% increase in the risk of dementia, while one standard deviation in entorhinal cortical thickness was associated with a 22% increase in the risk. However, Dr. Lee said, the interaction of entorhinal thickness and UPSIT score was only significant in the group of subjects who transitioned to dementia.

Dr. Richard Caselli, professor of neurology at the Mayo Clinic, Scottsdale, Ariz., commented on the limited clinical utility of the UPSIT in a video interview.

Neither Dr. Lee nor Dr. Kreisl had any financial declarations.

[email protected]

On Twitter @alz_gal

TORONTO – A scratch-and-sniff test that asks subjects to identify 40 odors and ranks olfaction is almost as powerful a predictor of Alzheimer’s disease as is a positive test for amyloid.

Low scores on the University of Pennsylvania Smell Identification Test (UPSIT) are linked to a thinning of the entorhinal cortex – the brain region where amyloid plaques are thought to first appear as Alzheimer’s disease takes hold, Seonjoo Lee, PhD, reported at the Alzheimer’s Association International Conference.

“The findings indirectly suggest that impairment in odor identification may precede thinning in the entorhinal cortex in the early clinical stage of AD,” she concluded.

According to William Kriesl, MD, poor UPSIT sores are also related to brain levels of amyloid beta and are almost as predictive of cognitive decline.

These sensory changes appear to be one of the earliest manifestations of Alzheimer’s disease, the researchers said at the Alzheimer’s Association International Conference. Their studies also suggest that the test has a place in the clinic as an easy and inexpensive screening tool for patients with memory complaints, Dr. Kreisl said at the Alzheimer’s Association International Conference.

The amyloid biomarker tests currently available are not suitable for wide dissemination. Amyloid brain scans are currently investigative; they are also invasive, expensive, and not covered by Medicare or any private insurance. Lumbar punctures are also invasive and expensive, and almost universally disliked by patients. Additionally, there is little consensus on how to interpret CSF amyloid levels.

“We need easy, noninvasive biomarkers that can be deployed in the clinic for patients who are concerned about their risk of memory decline,” said Dr. Kreisl of Columbia University Medical Center, New York. “Odor identification testing may provide to be a useful tool in helping physicians counsel patients who are concerned about this.”

His study concluded that the UPSIT predicted Alzheimer’s disease almost as well as invasive amyloid biomarkers. The scratch-and-sniff test asks subjects to identify 40 odors and ranks olfaction as normal, or mildly, moderately or severely impaired.

Dr. Kreisl examined the relationship between UPSIT and brain amyloid beta in 84 subjects, 58 of whom had mild cognitive impairment (MCI) at baseline. All of these subjects had either an amyloid brain scan or a lumbar puncture to measure amyloid in cerebrospinal fluid. They were followed for at least 6 months.

At follow-up, 67% of the group of participants showed cognitive decline. After correcting for age, gender, and education, patients who were amyloid-positive on imaging or in CSF were more than 7 times as likely to have experienced cognitive decline [Odds Ratio (OR) 7.3]. Overall, UPSIT score alone didn’t predict cognitive decline, Dr. Kreisl said. However, when it was imputed as a continuous variable, patients with a score of less than 35 on the 40-item test were four times more likely to show cognitive decline than those with a score of 35 or higher (OR 4).

In fact, these low UPSIT scores were much more common among amyloid-positive patients. Of the 38 patients who were positive for amyloid beta on either diagnostic test, 32 had an UPSIT score of less than 35 while six had a score of 35 or higher. Among the 46 amyloid-negative patients, 28 had low UPSIT scores and 18 had normal UPSIT scores.

Combining amyloid status and UPSIT in a single predictive model didn’t increase accuracy above that of either variable alone, which suggests olfactory dysfunction is not being completely driven by amyloid brain pathology.

“This makes sense because other factors like neurofibrillary tangle burden and other neurodegeneration are also involved in influencing how the UPSIT score predicts memory decline,” he said.

In a separate study, Dr. Lee examined the relationship of UPSIT performance to entorhinal cortical thickness in 397 cognitively normal subjects who were involved in the Washington Heights-Inwood Columbia Aging Project. These subjects took the UPSIT and had magnetic resonance brain imaging both at baseline and at 4 years’ follow-up. Over that time, 50 transitioned to dementia, and 49 of them were diagnosed with Alzheimer’s disease. Another 79 subjects experienced cognitive decline, which was defined as a decline of at least one standard deviation in the average of the three cognitive composite scores of memory, language and visuospatial domains.

In comparing the groups with and without dementia, Dr. Lee found significant differences in the follow-up UPSIT score (23 vs. 27) and entorhinal cortical thickness (2.9 vs. 3.1 mm).

One standard deviation in performance on the UPSIT score was associated with a significant 47% increase in the risk of dementia, while one standard deviation in entorhinal cortical thickness was associated with a 22% increase in the risk. However, Dr. Lee said, the interaction of entorhinal thickness and UPSIT score was only significant in the group of subjects who transitioned to dementia.

Dr. Richard Caselli, professor of neurology at the Mayo Clinic, Scottsdale, Ariz., commented on the limited clinical utility of the UPSIT in a video interview.

Neither Dr. Lee nor Dr. Kreisl had any financial declarations.

[email protected]

On Twitter @alz_gal

A psychiatric consultation service in an academic medical center usually is a robust and busy setting. In addition to expert faculty, the service is staffed by trainees (psychosomatic medicine fellows and psychiatry residents), nurse practitioners, and medical students. I have been drawn to this growing field, which is evolving hand in hand with advances in medical therapy (eg, new antineoplastic, antiretroviral, and anticonvulsant regimens) and surgical intervention (eg, heart, lung, and gut transplantation).

As a consultant, I have learned that we have an obligation to a dual clientele:

• the patient, through an established doctor–patient relationship
• the primary team, which requires our assistance or raises questions about management.

While working as a trainee in providing psychiatric consultative services, I have noted a number of ethical challenges that consultants face. Below are noteworthy examples.

Justice: Is less, more?

We live in an era of growing advocacy of the recognition, acceptance, and treatment of mental illness.¹ However, there does not appear to be enough psychiatric providers for the American population.² Regrettably, a timely psychiatric assessment is, for many, a unaffordable luxury; in some regions of the United States, the wait for an outpatient psychiatric appointment is longer than 6 months.³

When a patient is admitted to the hospital, admitting physicians often consider ordering a psychiatric consult if they suspect an underlying psychiatric disorder or if they would like an expert’s opinion on some matter—such as (1) medications already prescribed for the patient as an outpatient and (2) a patient’s decision-making capacity in complex situations—without reflecting on how much of a commodity this expert opinion is. (After all, in an ideal world, concerns about cost shouldn’t factor in to what we offer our patients.)

