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To the Editor: I would like to add three points to the excellent review of diabetes therapy and cancer risk by Drs. Sun, Kashyap, and Nasr in the October 2014 issue of Cleveland Clinic Journal of Medicine.1
First, a recent 10-year prospective observational study of more than 190,000 patients showed no increase in bladder cancer with exposure to or long-term use of pioglitazone vs comparator when smoking status was controlled. Although publicly released, these 10-year data have not yet been published.
Second, a recent paper2 from the US Food and Drug Administration and European Medicine Agency reviewed the pancreatic safety of incretin-based therapies. They concluded that there is no evidence that these agents increase the risk of pancreatitis or of pancreatic cancer. So I believe that the authors’ comment that pancreatitis is a “potential side effect” of these agents is not quite accurate.
Lastly, the authors cite no substantial evidence that would support their statement to avoid using glucagon-like protein 1 (GLP-1) receptor agonists in those with a personal history of differentiated thyroid cancer. Indeed these patients, if adequately treated, should have no remnant thyroid tissue. The rodent data indicate an effect of GLP-1 agonists on rodent C cells, not thyroid follicular cells.3 In addition, the prescribing information for these agents does not advise such a limitation on their use.
- Ching Sun GE, Kashyap SR, Nasr C. Diabetes therapy and cancer risk: where do we stand when treating patients? Cleve Clin J Med 2014; 81:620–628.
- Egan AG, Blind E, Dunder K, et al. Pancreatic safety of incretin-based drugs—FDA and EMA assessment. N Engl J Med 2014; 370:794–797.
- Knudsen L, Madsen LW, Andersen S, et al. Glucagon-like peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin release and C-cell proliferation. Endocrinology 2010; 151:1473–1486.
To the Editor: I would like to add three points to the excellent review of diabetes therapy and cancer risk by Drs. Sun, Kashyap, and Nasr in the October 2014 issue of Cleveland Clinic Journal of Medicine.1
First, a recent 10-year prospective observational study of more than 190,000 patients showed no increase in bladder cancer with exposure to or long-term use of pioglitazone vs comparator when smoking status was controlled. Although publicly released, these 10-year data have not yet been published.
Second, a recent paper2 from the US Food and Drug Administration and European Medicine Agency reviewed the pancreatic safety of incretin-based therapies. They concluded that there is no evidence that these agents increase the risk of pancreatitis or of pancreatic cancer. So I believe that the authors’ comment that pancreatitis is a “potential side effect” of these agents is not quite accurate.
Lastly, the authors cite no substantial evidence that would support their statement to avoid using glucagon-like protein 1 (GLP-1) receptor agonists in those with a personal history of differentiated thyroid cancer. Indeed these patients, if adequately treated, should have no remnant thyroid tissue. The rodent data indicate an effect of GLP-1 agonists on rodent C cells, not thyroid follicular cells.3 In addition, the prescribing information for these agents does not advise such a limitation on their use.
To the Editor: I would like to add three points to the excellent review of diabetes therapy and cancer risk by Drs. Sun, Kashyap, and Nasr in the October 2014 issue of Cleveland Clinic Journal of Medicine.1
First, a recent 10-year prospective observational study of more than 190,000 patients showed no increase in bladder cancer with exposure to or long-term use of pioglitazone vs comparator when smoking status was controlled. Although publicly released, these 10-year data have not yet been published.
Second, a recent paper2 from the US Food and Drug Administration and European Medicine Agency reviewed the pancreatic safety of incretin-based therapies. They concluded that there is no evidence that these agents increase the risk of pancreatitis or of pancreatic cancer. So I believe that the authors’ comment that pancreatitis is a “potential side effect” of these agents is not quite accurate.
Lastly, the authors cite no substantial evidence that would support their statement to avoid using glucagon-like protein 1 (GLP-1) receptor agonists in those with a personal history of differentiated thyroid cancer. Indeed these patients, if adequately treated, should have no remnant thyroid tissue. The rodent data indicate an effect of GLP-1 agonists on rodent C cells, not thyroid follicular cells.3 In addition, the prescribing information for these agents does not advise such a limitation on their use.
- Ching Sun GE, Kashyap SR, Nasr C. Diabetes therapy and cancer risk: where do we stand when treating patients? Cleve Clin J Med 2014; 81:620–628.
- Egan AG, Blind E, Dunder K, et al. Pancreatic safety of incretin-based drugs—FDA and EMA assessment. N Engl J Med 2014; 370:794–797.
- Knudsen L, Madsen LW, Andersen S, et al. Glucagon-like peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin release and C-cell proliferation. Endocrinology 2010; 151:1473–1486.
- Ching Sun GE, Kashyap SR, Nasr C. Diabetes therapy and cancer risk: where do we stand when treating patients? Cleve Clin J Med 2014; 81:620–628.
- Egan AG, Blind E, Dunder K, et al. Pancreatic safety of incretin-based drugs—FDA and EMA assessment. N Engl J Med 2014; 370:794–797.
- Knudsen L, Madsen LW, Andersen S, et al. Glucagon-like peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin release and C-cell proliferation. Endocrinology 2010; 151:1473–1486.