Michele G. Sullivan

VIENNA – Treatment with an insulin pump rather than insulin injections may help protect patients with type 2 diabetes from heart disease, a large registry study has determined.

Over a mean follow-up of about 7 years, the pump was associated with a 44% decrease in the risk of fatal cardiovascular disease. It also conferred a 29% decrease in the risk of death overall, Dr. Soffia Gudbjornsdottir said at the annual meeting of the European Association for the Study of Diabetes.

She used data extracted from the Swedish National Diabetes Registry, which was founded in 2005. It contains information on 95% of the country’s type 1 diabetes patients and is linked with national inpatient and death registries.

The study group comprised 18,168 patients, 2,441 of whom were using an insulin pump. There were some significant baseline differences between the pump users and the users of injectable insulin.

Pump users were younger (age at baseline 38 vs. 41 years), and more likely to be women. Those treated with the pump had better measures of blood pressure and lipids. They were more likely to exercise and less likely to smoke. Insulin injection users had higher rates of prior cardiovascular disease. However, a propensity matching score eliminated these differences and balanced the group, Dr. Gudbjornsdottir noted.

By 7 years, there had been few cardiovascular events or deaths – an expected finding, since the cohort was young. Fatal/nonfatal coronary heart disease had developed in 7% of the insulin injection users and 4% of the of pump users, a nonsignificant difference. Neither were there significant differences in fatal or nonfatal cardiovascular disease (8% vs. 5%) or noncardiovascular mortality (4% vs. 2%).

However, significant differences did appear in two other endpoints: fatal cardiovascular disease (3% vs. 1%) and total mortality (7% vs. 3%).

A multivariate regression model found several significant risk reductions associated with pump use, including fatal cardiovascular disease (hazard ratio, 0.56), and all-cause mortality (HR, 0.71).

There were no significant differences in the risks for fatal/nonfatal coronary heart disease, fatal/nonfatal cardiovascular disease, or noncardiovascular death.

During the discussion, Dr. Gudbjornsdottir addressed the concern of a treatment allocation bias due to some unknown variable in the group. “If we had such an unknown covariate, with, for example, a hazard ratio of 1.3, it would have had to be present in at least 80% of the insulin group and in none of the pump group to invalidate the results, so I would say our study findings are quite robust.”

She had no financial disclosures.

VIENNA – Treatment with an insulin pump rather than insulin injections may help protect patients with type 2 diabetes from heart disease, a large registry study has determined.

Over a mean follow-up of about 7 years, the pump was associated with a 44% decrease in the risk of fatal cardiovascular disease. It also conferred a 29% decrease in the risk of death overall, Dr. Soffia Gudbjornsdottir said at the annual meeting of the European Association for the Study of Diabetes.

She used data extracted from the Swedish National Diabetes Registry, which was founded in 2005. It contains information on 95% of the country’s type 1 diabetes patients and is linked with national inpatient and death registries.

The study group comprised 18,168 patients, 2,441 of whom were using an insulin pump. There were some significant baseline differences between the pump users and the users of injectable insulin.

Pump users were younger (age at baseline 38 vs. 41 years), and more likely to be women. Those treated with the pump had better measures of blood pressure and lipids. They were more likely to exercise and less likely to smoke. Insulin injection users had higher rates of prior cardiovascular disease. However, a propensity matching score eliminated these differences and balanced the group, Dr. Gudbjornsdottir noted.

By 7 years, there had been few cardiovascular events or deaths – an expected finding, since the cohort was young. Fatal/nonfatal coronary heart disease had developed in 7% of the insulin injection users and 4% of the of pump users, a nonsignificant difference. Neither were there significant differences in fatal or nonfatal cardiovascular disease (8% vs. 5%) or noncardiovascular mortality (4% vs. 2%).

However, significant differences did appear in two other endpoints: fatal cardiovascular disease (3% vs. 1%) and total mortality (7% vs. 3%).

A multivariate regression model found several significant risk reductions associated with pump use, including fatal cardiovascular disease (hazard ratio, 0.56), and all-cause mortality (HR, 0.71).

There were no significant differences in the risks for fatal/nonfatal coronary heart disease, fatal/nonfatal cardiovascular disease, or noncardiovascular death.

During the discussion, Dr. Gudbjornsdottir addressed the concern of a treatment allocation bias due to some unknown variable in the group. “If we had such an unknown covariate, with, for example, a hazard ratio of 1.3, it would have had to be present in at least 80% of the insulin group and in none of the pump group to invalidate the results, so I would say our study findings are quite robust.”

She had no financial disclosures.

VIENNA – Treatment with an insulin pump rather than insulin injections may help protect patients with type 2 diabetes from heart disease, a large registry study has determined.

Over a mean follow-up of about 7 years, the pump was associated with a 44% decrease in the risk of fatal cardiovascular disease. It also conferred a 29% decrease in the risk of death overall, Dr. Soffia Gudbjornsdottir said at the annual meeting of the European Association for the Study of Diabetes.

She used data extracted from the Swedish National Diabetes Registry, which was founded in 2005. It contains information on 95% of the country’s type 1 diabetes patients and is linked with national inpatient and death registries.

The study group comprised 18,168 patients, 2,441 of whom were using an insulin pump. There were some significant baseline differences between the pump users and the users of injectable insulin.

Pump users were younger (age at baseline 38 vs. 41 years), and more likely to be women. Those treated with the pump had better measures of blood pressure and lipids. They were more likely to exercise and less likely to smoke. Insulin injection users had higher rates of prior cardiovascular disease. However, a propensity matching score eliminated these differences and balanced the group, Dr. Gudbjornsdottir noted.

By 7 years, there had been few cardiovascular events or deaths – an expected finding, since the cohort was young. Fatal/nonfatal coronary heart disease had developed in 7% of the insulin injection users and 4% of the of pump users, a nonsignificant difference. Neither were there significant differences in fatal or nonfatal cardiovascular disease (8% vs. 5%) or noncardiovascular mortality (4% vs. 2%).

However, significant differences did appear in two other endpoints: fatal cardiovascular disease (3% vs. 1%) and total mortality (7% vs. 3%).

A multivariate regression model found several significant risk reductions associated with pump use, including fatal cardiovascular disease (hazard ratio, 0.56), and all-cause mortality (HR, 0.71).

There were no significant differences in the risks for fatal/nonfatal coronary heart disease, fatal/nonfatal cardiovascular disease, or noncardiovascular death.

During the discussion, Dr. Gudbjornsdottir addressed the concern of a treatment allocation bias due to some unknown variable in the group. “If we had such an unknown covariate, with, for example, a hazard ratio of 1.3, it would have had to be present in at least 80% of the insulin group and in none of the pump group to invalidate the results, so I would say our study findings are quite robust.”

She had no financial disclosures.

VIENNA – Treatment with an insulin pump rather than insulin injections may help protect patients with type 2 diabetes from heart disease, a large registry study has determined.

Over a mean follow-up of about 7 years, the pump was associated with a 44% decrease in the risk of fatal cardiovascular disease. It also conferred a 29% decrease in the risk of death overall, Dr. Soffia Gudbjornsdottir said at the annual meeting of the European Association for the Study of Diabetes.

She used data extracted from the Swedish National Diabetes Registry, which was founded in 2005. It contains information on 95% of the country’s type 1 diabetes patients and is linked with national inpatient and death registries.

The study group comprised 18,168 patients, 2,441 of whom were using an insulin pump. There were some significant baseline differences between the pump users and the users of injectable insulin.

Pump users were younger (age at baseline 38 vs. 41 years), and more likely to be women. Those treated with the pump had better measures of blood pressure and lipids. They were more likely to exercise and less likely to smoke. Insulin injection users had higher rates of prior cardiovascular disease. However, a propensity matching score eliminated these differences and balanced the group, Dr. Gudbjornsdottir noted.

By 7 years, there had been few cardiovascular events or deaths – an expected finding, since the cohort was young. Fatal/nonfatal coronary heart disease had developed in 7% of the insulin injection users and 4% of the of pump users, a nonsignificant difference. Neither were there significant differences in fatal or nonfatal cardiovascular disease (8% vs. 5%) or noncardiovascular mortality (4% vs. 2%).

However, significant differences did appear in two other endpoints: fatal cardiovascular disease (3% vs. 1%) and total mortality (7% vs. 3%).

A multivariate regression model found several significant risk reductions associated with pump use, including fatal cardiovascular disease (hazard ratio, 0.56), and all-cause mortality (HR, 0.71).

There were no significant differences in the risks for fatal/nonfatal coronary heart disease, fatal/nonfatal cardiovascular disease, or noncardiovascular death.

During the discussion, Dr. Gudbjornsdottir addressed the concern of a treatment allocation bias due to some unknown variable in the group. “If we had such an unknown covariate, with, for example, a hazard ratio of 1.3, it would have had to be present in at least 80% of the insulin group and in none of the pump group to invalidate the results, so I would say our study findings are quite robust.”

She had no financial disclosures.

[email protected]

On Twitter @alz_gal

VIENNA – Treatment with an insulin pump rather than insulin injections may help protect patients with type 2 diabetes from heart disease, a large registry study has determined.

Over a mean follow-up of about 7 years, the pump was associated with a 44% decrease in the risk of fatal cardiovascular disease. It also conferred a 29% decrease in the risk of death overall, Dr. Soffia Gudbjornsdottir said at the annual meeting of the European Association for the Study of Diabetes.

She used data extracted from the Swedish National Diabetes Registry, which was founded in 2005. It contains information on 95% of the country’s type 1 diabetes patients and is linked with national inpatient and death registries.

The study group comprised 18,168 patients, 2,441 of whom were using an insulin pump. There were some significant baseline differences between the pump users and the users of injectable insulin.

Pump users were younger (age at baseline 38 vs. 41 years), and more likely to be women. Those treated with the pump had better measures of blood pressure and lipids. They were more likely to exercise and less likely to smoke. Insulin injection users had higher rates of prior cardiovascular disease. However, a propensity matching score eliminated these differences and balanced the group, Dr. Gudbjornsdottir noted.

By 7 years, there had been few cardiovascular events or deaths – an expected finding, since the cohort was young. Fatal/nonfatal coronary heart disease had developed in 7% of the insulin injection users and 4% of the of pump users, a nonsignificant difference. Neither were there significant differences in fatal or nonfatal cardiovascular disease (8% vs. 5%) or noncardiovascular mortality (4% vs. 2%).

However, significant differences did appear in two other endpoints: fatal cardiovascular disease (3% vs. 1%) and total mortality (7% vs. 3%).

A multivariate regression model found several significant risk reductions associated with pump use, including fatal cardiovascular disease (hazard ratio, 0.56), and all-cause mortality (HR, 0.71).

There were no significant differences in the risks for fatal/nonfatal coronary heart disease, fatal/nonfatal cardiovascular disease, or noncardiovascular death.

During the discussion, Dr. Gudbjornsdottir addressed the concern of a treatment allocation bias due to some unknown variable in the group. “If we had such an unknown covariate, with, for example, a hazard ratio of 1.3, it would have had to be present in at least 80% of the insulin group and in none of the pump group to invalidate the results, so I would say our study findings are quite robust.”

She had no financial disclosures.

[email protected]

On Twitter @alz_gal

VIENNA – Treatment with an insulin pump rather than insulin injections may help protect patients with type 2 diabetes from heart disease, a large registry study has determined.

Over a mean follow-up of about 7 years, the pump was associated with a 44% decrease in the risk of fatal cardiovascular disease. It also conferred a 29% decrease in the risk of death overall, Dr. Soffia Gudbjornsdottir said at the annual meeting of the European Association for the Study of Diabetes.

She used data extracted from the Swedish National Diabetes Registry, which was founded in 2005. It contains information on 95% of the country’s type 1 diabetes patients and is linked with national inpatient and death registries.

The study group comprised 18,168 patients, 2,441 of whom were using an insulin pump. There were some significant baseline differences between the pump users and the users of injectable insulin.

Pump users were younger (age at baseline 38 vs. 41 years), and more likely to be women. Those treated with the pump had better measures of blood pressure and lipids. They were more likely to exercise and less likely to smoke. Insulin injection users had higher rates of prior cardiovascular disease. However, a propensity matching score eliminated these differences and balanced the group, Dr. Gudbjornsdottir noted.

By 7 years, there had been few cardiovascular events or deaths – an expected finding, since the cohort was young. Fatal/nonfatal coronary heart disease had developed in 7% of the insulin injection users and 4% of the of pump users, a nonsignificant difference. Neither were there significant differences in fatal or nonfatal cardiovascular disease (8% vs. 5%) or noncardiovascular mortality (4% vs. 2%).

However, significant differences did appear in two other endpoints: fatal cardiovascular disease (3% vs. 1%) and total mortality (7% vs. 3%).

A multivariate regression model found several significant risk reductions associated with pump use, including fatal cardiovascular disease (hazard ratio, 0.56), and all-cause mortality (HR, 0.71).

There were no significant differences in the risks for fatal/nonfatal coronary heart disease, fatal/nonfatal cardiovascular disease, or noncardiovascular death.

During the discussion, Dr. Gudbjornsdottir addressed the concern of a treatment allocation bias due to some unknown variable in the group. “If we had such an unknown covariate, with, for example, a hazard ratio of 1.3, it would have had to be present in at least 80% of the insulin group and in none of the pump group to invalidate the results, so I would say our study findings are quite robust.”