Different practitioners have different thresholds for requesting a psychiatric consultation; no clear guidelines or recommendations exist as to how to “calibrate” one’s self to be a good consultee. As psychiatrists, we rarely call for a cardiology consult just because a patient is hypertensive and takes a diuretic at home, or call in an orthopedic surgeon because a patient with a history of arthroplasty has knee pain today. Sometimes, however, it seems to me that our non-psychiatry colleagues don’t think twice to ask for our services if their patients have a history of mental illness, even if it’s well controlled.

There is no winning formula for calculating how many psychiatric providers and resources (represented by the clinical currencies of, respectively, full-time equivalents and relative value units) a consultation service should have, but efforts have been made to solve this mystery.⁴ Some institutions track, with different methods and variable accuracy, the number of consults they provide annually; others wing it. Lack of accuracy and standardization means that the system is prone to sacrificing quality for quantity in the provision of services, and to provide services in an inconsistent manner (think: better quality on slower days).

Nonmaleficence: Good intentions…

Within the U.S. health care system, a consulting psychiatrist must diagnose a billable condition to be reimbursed for a consult. But what if a so-called soft consult is requested and, after the evaluation, a major mental disorder that warranted our time and expertise can’t be identified?

That situation places the provider in an awkward position. Up-diagnosing might seem like a necessity to ensure reimbursement but, in a society that still stigmatizes mental illness, the health risks of charting a major mental disorder (and prescribing a vaguely warranted psychotropic) might outweigh the benefits for some patients, in the long run.

Coding systems can impact and complicate this scenario even more. We are required to comply with coding systems by providing as many predetermined historical and clinical details of any specific major mental disorder as we can document. As we become more detail-oriented, I wonder if we are losing touch with the reality of our patients’ suffering and deviating from the human emotional experience, as we focus on complying with the health care system and maximizing hospital reimbursement.

Beneficence: The care you would want for your loved ones

For me, an attractive aspect of becoming a psychiatric consultant in the medical setting was to function as a mental health ambassador, so to speak. We often evaluate patients who have never seen a psychiatrist before (eg, when there are symptoms of acute stress disorder in a trauma patient or postoperative delirium in a patient who does not have a psychiatric history). On those occasions, we have the opportunity to make an effective, long-lasting intervention with our clinical encounter, accurate diagnosis, medication recommendations, and outpatient referrals.

Sometimes, the best follow-up plans and intentions are undone by uneven discharge coordination efforts and limited community resources. Some medical institutions have become better at tracking reasons for re-hospitalization and at making post-discharge telephone calls to support good transition to outpatient services. Often, it is necessary to call on nonprofit organizations and public institutions to provide referral and crisis services, but we can always do a better job at offering our patients a comprehensive mental health treatment plan, even from the consultation arena.

Autonomy: Who is in control?

Psychiatry provides varying levels of intervention for acutely mentally ill patients. Laws and criteria for involuntary commitment and the use of psychotropic medication under such circumstances vary from state to state.⁵

In the consultation-liaison setting, we often co-manage patients with a neuropsychiatric disorder that precludes them from participating fully in medical decisions. Other times, patients come to our attention involuntarily (eg, by way of medical admission) having a high level of premorbid autonomy: They make their own life decisions, choose not to engage in psychiatric treatment, administer their funds (when they have them), and so on.

Complex ethical situations can arise when (1) there is disagreement between physician and patient and (2) payment for care or insurance coverage plays a role in disposition plans or long-term placement. Public institutions might have a modus operandi that allows for extra room to deliberate and keep the treatment conversation going—more so than for-profit health centers, where financial forces can sway providers’ judgment toward autonomy, regardless of what is best for the patient.

Summing up: Let’s be Hippocratic psychiatrists

As many forces continue to influence the way we practice the art and science of medicine and psychiatry, it’s important to pay close attention to ongoing challenges and utilize organized medicine to advocate for better ways of running an effective consultation service in an ethical manner. As a trainee and future psychosomatic medicine psychiatrist, I am committed to starting these conversations wherever I go.

We need novel ways to look at, question, understand, study, and review our clinical practice to effectively tackle these challenges as we continue advancing as a field.

A psychiatric consultation service in an academic medical center usually is a robust and busy setting. In addition to expert faculty, the service is staffed by trainees (psychosomatic medicine fellows and psychiatry residents), nurse practitioners, and medical students. I have been drawn to this growing field, which is evolving hand in hand with advances in medical therapy (eg, new antineoplastic, antiretroviral, and anticonvulsant regimens) and surgical intervention (eg, heart, lung, and gut transplantation).

As a consultant, I have learned that we have an obligation to a dual clientele:

• the patient, through an established doctor–patient relationship
• the primary team, which requires our assistance or raises questions about management.

While working as a trainee in providing psychiatric consultative services, I have noted a number of ethical challenges that consultants face. Below are noteworthy examples.

Justice: Is less, more?

We live in an era of growing advocacy of the recognition, acceptance, and treatment of mental illness.¹ However, there does not appear to be enough psychiatric providers for the American population.² Regrettably, a timely psychiatric assessment is, for many, a unaffordable luxury; in some regions of the United States, the wait for an outpatient psychiatric appointment is longer than 6 months.³

When a patient is admitted to the hospital, admitting physicians often consider ordering a psychiatric consult if they suspect an underlying psychiatric disorder or if they would like an expert’s opinion on some matter—such as (1) medications already prescribed for the patient as an outpatient and (2) a patient’s decision-making capacity in complex situations—without reflecting on how much of a commodity this expert opinion is. (After all, in an ideal world, concerns about cost shouldn’t factor in to what we offer our patients.)

Different practitioners have different thresholds for requesting a psychiatric consultation; no clear guidelines or recommendations exist as to how to “calibrate” one’s self to be a good consultee. As psychiatrists, we rarely call for a cardiology consult just because a patient is hypertensive and takes a diuretic at home, or call in an orthopedic surgeon because a patient with a history of arthroplasty has knee pain today. Sometimes, however, it seems to me that our non-psychiatry colleagues don’t think twice to ask for our services if their patients have a history of mental illness, even if it’s well controlled.

There is no winning formula for calculating how many psychiatric providers and resources (represented by the clinical currencies of, respectively, full-time equivalents and relative value units) a consultation service should have, but efforts have been made to solve this mystery.⁴ Some institutions track, with different methods and variable accuracy, the number of consults they provide annually; others wing it. Lack of accuracy and standardization means that the system is prone to sacrificing quality for quantity in the provision of services, and to provide services in an inconsistent manner (think: better quality on slower days).

