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Diabetes therapy and cancer risk
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.
Bariatric surgery, vitamin C, and kidney stones
To the Editor: I read with interest the excellent review by Dr. Kashyap and coauthors of bariatric surgery for patients with type 2 diabetes.1 I am writing to contribute an additional caveat to their otherwise detailed list of postoperative complications—the increased risk of nephrolithiasis.2,3 The majority of kidney stones that develop after bariatric surgery tend to be composed of calcium oxalate. Increased intestinal absorption of oxalate appears to promote hyperoxaluria.2,3
Vitamin C deficiency is not usual after bariatric surgery, and the dietary reference intake of vitamin C for adults is no more than 90 mg. Therefore, I was surprised to see Dr. Kashyap recommend supplementation with vitamin C 500 mg daily (in Table 4 of her article). In my practice I have avoided supplemental vitamin C, other than that in a multivitamin, because of the risk of increasing urinary oxalate and stone formation.4
Iron deficiency can be a challenge after bariatric surgery. Although they do not state it in the review, the authors may believe that additional vitamin C can improve iron absorption. However, there are no compelling data of which I am aware for this belief in patients who have undergone gastric bypass,5 and the benefit of taking vitamin C along with iron in otherwise normal people with iron deficiency remains controversial.6
- Kashyap SR, Gatmaitan P, Brethauer S, Schauer P. Bariatric surgery for type 2 diabetes: weighing the impact for obese patients. Cleve Clin J Med 2010; 77:468–476.
- Lieske JC, Kumar R, Collazo-Clavell ML. Nephrolithiasis after bariatric surgery for obesity. Semin Nephrol 2008; 28:163–173.
- Asplin JR, Coe FL. Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. J Urol 2007; 177:565–569.
- Massey LK, Liebman M, Kynast-Gales SA. Ascorbate increases human oxaluria and kidney stone risk. J Nutr 2005; 135:1673–1677.
- Rhode BM, Shustik C, Christou NV, MacLean LD. Iron absorption and therapy after gastric bypass. Obes Surg 1999; 9:17–21.
- Hunt JR, Gallagher SK, Johnson LK. Effect of ascorbic acid on apparent iron absorption by women with low iron stores. Am J Clin Nutr 1994; 59:1381–1385.
To the Editor: I read with interest the excellent review by Dr. Kashyap and coauthors of bariatric surgery for patients with type 2 diabetes.1 I am writing to contribute an additional caveat to their otherwise detailed list of postoperative complications—the increased risk of nephrolithiasis.2,3 The majority of kidney stones that develop after bariatric surgery tend to be composed of calcium oxalate. Increased intestinal absorption of oxalate appears to promote hyperoxaluria.2,3
Vitamin C deficiency is not usual after bariatric surgery, and the dietary reference intake of vitamin C for adults is no more than 90 mg. Therefore, I was surprised to see Dr. Kashyap recommend supplementation with vitamin C 500 mg daily (in Table 4 of her article). In my practice I have avoided supplemental vitamin C, other than that in a multivitamin, because of the risk of increasing urinary oxalate and stone formation.4
Iron deficiency can be a challenge after bariatric surgery. Although they do not state it in the review, the authors may believe that additional vitamin C can improve iron absorption. However, there are no compelling data of which I am aware for this belief in patients who have undergone gastric bypass,5 and the benefit of taking vitamin C along with iron in otherwise normal people with iron deficiency remains controversial.6
To the Editor: I read with interest the excellent review by Dr. Kashyap and coauthors of bariatric surgery for patients with type 2 diabetes.1 I am writing to contribute an additional caveat to their otherwise detailed list of postoperative complications—the increased risk of nephrolithiasis.2,3 The majority of kidney stones that develop after bariatric surgery tend to be composed of calcium oxalate. Increased intestinal absorption of oxalate appears to promote hyperoxaluria.2,3
Vitamin C deficiency is not usual after bariatric surgery, and the dietary reference intake of vitamin C for adults is no more than 90 mg. Therefore, I was surprised to see Dr. Kashyap recommend supplementation with vitamin C 500 mg daily (in Table 4 of her article). In my practice I have avoided supplemental vitamin C, other than that in a multivitamin, because of the risk of increasing urinary oxalate and stone formation.4
Iron deficiency can be a challenge after bariatric surgery. Although they do not state it in the review, the authors may believe that additional vitamin C can improve iron absorption. However, there are no compelling data of which I am aware for this belief in patients who have undergone gastric bypass,5 and the benefit of taking vitamin C along with iron in otherwise normal people with iron deficiency remains controversial.6
- Kashyap SR, Gatmaitan P, Brethauer S, Schauer P. Bariatric surgery for type 2 diabetes: weighing the impact for obese patients. Cleve Clin J Med 2010; 77:468–476.
- Lieske JC, Kumar R, Collazo-Clavell ML. Nephrolithiasis after bariatric surgery for obesity. Semin Nephrol 2008; 28:163–173.
- Asplin JR, Coe FL. Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. J Urol 2007; 177:565–569.
- Massey LK, Liebman M, Kynast-Gales SA. Ascorbate increases human oxaluria and kidney stone risk. J Nutr 2005; 135:1673–1677.
- Rhode BM, Shustik C, Christou NV, MacLean LD. Iron absorption and therapy after gastric bypass. Obes Surg 1999; 9:17–21.
- Hunt JR, Gallagher SK, Johnson LK. Effect of ascorbic acid on apparent iron absorption by women with low iron stores. Am J Clin Nutr 1994; 59:1381–1385.
- Kashyap SR, Gatmaitan P, Brethauer S, Schauer P. Bariatric surgery for type 2 diabetes: weighing the impact for obese patients. Cleve Clin J Med 2010; 77:468–476.
- Lieske JC, Kumar R, Collazo-Clavell ML. Nephrolithiasis after bariatric surgery for obesity. Semin Nephrol 2008; 28:163–173.
- Asplin JR, Coe FL. Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. J Urol 2007; 177:565–569.
- Massey LK, Liebman M, Kynast-Gales SA. Ascorbate increases human oxaluria and kidney stone risk. J Nutr 2005; 135:1673–1677.
- Rhode BM, Shustik C, Christou NV, MacLean LD. Iron absorption and therapy after gastric bypass. Obes Surg 1999; 9:17–21.
- Hunt JR, Gallagher SK, Johnson LK. Effect of ascorbic acid on apparent iron absorption by women with low iron stores. Am J Clin Nutr 1994; 59:1381–1385.