She had no financial disclosures.

[email protected]

On Twitter @alz_gal

A fluorocuracil-based first-line chemotherapy regimen demonstrated acceptable response and survival outcomes and was less toxic and better tolerated than an epirubicin-based regimen for patients with advanced gastric cancers, Dr. Rosine Guimbaud and her colleagues reported in the October issue of the Journal of Clinical Oncology.

In a trial, conducted at 71 centers in France, 416 patients with advanced or metastatic gastric adenocarcinomas were randomized to receive fluorouracil, leucovorin, and irinotecan (FOLFIRI) or epirubicin, cisplatin, and capecitabine (ECX). After a median follow-up of 31 months, the median time to treatment failure was significantly longer with FOLFIRI than with ECX (5.1 vs. 4.2 months; P = .008), though there was no significant difference between the two groups in median progression-free or overall survival.

The rate of grade 3-4 toxicity was signficantly lower with FOLFIRI (69% vs. 84%; P less than .001), Toxicity leading to discontinuation occurred in 4% of the FOLFIRI group and 14.5% of the ECX group. Toxicity-related deaths occurred in two patients taking FOLFIRI and seven taking ECX.

The findings of the trial support retiring the use of the epirubicin-based regimen for patients with advanced gastric cancers, wrote Dr. Guimbaud of the Centre Hospitalier Universitaire de Toulouse (France) and her coauthors (J. Clin. Oncol. 2014 [doi:10.1200/JCO.2013.54.1011]).

“The utility of epirubicin is called into question; many continue to debate whether anthracyclines should be used for therapy, given their toxicity. Our results support abandoning their use,” they said.

Dr. Guimbaud disclosed financial ties with Roche; many of the coauthors also disclosed relationships with Roche and other pharmaceutical companies.

[email protected]

On Twitter @alz_gal

A fluorocuracil-based first-line chemotherapy regimen demonstrated acceptable response and survival outcomes and was less toxic and better tolerated than an epirubicin-based regimen for patients with advanced gastric cancers, Dr. Rosine Guimbaud and her colleagues reported in the October issue of the Journal of Clinical Oncology.

In a trial, conducted at 71 centers in France, 416 patients with advanced or metastatic gastric adenocarcinomas were randomized to receive fluorouracil, leucovorin, and irinotecan (FOLFIRI) or epirubicin, cisplatin, and capecitabine (ECX). After a median follow-up of 31 months, the median time to treatment failure was significantly longer with FOLFIRI than with ECX (5.1 vs. 4.2 months; P = .008), though there was no significant difference between the two groups in median progression-free or overall survival.

The rate of grade 3-4 toxicity was signficantly lower with FOLFIRI (69% vs. 84%; P less than .001), Toxicity leading to discontinuation occurred in 4% of the FOLFIRI group and 14.5% of the ECX group. Toxicity-related deaths occurred in two patients taking FOLFIRI and seven taking ECX.

The findings of the trial support retiring the use of the epirubicin-based regimen for patients with advanced gastric cancers, wrote Dr. Guimbaud of the Centre Hospitalier Universitaire de Toulouse (France) and her coauthors (J. Clin. Oncol. 2014 [doi:10.1200/JCO.2013.54.1011]).

“The utility of epirubicin is called into question; many continue to debate whether anthracyclines should be used for therapy, given their toxicity. Our results support abandoning their use,” they said.

Dr. Guimbaud disclosed financial ties with Roche; many of the coauthors also disclosed relationships with Roche and other pharmaceutical companies.

[email protected]

On Twitter @alz_gal

A fluorocuracil-based first-line chemotherapy regimen demonstrated acceptable response and survival outcomes and was less toxic and better tolerated than an epirubicin-based regimen for patients with advanced gastric cancers, Dr. Rosine Guimbaud and her colleagues reported in the October issue of the Journal of Clinical Oncology.

In a trial, conducted at 71 centers in France, 416 patients with advanced or metastatic gastric adenocarcinomas were randomized to receive fluorouracil, leucovorin, and irinotecan (FOLFIRI) or epirubicin, cisplatin, and capecitabine (ECX). After a median follow-up of 31 months, the median time to treatment failure was significantly longer with FOLFIRI than with ECX (5.1 vs. 4.2 months; P = .008), though there was no significant difference between the two groups in median progression-free or overall survival.

The rate of grade 3-4 toxicity was signficantly lower with FOLFIRI (69% vs. 84%; P less than .001), Toxicity leading to discontinuation occurred in 4% of the FOLFIRI group and 14.5% of the ECX group. Toxicity-related deaths occurred in two patients taking FOLFIRI and seven taking ECX.

The findings of the trial support retiring the use of the epirubicin-based regimen for patients with advanced gastric cancers, wrote Dr. Guimbaud of the Centre Hospitalier Universitaire de Toulouse (France) and her coauthors (J. Clin. Oncol. 2014 [doi:10.1200/JCO.2013.54.1011]).

“The utility of epirubicin is called into question; many continue to debate whether anthracyclines should be used for therapy, given their toxicity. Our results support abandoning their use,” they said.

Dr. Guimbaud disclosed financial ties with Roche; many of the coauthors also disclosed relationships with Roche and other pharmaceutical companies.

[email protected]

On Twitter @alz_gal

BALTIMORE– Amitriptyline decreased pain and improved function significantly more than did pregabalin in a randomized trial of patients with chronic low back pain.

Almost 60% of patients taking the tricyclic antidepressant experienced at least a 50% decrease in pain on a visual analog pain scale, compared with 38% of those taking pregabalin, Dr. Jayantee Kalita reported at the annual meeting of the American Neurological Association.

The study is the first to examine amitriptyline in low back pain, a chronic pain condition that can be debilitating in its duration and severity and is notoriously difficult to control, said Dr. Kalita, a neurologist at the Sanjay Gandhi Post Graduate Institute of Medicine, Lucknow, India.

A 2011 systematic review found 17 randomized controlled trials of pharmacologic treatments for chronic low back pain (Eur. Spine J. 2011;20:40-50). These examined the benefits of nonsteroidal anti-inflammatory drugs, antidepressants, and opioids. The best results were obtained with acetaminophen and opioids, but there were dose-limiting side effects, and pain rebounded when the treatment was discontinued. The studies that examined antidepressants found them to be no more effective than placebo.

Dr. Kalita and her colleagues randomized 200 patients with chronic low back pain to amitriptyline or pregabalin for 14 weeks. Amitriptyline was started at 10 mg once a day and increased to a maximum of 50 mg as needed. Pregabalin was started at 75 mg twice a day and increased to a maximum of 300 mg twice a day if needed.

The cohort had a mean age of 41 years, with a median 35 months of back pain, although one patient had experienced 30 years of back pain. Pain was idiopathic and experienced as radiculopathy (48%), localized (46%), or as lower crossed syndrome (6%).

Most patients (115) lived in rural areas. Risk factors included diabetes (9 patients), hypertension (15), smoking (39), and tobacco use (65).

At baseline, both treatment groups reported their pain as a median of 7 on a 10-point visual analog scale. The mean score on the Oswestry Disability Index (ODI) was 40%, indicating severe pain that limits work, travel, personal care, social life, sexual activity, and sleep.By 6 weeks into the trial, pain scores in the amitriptyline group had decreased from 7 to 4, a significant improvement. By the end of 14 weeks, scores had decreased to about 3, which was significantly better than the scores both at 6 weeks and at baseline.

In the pregabalin group, the pain score dropped from 7 to 5, which was not a significant change. During weeks 6-14, scores dropped another half-point, to around 4.5. This was a significant improvement from baseline, but not from week 6.

The ODI score also improved more in patients taking amitriptyline. From a median of about 43%, the index dropped to about 30% at 6 weeks and 20% at 14 weeks. A 20% score indicates minimal disability; patients need no assistance with activities of daily living and experience minimal life interruptions from pain.

Disability also improved in the pregabalin group, dropping from about 40% at baseline to 35% at 6 weeks, and then to about 25% at 14 weeks. This score falls in the moderate disability range. Patients may need help with some daily activities, and may be off work. The final score was also a significant improvement over baseline, although it was not as robust as with the amitriptyline group, Dr. Kalita noted.

In the intent-to-treat analysis, 57% of the amitriptyline group and 39% of the pregabalin group experienced a pain scale decrease of at least 50%. There was at least a 20% improvement in the disability scores of 67% of the amitriptyline group and 48% of the pregabalin group.

Side effects included sedation, vertigo, dry mouth, skin rash, and restlessness. Significantly more patients who took pregabalin had at least one side effect (eight patients vs. three patients). Sedation was most common, occurring in 10 patients who took amitriptyline and 4 who took pregabalin.

Dr. Kalita had no financial disclosures.

[email protected] 


On Twitter @alz_gal

BALTIMORE– Amitriptyline decreased pain and improved function significantly more than did pregabalin in a randomized trial of patients with chronic low back pain.

Almost 60% of patients taking the tricyclic antidepressant experienced at least a 50% decrease in pain on a visual analog pain scale, compared with 38% of those taking pregabalin, Dr. Jayantee Kalita reported at the annual meeting of the American Neurological Association.

The study is the first to examine amitriptyline in low back pain, a chronic pain condition that can be debilitating in its duration and severity and is notoriously difficult to control, said Dr. Kalita, a neurologist at the Sanjay Gandhi Post Graduate Institute of Medicine, Lucknow, India.

A 2011 systematic review found 17 randomized controlled trials of pharmacologic treatments for chronic low back pain (Eur. Spine J. 2011;20:40-50). These examined the benefits of nonsteroidal anti-inflammatory drugs, antidepressants, and opioids. The best results were obtained with acetaminophen and opioids, but there were dose-limiting side effects, and pain rebounded when the treatment was discontinued. The studies that examined antidepressants found them to be no more effective than placebo.

Dr. Kalita and her colleagues randomized 200 patients with chronic low back pain to amitriptyline or pregabalin for 14 weeks. Amitriptyline was started at 10 mg once a day and increased to a maximum of 50 mg as needed. Pregabalin was started at 75 mg twice a day and increased to a maximum of 300 mg twice a day if needed.

The cohort had a mean age of 41 years, with a median 35 months of back pain, although one patient had experienced 30 years of back pain. Pain was idiopathic and experienced as radiculopathy (48%), localized (46%), or as lower crossed syndrome (6%).

Most patients (115) lived in rural areas. Risk factors included diabetes (9 patients), hypertension (15), smoking (39), and tobacco use (65).

At baseline, both treatment groups reported their pain as a median of 7 on a 10-point visual analog scale. The mean score on the Oswestry Disability Index (ODI) was 40%, indicating severe pain that limits work, travel, personal care, social life, sexual activity, and sleep.By 6 weeks into the trial, pain scores in the amitriptyline group had decreased from 7 to 4, a significant improvement. By the end of 14 weeks, scores had decreased to about 3, which was significantly better than the scores both at 6 weeks and at baseline.

In the pregabalin group, the pain score dropped from 7 to 5, which was not a significant change. During weeks 6-14, scores dropped another half-point, to around 4.5. This was a significant improvement from baseline, but not from week 6.

The ODI score also improved more in patients taking amitriptyline. From a median of about 43%, the index dropped to about 30% at 6 weeks and 20% at 14 weeks. A 20% score indicates minimal disability; patients need no assistance with activities of daily living and experience minimal life interruptions from pain.

Disability also improved in the pregabalin group, dropping from about 40% at baseline to 35% at 6 weeks, and then to about 25% at 14 weeks. This score falls in the moderate disability range. Patients may need help with some daily activities, and may be off work. The final score was also a significant improvement over baseline, although it was not as robust as with the amitriptyline group, Dr. Kalita noted.

In the intent-to-treat analysis, 57% of the amitriptyline group and 39% of the pregabalin group experienced a pain scale decrease of at least 50%. There was at least a 20% improvement in the disability scores of 67% of the amitriptyline group and 48% of the pregabalin group.

Side effects included sedation, vertigo, dry mouth, skin rash, and restlessness. Significantly more patients who took pregabalin had at least one side effect (eight patients vs. three patients). Sedation was most common, occurring in 10 patients who took amitriptyline and 4 who took pregabalin.

Dr. Kalita had no financial disclosures.

[email protected] 


On Twitter @alz_gal

BALTIMORE– Amitriptyline decreased pain and improved function significantly more than did pregabalin in a randomized trial of patients with chronic low back pain.

Almost 60% of patients taking the tricyclic antidepressant experienced at least a 50% decrease in pain on a visual analog pain scale, compared with 38% of those taking pregabalin, Dr. Jayantee Kalita reported at the annual meeting of the American Neurological Association.

The study is the first to examine amitriptyline in low back pain, a chronic pain condition that can be debilitating in its duration and severity and is notoriously difficult to control, said Dr. Kalita, a neurologist at the Sanjay Gandhi Post Graduate Institute of Medicine, Lucknow, India.

A 2011 systematic review found 17 randomized controlled trials of pharmacologic treatments for chronic low back pain (Eur. Spine J. 2011;20:40-50). These examined the benefits of nonsteroidal anti-inflammatory drugs, antidepressants, and opioids. The best results were obtained with acetaminophen and opioids, but there were dose-limiting side effects, and pain rebounded when the treatment was discontinued. The studies that examined antidepressants found them to be no more effective than placebo.