Nonmaleficence: Good intentions…

Within the U.S. health care system, a consulting psychiatrist must diagnose a billable condition to be reimbursed for a consult. But what if a so-called soft consult is requested and, after the evaluation, a major mental disorder that warranted our time and expertise can’t be identified?

That situation places the provider in an awkward position. Up-diagnosing might seem like a necessity to ensure reimbursement but, in a society that still stigmatizes mental illness, the health risks of charting a major mental disorder (and prescribing a vaguely warranted psychotropic) might outweigh the benefits for some patients, in the long run.

Coding systems can impact and complicate this scenario even more. We are required to comply with coding systems by providing as many predetermined historical and clinical details of any specific major mental disorder as we can document. As we become more detail-oriented, I wonder if we are losing touch with the reality of our patients’ suffering and deviating from the human emotional experience, as we focus on complying with the health care system and maximizing hospital reimbursement.

Beneficence: The care you would want for your loved ones

For me, an attractive aspect of becoming a psychiatric consultant in the medical setting was to function as a mental health ambassador, so to speak. We often evaluate patients who have never seen a psychiatrist before (eg, when there are symptoms of acute stress disorder in a trauma patient or postoperative delirium in a patient who does not have a psychiatric history). On those occasions, we have the opportunity to make an effective, long-lasting intervention with our clinical encounter, accurate diagnosis, medication recommendations, and outpatient referrals.

Sometimes, the best follow-up plans and intentions are undone by uneven discharge coordination efforts and limited community resources. Some medical institutions have become better at tracking reasons for re-hospitalization and at making post-discharge telephone calls to support good transition to outpatient services. Often, it is necessary to call on nonprofit organizations and public institutions to provide referral and crisis services, but we can always do a better job at offering our patients a comprehensive mental health treatment plan, even from the consultation arena.

Autonomy: Who is in control?

Psychiatry provides varying levels of intervention for acutely mentally ill patients. Laws and criteria for involuntary commitment and the use of psychotropic medication under such circumstances vary from state to state.⁵

In the consultation-liaison setting, we often co-manage patients with a neuropsychiatric disorder that precludes them from participating fully in medical decisions. Other times, patients come to our attention involuntarily (eg, by way of medical admission) having a high level of premorbid autonomy: They make their own life decisions, choose not to engage in psychiatric treatment, administer their funds (when they have them), and so on.

Complex ethical situations can arise when (1) there is disagreement between physician and patient and (2) payment for care or insurance coverage plays a role in disposition plans or long-term placement. Public institutions might have a modus operandi that allows for extra room to deliberate and keep the treatment conversation going—more so than for-profit health centers, where financial forces can sway providers’ judgment toward autonomy, regardless of what is best for the patient.

Summing up: Let’s be Hippocratic psychiatrists

As many forces continue to influence the way we practice the art and science of medicine and psychiatry, it’s important to pay close attention to ongoing challenges and utilize organized medicine to advocate for better ways of running an effective consultation service in an ethical manner. As a trainee and future psychosomatic medicine psychiatrist, I am committed to starting these conversations wherever I go.

We need novel ways to look at, question, understand, study, and review our clinical practice to effectively tackle these challenges as we continue advancing as a field.

A psychiatric consultation service in an academic medical center usually is a robust and busy setting. In addition to expert faculty, the service is staffed by trainees (psychosomatic medicine fellows and psychiatry residents), nurse practitioners, and medical students. I have been drawn to this growing field, which is evolving hand in hand with advances in medical therapy (eg, new antineoplastic, antiretroviral, and anticonvulsant regimens) and surgical intervention (eg, heart, lung, and gut transplantation).

As a consultant, I have learned that we have an obligation to a dual clientele:

• the patient, through an established doctor–patient relationship
• the primary team, which requires our assistance or raises questions about management.

While working as a trainee in providing psychiatric consultative services, I have noted a number of ethical challenges that consultants face. Below are noteworthy examples.

Justice: Is less, more?

We live in an era of growing advocacy of the recognition, acceptance, and treatment of mental illness.¹ However, there does not appear to be enough psychiatric providers for the American population.² Regrettably, a timely psychiatric assessment is, for many, a unaffordable luxury; in some regions of the United States, the wait for an outpatient psychiatric appointment is longer than 6 months.³

When a patient is admitted to the hospital, admitting physicians often consider ordering a psychiatric consult if they suspect an underlying psychiatric disorder or if they would like an expert’s opinion on some matter—such as (1) medications already prescribed for the patient as an outpatient and (2) a patient’s decision-making capacity in complex situations—without reflecting on how much of a commodity this expert opinion is. (After all, in an ideal world, concerns about cost shouldn’t factor in to what we offer our patients.)

Different practitioners have different thresholds for requesting a psychiatric consultation; no clear guidelines or recommendations exist as to how to “calibrate” one’s self to be a good consultee. As psychiatrists, we rarely call for a cardiology consult just because a patient is hypertensive and takes a diuretic at home, or call in an orthopedic surgeon because a patient with a history of arthroplasty has knee pain today. Sometimes, however, it seems to me that our non-psychiatry colleagues don’t think twice to ask for our services if their patients have a history of mental illness, even if it’s well controlled.

There is no winning formula for calculating how many psychiatric providers and resources (represented by the clinical currencies of, respectively, full-time equivalents and relative value units) a consultation service should have, but efforts have been made to solve this mystery.⁴ Some institutions track, with different methods and variable accuracy, the number of consults they provide annually; others wing it. Lack of accuracy and standardization means that the system is prone to sacrificing quality for quantity in the provision of services, and to provide services in an inconsistent manner (think: better quality on slower days).

Nonmaleficence: Good intentions…

Within the U.S. health care system, a consulting psychiatrist must diagnose a billable condition to be reimbursed for a consult. But what if a so-called soft consult is requested and, after the evaluation, a major mental disorder that warranted our time and expertise can’t be identified?

That situation places the provider in an awkward position. Up-diagnosing might seem like a necessity to ensure reimbursement but, in a society that still stigmatizes mental illness, the health risks of charting a major mental disorder (and prescribing a vaguely warranted psychotropic) might outweigh the benefits for some patients, in the long run.

Coding systems can impact and complicate this scenario even more. We are required to comply with coding systems by providing as many predetermined historical and clinical details of any specific major mental disorder as we can document. As we become more detail-oriented, I wonder if we are losing touch with the reality of our patients’ suffering and deviating from the human emotional experience, as we focus on complying with the health care system and maximizing hospital reimbursement.

