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Granulomatosis with polyangiitis (GPA) typically presents with upper or lower respiratory tract symptoms and/or with renal involvement. Although it can affect the peripheral nervous system frequently, with mononeuritis multiplex being the most common pattern, the occurrence of peripheral sensory-motor polyneuropathy as a presenting manifestation is distinctly rare. Prevalence of digital gangrene is also extremely rare in GPA. We describe a 46-year-old woman presenting with severe peripheral sensorimotor polyneuropathy affecting bilateral lower limbs preceded by a purpuric skin rash and multiple painful ulcers confined to the lower limbs. She had evidence of digital ischemia affecting multiple toes and dry gangrene of the left 4th toe. Diagnosis of GPA was made based on skin biopsy, positive ANCA serology, and clinical criteria. She made a good recovery following aggressive immunosuppressive treatment with methylprednisolone and cyclophosphamide and was maintained on prednisolone and azathioprine. This case highlights the importance of suspecting GPA in a patient presenting with sensorimotor polyneuropathy and/or digital ischemia even in the absence of more classic presenting features and underlies the necessity of accurate differential diagnosis in evaluating a case of peripheral neuropathy.

Osmotic demyelination syndrome (ODS) is a rare and potentially treatable cause of secondary parkinsonism. Rapid correction of chronic hyponatremia is the most common culprit. We report a 65-year-old man presenting with parkinsonism and pyramidal tract signs 3 weeks following rapid correction of chronic diuretic induced hyponatremia. His MRI brain revealed typical features of ODS involving pons and bilateral basal ganglia excluding globus pallidi. He was successfully treated with dopaminergic drugs. ODS should be considered as a cause of secondary Parkinson’s disease and the symptoms of ODS can appear as late as 3 weeks after correction of hyponatremia. Chronic hyponatremia should be corrected with great caution in order to prevent ODS especially when there is coexistent hypokalemia.

This study evaluated the effects of zinc supplementation on glycemic control, other cardiometabolic and anthropometric parameters, and disease progression in prediabetes.A randomized double-blind placebo-controlled Phase 2 clinical trial was conducted over a 12-month period in 200 subjects (43% male; mean [± SD] age 51.8 ± 7.3 years), randomly assigned (1: 1) to the treatment or control group. The treatment group received zinc (20 mg daily). Subjects were evaluated at baseline and at 1, 3, 6, and 12 months. The primary outcome was the change in glycemic control from baseline. Multiple regression analyses were performed, with change in outcome variables after intervention from baseline used as continuous dependent variables.In both groups, mean serum zinc concentrations prior to the trial were below normal (15.29-21.41 μmol/L). During the 12-month follow-up, a significantly higher percentage of participants developed type 2 diabetes in the control compared with zinc-treated group (25.0% vs 11.0% respectively; P = 0.016). Fasting plasma glucose (FPG), 2-h glucose levels in the oral glucose tolerance test (OGTT), homeostasis model assessment of insulin resistance (HOMA-IR), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) were significantly lower in the treated group, with significant improvement in β-cell function. In all four regression models, the best predictor of the dependent variables (i.e. change in FPG, 2-h glucose in the OGTT, HOMA-IR, and homeostatic model assessment of β-cell function) was zinc treatment.Zinc supplementation reduced blood glucose and insulin resistance while improving β-cell function. Furthermore, supplementation reduced disease progression to diabetes and had beneficial effects on TC and LDL-C.