Dr. Kalita and her colleagues randomized 200 patients with chronic low back pain to amitriptyline or pregabalin for 14 weeks. Amitriptyline was started at 10 mg once a day and increased to a maximum of 50 mg as needed. Pregabalin was started at 75 mg twice a day and increased to a maximum of 300 mg twice a day if needed.

The cohort had a mean age of 41 years, with a median 35 months of back pain, although one patient had experienced 30 years of back pain. Pain was idiopathic and experienced as radiculopathy (48%), localized (46%), or as lower crossed syndrome (6%).

Most patients (115) lived in rural areas. Risk factors included diabetes (9 patients), hypertension (15), smoking (39), and tobacco use (65).

At baseline, both treatment groups reported their pain as a median of 7 on a 10-point visual analog scale. The mean score on the Oswestry Disability Index (ODI) was 40%, indicating severe pain that limits work, travel, personal care, social life, sexual activity, and sleep.By 6 weeks into the trial, pain scores in the amitriptyline group had decreased from 7 to 4, a significant improvement. By the end of 14 weeks, scores had decreased to about 3, which was significantly better than the scores both at 6 weeks and at baseline.

In the pregabalin group, the pain score dropped from 7 to 5, which was not a significant change. During weeks 6-14, scores dropped another half-point, to around 4.5. This was a significant improvement from baseline, but not from week 6.

The ODI score also improved more in patients taking amitriptyline. From a median of about 43%, the index dropped to about 30% at 6 weeks and 20% at 14 weeks. A 20% score indicates minimal disability; patients need no assistance with activities of daily living and experience minimal life interruptions from pain.

Disability also improved in the pregabalin group, dropping from about 40% at baseline to 35% at 6 weeks, and then to about 25% at 14 weeks. This score falls in the moderate disability range. Patients may need help with some daily activities, and may be off work. The final score was also a significant improvement over baseline, although it was not as robust as with the amitriptyline group, Dr. Kalita noted.

In the intent-to-treat analysis, 57% of the amitriptyline group and 39% of the pregabalin group experienced a pain scale decrease of at least 50%. There was at least a 20% improvement in the disability scores of 67% of the amitriptyline group and 48% of the pregabalin group.

Side effects included sedation, vertigo, dry mouth, skin rash, and restlessness. Significantly more patients who took pregabalin had at least one side effect (eight patients vs. three patients). Sedation was most common, occurring in 10 patients who took amitriptyline and 4 who took pregabalin.

Dr. Kalita had no financial disclosures.

[email protected] 


On Twitter @alz_gal

An overabundance of orexin ­– a protein that helps regulate normal sleep and waking – appears linked to rising tau levels in Alzheimer’s disease, according to findings published online Oct. 13 in JAMA Neurology.

Orexin levels showed a tight positive correlation with tau – a protein that correlates positively with cognitive decline in the disease – in the cerebrospinal fluid of Alzheimer’s patients, according to a study by Dr. Claudio Liguori and associates. In addition, the sleep dysregulation characteristic of Alzheimer’s patients is tightly correlated with both increased orexin and tau levels.

“Our study has shown that, in Alzheimer’s disease, increased CSF orexin levels are linked to a parallel sleep deterioration, which appears to be related to cognitive decline,” the authors wrote. “Hence, our results demonstrate that, in [Alzheimer’s], orexinergic output and function seem to be over-expressed with disease progression and severity, possibly owing to an imbalance in the neurotransmitter networks regulating the wake-sleep cycle toward the orexinergic system promoting wakefulness.”

The physiologic interplay isn’t completely understood, said Dr. Ligouri of the University of Rome Tor Vergata. But since orexinergic neurons interact with cholinergic pathways, sleep impairment might be related to the damaged cholinergic feedback characteristic of Alzheimer’s, the researchers noted (JAMA Neurol. 2014 Oct. 13 [doi:10.1001/jamaneurol.2014.2510]).

The case-control study comprised 48 drug-naive Alzheimer’s patients (21 mild and 27 moderate-severe) and 29 matched controls. All patients underwent polysomnography and lumbar puncture for CSF tau, beta amyloid peptide 1-42, and orexin.

Compared with controls, patients showed the characteristic increased CSF tau and decreased amyloid levels. Patients with moderate to severe Alzheimer’s had significantly higher CSF orexin levels than did controls (154.36 pg/mL vs. 131.03 pg/mL), but the difference between controls and patients with mild disease was not significant, Dr. Ligouri and associates reported.

The patients with moderate to severe disease also displayed earlier bedtimes, reduced sleep efficiency and REM sleep, and increased wakefulness after sleep onset, compared with controls and patients with mild disease, they said.

Orexin and both total and phosphorylated tau positively correlated in those with moderate to severe disease, although beta-amyloid peptide 1-42 showed no such pattern. No such relationship was noted in patients with mild disease or in controls.

Although there were no direct connections between cognitive scores and orexin levels, increased orexin correlated directly with increased sleep onset latency and wakefulness after sleep onset, and with decreased sleep efficiency and REM time. Increased t-tau correlated with increased time in stage 1 of non-REM sleep, but decreased time in stage 3 of non-REM sleep.

Recent studies suggest that sleep plays an important role in clearing the brain of beta amyloid 1-42 fragments before they aggregate into neurotoxic plaques. “Therefore, the sleep impairment in Alzheimer’s disease could be considered an additional detrimental factor for pathologic amyloid findings, thus worsening the neurodegeneration,” Dr. Liguori and coauthors wrote.

None of the investigators had any financial disclosures.

[email protected]

On Twitter @alz_gal

An overabundance of orexin ­– a protein that helps regulate normal sleep and waking – appears linked to rising tau levels in Alzheimer’s disease, according to findings published online Oct. 13 in JAMA Neurology.

Orexin levels showed a tight positive correlation with tau – a protein that correlates positively with cognitive decline in the disease – in the cerebrospinal fluid of Alzheimer’s patients, according to a study by Dr. Claudio Liguori and associates. In addition, the sleep dysregulation characteristic of Alzheimer’s patients is tightly correlated with both increased orexin and tau levels.

“Our study has shown that, in Alzheimer’s disease, increased CSF orexin levels are linked to a parallel sleep deterioration, which appears to be related to cognitive decline,” the authors wrote. “Hence, our results demonstrate that, in [Alzheimer’s], orexinergic output and function seem to be over-expressed with disease progression and severity, possibly owing to an imbalance in the neurotransmitter networks regulating the wake-sleep cycle toward the orexinergic system promoting wakefulness.”

The physiologic interplay isn’t completely understood, said Dr. Ligouri of the University of Rome Tor Vergata. But since orexinergic neurons interact with cholinergic pathways, sleep impairment might be related to the damaged cholinergic feedback characteristic of Alzheimer’s, the researchers noted (JAMA Neurol. 2014 Oct. 13 [doi:10.1001/jamaneurol.2014.2510]).

The case-control study comprised 48 drug-naive Alzheimer’s patients (21 mild and 27 moderate-severe) and 29 matched controls. All patients underwent polysomnography and lumbar puncture for CSF tau, beta amyloid peptide 1-42, and orexin.

Compared with controls, patients showed the characteristic increased CSF tau and decreased amyloid levels. Patients with moderate to severe Alzheimer’s had significantly higher CSF orexin levels than did controls (154.36 pg/mL vs. 131.03 pg/mL), but the difference between controls and patients with mild disease was not significant, Dr. Ligouri and associates reported.

The patients with moderate to severe disease also displayed earlier bedtimes, reduced sleep efficiency and REM sleep, and increased wakefulness after sleep onset, compared with controls and patients with mild disease, they said.

Orexin and both total and phosphorylated tau positively correlated in those with moderate to severe disease, although beta-amyloid peptide 1-42 showed no such pattern. No such relationship was noted in patients with mild disease or in controls.

Although there were no direct connections between cognitive scores and orexin levels, increased orexin correlated directly with increased sleep onset latency and wakefulness after sleep onset, and with decreased sleep efficiency and REM time. Increased t-tau correlated with increased time in stage 1 of non-REM sleep, but decreased time in stage 3 of non-REM sleep.

Recent studies suggest that sleep plays an important role in clearing the brain of beta amyloid 1-42 fragments before they aggregate into neurotoxic plaques. “Therefore, the sleep impairment in Alzheimer’s disease could be considered an additional detrimental factor for pathologic amyloid findings, thus worsening the neurodegeneration,” Dr. Liguori and coauthors wrote.

None of the investigators had any financial disclosures.

[email protected]

On Twitter @alz_gal

An overabundance of orexin ­– a protein that helps regulate normal sleep and waking – appears linked to rising tau levels in Alzheimer’s disease, according to findings published online Oct. 13 in JAMA Neurology.

Orexin levels showed a tight positive correlation with tau – a protein that correlates positively with cognitive decline in the disease – in the cerebrospinal fluid of Alzheimer’s patients, according to a study by Dr. Claudio Liguori and associates. In addition, the sleep dysregulation characteristic of Alzheimer’s patients is tightly correlated with both increased orexin and tau levels.

“Our study has shown that, in Alzheimer’s disease, increased CSF orexin levels are linked to a parallel sleep deterioration, which appears to be related to cognitive decline,” the authors wrote. “Hence, our results demonstrate that, in [Alzheimer’s], orexinergic output and function seem to be over-expressed with disease progression and severity, possibly owing to an imbalance in the neurotransmitter networks regulating the wake-sleep cycle toward the orexinergic system promoting wakefulness.”

The physiologic interplay isn’t completely understood, said Dr. Ligouri of the University of Rome Tor Vergata. But since orexinergic neurons interact with cholinergic pathways, sleep impairment might be related to the damaged cholinergic feedback characteristic of Alzheimer’s, the researchers noted (JAMA Neurol. 2014 Oct. 13 [doi:10.1001/jamaneurol.2014.2510]).

The case-control study comprised 48 drug-naive Alzheimer’s patients (21 mild and 27 moderate-severe) and 29 matched controls. All patients underwent polysomnography and lumbar puncture for CSF tau, beta amyloid peptide 1-42, and orexin.

Compared with controls, patients showed the characteristic increased CSF tau and decreased amyloid levels. Patients with moderate to severe Alzheimer’s had significantly higher CSF orexin levels than did controls (154.36 pg/mL vs. 131.03 pg/mL), but the difference between controls and patients with mild disease was not significant, Dr. Ligouri and associates reported.

The patients with moderate to severe disease also displayed earlier bedtimes, reduced sleep efficiency and REM sleep, and increased wakefulness after sleep onset, compared with controls and patients with mild disease, they said.

Orexin and both total and phosphorylated tau positively correlated in those with moderate to severe disease, although beta-amyloid peptide 1-42 showed no such pattern. No such relationship was noted in patients with mild disease or in controls.

Although there were no direct connections between cognitive scores and orexin levels, increased orexin correlated directly with increased sleep onset latency and wakefulness after sleep onset, and with decreased sleep efficiency and REM time. Increased t-tau correlated with increased time in stage 1 of non-REM sleep, but decreased time in stage 3 of non-REM sleep.

Recent studies suggest that sleep plays an important role in clearing the brain of beta amyloid 1-42 fragments before they aggregate into neurotoxic plaques. “Therefore, the sleep impairment in Alzheimer’s disease could be considered an additional detrimental factor for pathologic amyloid findings, thus worsening the neurodegeneration,” Dr. Liguori and coauthors wrote.

None of the investigators had any financial disclosures.

[email protected]

On Twitter @alz_gal

BALTIMORE – A hand-held vagal nerve stimulator significantly decreased the frequency of cluster headache attacks per week, compared with the usual standard of care, based on data from a randomized trial of 97 patients.

The noninvasive device, called gammaCore, was associated with seven fewer weekly headache attacks when used in conjunction with sumatriptan and oxygen – significantly better than the one-attack reduction achieved with standard therapy alone, Eric Liebler reported at the annual meeting of the American Neurological Association.

Michele G. Sullivan/Frontline Medical Media

“In this 2-month study, the external vagal nerve stimulator effected a significant improvement in the reduced rate of attacks and the 50% responder rate, with very few device-related adverse events,” said Mr. Liebler, vice president of scientific, medical, and governmental affairs for electroCore, the New Jersey–based company that manufactures the device.

The gammaCore device is used in Europe for the treatment of primary headache disorders. The device, which transmits mild current to the vagal nerve, is a small, hand-held unit that the patient uses twice each day. It’s thought to work by suppressing excessive extracellular glutamate in the trigeminal nucleus caudalis – a phenomenon that seems to stimulate trigeminal sensitization in migraine.

Patients are instructed to activate the device over the carotid pulse point on the neck for about 90 seconds. A conductive gel helps transmit mild current to the vagal nerve.

The 2-month Prevention and Acute Treatment of Chronic Cluster Headache (PREVA) trial examined the use of gammaCore in treating cluster headaches. The cohort included 97 patients who were randomized to the device plus the standard therapy or to standard therapy alone. At the end of the first month, patients in the combination group continued for another month while those in the standard-care group were offered a month of combination therapy.

The primary endpoint was the reduction in cluster headache attacks per week during the last 2 weeks of each month. Secondary endpoints included the number of patients with at least a 50% reduction in the number of cluster headaches per month and changes in the use of acute medications. The study also examined device safety and tolerability. Attack pain and duration are being assessed in a separate study, Mr. Liebler noted.