Beneficence: The care you would want for your loved ones

For me, an attractive aspect of becoming a psychiatric consultant in the medical setting was to function as a mental health ambassador, so to speak. We often evaluate patients who have never seen a psychiatrist before (eg, when there are symptoms of acute stress disorder in a trauma patient or postoperative delirium in a patient who does not have a psychiatric history). On those occasions, we have the opportunity to make an effective, long-lasting intervention with our clinical encounter, accurate diagnosis, medication recommendations, and outpatient referrals.

Sometimes, the best follow-up plans and intentions are undone by uneven discharge coordination efforts and limited community resources. Some medical institutions have become better at tracking reasons for re-hospitalization and at making post-discharge telephone calls to support good transition to outpatient services. Often, it is necessary to call on nonprofit organizations and public institutions to provide referral and crisis services, but we can always do a better job at offering our patients a comprehensive mental health treatment plan, even from the consultation arena.

Autonomy: Who is in control?

Psychiatry provides varying levels of intervention for acutely mentally ill patients. Laws and criteria for involuntary commitment and the use of psychotropic medication under such circumstances vary from state to state.⁵

In the consultation-liaison setting, we often co-manage patients with a neuropsychiatric disorder that precludes them from participating fully in medical decisions. Other times, patients come to our attention involuntarily (eg, by way of medical admission) having a high level of premorbid autonomy: They make their own life decisions, choose not to engage in psychiatric treatment, administer their funds (when they have them), and so on.

Complex ethical situations can arise when (1) there is disagreement between physician and patient and (2) payment for care or insurance coverage plays a role in disposition plans or long-term placement. Public institutions might have a modus operandi that allows for extra room to deliberate and keep the treatment conversation going—more so than for-profit health centers, where financial forces can sway providers’ judgment toward autonomy, regardless of what is best for the patient.

Summing up: Let’s be Hippocratic psychiatrists

As many forces continue to influence the way we practice the art and science of medicine and psychiatry, it’s important to pay close attention to ongoing challenges and utilize organized medicine to advocate for better ways of running an effective consultation service in an ethical manner. As a trainee and future psychosomatic medicine psychiatrist, I am committed to starting these conversations wherever I go.

We need novel ways to look at, question, understand, study, and review our clinical practice to effectively tackle these challenges as we continue advancing as a field.

Two different doses of the humanized monoclonal antibody ixekizumab improved signs and symptoms of active psoriatic arthritis in a phase III manufacturer-sponsored trial of patients who had not taken a biologic drug before.

The agent selectively binds and neutralizes interleukin (IL)-17A, which promotes joint inflammation and damage via several mechanisms. So the study findings support the view that IL-17A is a key cytokine in the pathogenesis of psoriatic arthritis and an appropriate therapeutic target, said Philip J. Mease, MD, of the department of rheumatology at Swedish Medical Center and the University of Washington, Seattle, and his associates.

They are performing the ongoing, 3-year, randomized, double-blind trial (SPIRIT-P1) comparing responses with an 80-mg dose of ixekizumab every 2 weeks (103 patients), an 80-mg dose every 4 weeks (107 patients), a 40-mg dose of adalimumab (Humira) every 2 weeks (101 patients, active control group), and matching placebo (106 patients, placebo-control group). Each of the two ixekizumab arms received a starting dose of 160 mg given as two injections at week 0. This report presented the findings after the initial 24-week, double-blind treatment period of the trial.

The study participants are adults with active psoriatic arthritis who had never been treated with biologic agents and who continued taking their usual doses of conventional disease-modifying antirheumatic drugs, oral corticosteroids, opiates, and/or nonsteroidal anti-inflammatory drugs/Cox-2 inhibitors during the study. The mean patient age was 49.5 years. Of the 382 who completed this portion of the study, 57 showed an inadequate response and required rescue medication, including 10 on the lower dose of ixekizumab, 11 on the higher dose of ixekizumab, 9 taking adalimumab, and 27 taking placebo.

The primary efficacy endpoint, ACR20 response at week 24, was met by 62.1% of the higher-dose ixekizumab group, 57.9% of the lower-dose ixekizumab group, and 57.4% of the adalimumab group, all of which were significantly greater than the 30.2% rate in the placebo group. Both doses of the study drug as well as the active control drug also improved secondary endpoints: reducing mean levels of disease activity as measured by the 28-joint Disease Activity Score using on C-reactive protein, improving patient-reported physical function on the Health Assessment Questionnaire–Disability Index, and improving disease-related physical health as measured by the SF-36, the investigators said (Ann Rheum Dis. 2016 Aug 23. doi: 10.1136/annrheumdis-2016-209709).

In addition, the progression of structural joint damage, as assessed on radiographs of bone erosions and joint-space narrowing in the hands and feet, was significantly less with the three active treatments than with placebo. Among patients with the most extensive disease, a significantly greater percentage achieved Psoriasis Area and Severity Index 75 level of improvement with the three active treatments than with placebo. And among patients with nail involvement, mean improvements in Nail Psoriasis Severity Index scores were significantly higher with the three active treatments than with placebo.

Adverse effects included grade 1 and 2 neutropenia, herpes zoster involving the eyelid, gastroenteritis, esophageal candidiasis, and depression-related symptoms. All infections resolved with treatment, and none required discontinuation of the study drug.

This study was funded and sponsored by Eli Lilly, maker of ixekizumab. Dr. Mease reported receiving grants, personal fees, and other support from Eli Lilly, AbbVie, Amgen, Bristol Myers Squibb, Celgene, Crescendo, Genentech, Janssen, Pfizer, UCB Pharma, Merck, Novartis, and Corrona. His associates reported ties to numerous industry sources.

Two different doses of the humanized monoclonal antibody ixekizumab improved signs and symptoms of active psoriatic arthritis in a phase III manufacturer-sponsored trial of patients who had not taken a biologic drug before.

The agent selectively binds and neutralizes interleukin (IL)-17A, which promotes joint inflammation and damage via several mechanisms. So the study findings support the view that IL-17A is a key cytokine in the pathogenesis of psoriatic arthritis and an appropriate therapeutic target, said Philip J. Mease, MD, of the department of rheumatology at Swedish Medical Center and the University of Washington, Seattle, and his associates.

They are performing the ongoing, 3-year, randomized, double-blind trial (SPIRIT-P1) comparing responses with an 80-mg dose of ixekizumab every 2 weeks (103 patients), an 80-mg dose every 4 weeks (107 patients), a 40-mg dose of adalimumab (Humira) every 2 weeks (101 patients, active control group), and matching placebo (106 patients, placebo-control group). Each of the two ixekizumab arms received a starting dose of 160 mg given as two injections at week 0. This report presented the findings after the initial 24-week, double-blind treatment period of the trial.

