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A case of secondary diabetes mellitus associated with chronic arsenic toxicity
Author(s) -
John M. Moorman,
Melanie L. Boros,
Daniela Ciltea,
Josephine A. Taverna,
Nairmeen Haller
Publication year - 2016
Publication title -
case reports in internal medicine
Language(s) - English
Resource type - Journals
eISSN - 2332-7251
pISSN - 2332-7243
DOI - 10.5430/crim.v3n4p55
Subject(s) - medicine , diabetes mellitus , anorexia , hypoglycemia , arsenic poisoning , arsenic toxicity , toxicity , gastroenterology , population , creatinine , arsenic , surgery , endocrinology , environmental health , materials science , metallurgy
Chronic arsenic exposure leads to systemic illness involving multiple organ systems, and has been associated with the development of diabetes mellitus (DM).  While the majority of the literature surrounding arsenic-induced DM is from areas where the arsenic content of drinking water is high, population-based studies in North America have shown a similar association.  Here, we present a case of newly-diagnosed DM thought to be secondary to chronic arsenic exposure. The patient was a previously healthy 54-year-old female who presented with progressive fatigue, weight loss and anorexia, and eventually developed colitis, cachexia, skin eruptions, and alopecia.  She was also diagnosed with DM, and treatment was complicated by episodes of severe hyper- and hypoglycemia.  She was evaluated for autoimmune, rheumatologic, oncologic, and infectious etiologies of her symptoms, all of which were negative.  Also negative was an extensive workup for secondary causes of DM.  During her final hospitalization, she underwent a workup for heavy metal toxicity, which revealed elevated serum (11 mcg/L, reference range < 5 mcg/L) and urine (233.5 mcg/gram creatinine, reference range < 50 mcg/gram creatinine) arsenic levels.  A diagnosis of arsenic toxicity was made, and the patient underwent chelation therapy with British anti-Lewisite (BAL). This is an interesting case of DM that was thought to be secondary to chronic arsenic exposure.  While BAL was effective at lowering arsenic levels, we were unable to observe clinical improvement due to the patient’s death shortly after completion of therapy.  In cases where other secondary causes of DM are ruled out, it may be prudent to evaluate for heavy metal toxicity to allow for early diagnosis and initiation of treatment.  Further studies are needed to determine the efficacy of different treatment strategies for arsenic-induced DM, and whether resolution of arsenic toxicity will reverse the diabetogenic effects.

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