The mean age of the patients was approximately 44 years. Most were using medications (90%) and oxygen (68%), and the mean duration of their cluster headaches at baseline was about 28 minutes when they used these treatments. Without medications and oxygen, the headaches lasted a mean of 100 minutes. These patients expereinced about 70 cluster attacks in the month before randomization.

Patients in the combination group experienced a significant reduction in the number of cluster headache attacks per week (from 16 to 9 attacks). The change among those taking standard therapy alone was not significant (from 16 to 15 attacks).

In the intent-to-treat population, 38% of the combination group achieved at least a 50% decrease in headache days, compared with 8% of the standard-therapy group – a significant difference. In the full analysis, the device response numbers were better – 46% vs. 8%. The per protocol analysis included only those patients who used the device as instructed at least 80% of the time. The 50% responder rate in that group was 52% vs. 9% of the standard-treatment group.

Among the combination-therapy group, the use of rescue medications decreased significantly: from 7 to 3 times per month for subcutaneous sumatriptan and from 16 to 6 times per month for oxygen. Rescue-medication use was virtually unchanged among those who used standard therapy only.

Safety and tolerability was good. Most of the patients using the device (44) did experience an adverse event. Device-related events included dizziness (3), oropharyngeal pain (3), and neck pain (3). These events probably occurred because electrical current tends to spread to neck muscles, Mr. Liebler said. The sensations were transitory, he added.

Dr. Peter Goadsby, director of the headache center at the University of California, San Francisco, said that he has been “surprised” at the positive results seen in European patients. “These are medication-refractory patients, and about half of them had significant reductions in the frequency and severity of their cluster headaches, with a simultaneous decrease in the need for oxygen and steroids. They also seemed to feel that their steroids worked more efficiently,” when used in conjunction with the device, he said.

The study was sponsored by electroCore, and Mr. Liebler is a full-time employee of electroCore. Dr. Goadsby has served as a consultant for a number of pharmaceutical companies.

[email protected]

On Twitter @alz_gal

BALTIMORE – A hand-held vagal nerve stimulator significantly decreased the frequency of cluster headache attacks per week, compared with the usual standard of care, based on data from a randomized trial of 97 patients.

The noninvasive device, called gammaCore, was associated with seven fewer weekly headache attacks when used in conjunction with sumatriptan and oxygen – significantly better than the one-attack reduction achieved with standard therapy alone, Eric Liebler reported at the annual meeting of the American Neurological Association.

Michele G. Sullivan/Frontline Medical Media

“In this 2-month study, the external vagal nerve stimulator effected a significant improvement in the reduced rate of attacks and the 50% responder rate, with very few device-related adverse events,” said Mr. Liebler, vice president of scientific, medical, and governmental affairs for electroCore, the New Jersey–based company that manufactures the device.

The gammaCore device is used in Europe for the treatment of primary headache disorders. The device, which transmits mild current to the vagal nerve, is a small, hand-held unit that the patient uses twice each day. It’s thought to work by suppressing excessive extracellular glutamate in the trigeminal nucleus caudalis – a phenomenon that seems to stimulate trigeminal sensitization in migraine.

Patients are instructed to activate the device over the carotid pulse point on the neck for about 90 seconds. A conductive gel helps transmit mild current to the vagal nerve.

The 2-month Prevention and Acute Treatment of Chronic Cluster Headache (PREVA) trial examined the use of gammaCore in treating cluster headaches. The cohort included 97 patients who were randomized to the device plus the standard therapy or to standard therapy alone. At the end of the first month, patients in the combination group continued for another month while those in the standard-care group were offered a month of combination therapy.

The primary endpoint was the reduction in cluster headache attacks per week during the last 2 weeks of each month. Secondary endpoints included the number of patients with at least a 50% reduction in the number of cluster headaches per month and changes in the use of acute medications. The study also examined device safety and tolerability. Attack pain and duration are being assessed in a separate study, Mr. Liebler noted.

The mean age of the patients was approximately 44 years. Most were using medications (90%) and oxygen (68%), and the mean duration of their cluster headaches at baseline was about 28 minutes when they used these treatments. Without medications and oxygen, the headaches lasted a mean of 100 minutes. These patients expereinced about 70 cluster attacks in the month before randomization.

Patients in the combination group experienced a significant reduction in the number of cluster headache attacks per week (from 16 to 9 attacks). The change among those taking standard therapy alone was not significant (from 16 to 15 attacks).

In the intent-to-treat population, 38% of the combination group achieved at least a 50% decrease in headache days, compared with 8% of the standard-therapy group – a significant difference. In the full analysis, the device response numbers were better – 46% vs. 8%. The per protocol analysis included only those patients who used the device as instructed at least 80% of the time. The 50% responder rate in that group was 52% vs. 9% of the standard-treatment group.

Among the combination-therapy group, the use of rescue medications decreased significantly: from 7 to 3 times per month for subcutaneous sumatriptan and from 16 to 6 times per month for oxygen. Rescue-medication use was virtually unchanged among those who used standard therapy only.

Safety and tolerability was good. Most of the patients using the device (44) did experience an adverse event. Device-related events included dizziness (3), oropharyngeal pain (3), and neck pain (3). These events probably occurred because electrical current tends to spread to neck muscles, Mr. Liebler said. The sensations were transitory, he added.

Dr. Peter Goadsby, director of the headache center at the University of California, San Francisco, said that he has been “surprised” at the positive results seen in European patients. “These are medication-refractory patients, and about half of them had significant reductions in the frequency and severity of their cluster headaches, with a simultaneous decrease in the need for oxygen and steroids. They also seemed to feel that their steroids worked more efficiently,” when used in conjunction with the device, he said.

The study was sponsored by electroCore, and Mr. Liebler is a full-time employee of electroCore. Dr. Goadsby has served as a consultant for a number of pharmaceutical companies.

[email protected]

On Twitter @alz_gal

BALTIMORE – A hand-held vagal nerve stimulator significantly decreased the frequency of cluster headache attacks per week, compared with the usual standard of care, based on data from a randomized trial of 97 patients.

The noninvasive device, called gammaCore, was associated with seven fewer weekly headache attacks when used in conjunction with sumatriptan and oxygen – significantly better than the one-attack reduction achieved with standard therapy alone, Eric Liebler reported at the annual meeting of the American Neurological Association.

Michele G. Sullivan/Frontline Medical Media

“In this 2-month study, the external vagal nerve stimulator effected a significant improvement in the reduced rate of attacks and the 50% responder rate, with very few device-related adverse events,” said Mr. Liebler, vice president of scientific, medical, and governmental affairs for electroCore, the New Jersey–based company that manufactures the device.

The gammaCore device is used in Europe for the treatment of primary headache disorders. The device, which transmits mild current to the vagal nerve, is a small, hand-held unit that the patient uses twice each day. It’s thought to work by suppressing excessive extracellular glutamate in the trigeminal nucleus caudalis – a phenomenon that seems to stimulate trigeminal sensitization in migraine.

Patients are instructed to activate the device over the carotid pulse point on the neck for about 90 seconds. A conductive gel helps transmit mild current to the vagal nerve.

The 2-month Prevention and Acute Treatment of Chronic Cluster Headache (PREVA) trial examined the use of gammaCore in treating cluster headaches. The cohort included 97 patients who were randomized to the device plus the standard therapy or to standard therapy alone. At the end of the first month, patients in the combination group continued for another month while those in the standard-care group were offered a month of combination therapy.

The primary endpoint was the reduction in cluster headache attacks per week during the last 2 weeks of each month. Secondary endpoints included the number of patients with at least a 50% reduction in the number of cluster headaches per month and changes in the use of acute medications. The study also examined device safety and tolerability. Attack pain and duration are being assessed in a separate study, Mr. Liebler noted.

The mean age of the patients was approximately 44 years. Most were using medications (90%) and oxygen (68%), and the mean duration of their cluster headaches at baseline was about 28 minutes when they used these treatments. Without medications and oxygen, the headaches lasted a mean of 100 minutes. These patients expereinced about 70 cluster attacks in the month before randomization.

Patients in the combination group experienced a significant reduction in the number of cluster headache attacks per week (from 16 to 9 attacks). The change among those taking standard therapy alone was not significant (from 16 to 15 attacks).

In the intent-to-treat population, 38% of the combination group achieved at least a 50% decrease in headache days, compared with 8% of the standard-therapy group – a significant difference. In the full analysis, the device response numbers were better – 46% vs. 8%. The per protocol analysis included only those patients who used the device as instructed at least 80% of the time. The 50% responder rate in that group was 52% vs. 9% of the standard-treatment group.

Among the combination-therapy group, the use of rescue medications decreased significantly: from 7 to 3 times per month for subcutaneous sumatriptan and from 16 to 6 times per month for oxygen. Rescue-medication use was virtually unchanged among those who used standard therapy only.

Safety and tolerability was good. Most of the patients using the device (44) did experience an adverse event. Device-related events included dizziness (3), oropharyngeal pain (3), and neck pain (3). These events probably occurred because electrical current tends to spread to neck muscles, Mr. Liebler said. The sensations were transitory, he added.

Dr. Peter Goadsby, director of the headache center at the University of California, San Francisco, said that he has been “surprised” at the positive results seen in European patients. “These are medication-refractory patients, and about half of them had significant reductions in the frequency and severity of their cluster headaches, with a simultaneous decrease in the need for oxygen and steroids. They also seemed to feel that their steroids worked more efficiently,” when used in conjunction with the device, he said.

The study was sponsored by electroCore, and Mr. Liebler is a full-time employee of electroCore. Dr. Goadsby has served as a consultant for a number of pharmaceutical companies.

[email protected]

On Twitter @alz_gal

VIENNA – Most of the increased risk of cancer associated with diabetes appears in the first year or so after diabetes diagnosis, suggesting that it’s mainly attributable to increased medical surveillance.

Three studies presented at the annual meeting of the European Association for the Study of Diabetes came to similar conclusions, which seemed to hold for both genders, for obesity-driven and non–obesity-driven cancers, and for patients with type 1 as well as type 2 diabetes – a new finding, according to Mr. Bendix Carstensen.

His large, population-based study found no overall excess risk of cancers among type 1 diabetes patients, compared with the general population.

“Based on this, we can exclude a major carcinogenic effect of exogenous insulin among those with type 1 diabetes, because if there was such an effect we would see some substantial increases in at least some cancers,” said Mr. Carstensen, an epidemiologist at the Steno Diabetes Center in Gentofte, Denmark.

Cancer and type 1 diabetes

The study examined cancer rates in patients with type 1 diabetes from five countries: Australia, Denmark, Finland, Scotland, and Sweden. Type 1 diabetes was defined as a diabetes diagnosis that occurred before age 30. In general, these registries contained patients who were still younger than 60 years. Despite the very large 4.6 million person-years of follow-up, the databases represent a population that does not exhibit the typical age-related increase in cancer risk – a slight limitation of the study, Mr. Carstensen noted.

The databases identified 9,369 cases of cancer among patients with type 1 diabetes. They were classified by gender, age, date of cancer diagnosis, and cancer rate, compared with that of the country’s entire population stratified by the same variables.

The crude rate of cancers in all the diabetes patients combined was no different from that of the general populations, with a risk ratio of 1.00 for men and 1.04 for women.

When cancers were examined by site and gender, some significant differences did arise between the diabetic and nondiabetic groups. Stomach cancer was 19% more likely in men and 75% more likely in women. The risk of pancreatic cancer was 70% increased in men and 36% in women. The risk of liver cancer was about doubled in each gender, and for kidney cancer, the risk was 29% in men and 42% in women. For women, there was a 53% increase in the risk of endometrial cancer.

In the time-dependent analysis, Mr. Carstensen found that almost all of the cancers diagnoses were made in the first year after diabetes was diagnosed and dropped rapidly thereafter. The extended time curve showed no lasting impact of diabetes on overall cancer incidence.

A more specific analysis looked at the time-dependent rate ratios of prostate and colorectal cancers for men, and breast, endometrial, and colorectal cancers in women. Each curve showed the high rate ratio in the first few years, followed by a drop-off and no lasting impact.

There were also no lasting impacts of diabetes on lung cancer, melanoma, or non-Hodgkins lymphoma in either gender.

“We did see an elevated site-specific cancer pattern in patients with type 1 diabetes, but no overall excess,” he said. “For these patients, the total cancer occurrence is not really different from population rates.”

Detection bias in diabetes and obesity

Another large, population-based study came to a similar conclusion for those with type 2 diabetes. In fact, “Detection bias may be the main cause of the increased cancer incidence among patients with diabetes,” Dr. Kirstin De Bruijn said.

She presented a subanalysis of the ongoing Rotterdam Study. The Rotterdam Study, launched in 1990, is investigating determinants of disease in residents aged 55 years and older. It now comprises about 11,000 subjects. Dr. De Bruijn of Erasmus University, Rotterdam, the Netherlands, investigated the association of cancer and diabetes in 10,181 patients. Of these, 906 had an incident type 2 diabetes diagnosis, and 2,238 had an incident cancer diagnosis during the mean follow-up period of 11 years. She looked at the incidence of breast, prostate, pancreatic, lung, and colorectal cancers.