The study participants are adults with active psoriatic arthritis who had never been treated with biologic agents and who continued taking their usual doses of conventional disease-modifying antirheumatic drugs, oral corticosteroids, opiates, and/or nonsteroidal anti-inflammatory drugs/Cox-2 inhibitors during the study. The mean patient age was 49.5 years. Of the 382 who completed this portion of the study, 57 showed an inadequate response and required rescue medication, including 10 on the lower dose of ixekizumab, 11 on the higher dose of ixekizumab, 9 taking adalimumab, and 27 taking placebo.

The primary efficacy endpoint, ACR20 response at week 24, was met by 62.1% of the higher-dose ixekizumab group, 57.9% of the lower-dose ixekizumab group, and 57.4% of the adalimumab group, all of which were significantly greater than the 30.2% rate in the placebo group. Both doses of the study drug as well as the active control drug also improved secondary endpoints: reducing mean levels of disease activity as measured by the 28-joint Disease Activity Score using on C-reactive protein, improving patient-reported physical function on the Health Assessment Questionnaire–Disability Index, and improving disease-related physical health as measured by the SF-36, the investigators said (Ann Rheum Dis. 2016 Aug 23. doi: 10.1136/annrheumdis-2016-209709).

In addition, the progression of structural joint damage, as assessed on radiographs of bone erosions and joint-space narrowing in the hands and feet, was significantly less with the three active treatments than with placebo. Among patients with the most extensive disease, a significantly greater percentage achieved Psoriasis Area and Severity Index 75 level of improvement with the three active treatments than with placebo. And among patients with nail involvement, mean improvements in Nail Psoriasis Severity Index scores were significantly higher with the three active treatments than with placebo.

Adverse effects included grade 1 and 2 neutropenia, herpes zoster involving the eyelid, gastroenteritis, esophageal candidiasis, and depression-related symptoms. All infections resolved with treatment, and none required discontinuation of the study drug.

This study was funded and sponsored by Eli Lilly, maker of ixekizumab. Dr. Mease reported receiving grants, personal fees, and other support from Eli Lilly, AbbVie, Amgen, Bristol Myers Squibb, Celgene, Crescendo, Genentech, Janssen, Pfizer, UCB Pharma, Merck, Novartis, and Corrona. His associates reported ties to numerous industry sources.

Two different doses of the humanized monoclonal antibody ixekizumab improved signs and symptoms of active psoriatic arthritis in a phase III manufacturer-sponsored trial of patients who had not taken a biologic drug before.

The agent selectively binds and neutralizes interleukin (IL)-17A, which promotes joint inflammation and damage via several mechanisms. So the study findings support the view that IL-17A is a key cytokine in the pathogenesis of psoriatic arthritis and an appropriate therapeutic target, said Philip J. Mease, MD, of the department of rheumatology at Swedish Medical Center and the University of Washington, Seattle, and his associates.

They are performing the ongoing, 3-year, randomized, double-blind trial (SPIRIT-P1) comparing responses with an 80-mg dose of ixekizumab every 2 weeks (103 patients), an 80-mg dose every 4 weeks (107 patients), a 40-mg dose of adalimumab (Humira) every 2 weeks (101 patients, active control group), and matching placebo (106 patients, placebo-control group). Each of the two ixekizumab arms received a starting dose of 160 mg given as two injections at week 0. This report presented the findings after the initial 24-week, double-blind treatment period of the trial.

The study participants are adults with active psoriatic arthritis who had never been treated with biologic agents and who continued taking their usual doses of conventional disease-modifying antirheumatic drugs, oral corticosteroids, opiates, and/or nonsteroidal anti-inflammatory drugs/Cox-2 inhibitors during the study. The mean patient age was 49.5 years. Of the 382 who completed this portion of the study, 57 showed an inadequate response and required rescue medication, including 10 on the lower dose of ixekizumab, 11 on the higher dose of ixekizumab, 9 taking adalimumab, and 27 taking placebo.

The primary efficacy endpoint, ACR20 response at week 24, was met by 62.1% of the higher-dose ixekizumab group, 57.9% of the lower-dose ixekizumab group, and 57.4% of the adalimumab group, all of which were significantly greater than the 30.2% rate in the placebo group. Both doses of the study drug as well as the active control drug also improved secondary endpoints: reducing mean levels of disease activity as measured by the 28-joint Disease Activity Score using on C-reactive protein, improving patient-reported physical function on the Health Assessment Questionnaire–Disability Index, and improving disease-related physical health as measured by the SF-36, the investigators said (Ann Rheum Dis. 2016 Aug 23. doi: 10.1136/annrheumdis-2016-209709).

In addition, the progression of structural joint damage, as assessed on radiographs of bone erosions and joint-space narrowing in the hands and feet, was significantly less with the three active treatments than with placebo. Among patients with the most extensive disease, a significantly greater percentage achieved Psoriasis Area and Severity Index 75 level of improvement with the three active treatments than with placebo. And among patients with nail involvement, mean improvements in Nail Psoriasis Severity Index scores were significantly higher with the three active treatments than with placebo.

Adverse effects included grade 1 and 2 neutropenia, herpes zoster involving the eyelid, gastroenteritis, esophageal candidiasis, and depression-related symptoms. All infections resolved with treatment, and none required discontinuation of the study drug.

This study was funded and sponsored by Eli Lilly, maker of ixekizumab. Dr. Mease reported receiving grants, personal fees, and other support from Eli Lilly, AbbVie, Amgen, Bristol Myers Squibb, Celgene, Crescendo, Genentech, Janssen, Pfizer, UCB Pharma, Merck, Novartis, and Corrona. His associates reported ties to numerous industry sources.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Walking around the Cardiac Intensive Care Unit (CICU) with one of my heart failure colleagues, I was struck by the relative absence of patients with acute myocardial infarctions. Over the past 50 years, they have been replaced by patients with advanced heart failure, many of whom had been implanted with left ventricular assist devices or connected to a variety of extracorporeal support devices.

Although some of the patients were new New York Heart Association class IV patients, many had been treated for years with beta-blockers and renal ACE inhibitors or aldosterone antagonists. Their disease had now recurred and progressed despite what I had presumed to be curative drug therapy. They were experiencing the relentless progression of heart failure despite treatment that was developed almost 20 years ago and which has not advanced much since then. Many cardiologists of my generation presumed that heart failure was no longer a problem even though we knew that annual mortality rates of heart failure remained in the 10% range and that its incidence was increasing.

It has become clear to many of us that there has been little advance in the treatment of heart failure since the introduction of those 20th century drugs, notwithstanding the importance of the development of end stage cardiac support devices.

