Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 57-year-old man was admitted to our hospital complaining of poor appetite. He had been diagnosed with diabetes mellitus and was anti-GAD antibody (GAD-Ab) negative 1 year previously, at the age of 56 years old. Abdominal CT revealed pancreas tail swelling; elastase-I level was elevated and he was diagnosed with pancreatitis. The level of GAD-Ab was increased and HLA haplotype was DRB1*0901-DQB1*0303, which is seen frequently in type 1 diabetic Japanese patients. However, his endogenous insulin secretion ability was not deteriorated. After elastase-I level and pancreas swelling improved, GAD-Ab returned to a normal range. One year after the onset of pancreas swelling, he was still not in an insulin-dependent state. In this case, transient GAD-Ab positivity with susceptible haplotype for type 1 diabetes mellitus might have been induced by a GAD antigen discharged from the destroyed islet due to pancreatitis.
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PMID:Transient anti-GAD antibody positivity and acute pancreatitis with pancreas tail swelling in a patient with susceptible haplotype for type 1 diabetes mellitus. 1988 Dec 42

BACKGROUND Medications are one of the most common causes of acute kidney injury (AKI). Elderly patients with diabetes mellitus and chronic kidney disease seem to be at particularly high risk for development of medication-induced AKI. Among antibiotics, the most commonly implicated agents are aminoglycosides, cephalosporins, trimethoprim-sulfamethoxazole, acyclovir, and amphotericin. Despite its widespread use, clindamycin has been rarely associated with AKI. CASE REPORT A 52-year-old male patient with type II insulin dependent diabetes mellitus without diabetic nephropathy was treated with clindamycin for chronic osteomyelitis. Five days following initiation of therapy, he developed nausea, poor appetite, decrease in urine output, and profound generalized weakness. His symptoms were initially attributed to gastrointestinal side effects of clindamycin and he was advised to take it with food and to hydrate himself vigorously. Despite this change, his symptoms progressed and he developed hematuria and AKI which prompted hospital admission. Extensive workup for AKI that included evaluation for pre-renal, intrinsic renal, and post-renal etiologies failed to point to other etiologies apart from clindamycin-induced AKI. Following cessation of medication and temporary renal replacement therapy (RRT), his renal function returned to baseline. CONCLUSIONS We present a case of clindamycin-induced AKI that was diagnosed after a delay due to uremia symptoms being mistakenly attributed to gastrointestinal side effects of clindamycin. Although rare, clindamycin can be a cause of AKI and clinician should be aware of this association in order to recognize and treat it in timely manner.
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PMID:Clindamycin: An Unusual Cause of Acute Kidney Injury. 3079 34