In the overall analysis, the risk of any cancer was 30% increased in the patients with diabetes. This risk was attenuated, but remained statistically significant, in the fully adjusted model (hazard ratio, 1.2). In a cancer-specific analysis, however, only the risk of pancreatic cancer was significantly elevated (HR, 3.6 in the adjusted model). The risk of prostate cancer was 30% lower than that of the general population, but that was not a significant finding, she added.

She then looked at a time-dependent model that split the follow-up period into epochs according to time since diabetes diagnosis (up to 3 months, 3 months to 5 years, and more than 5 years).

The overall risk of a cancer diagnosis was more than three times higher in the first 3 months. It remained significantly elevated, though less so, in the first 5 years (HR, 1.5), and then fell off.

When the individual cancers were considered, only pancreatic cancer was significantly more common among the diabetes patients, and was almost 29 times more likely to be diagnosed in the first 3 months. However, Dr. De Bruijn noted, it’s tough to tease out that particular relationship, since the obesity that accompanies type 2 diabetes can also drive the development of pancreatic cancer.

Ellena Badrick, a researcher at the University of Manchester (England), also examined the idea of detection bias in a population database, exploring the time-dependent relationships for obesity-related cancers, compared with those not related to obesity.

She found 10,315 patients who were diagnosed with type 2 diabetes from 1995 to 2010. These were compared with 20,630 controls chosen from the same period. Obesity-related cancers were considered to be breast, endometrial, ovarian, renal, esophageal, pancreatic, and gallbladder.

There were 1,349 cancers among the patients with diabetes, of which 323 were related to obesity. Among the controls, there were 3,218 cancers, of which 634 were obesity related.

She also split her follow-up period into epochs since diabetes diagnosis: up to 6 months, 6-12 months, 12-24 months, 24 months-5 years, and beyond. Cancer incidence was reported as cases per 1,000 person/epoch.

There was a much higher detection rate overall in the first 6 months after diagnosis – more than 100 cases per 1,000 person-epoch. After 6 months, this dropped to less than 20 cases per 1,000 person-epoch. The incidence did increase over the follow-up period, but she said that reflected the expected age-related pattern.

The same pattern emerged when looking at obesity- vs. non–obesity-related cancers. In the first 6 months, the incidence of obesity-related cancer hovered around 30 per 1,000 person-epoch. By 1 year this had dropped to near zero. For non–obesity-related cancers, the incidence rate was much higher in the first 6 months, at nearly 80 per person/epoch. But this also dropped to near zero by 1 year. Both incidence curves followed the same slow increase as the subjects aged.

Over the entire follow-up, 27% of all the obesity-related cancers and 73% of the non–obesity-related cancers were diagnosed within the first year after a diagnosis of type 2 diabetes.

When cancers diagnosed during the first 2 years were excluded, patients with type 2 diabetes had a 43% increase in the risk of developing an obesity-related cancer during the study. There was no increased risk, however, in developing a cancer not related to obesity.

“This suggests that in patients with type 2 diabetes, cancer risk-reduction strategies should be targeted against obesity-related cancers,” Ms. Badrick said.

Mr. Carstensen is an employee of the Steno Diabetes Center, which is owned by Novo Nordisk. He disclosed that he owns stock in the company. Dr. De Bruijn and Ms. Badrick had no financial disclosures.

VIENNA – Most of the increased risk of cancer associated with diabetes appears in the first year or so after diabetes diagnosis, suggesting that it’s mainly attributable to increased medical surveillance.

Three studies presented at the annual meeting of the European Association for the Study of Diabetes came to similar conclusions, which seemed to hold for both genders, for obesity-driven and non–obesity-driven cancers, and for patients with type 1 as well as type 2 diabetes – a new finding, according to Mr. Bendix Carstensen.

His large, population-based study found no overall excess risk of cancers among type 1 diabetes patients, compared with the general population.

“Based on this, we can exclude a major carcinogenic effect of exogenous insulin among those with type 1 diabetes, because if there was such an effect we would see some substantial increases in at least some cancers,” said Mr. Carstensen, an epidemiologist at the Steno Diabetes Center in Gentofte, Denmark.

Cancer and type 1 diabetes

The study examined cancer rates in patients with type 1 diabetes from five countries: Australia, Denmark, Finland, Scotland, and Sweden. Type 1 diabetes was defined as a diabetes diagnosis that occurred before age 30. In general, these registries contained patients who were still younger than 60 years. Despite the very large 4.6 million person-years of follow-up, the databases represent a population that does not exhibit the typical age-related increase in cancer risk – a slight limitation of the study, Mr. Carstensen noted.

The databases identified 9,369 cases of cancer among patients with type 1 diabetes. They were classified by gender, age, date of cancer diagnosis, and cancer rate, compared with that of the country’s entire population stratified by the same variables.

The crude rate of cancers in all the diabetes patients combined was no different from that of the general populations, with a risk ratio of 1.00 for men and 1.04 for women.

When cancers were examined by site and gender, some significant differences did arise between the diabetic and nondiabetic groups. Stomach cancer was 19% more likely in men and 75% more likely in women. The risk of pancreatic cancer was 70% increased in men and 36% in women. The risk of liver cancer was about doubled in each gender, and for kidney cancer, the risk was 29% in men and 42% in women. For women, there was a 53% increase in the risk of endometrial cancer.

In the time-dependent analysis, Mr. Carstensen found that almost all of the cancers diagnoses were made in the first year after diabetes was diagnosed and dropped rapidly thereafter. The extended time curve showed no lasting impact of diabetes on overall cancer incidence.

A more specific analysis looked at the time-dependent rate ratios of prostate and colorectal cancers for men, and breast, endometrial, and colorectal cancers in women. Each curve showed the high rate ratio in the first few years, followed by a drop-off and no lasting impact.

There were also no lasting impacts of diabetes on lung cancer, melanoma, or non-Hodgkins lymphoma in either gender.

“We did see an elevated site-specific cancer pattern in patients with type 1 diabetes, but no overall excess,” he said. “For these patients, the total cancer occurrence is not really different from population rates.”

Detection bias in diabetes and obesity

Another large, population-based study came to a similar conclusion for those with type 2 diabetes. In fact, “Detection bias may be the main cause of the increased cancer incidence among patients with diabetes,” Dr. Kirstin De Bruijn said.

She presented a subanalysis of the ongoing Rotterdam Study. The Rotterdam Study, launched in 1990, is investigating determinants of disease in residents aged 55 years and older. It now comprises about 11,000 subjects. Dr. De Bruijn of Erasmus University, Rotterdam, the Netherlands, investigated the association of cancer and diabetes in 10,181 patients. Of these, 906 had an incident type 2 diabetes diagnosis, and 2,238 had an incident cancer diagnosis during the mean follow-up period of 11 years. She looked at the incidence of breast, prostate, pancreatic, lung, and colorectal cancers.

In the overall analysis, the risk of any cancer was 30% increased in the patients with diabetes. This risk was attenuated, but remained statistically significant, in the fully adjusted model (hazard ratio, 1.2). In a cancer-specific analysis, however, only the risk of pancreatic cancer was significantly elevated (HR, 3.6 in the adjusted model). The risk of prostate cancer was 30% lower than that of the general population, but that was not a significant finding, she added.

She then looked at a time-dependent model that split the follow-up period into epochs according to time since diabetes diagnosis (up to 3 months, 3 months to 5 years, and more than 5 years).

The overall risk of a cancer diagnosis was more than three times higher in the first 3 months. It remained significantly elevated, though less so, in the first 5 years (HR, 1.5), and then fell off.

When the individual cancers were considered, only pancreatic cancer was significantly more common among the diabetes patients, and was almost 29 times more likely to be diagnosed in the first 3 months. However, Dr. De Bruijn noted, it’s tough to tease out that particular relationship, since the obesity that accompanies type 2 diabetes can also drive the development of pancreatic cancer.

Ellena Badrick, a researcher at the University of Manchester (England), also examined the idea of detection bias in a population database, exploring the time-dependent relationships for obesity-related cancers, compared with those not related to obesity.

She found 10,315 patients who were diagnosed with type 2 diabetes from 1995 to 2010. These were compared with 20,630 controls chosen from the same period. Obesity-related cancers were considered to be breast, endometrial, ovarian, renal, esophageal, pancreatic, and gallbladder.

There were 1,349 cancers among the patients with diabetes, of which 323 were related to obesity. Among the controls, there were 3,218 cancers, of which 634 were obesity related.

She also split her follow-up period into epochs since diabetes diagnosis: up to 6 months, 6-12 months, 12-24 months, 24 months-5 years, and beyond. Cancer incidence was reported as cases per 1,000 person/epoch.

There was a much higher detection rate overall in the first 6 months after diagnosis – more than 100 cases per 1,000 person-epoch. After 6 months, this dropped to less than 20 cases per 1,000 person-epoch. The incidence did increase over the follow-up period, but she said that reflected the expected age-related pattern.

The same pattern emerged when looking at obesity- vs. non–obesity-related cancers. In the first 6 months, the incidence of obesity-related cancer hovered around 30 per 1,000 person-epoch. By 1 year this had dropped to near zero. For non–obesity-related cancers, the incidence rate was much higher in the first 6 months, at nearly 80 per person/epoch. But this also dropped to near zero by 1 year. Both incidence curves followed the same slow increase as the subjects aged.

Over the entire follow-up, 27% of all the obesity-related cancers and 73% of the non–obesity-related cancers were diagnosed within the first year after a diagnosis of type 2 diabetes.

When cancers diagnosed during the first 2 years were excluded, patients with type 2 diabetes had a 43% increase in the risk of developing an obesity-related cancer during the study. There was no increased risk, however, in developing a cancer not related to obesity.

“This suggests that in patients with type 2 diabetes, cancer risk-reduction strategies should be targeted against obesity-related cancers,” Ms. Badrick said.

Mr. Carstensen is an employee of the Steno Diabetes Center, which is owned by Novo Nordisk. He disclosed that he owns stock in the company. Dr. De Bruijn and Ms. Badrick had no financial disclosures.

VIENNA – Most of the increased risk of cancer associated with diabetes appears in the first year or so after diabetes diagnosis, suggesting that it’s mainly attributable to increased medical surveillance.

Three studies presented at the annual meeting of the European Association for the Study of Diabetes came to similar conclusions, which seemed to hold for both genders, for obesity-driven and non–obesity-driven cancers, and for patients with type 1 as well as type 2 diabetes – a new finding, according to Mr. Bendix Carstensen.

His large, population-based study found no overall excess risk of cancers among type 1 diabetes patients, compared with the general population.

“Based on this, we can exclude a major carcinogenic effect of exogenous insulin among those with type 1 diabetes, because if there was such an effect we would see some substantial increases in at least some cancers,” said Mr. Carstensen, an epidemiologist at the Steno Diabetes Center in Gentofte, Denmark.

Cancer and type 1 diabetes

The study examined cancer rates in patients with type 1 diabetes from five countries: Australia, Denmark, Finland, Scotland, and Sweden. Type 1 diabetes was defined as a diabetes diagnosis that occurred before age 30. In general, these registries contained patients who were still younger than 60 years. Despite the very large 4.6 million person-years of follow-up, the databases represent a population that does not exhibit the typical age-related increase in cancer risk – a slight limitation of the study, Mr. Carstensen noted.

The databases identified 9,369 cases of cancer among patients with type 1 diabetes. They were classified by gender, age, date of cancer diagnosis, and cancer rate, compared with that of the country’s entire population stratified by the same variables.

The crude rate of cancers in all the diabetes patients combined was no different from that of the general populations, with a risk ratio of 1.00 for men and 1.04 for women.

When cancers were examined by site and gender, some significant differences did arise between the diabetic and nondiabetic groups. Stomach cancer was 19% more likely in men and 75% more likely in women. The risk of pancreatic cancer was 70% increased in men and 36% in women. The risk of liver cancer was about doubled in each gender, and for kidney cancer, the risk was 29% in men and 42% in women. For women, there was a 53% increase in the risk of endometrial cancer.

In the time-dependent analysis, Mr. Carstensen found that almost all of the cancers diagnoses were made in the first year after diabetes was diagnosed and dropped rapidly thereafter. The extended time curve showed no lasting impact of diabetes on overall cancer incidence.

A more specific analysis looked at the time-dependent rate ratios of prostate and colorectal cancers for men, and breast, endometrial, and colorectal cancers in women. Each curve showed the high rate ratio in the first few years, followed by a drop-off and no lasting impact.

There were also no lasting impacts of diabetes on lung cancer, melanoma, or non-Hodgkins lymphoma in either gender.

“We did see an elevated site-specific cancer pattern in patients with type 1 diabetes, but no overall excess,” he said. “For these patients, the total cancer occurrence is not really different from population rates.”

Detection bias in diabetes and obesity

Another large, population-based study came to a similar conclusion for those with type 2 diabetes. In fact, “Detection bias may be the main cause of the increased cancer incidence among patients with diabetes,” Dr. Kirstin De Bruijn said.

She presented a subanalysis of the ongoing Rotterdam Study. The Rotterdam Study, launched in 1990, is investigating determinants of disease in residents aged 55 years and older. It now comprises about 11,000 subjects. Dr. De Bruijn of Erasmus University, Rotterdam, the Netherlands, investigated the association of cancer and diabetes in 10,181 patients. Of these, 906 had an incident type 2 diabetes diagnosis, and 2,238 had an incident cancer diagnosis during the mean follow-up period of 11 years. She looked at the incidence of breast, prostate, pancreatic, lung, and colorectal cancers.