It seems our success in treating patients with ischemic heart disease had only delayed the expression and progression of cardiac dysfunction. Even with our success in treating patients with nonischemic heart failure, whatever that is, after reaching a brief plateau with drug therapy, they often experienced recurrence. It is true that many patients had improved as a result of drug therapy and that progression had been arrested and in some patients heart failure had actually been reversed. But many, like the patients I saw in our CICU, had progressed to advanced heart failure with little to be offered other than end-stage device therapy or heart transplantation. Both of these outcomes, although lifesaving, represent therapeutic failures.

It is time that we refocus our efforts on the treatment and eradication of heart failure. Although a number of contemporary treatment strategies have been developed, for the most part they have only resulted in modest additive benefit. We need to reconsider the protection of the heart during and after an ischemic event and prevent the insidious progression of ischemia in those patients with chronic coronary heart disease. In addition we need to direct our research to understand the pathophysiology of the “heart” in heart failure and to unlock the mysticism associated with the many etiologies of idiopathic nonischemic heart failure. Our knowledge in this disease or diseases is embarrassingly poor.

It is time to move on from the 20th century drug foundation of therapy based on neurohumoral control, to a 21st century understanding of the cellular and molecular targets affecting cardiac function. Recent investigations of collagen synthesis and degradation, cardiac energetics, and mitochondrial function have provided provocative information but represent only forays into the vast unknown mechanism of heart failure. The solution to worldwide heart failure is not in device therapy for everyone but in a deeper understanding of the mechanisms of heart failure and its application to therapy.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

ROME – Combined exposure to low LDL cholesterol and systolic blood pressure is associated with multiplicative and cumulative effects over time, Brian A. Ference, MD, said in a video interview at the annual congress of the European Society of Cardiology.

Indeed, long-term exposure to a combined 1-mmol/L lower LDL cholesterol and 10-mm Hg lower systolic BP was associated with up to a 90% lower risk of major cardiovascular events in the “naturally randomized” study he presented. The investigators used the 102,000 participants’ genetic LDL and BP scores in a Mendelian design.

If these lower LDL and blood pressure levels are sustained over decades, “those cumulative effects multiply, resulting in potentially dramatic reductions in the lifetime risk of cardiovascular events from even modestly lower levels of LDL and systolic blood pressure,” Dr. Ference of Wayne State University, Detroit, told reporter Bruce Jancin.

[email protected]

ROME – Combined exposure to low LDL cholesterol and systolic blood pressure is associated with multiplicative and cumulative effects over time, Brian A. Ference, MD, said in a video interview at the annual congress of the European Society of Cardiology.

Indeed, long-term exposure to a combined 1-mmol/L lower LDL cholesterol and 10-mm Hg lower systolic BP was associated with up to a 90% lower risk of major cardiovascular events in the “naturally randomized” study he presented. The investigators used the 102,000 participants’ genetic LDL and BP scores in a Mendelian design.

If these lower LDL and blood pressure levels are sustained over decades, “those cumulative effects multiply, resulting in potentially dramatic reductions in the lifetime risk of cardiovascular events from even modestly lower levels of LDL and systolic blood pressure,” Dr. Ference of Wayne State University, Detroit, told reporter Bruce Jancin.

[email protected]

ROME – Combined exposure to low LDL cholesterol and systolic blood pressure is associated with multiplicative and cumulative effects over time, Brian A. Ference, MD, said in a video interview at the annual congress of the European Society of Cardiology.

Indeed, long-term exposure to a combined 1-mmol/L lower LDL cholesterol and 10-mm Hg lower systolic BP was associated with up to a 90% lower risk of major cardiovascular events in the “naturally randomized” study he presented. The investigators used the 102,000 participants’ genetic LDL and BP scores in a Mendelian design.

If these lower LDL and blood pressure levels are sustained over decades, “those cumulative effects multiply, resulting in potentially dramatic reductions in the lifetime risk of cardiovascular events from even modestly lower levels of LDL and systolic blood pressure,” Dr. Ference of Wayne State University, Detroit, told reporter Bruce Jancin.

[email protected]

ANNAPOLIS, MD. – The definition of taking a thorough travel history has expanded with the spread of Zika.

Physicians “need to focus not only on patients’ travel histories, but also the travel histories and future travel plans of our patients’ sexual partners,” Ilona T. Goldfarb, a perinatologist at Massachusetts General Hospital, Boston, said in an interview. “We cannot rely on our patients to just [offer] that they’ve been in the Caribbean. We have to ask them diligently, and at every visit.”

Dr. Goldfarb added that immigration is a risk for Zika exposure, and may be a barrier to accurate history taking. In these cases, travel history will need to be performed in the patient’s spoken language to ensure accuracy, Dr. Goldfarb said. To track and communicate Zika information, Dr. Goldfarb and her colleagues have developed a three-part response based on their experience with previous infectious disease emergencies:

1. Communication. The practice is in regular communication with the Centers for Disease Control and Prevention and the state public health department to ensure they are up to date on all guidelines.

2. Education. Dr. Goldfarb and her practice colleagues routinely brief each other and patients on any new information, including recommended testing and guidelines, as well as travel warnings.

3. Tracking. Clinicians use a tracking worksheet for every patient screened for potential Zika exposure, allowing them to prospectively and retrospectively review patients. This has already proven useful, Dr. Goldfarb said, when the CDC changed its guidance around testing of asymptomatic patients.

In a presentation at the annual scientific meeting of the Infectious Diseases Society for Obstetrics and Gynecology, Dr. Goldfarb presented the data that she and her colleagues have collected so far on patients with Zika exposure.

As of Aug. 10, 2016, the practice had screened 142 women for Zika virus exposure since January 2016. More than 80% of the exposure came from travel to Zika-endemic areas. There have been few cases of exposure reported through sex, but Dr. Goldfarb said she thinks this type of exposure has been underreported because the link between infection and sex was not known until more recently.

Of the patients screened, 87% were appropriate candidates for Zika virus serum testing under CDC guidelines. There have been four positive serum tests for Zika exposure in Dr. Goldfarb’s patients so far.

In the one live birth, the newborn showed no visible signs of abnormalities. Testing revealed Zika virus RNA in the placenta, but not in the cord blood. The other three pregnancies were either terminated or associated with miscarriages. Again, Zika was detected in the placentas, but not in the fetuses.

Testing protocols have been a moving target since the outbreak began, according to Dr. Goldfarb. Some patients who call or are screened for possible exposure “are not actually eligible for testing because of the time frame or location of travel.”

To make sure that appropriate testing is being performed, Dr. Goldfarb advised designating an in-practice “Zika expert.” In her own practice, Dr. Goldfarb and one other colleague handle all Zika screening and inquiries from patients and colleagues. “This has greatly improved our efficiency and the experience for the patients,” she said in an interview.

