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ABSTRACT: Objective: To demonstrate important points regarding the possible hypoglycemic effects of sulfasalazine and suggest possible underlying mechanism(s) accounting for sulfasalazine-induced hypoglycemia.Methods: We describe a case of reversible sulfasalazine-induced hypoglycemia, review the literature, and discuss a potential mechanism accounting for sulfasalazine-induced hypoglycemia.Results: A 63-year-old man with Crohn disease treated with sulfasalazine and type 2 diabetes complicated by end-stage renal disease was admitted for treatment of persistent hypoglycemia. Insulinoma was initially suspected, but localization studies including endoscopic ultrasound were negative. This raised the possibility of sulfasalazine-induced hypoglycemia. Three days after sulfasalazine was stopped, he became normoglycemic. Hypoglycemia has not recurred since discontinuing sulfasalazine.Conclusion: Clinicians should be aware of the potential hypoglycemic effect of sulfasalazine. Doses should be reduced in patients with impaired renal function, and it should be discontinued if otherwise unexplained hypoglycemia develops.Abbreviations: CT = computed tomography; ESRD = end-stage renal disease

ABSTRACT: Objective: To discuss the prevalence of hyperhidrosis, its association with proton pump inhibitor (PPI) use, and possible underlying mechanism(s) accounting for PPI-induced hyperhidrosis.Methods: We describe 2 patients who presented with hyperhidrosis while on PPI therapy, review the literature regarding PPI-associated hyperhidrosis, discuss a potential mechanism, and provide recommendations for hyperhidrosis evaluation in the setting of PPI use.Results: A 62-year-old man (case 1) presented with hyperhidrosis. Biochemical workup was nondiagnostic except for elevated chromogranin A (CgA) levels. He had been taking lansoprazole. Since PPI therapy can increase CgA levels, lansoprazole was discontinued. CgA levels decreased by 2 weeks, and hyperhidrosis resolved within 4 weeks. Symptoms recurred once PPI therapy was restarted. An 83-year-old man (case 2) presented with hyperhidrosis. He had been on omeprazole for 9 months. Omeprazole was held before performing extensive biochemical workup. Hyperhidrosis resolved after 5 days and recurred within 3 days of re-introducing omeprazole. Omeprazole was switched to ranitidine, and hyperhidrosis resolved within 1 month.Conclusion: PPI-induced hyperhidrosis is an uncommon side effect, and a mechanism has not been described. CgA is a precursor of several bioactive peptides, and levels increase while on PPIs. Expression of CgA has been identified on sweat glands and ducts. Elevated CgA levels may play a functional role in PPI-induced hyperhidrosis, but this remains to be demonstrated. In the absence of an apparent cause of hyperhidrosis in a patient on PPI therapy, a trial off PPI should be considered prior to embarking on costly and extensive workup.Abbreviations: CgA = chromogranin A; ECL = enterochromaffin-like; GERD = gastroesophageal reflux disease; PPI = proton pump inhibitor