In the overall analysis, the risk of any cancer was 30% increased in the patients with diabetes. This risk was attenuated, but remained statistically significant, in the fully adjusted model (hazard ratio, 1.2). In a cancer-specific analysis, however, only the risk of pancreatic cancer was significantly elevated (HR, 3.6 in the adjusted model). The risk of prostate cancer was 30% lower than that of the general population, but that was not a significant finding, she added.

She then looked at a time-dependent model that split the follow-up period into epochs according to time since diabetes diagnosis (up to 3 months, 3 months to 5 years, and more than 5 years).

The overall risk of a cancer diagnosis was more than three times higher in the first 3 months. It remained significantly elevated, though less so, in the first 5 years (HR, 1.5), and then fell off.

When the individual cancers were considered, only pancreatic cancer was significantly more common among the diabetes patients, and was almost 29 times more likely to be diagnosed in the first 3 months. However, Dr. De Bruijn noted, it’s tough to tease out that particular relationship, since the obesity that accompanies type 2 diabetes can also drive the development of pancreatic cancer.

Ellena Badrick, a researcher at the University of Manchester (England), also examined the idea of detection bias in a population database, exploring the time-dependent relationships for obesity-related cancers, compared with those not related to obesity.

She found 10,315 patients who were diagnosed with type 2 diabetes from 1995 to 2010. These were compared with 20,630 controls chosen from the same period. Obesity-related cancers were considered to be breast, endometrial, ovarian, renal, esophageal, pancreatic, and gallbladder.

There were 1,349 cancers among the patients with diabetes, of which 323 were related to obesity. Among the controls, there were 3,218 cancers, of which 634 were obesity related.

She also split her follow-up period into epochs since diabetes diagnosis: up to 6 months, 6-12 months, 12-24 months, 24 months-5 years, and beyond. Cancer incidence was reported as cases per 1,000 person/epoch.

There was a much higher detection rate overall in the first 6 months after diagnosis – more than 100 cases per 1,000 person-epoch. After 6 months, this dropped to less than 20 cases per 1,000 person-epoch. The incidence did increase over the follow-up period, but she said that reflected the expected age-related pattern.

The same pattern emerged when looking at obesity- vs. non–obesity-related cancers. In the first 6 months, the incidence of obesity-related cancer hovered around 30 per 1,000 person-epoch. By 1 year this had dropped to near zero. For non–obesity-related cancers, the incidence rate was much higher in the first 6 months, at nearly 80 per person/epoch. But this also dropped to near zero by 1 year. Both incidence curves followed the same slow increase as the subjects aged.

Over the entire follow-up, 27% of all the obesity-related cancers and 73% of the non–obesity-related cancers were diagnosed within the first year after a diagnosis of type 2 diabetes.

When cancers diagnosed during the first 2 years were excluded, patients with type 2 diabetes had a 43% increase in the risk of developing an obesity-related cancer during the study. There was no increased risk, however, in developing a cancer not related to obesity.

“This suggests that in patients with type 2 diabetes, cancer risk-reduction strategies should be targeted against obesity-related cancers,” Ms. Badrick said.

Mr. Carstensen is an employee of the Steno Diabetes Center, which is owned by Novo Nordisk. He disclosed that he owns stock in the company. Dr. De Bruijn and Ms. Badrick had no financial disclosures.

VIENNA – Most of the increased risk of cancer associated with diabetes appears in the first year or so after diabetes diagnosis, suggesting that it’s mainly attributable to increased medical surveillance.

Three studies presented at the annual meeting of the European Association for the Study of Diabetes came to similar conclusions, which seemed to hold for both genders, for obesity-driven and non–obesity-driven cancers, and for patients with type 1 as well as type 2 diabetes – a new finding, according to Mr. Bendix Carstensen.

His large, population-based study found no overall excess risk of cancers among type 1 diabetes patients, compared with the general population.

“Based on this, we can exclude a major carcinogenic effect of exogenous insulin among those with type 1 diabetes, because if there was such an effect we would see some substantial increases in at least some cancers,” said Mr. Carstensen, an epidemiologist at the Steno Diabetes Center in Gentofte, Denmark.

Cancer and type 1 diabetes

The study examined cancer rates in patients with type 1 diabetes from five countries: Australia, Denmark, Finland, Scotland, and Sweden. Type 1 diabetes was defined as a diabetes diagnosis that occurred before age 30. In general, these registries contained patients who were still younger than 60 years. Despite the very large 4.6 million person-years of follow-up, the databases represent a population that does not exhibit the typical age-related increase in cancer risk – a slight limitation of the study, Mr. Carstensen noted.

The databases identified 9,369 cases of cancer among patients with type 1 diabetes. They were classified by gender, age, date of cancer diagnosis, and cancer rate, compared with that of the country’s entire population stratified by the same variables.

The crude rate of cancers in all the diabetes patients combined was no different from that of the general populations, with a risk ratio of 1.00 for men and 1.04 for women.

When cancers were examined by site and gender, some significant differences did arise between the diabetic and nondiabetic groups. Stomach cancer was 19% more likely in men and 75% more likely in women. The risk of pancreatic cancer was 70% increased in men and 36% in women. The risk of liver cancer was about doubled in each gender, and for kidney cancer, the risk was 29% in men and 42% in women. For women, there was a 53% increase in the risk of endometrial cancer.

In the time-dependent analysis, Mr. Carstensen found that almost all of the cancers diagnoses were made in the first year after diabetes was diagnosed and dropped rapidly thereafter. The extended time curve showed no lasting impact of diabetes on overall cancer incidence.

A more specific analysis looked at the time-dependent rate ratios of prostate and colorectal cancers for men, and breast, endometrial, and colorectal cancers in women. Each curve showed the high rate ratio in the first few years, followed by a drop-off and no lasting impact.

There were also no lasting impacts of diabetes on lung cancer, melanoma, or non-Hodgkins lymphoma in either gender.

“We did see an elevated site-specific cancer pattern in patients with type 1 diabetes, but no overall excess,” he said. “For these patients, the total cancer occurrence is not really different from population rates.”

Detection bias in diabetes and obesity

Another large, population-based study came to a similar conclusion for those with type 2 diabetes. In fact, “Detection bias may be the main cause of the increased cancer incidence among patients with diabetes,” Dr. Kirstin De Bruijn said.

She presented a subanalysis of the ongoing Rotterdam Study. The Rotterdam Study, launched in 1990, is investigating determinants of disease in residents aged 55 years and older. It now comprises about 11,000 subjects. Dr. De Bruijn of Erasmus University, Rotterdam, the Netherlands, investigated the association of cancer and diabetes in 10,181 patients. Of these, 906 had an incident type 2 diabetes diagnosis, and 2,238 had an incident cancer diagnosis during the mean follow-up period of 11 years. She looked at the incidence of breast, prostate, pancreatic, lung, and colorectal cancers.

In the overall analysis, the risk of any cancer was 30% increased in the patients with diabetes. This risk was attenuated, but remained statistically significant, in the fully adjusted model (hazard ratio, 1.2). In a cancer-specific analysis, however, only the risk of pancreatic cancer was significantly elevated (HR, 3.6 in the adjusted model). The risk of prostate cancer was 30% lower than that of the general population, but that was not a significant finding, she added.

She then looked at a time-dependent model that split the follow-up period into epochs according to time since diabetes diagnosis (up to 3 months, 3 months to 5 years, and more than 5 years).

The overall risk of a cancer diagnosis was more than three times higher in the first 3 months. It remained significantly elevated, though less so, in the first 5 years (HR, 1.5), and then fell off.

When the individual cancers were considered, only pancreatic cancer was significantly more common among the diabetes patients, and was almost 29 times more likely to be diagnosed in the first 3 months. However, Dr. De Bruijn noted, it’s tough to tease out that particular relationship, since the obesity that accompanies type 2 diabetes can also drive the development of pancreatic cancer.

Ellena Badrick, a researcher at the University of Manchester (England), also examined the idea of detection bias in a population database, exploring the time-dependent relationships for obesity-related cancers, compared with those not related to obesity.

She found 10,315 patients who were diagnosed with type 2 diabetes from 1995 to 2010. These were compared with 20,630 controls chosen from the same period. Obesity-related cancers were considered to be breast, endometrial, ovarian, renal, esophageal, pancreatic, and gallbladder.

There were 1,349 cancers among the patients with diabetes, of which 323 were related to obesity. Among the controls, there were 3,218 cancers, of which 634 were obesity related.

She also split her follow-up period into epochs since diabetes diagnosis: up to 6 months, 6-12 months, 12-24 months, 24 months-5 years, and beyond. Cancer incidence was reported as cases per 1,000 person/epoch.

There was a much higher detection rate overall in the first 6 months after diagnosis – more than 100 cases per 1,000 person-epoch. After 6 months, this dropped to less than 20 cases per 1,000 person-epoch. The incidence did increase over the follow-up period, but she said that reflected the expected age-related pattern.

The same pattern emerged when looking at obesity- vs. non–obesity-related cancers. In the first 6 months, the incidence of obesity-related cancer hovered around 30 per 1,000 person-epoch. By 1 year this had dropped to near zero. For non–obesity-related cancers, the incidence rate was much higher in the first 6 months, at nearly 80 per person/epoch. But this also dropped to near zero by 1 year. Both incidence curves followed the same slow increase as the subjects aged.

Over the entire follow-up, 27% of all the obesity-related cancers and 73% of the non–obesity-related cancers were diagnosed within the first year after a diagnosis of type 2 diabetes.

When cancers diagnosed during the first 2 years were excluded, patients with type 2 diabetes had a 43% increase in the risk of developing an obesity-related cancer during the study. There was no increased risk, however, in developing a cancer not related to obesity.

“This suggests that in patients with type 2 diabetes, cancer risk-reduction strategies should be targeted against obesity-related cancers,” Ms. Badrick said.

Mr. Carstensen is an employee of the Steno Diabetes Center, which is owned by Novo Nordisk. He disclosed that he owns stock in the company. Dr. De Bruijn and Ms. Badrick had no financial disclosures.

[email protected]

On Twitter @alz_gal

VIENNA – Most of the increased risk of cancer associated with diabetes appears in the first year or so after diabetes diagnosis, suggesting that it’s mainly attributable to increased medical surveillance.

Three studies presented at the annual meeting of the European Association for the Study of Diabetes came to similar conclusions, which seemed to hold for both genders, for obesity-driven and non–obesity-driven cancers, and for patients with type 1 as well as type 2 diabetes – a new finding, according to Mr. Bendix Carstensen.

His large, population-based study found no overall excess risk of cancers among type 1 diabetes patients, compared with the general population.

“Based on this, we can exclude a major carcinogenic effect of exogenous insulin among those with type 1 diabetes, because if there was such an effect we would see some substantial increases in at least some cancers,” said Mr. Carstensen, an epidemiologist at the Steno Diabetes Center in Gentofte, Denmark.

Cancer and type 1 diabetes

The study examined cancer rates in patients with type 1 diabetes from five countries: Australia, Denmark, Finland, Scotland, and Sweden. Type 1 diabetes was defined as a diabetes diagnosis that occurred before age 30. In general, these registries contained patients who were still younger than 60 years. Despite the very large 4.6 million person-years of follow-up, the databases represent a population that does not exhibit the typical age-related increase in cancer risk – a slight limitation of the study, Mr. Carstensen noted.

The databases identified 9,369 cases of cancer among patients with type 1 diabetes. They were classified by gender, age, date of cancer diagnosis, and cancer rate, compared with that of the country’s entire population stratified by the same variables.

The crude rate of cancers in all the diabetes patients combined was no different from that of the general populations, with a risk ratio of 1.00 for men and 1.04 for women.

When cancers were examined by site and gender, some significant differences did arise between the diabetic and nondiabetic groups. Stomach cancer was 19% more likely in men and 75% more likely in women. The risk of pancreatic cancer was 70% increased in men and 36% in women. The risk of liver cancer was about doubled in each gender, and for kidney cancer, the risk was 29% in men and 42% in women. For women, there was a 53% increase in the risk of endometrial cancer.

In the time-dependent analysis, Mr. Carstensen found that almost all of the cancers diagnoses were made in the first year after diabetes was diagnosed and dropped rapidly thereafter. The extended time curve showed no lasting impact of diabetes on overall cancer incidence.

A more specific analysis looked at the time-dependent rate ratios of prostate and colorectal cancers for men, and breast, endometrial, and colorectal cancers in women. Each curve showed the high rate ratio in the first few years, followed by a drop-off and no lasting impact.

There were also no lasting impacts of diabetes on lung cancer, melanoma, or non-Hodgkins lymphoma in either gender.

“We did see an elevated site-specific cancer pattern in patients with type 1 diabetes, but no overall excess,” he said. “For these patients, the total cancer occurrence is not really different from population rates.”

Detection bias in diabetes and obesity

Another large, population-based study came to a similar conclusion for those with type 2 diabetes. In fact, “Detection bias may be the main cause of the increased cancer incidence among patients with diabetes,” Dr. Kirstin De Bruijn said.