The Massachusetts Department of Public Health is piloting a program with Dr. Goldfarb’s practice to determine if using the “designated expert” approach will improve laboratory wait times, compared with the standard protocol of having clinicians obtain approval from a state epidemiologist before sending patient serum samples for testing.

It has taken from 2 to 68 days to receive test results from the state lab, although a period of 17 days is typical, Dr. Goldfarb reported. The process has improved since last March when state health officials ramped up their capacity, she said.

As of Aug. 10, Dr. Goldfarb’s practice has performed 107 ultrasounds for patients with suspected Zika virus, averaging 3 per patient. Across all ultrasounds, there were three abnormalities, including one case of bilateral ventriculomegaly. Earlier in that pregnancy, the patient had tested negative for Zika on real-time reverse transcription polymerase chain reaction testing, which simultaneously screens for dengue, chikungunya, and Zika. Serum testing was also negative for Zika in the two other pregnancies with fetal abnormalities.

Dr. Goldfarb said she couldn’t quantify how much time is being spent on Zika screening and counseling since that is not being tracked, but she estimated that her practice takes between three and five calls or questions per day regarding the virus.

[email protected]

On Twitter @whitneymcknight

ANNAPOLIS, MD. – The definition of taking a thorough travel history has expanded with the spread of Zika.

Physicians “need to focus not only on patients’ travel histories, but also the travel histories and future travel plans of our patients’ sexual partners,” Ilona T. Goldfarb, a perinatologist at Massachusetts General Hospital, Boston, said in an interview. “We cannot rely on our patients to just [offer] that they’ve been in the Caribbean. We have to ask them diligently, and at every visit.”

Dr. Goldfarb added that immigration is a risk for Zika exposure, and may be a barrier to accurate history taking. In these cases, travel history will need to be performed in the patient’s spoken language to ensure accuracy, Dr. Goldfarb said. To track and communicate Zika information, Dr. Goldfarb and her colleagues have developed a three-part response based on their experience with previous infectious disease emergencies:

1. Communication. The practice is in regular communication with the Centers for Disease Control and Prevention and the state public health department to ensure they are up to date on all guidelines.

2. Education. Dr. Goldfarb and her practice colleagues routinely brief each other and patients on any new information, including recommended testing and guidelines, as well as travel warnings.

3. Tracking. Clinicians use a tracking worksheet for every patient screened for potential Zika exposure, allowing them to prospectively and retrospectively review patients. This has already proven useful, Dr. Goldfarb said, when the CDC changed its guidance around testing of asymptomatic patients.

In a presentation at the annual scientific meeting of the Infectious Diseases Society for Obstetrics and Gynecology, Dr. Goldfarb presented the data that she and her colleagues have collected so far on patients with Zika exposure.

As of Aug. 10, 2016, the practice had screened 142 women for Zika virus exposure since January 2016. More than 80% of the exposure came from travel to Zika-endemic areas. There have been few cases of exposure reported through sex, but Dr. Goldfarb said she thinks this type of exposure has been underreported because the link between infection and sex was not known until more recently.

Of the patients screened, 87% were appropriate candidates for Zika virus serum testing under CDC guidelines. There have been four positive serum tests for Zika exposure in Dr. Goldfarb’s patients so far.

In the one live birth, the newborn showed no visible signs of abnormalities. Testing revealed Zika virus RNA in the placenta, but not in the cord blood. The other three pregnancies were either terminated or associated with miscarriages. Again, Zika was detected in the placentas, but not in the fetuses.

Testing protocols have been a moving target since the outbreak began, according to Dr. Goldfarb. Some patients who call or are screened for possible exposure “are not actually eligible for testing because of the time frame or location of travel.”

To make sure that appropriate testing is being performed, Dr. Goldfarb advised designating an in-practice “Zika expert.” In her own practice, Dr. Goldfarb and one other colleague handle all Zika screening and inquiries from patients and colleagues. “This has greatly improved our efficiency and the experience for the patients,” she said in an interview.

The Massachusetts Department of Public Health is piloting a program with Dr. Goldfarb’s practice to determine if using the “designated expert” approach will improve laboratory wait times, compared with the standard protocol of having clinicians obtain approval from a state epidemiologist before sending patient serum samples for testing.

It has taken from 2 to 68 days to receive test results from the state lab, although a period of 17 days is typical, Dr. Goldfarb reported. The process has improved since last March when state health officials ramped up their capacity, she said.

As of Aug. 10, Dr. Goldfarb’s practice has performed 107 ultrasounds for patients with suspected Zika virus, averaging 3 per patient. Across all ultrasounds, there were three abnormalities, including one case of bilateral ventriculomegaly. Earlier in that pregnancy, the patient had tested negative for Zika on real-time reverse transcription polymerase chain reaction testing, which simultaneously screens for dengue, chikungunya, and Zika. Serum testing was also negative for Zika in the two other pregnancies with fetal abnormalities.

Dr. Goldfarb said she couldn’t quantify how much time is being spent on Zika screening and counseling since that is not being tracked, but she estimated that her practice takes between three and five calls or questions per day regarding the virus.

[email protected]

On Twitter @whitneymcknight

ANNAPOLIS, MD. – The definition of taking a thorough travel history has expanded with the spread of Zika.

Physicians “need to focus not only on patients’ travel histories, but also the travel histories and future travel plans of our patients’ sexual partners,” Ilona T. Goldfarb, a perinatologist at Massachusetts General Hospital, Boston, said in an interview. “We cannot rely on our patients to just [offer] that they’ve been in the Caribbean. We have to ask them diligently, and at every visit.”

Dr. Goldfarb added that immigration is a risk for Zika exposure, and may be a barrier to accurate history taking. In these cases, travel history will need to be performed in the patient’s spoken language to ensure accuracy, Dr. Goldfarb said. To track and communicate Zika information, Dr. Goldfarb and her colleagues have developed a three-part response based on their experience with previous infectious disease emergencies:

1. Communication. The practice is in regular communication with the Centers for Disease Control and Prevention and the state public health department to ensure they are up to date on all guidelines.

2. Education. Dr. Goldfarb and her practice colleagues routinely brief each other and patients on any new information, including recommended testing and guidelines, as well as travel warnings.

3. Tracking. Clinicians use a tracking worksheet for every patient screened for potential Zika exposure, allowing them to prospectively and retrospectively review patients. This has already proven useful, Dr. Goldfarb said, when the CDC changed its guidance around testing of asymptomatic patients.

