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The aim of this study was to investigate factors associated with sarcopenia among elderly patients with poorly controlled diabetes mellitus (DM). We retrospectively analyzed 41 patients with type 2 DM, aged ≥65 years who required diabetes education hospitalization. Patients were classified into two groups according to the presence or absence of a weakened hand grip, and clinical characteristics were compared. Patients with a weakened hand grip ( n = 21) scored worse on a mini-mental state examination (24.3 vs. 26.5, p = 0.04), showed a higher prevalence of diabetic peripheral neuropathy (76% vs. 40%, p = 0.03), and had a higher serum phosphorus concentration (3.8 vs. 3.3 mg/dL, p < 0.01) compared to those without a weakened hand grip ( n = 20). The serum phosphorus concentration was inversely correlated to hand grip strength ( r = -0.501, p < 0.001) among the total of 41 patients. This inverse association was also confirmed after adjusting the effects of estimated glomerular filtration rate, age, and glycated hemoglobin. Thus, cognitive impairment, diabetic peripheral neuropathy, and high serum phosphorus concentrations are associated with hand grip weakness in elderly patients with type 2 DM.

Hyponatremia associated with low-dose trimethoprim in patients on concomitant systemic corticosteroid therapy has rarely been reported. Here, we describe a 57-year-old woman with a history of diabetes mellitus and hypertension treated with telmisartan, who presented with progressive visual impairment of the left eye due to anti-aquaporin-4 antibody-positive optic neuritis. The patient received pulsed intravenous methylprednisolone followed by oral prednisolone at 30 mg/day and trimethoprim-sulfamethoxazole prophylaxis (160 mg and 800 mg daily). Her serum sodium level steadily decreased, and the potassium level was slightly elevated despite well-preserved renal function. This state persisted even after telmisartan discontinuation. In addition to hypotonic hyponatremia (125 mEq/L) with natriuresis, hyperkalemic renal tubular acidosis was diagnosed based on normal anion gap metabolic acidosis and hyperkalemia with low urinary potassium excretion. After trimethoprim-sulfamethoxazole cessation, electrolytes and acid-base imbalances swiftly recovered. We can conclude that caution must be exercised when treating such patients, because even low-dose trimethoprim may cause hyponatremia concomitant with hyperkalemic renal tubular acidosis, despite the mineralocorticoid effects of systemic corticosteroids.