She presented a subanalysis of the ongoing Rotterdam Study. The Rotterdam Study, launched in 1990, is investigating determinants of disease in residents aged 55 years and older. It now comprises about 11,000 subjects. Dr. De Bruijn of Erasmus University, Rotterdam, the Netherlands, investigated the association of cancer and diabetes in 10,181 patients. Of these, 906 had an incident type 2 diabetes diagnosis, and 2,238 had an incident cancer diagnosis during the mean follow-up period of 11 years. She looked at the incidence of breast, prostate, pancreatic, lung, and colorectal cancers.

In the overall analysis, the risk of any cancer was 30% increased in the patients with diabetes. This risk was attenuated, but remained statistically significant, in the fully adjusted model (hazard ratio, 1.2). In a cancer-specific analysis, however, only the risk of pancreatic cancer was significantly elevated (HR, 3.6 in the adjusted model). The risk of prostate cancer was 30% lower than that of the general population, but that was not a significant finding, she added.

She then looked at a time-dependent model that split the follow-up period into epochs according to time since diabetes diagnosis (up to 3 months, 3 months to 5 years, and more than 5 years).

The overall risk of a cancer diagnosis was more than three times higher in the first 3 months. It remained significantly elevated, though less so, in the first 5 years (HR, 1.5), and then fell off.

When the individual cancers were considered, only pancreatic cancer was significantly more common among the diabetes patients, and was almost 29 times more likely to be diagnosed in the first 3 months. However, Dr. De Bruijn noted, it’s tough to tease out that particular relationship, since the obesity that accompanies type 2 diabetes can also drive the development of pancreatic cancer.

Ellena Badrick, a researcher at the University of Manchester (England), also examined the idea of detection bias in a population database, exploring the time-dependent relationships for obesity-related cancers, compared with those not related to obesity.

She found 10,315 patients who were diagnosed with type 2 diabetes from 1995 to 2010. These were compared with 20,630 controls chosen from the same period. Obesity-related cancers were considered to be breast, endometrial, ovarian, renal, esophageal, pancreatic, and gallbladder.

There were 1,349 cancers among the patients with diabetes, of which 323 were related to obesity. Among the controls, there were 3,218 cancers, of which 634 were obesity related.

She also split her follow-up period into epochs since diabetes diagnosis: up to 6 months, 6-12 months, 12-24 months, 24 months-5 years, and beyond. Cancer incidence was reported as cases per 1,000 person/epoch.

There was a much higher detection rate overall in the first 6 months after diagnosis – more than 100 cases per 1,000 person-epoch. After 6 months, this dropped to less than 20 cases per 1,000 person-epoch. The incidence did increase over the follow-up period, but she said that reflected the expected age-related pattern.

The same pattern emerged when looking at obesity- vs. non–obesity-related cancers. In the first 6 months, the incidence of obesity-related cancer hovered around 30 per 1,000 person-epoch. By 1 year this had dropped to near zero. For non–obesity-related cancers, the incidence rate was much higher in the first 6 months, at nearly 80 per person/epoch. But this also dropped to near zero by 1 year. Both incidence curves followed the same slow increase as the subjects aged.

Over the entire follow-up, 27% of all the obesity-related cancers and 73% of the non–obesity-related cancers were diagnosed within the first year after a diagnosis of type 2 diabetes.

When cancers diagnosed during the first 2 years were excluded, patients with type 2 diabetes had a 43% increase in the risk of developing an obesity-related cancer during the study. There was no increased risk, however, in developing a cancer not related to obesity.

“This suggests that in patients with type 2 diabetes, cancer risk-reduction strategies should be targeted against obesity-related cancers,” Ms. Badrick said.

Mr. Carstensen is an employee of the Steno Diabetes Center, which is owned by Novo Nordisk. He disclosed that he owns stock in the company. Dr. De Bruijn and Ms. Badrick had no financial disclosures.

[email protected]

On Twitter @alz_gal

VIENNA – Most of the increased risk of cancer associated with diabetes appears in the first year or so after diabetes diagnosis, suggesting that it’s mainly attributable to increased medical surveillance.

Three studies presented at the annual meeting of the European Association for the Study of Diabetes came to similar conclusions, which seemed to hold for both genders, for obesity-driven and non–obesity-driven cancers, and for patients with type 1 as well as type 2 diabetes – a new finding, according to Mr. Bendix Carstensen.

His large, population-based study found no overall excess risk of cancers among type 1 diabetes patients, compared with the general population.

“Based on this, we can exclude a major carcinogenic effect of exogenous insulin among those with type 1 diabetes, because if there was such an effect we would see some substantial increases in at least some cancers,” said Mr. Carstensen, an epidemiologist at the Steno Diabetes Center in Gentofte, Denmark.

Cancer and type 1 diabetes

The study examined cancer rates in patients with type 1 diabetes from five countries: Australia, Denmark, Finland, Scotland, and Sweden. Type 1 diabetes was defined as a diabetes diagnosis that occurred before age 30. In general, these registries contained patients who were still younger than 60 years. Despite the very large 4.6 million person-years of follow-up, the databases represent a population that does not exhibit the typical age-related increase in cancer risk – a slight limitation of the study, Mr. Carstensen noted.

The databases identified 9,369 cases of cancer among patients with type 1 diabetes. They were classified by gender, age, date of cancer diagnosis, and cancer rate, compared with that of the country’s entire population stratified by the same variables.

The crude rate of cancers in all the diabetes patients combined was no different from that of the general populations, with a risk ratio of 1.00 for men and 1.04 for women.

When cancers were examined by site and gender, some significant differences did arise between the diabetic and nondiabetic groups. Stomach cancer was 19% more likely in men and 75% more likely in women. The risk of pancreatic cancer was 70% increased in men and 36% in women. The risk of liver cancer was about doubled in each gender, and for kidney cancer, the risk was 29% in men and 42% in women. For women, there was a 53% increase in the risk of endometrial cancer.

In the time-dependent analysis, Mr. Carstensen found that almost all of the cancers diagnoses were made in the first year after diabetes was diagnosed and dropped rapidly thereafter. The extended time curve showed no lasting impact of diabetes on overall cancer incidence.

A more specific analysis looked at the time-dependent rate ratios of prostate and colorectal cancers for men, and breast, endometrial, and colorectal cancers in women. Each curve showed the high rate ratio in the first few years, followed by a drop-off and no lasting impact.

There were also no lasting impacts of diabetes on lung cancer, melanoma, or non-Hodgkins lymphoma in either gender.

“We did see an elevated site-specific cancer pattern in patients with type 1 diabetes, but no overall excess,” he said. “For these patients, the total cancer occurrence is not really different from population rates.”

Detection bias in diabetes and obesity

Another large, population-based study came to a similar conclusion for those with type 2 diabetes. In fact, “Detection bias may be the main cause of the increased cancer incidence among patients with diabetes,” Dr. Kirstin De Bruijn said.

She presented a subanalysis of the ongoing Rotterdam Study. The Rotterdam Study, launched in 1990, is investigating determinants of disease in residents aged 55 years and older. It now comprises about 11,000 subjects. Dr. De Bruijn of Erasmus University, Rotterdam, the Netherlands, investigated the association of cancer and diabetes in 10,181 patients. Of these, 906 had an incident type 2 diabetes diagnosis, and 2,238 had an incident cancer diagnosis during the mean follow-up period of 11 years. She looked at the incidence of breast, prostate, pancreatic, lung, and colorectal cancers.

In the overall analysis, the risk of any cancer was 30% increased in the patients with diabetes. This risk was attenuated, but remained statistically significant, in the fully adjusted model (hazard ratio, 1.2). In a cancer-specific analysis, however, only the risk of pancreatic cancer was significantly elevated (HR, 3.6 in the adjusted model). The risk of prostate cancer was 30% lower than that of the general population, but that was not a significant finding, she added.

She then looked at a time-dependent model that split the follow-up period into epochs according to time since diabetes diagnosis (up to 3 months, 3 months to 5 years, and more than 5 years).

The overall risk of a cancer diagnosis was more than three times higher in the first 3 months. It remained significantly elevated, though less so, in the first 5 years (HR, 1.5), and then fell off.

When the individual cancers were considered, only pancreatic cancer was significantly more common among the diabetes patients, and was almost 29 times more likely to be diagnosed in the first 3 months. However, Dr. De Bruijn noted, it’s tough to tease out that particular relationship, since the obesity that accompanies type 2 diabetes can also drive the development of pancreatic cancer.

Ellena Badrick, a researcher at the University of Manchester (England), also examined the idea of detection bias in a population database, exploring the time-dependent relationships for obesity-related cancers, compared with those not related to obesity.

She found 10,315 patients who were diagnosed with type 2 diabetes from 1995 to 2010. These were compared with 20,630 controls chosen from the same period. Obesity-related cancers were considered to be breast, endometrial, ovarian, renal, esophageal, pancreatic, and gallbladder.

There were 1,349 cancers among the patients with diabetes, of which 323 were related to obesity. Among the controls, there were 3,218 cancers, of which 634 were obesity related.

She also split her follow-up period into epochs since diabetes diagnosis: up to 6 months, 6-12 months, 12-24 months, 24 months-5 years, and beyond. Cancer incidence was reported as cases per 1,000 person/epoch.

There was a much higher detection rate overall in the first 6 months after diagnosis – more than 100 cases per 1,000 person-epoch. After 6 months, this dropped to less than 20 cases per 1,000 person-epoch. The incidence did increase over the follow-up period, but she said that reflected the expected age-related pattern.

The same pattern emerged when looking at obesity- vs. non–obesity-related cancers. In the first 6 months, the incidence of obesity-related cancer hovered around 30 per 1,000 person-epoch. By 1 year this had dropped to near zero. For non–obesity-related cancers, the incidence rate was much higher in the first 6 months, at nearly 80 per person/epoch. But this also dropped to near zero by 1 year. Both incidence curves followed the same slow increase as the subjects aged.

Over the entire follow-up, 27% of all the obesity-related cancers and 73% of the non–obesity-related cancers were diagnosed within the first year after a diagnosis of type 2 diabetes.

When cancers diagnosed during the first 2 years were excluded, patients with type 2 diabetes had a 43% increase in the risk of developing an obesity-related cancer during the study. There was no increased risk, however, in developing a cancer not related to obesity.

“This suggests that in patients with type 2 diabetes, cancer risk-reduction strategies should be targeted against obesity-related cancers,” Ms. Badrick said.

Mr. Carstensen is an employee of the Steno Diabetes Center, which is owned by Novo Nordisk. He disclosed that he owns stock in the company. Dr. De Bruijn and Ms. Badrick had no financial disclosures.

[email protected]

On Twitter @alz_gal

Using a 70-gene signature screening tool for adjuvant chemotherapy decisions cost significantly more than did other methods, including giving chemotherapy to all patients, but did not confer any additional advantages in survival or quality of life, for women with node-negative breast cancer.

The estimated cost per woman with a node-negative tumor was 12,780 euros for using the MammaPrint test – significantly higher than either an online decision tool, or a strategy of systematic chemotherapy for all, according to Julia Bonastre, Ph.D., and her colleagues (J. Clin. Oncol. 2014 October [doi:10.1200/JCO.2013.54.9931]).

©Kativ/iStockphoto

The study compared cost and clinical outcomes among 307 women treated for node-negative breast cancers as part of a MammaPrint validation trial. Chemotherapy choice was guided either by MammaPrint, the Adjuvant! Online program, or a scheme of systematic chemotherapy for every patient.

The mean cost of the 70-gene MammaPrint profile was 12,780 euros; the mean cost of Adjuvant! Online, 10,743 euros; and the mean cost of systematic chemotherapy, 12,123 euros. Over the 10-year follow-up period, there were no differences in life-years or quality-adjusted life-years.

Treatment de-escalation is critical for ensuring high-quality survivorship over the long term, wrote Dr. Bonastre of Gustave Roussy Institute of Oncology, Paris, and her associates. “However, our study shows that the health benefits associated with the use of molecular tests are modest. In addition, the high price of these tests results in poor value for the money, limiting their usefulness in routine practice,” they said.

The study was funded by the French National Cancer Institute, and the authors reported no conflicts of interest.

[email protected]

On Twitter @alz_gal

Using a 70-gene signature screening tool for adjuvant chemotherapy decisions cost significantly more than did other methods, including giving chemotherapy to all patients, but did not confer any additional advantages in survival or quality of life, for women with node-negative breast cancer.

The estimated cost per woman with a node-negative tumor was 12,780 euros for using the MammaPrint test – significantly higher than either an online decision tool, or a strategy of systematic chemotherapy for all, according to Julia Bonastre, Ph.D., and her colleagues (J. Clin. Oncol. 2014 October [doi:10.1200/JCO.2013.54.9931]).

©Kativ/iStockphoto

The study compared cost and clinical outcomes among 307 women treated for node-negative breast cancers as part of a MammaPrint validation trial. Chemotherapy choice was guided either by MammaPrint, the Adjuvant! Online program, or a scheme of systematic chemotherapy for every patient.

The mean cost of the 70-gene MammaPrint profile was 12,780 euros; the mean cost of Adjuvant! Online, 10,743 euros; and the mean cost of systematic chemotherapy, 12,123 euros. Over the 10-year follow-up period, there were no differences in life-years or quality-adjusted life-years.