In a presentation at the annual scientific meeting of the Infectious Diseases Society for Obstetrics and Gynecology, Dr. Goldfarb presented the data that she and her colleagues have collected so far on patients with Zika exposure.

As of Aug. 10, 2016, the practice had screened 142 women for Zika virus exposure since January 2016. More than 80% of the exposure came from travel to Zika-endemic areas. There have been few cases of exposure reported through sex, but Dr. Goldfarb said she thinks this type of exposure has been underreported because the link between infection and sex was not known until more recently.

Of the patients screened, 87% were appropriate candidates for Zika virus serum testing under CDC guidelines. There have been four positive serum tests for Zika exposure in Dr. Goldfarb’s patients so far.

In the one live birth, the newborn showed no visible signs of abnormalities. Testing revealed Zika virus RNA in the placenta, but not in the cord blood. The other three pregnancies were either terminated or associated with miscarriages. Again, Zika was detected in the placentas, but not in the fetuses.

Testing protocols have been a moving target since the outbreak began, according to Dr. Goldfarb. Some patients who call or are screened for possible exposure “are not actually eligible for testing because of the time frame or location of travel.”

To make sure that appropriate testing is being performed, Dr. Goldfarb advised designating an in-practice “Zika expert.” In her own practice, Dr. Goldfarb and one other colleague handle all Zika screening and inquiries from patients and colleagues. “This has greatly improved our efficiency and the experience for the patients,” she said in an interview.

The Massachusetts Department of Public Health is piloting a program with Dr. Goldfarb’s practice to determine if using the “designated expert” approach will improve laboratory wait times, compared with the standard protocol of having clinicians obtain approval from a state epidemiologist before sending patient serum samples for testing.

It has taken from 2 to 68 days to receive test results from the state lab, although a period of 17 days is typical, Dr. Goldfarb reported. The process has improved since last March when state health officials ramped up their capacity, she said.

As of Aug. 10, Dr. Goldfarb’s practice has performed 107 ultrasounds for patients with suspected Zika virus, averaging 3 per patient. Across all ultrasounds, there were three abnormalities, including one case of bilateral ventriculomegaly. Earlier in that pregnancy, the patient had tested negative for Zika on real-time reverse transcription polymerase chain reaction testing, which simultaneously screens for dengue, chikungunya, and Zika. Serum testing was also negative for Zika in the two other pregnancies with fetal abnormalities.

Dr. Goldfarb said she couldn’t quantify how much time is being spent on Zika screening and counseling since that is not being tracked, but she estimated that her practice takes between three and five calls or questions per day regarding the virus.

[email protected]

On Twitter @whitneymcknight

The editors of the Journal of Vascular Surgery Publications are seeking nominations, including self-nominations, for multiple editorial positions. All applicants must be active or senior members of the Society for Vascular Surgery. Prior service on the JVS editorial board is preferred. An annual financial stipend is provided for these editorial roles.

More information about each of the positions listed below can be found in this online document.

Assistant editor of abstracts and book reviews. This editor selects non-JVS abstracts and writes short commentaries for those abstracts for publication in the JVS and JVS-VL. This editor will also write and solicit book reviews.

Assistant editor of social media and press releases. This position requires writing short press release articles for the JVS Journals and drafting Facebook, Twitter and LinkedIn posts to promote JVS content.

Assistant editor of reviews for the Journal of Vascular Surgery. The assistant editor solicits review articles and manages the peer-review process for systematic reviews, meta-analyses, and evidence summaries.

Associate basic science editor for the JVS and the JVSVL. This associate editor manages the peer-review process and makes the final decision on manuscript publication for about 200 basic science submissions a year.

Associate editor of the Journal of Vascular Surgery. The JVS associate editor manages the peer-review process of about 600 submissions a year, recommending a final decision to the editors regarding the publication of a submission.

If you would like to apply for one of these editorial positions, please send your name and a brief summary of your qualifications Jessica McEwan, JVS managing editor at: [email protected]. The deadline for applications is Oct. 1, 2016.

The editors of the Journal of Vascular Surgery Publications are seeking nominations, including self-nominations, for multiple editorial positions. All applicants must be active or senior members of the Society for Vascular Surgery. Prior service on the JVS editorial board is preferred. An annual financial stipend is provided for these editorial roles.

More information about each of the positions listed below can be found in this online document.

Assistant editor of abstracts and book reviews. This editor selects non-JVS abstracts and writes short commentaries for those abstracts for publication in the JVS and JVS-VL. This editor will also write and solicit book reviews.

Assistant editor of social media and press releases. This position requires writing short press release articles for the JVS Journals and drafting Facebook, Twitter and LinkedIn posts to promote JVS content.

Assistant editor of reviews for the Journal of Vascular Surgery. The assistant editor solicits review articles and manages the peer-review process for systematic reviews, meta-analyses, and evidence summaries.

Associate basic science editor for the JVS and the JVSVL. This associate editor manages the peer-review process and makes the final decision on manuscript publication for about 200 basic science submissions a year.

Associate editor of the Journal of Vascular Surgery. The JVS associate editor manages the peer-review process of about 600 submissions a year, recommending a final decision to the editors regarding the publication of a submission.

If you would like to apply for one of these editorial positions, please send your name and a brief summary of your qualifications Jessica McEwan, JVS managing editor at: [email protected]. The deadline for applications is Oct. 1, 2016.

The editors of the Journal of Vascular Surgery Publications are seeking nominations, including self-nominations, for multiple editorial positions. All applicants must be active or senior members of the Society for Vascular Surgery. Prior service on the JVS editorial board is preferred. An annual financial stipend is provided for these editorial roles.

More information about each of the positions listed below can be found in this online document.

Assistant editor of abstracts and book reviews. This editor selects non-JVS abstracts and writes short commentaries for those abstracts for publication in the JVS and JVS-VL. This editor will also write and solicit book reviews.

Assistant editor of social media and press releases. This position requires writing short press release articles for the JVS Journals and drafting Facebook, Twitter and LinkedIn posts to promote JVS content.

Assistant editor of reviews for the Journal of Vascular Surgery. The assistant editor solicits review articles and manages the peer-review process for systematic reviews, meta-analyses, and evidence summaries.

Associate basic science editor for the JVS and the JVSVL. This associate editor manages the peer-review process and makes the final decision on manuscript publication for about 200 basic science submissions a year.

Associate editor of the Journal of Vascular Surgery. The JVS associate editor manages the peer-review process of about 600 submissions a year, recommending a final decision to the editors regarding the publication of a submission.

If you would like to apply for one of these editorial positions, please send your name and a brief summary of your qualifications Jessica McEwan, JVS managing editor at: [email protected]. The deadline for applications is Oct. 1, 2016.