Treatment de-escalation is critical for ensuring high-quality survivorship over the long term, wrote Dr. Bonastre of Gustave Roussy Institute of Oncology, Paris, and her associates. “However, our study shows that the health benefits associated with the use of molecular tests are modest. In addition, the high price of these tests results in poor value for the money, limiting their usefulness in routine practice,” they said.

The study was funded by the French National Cancer Institute, and the authors reported no conflicts of interest.

[email protected]

On Twitter @alz_gal

Using a 70-gene signature screening tool for adjuvant chemotherapy decisions cost significantly more than did other methods, including giving chemotherapy to all patients, but did not confer any additional advantages in survival or quality of life, for women with node-negative breast cancer.

The estimated cost per woman with a node-negative tumor was 12,780 euros for using the MammaPrint test – significantly higher than either an online decision tool, or a strategy of systematic chemotherapy for all, according to Julia Bonastre, Ph.D., and her colleagues (J. Clin. Oncol. 2014 October [doi:10.1200/JCO.2013.54.9931]).

©Kativ/iStockphoto

The study compared cost and clinical outcomes among 307 women treated for node-negative breast cancers as part of a MammaPrint validation trial. Chemotherapy choice was guided either by MammaPrint, the Adjuvant! Online program, or a scheme of systematic chemotherapy for every patient.

The mean cost of the 70-gene MammaPrint profile was 12,780 euros; the mean cost of Adjuvant! Online, 10,743 euros; and the mean cost of systematic chemotherapy, 12,123 euros. Over the 10-year follow-up period, there were no differences in life-years or quality-adjusted life-years.

Treatment de-escalation is critical for ensuring high-quality survivorship over the long term, wrote Dr. Bonastre of Gustave Roussy Institute of Oncology, Paris, and her associates. “However, our study shows that the health benefits associated with the use of molecular tests are modest. In addition, the high price of these tests results in poor value for the money, limiting their usefulness in routine practice,” they said.

The study was funded by the French National Cancer Institute, and the authors reported no conflicts of interest.

[email protected]

On Twitter @alz_gal

VIENNA – A concerning number of women with gestational diabetes may not be getting optimal retinal care during their pregnancy.

About 11% of women in an Irish observational cohort study received just one retinal exam of the two that are recommended during pregnancy and 29% received no exam, Dr. Aoife Maria Egan said at the annual meeting of the European Association for the Study of Diabetes.

Women who attended prepregnancy care clinics were most likely to get appropriate screening. “This is probably because they had been made aware of what would be expected for them during pregnancy,” said Dr. Egan of the University Hospital Galway (Ireland).

Michele G. Sullivan/Frontline Medical News

The study was an offshoot of the ongoing Atlantic Diabetes in Pregnancy (DIP) project, which examines the outcomes of pregnancy for women with type 1 and type 2 diabetes and the factors influencing these outcomes. It was created in 2005 and provides universal screening for gestational diabetes as part of its outcomes research. The retinopathy study covered 2006-2012.

Adequate retinopathy evaluation was considered to be at least two retinal exams conducted in separate trimesters. Each exam consisted of tests of visual acuity, dilation, and opthalmologic exams and retinal images that were reviewed by an accredited retinal grader.

DIP considered four grades of retinopathy, which have been defined by the National Screening Committee in the United Kingdom: none (R0), background (R1), preproliferative (R2), and proliferative (R3). Additionally, macular edema is graded as present or absent. Progression was considered to be a change from one retinopathy grade to the next or the development of new macular edema.

The study group consisted of 341 women with gestational diabetes (68% type 1). Most of these (90%) were white. They averaged 31 years of age, with a history of two pregnancies. There were 296 live births (87%). The final analysis included 307 women who delivered after 22 weeks.

Most of the women (60%) did have an adequate evaluation. However, 11% had only one exam and 29% had no exam, Dr. Egan said.

There were a few significant differences between those who had adequate retinal exams and those who did not. Women who had two exams were more likely to have type 1 diabetes (72% vs. 61% without adequate exams) and white (94% vs. 85%). They had a longer duration of diabetics (11 vs. 9 years). More of them had attended a prepregnancy center (56% vs. 17%) and were taking folic acid (70% vs. 54%), she reported.

A multivariate analysis determined that attending the prepregnancy clinic was the strongest predictive factor, increasing the likelihood of adequate screening by more than six times.

Of those who had an adequate exam, 74% did not progress during their pregnancy and 26% did. Of those 48 who progressed, the largest portion (26) went from R0 to R1. R1 to R2 progression occurred in seven patients, and R1/R2 to R3 in six. Six patients developed a new maculopathy and three had worsening maculopathy.

Several significant differences emerged when comparing those who progressed with those who did not. The women with worsening retinopathy had a longer duration of diabetes (14 vs. 10 years) and higher systolic blood pressure at baseline (129 vs. 122 mm Hg).

They also had higher baseline hemoglobin A1c (7.7% vs. 7%) and a greater change in HbA1cduring the pregnancy (1.38% vs. 0.74%). An HbA1creduction between the first and third trimester was associated with a doubling in the risk of progression. Those who had a higher reduction of HbA1cbetween trimesters one and three were more than twice as likely to have retinopathy progression.

This highlights the dilemma clinicians face when trying to balance maternal and fetal risks of glycemic control, Dr. Egan said. Women who present with poor glycemic control should moderate that to optimize fetal health, but lowering HbA1ccan predispose the mother to retinopathic changes.

“We try and target tight control and monitor the ones we know are at risk for retinopathy progression very closely,” she said.

Whether that makes any long-term difference is still an unknown. “Some studies have shown that, while pregnancy might accelerate retinopathy, in the long run women end up even in that regard. Six or seven years down the road, everyone looks the same,” she noted.

The DIP program is funded by the Health Research Board of Ireland. Dr. Egan had no financial disclosures.

[email protected]

On Twitter @alz_gal

VIENNA – A concerning number of women with gestational diabetes may not be getting optimal retinal care during their pregnancy.

About 11% of women in an Irish observational cohort study received just one retinal exam of the two that are recommended during pregnancy and 29% received no exam, Dr. Aoife Maria Egan said at the annual meeting of the European Association for the Study of Diabetes.

Women who attended prepregnancy care clinics were most likely to get appropriate screening. “This is probably because they had been made aware of what would be expected for them during pregnancy,” said Dr. Egan of the University Hospital Galway (Ireland).

Michele G. Sullivan/Frontline Medical News

The study was an offshoot of the ongoing Atlantic Diabetes in Pregnancy (DIP) project, which examines the outcomes of pregnancy for women with type 1 and type 2 diabetes and the factors influencing these outcomes. It was created in 2005 and provides universal screening for gestational diabetes as part of its outcomes research. The retinopathy study covered 2006-2012.

Adequate retinopathy evaluation was considered to be at least two retinal exams conducted in separate trimesters. Each exam consisted of tests of visual acuity, dilation, and opthalmologic exams and retinal images that were reviewed by an accredited retinal grader.

DIP considered four grades of retinopathy, which have been defined by the National Screening Committee in the United Kingdom: none (R0), background (R1), preproliferative (R2), and proliferative (R3). Additionally, macular edema is graded as present or absent. Progression was considered to be a change from one retinopathy grade to the next or the development of new macular edema.

The study group consisted of 341 women with gestational diabetes (68% type 1). Most of these (90%) were white. They averaged 31 years of age, with a history of two pregnancies. There were 296 live births (87%). The final analysis included 307 women who delivered after 22 weeks.

Most of the women (60%) did have an adequate evaluation. However, 11% had only one exam and 29% had no exam, Dr. Egan said.

There were a few significant differences between those who had adequate retinal exams and those who did not. Women who had two exams were more likely to have type 1 diabetes (72% vs. 61% without adequate exams) and white (94% vs. 85%). They had a longer duration of diabetics (11 vs. 9 years). More of them had attended a prepregnancy center (56% vs. 17%) and were taking folic acid (70% vs. 54%), she reported.

A multivariate analysis determined that attending the prepregnancy clinic was the strongest predictive factor, increasing the likelihood of adequate screening by more than six times.

Of those who had an adequate exam, 74% did not progress during their pregnancy and 26% did. Of those 48 who progressed, the largest portion (26) went from R0 to R1. R1 to R2 progression occurred in seven patients, and R1/R2 to R3 in six. Six patients developed a new maculopathy and three had worsening maculopathy.

Several significant differences emerged when comparing those who progressed with those who did not. The women with worsening retinopathy had a longer duration of diabetes (14 vs. 10 years) and higher systolic blood pressure at baseline (129 vs. 122 mm Hg).

They also had higher baseline hemoglobin A1c (7.7% vs. 7%) and a greater change in HbA1cduring the pregnancy (1.38% vs. 0.74%). An HbA1creduction between the first and third trimester was associated with a doubling in the risk of progression. Those who had a higher reduction of HbA1cbetween trimesters one and three were more than twice as likely to have retinopathy progression.

This highlights the dilemma clinicians face when trying to balance maternal and fetal risks of glycemic control, Dr. Egan said. Women who present with poor glycemic control should moderate that to optimize fetal health, but lowering HbA1ccan predispose the mother to retinopathic changes.

“We try and target tight control and monitor the ones we know are at risk for retinopathy progression very closely,” she said.

Whether that makes any long-term difference is still an unknown. “Some studies have shown that, while pregnancy might accelerate retinopathy, in the long run women end up even in that regard. Six or seven years down the road, everyone looks the same,” she noted.

The DIP program is funded by the Health Research Board of Ireland. Dr. Egan had no financial disclosures.

[email protected]

On Twitter @alz_gal

VIENNA – A concerning number of women with gestational diabetes may not be getting optimal retinal care during their pregnancy.

About 11% of women in an Irish observational cohort study received just one retinal exam of the two that are recommended during pregnancy and 29% received no exam, Dr. Aoife Maria Egan said at the annual meeting of the European Association for the Study of Diabetes.

Women who attended prepregnancy care clinics were most likely to get appropriate screening. “This is probably because they had been made aware of what would be expected for them during pregnancy,” said Dr. Egan of the University Hospital Galway (Ireland).

Michele G. Sullivan/Frontline Medical News

The study was an offshoot of the ongoing Atlantic Diabetes in Pregnancy (DIP) project, which examines the outcomes of pregnancy for women with type 1 and type 2 diabetes and the factors influencing these outcomes. It was created in 2005 and provides universal screening for gestational diabetes as part of its outcomes research. The retinopathy study covered 2006-2012.

Adequate retinopathy evaluation was considered to be at least two retinal exams conducted in separate trimesters. Each exam consisted of tests of visual acuity, dilation, and opthalmologic exams and retinal images that were reviewed by an accredited retinal grader.

DIP considered four grades of retinopathy, which have been defined by the National Screening Committee in the United Kingdom: none (R0), background (R1), preproliferative (R2), and proliferative (R3). Additionally, macular edema is graded as present or absent. Progression was considered to be a change from one retinopathy grade to the next or the development of new macular edema.

The study group consisted of 341 women with gestational diabetes (68% type 1). Most of these (90%) were white. They averaged 31 years of age, with a history of two pregnancies. There were 296 live births (87%). The final analysis included 307 women who delivered after 22 weeks.

Most of the women (60%) did have an adequate evaluation. However, 11% had only one exam and 29% had no exam, Dr. Egan said.

There were a few significant differences between those who had adequate retinal exams and those who did not. Women who had two exams were more likely to have type 1 diabetes (72% vs. 61% without adequate exams) and white (94% vs. 85%). They had a longer duration of diabetics (11 vs. 9 years). More of them had attended a prepregnancy center (56% vs. 17%) and were taking folic acid (70% vs. 54%), she reported.

A multivariate analysis determined that attending the prepregnancy clinic was the strongest predictive factor, increasing the likelihood of adequate screening by more than six times.

Of those who had an adequate exam, 74% did not progress during their pregnancy and 26% did. Of those 48 who progressed, the largest portion (26) went from R0 to R1. R1 to R2 progression occurred in seven patients, and R1/R2 to R3 in six. Six patients developed a new maculopathy and three had worsening maculopathy.

Several significant differences emerged when comparing those who progressed with those who did not. The women with worsening retinopathy had a longer duration of diabetes (14 vs. 10 years) and higher systolic blood pressure at baseline (129 vs. 122 mm Hg).

They also had higher baseline hemoglobin A1c (7.7% vs. 7%) and a greater change in HbA1cduring the pregnancy (1.38% vs. 0.74%). An HbA1creduction between the first and third trimester was associated with a doubling in the risk of progression. Those who had a higher reduction of HbA1cbetween trimesters one and three were more than twice as likely to have retinopathy progression.

This highlights the dilemma clinicians face when trying to balance maternal and fetal risks of glycemic control, Dr. Egan said. Women who present with poor glycemic control should moderate that to optimize fetal health, but lowering HbA1ccan predispose the mother to retinopathic changes.

“We try and target tight control and monitor the ones we know are at risk for retinopathy progression very closely,” she said.

Whether that makes any long-term difference is still an unknown. “Some studies have shown that, while pregnancy might accelerate retinopathy, in the long run women end up even in that regard. Six or seven years down the road, everyone looks the same,” she noted.

The DIP program is funded by the Health Research Board of Ireland. Dr. Egan had no financial disclosures.

[email protected]

On Twitter @alz_gal