Rosiglitazone improved both plasma glucose and blood pressure levels, probably by attenuation of hyperinsulinemia and sympathetic activity, while Glibenclamide worsened blood pressure control possibly by elevation of insulin levels and activation of the sympathetic system.
Some recent studies have shown that clozapine (CLZ) has myopathic side effects and causes alterations in motor force control. The aim of this study was to evaluate the neurologic and electrophysiologic characteristics of patients with schizophrenia who are undergoing long-term CLZ treatment. Ninety-four patients with schizophrenia treated with CLZ for 18.2 +/- 15.5 months were studied retrospectively and prospectively (40% and 60%, respectively) for serum creatine kinase (CK) levels before and after initiation of CLZ treatment. An electrodiagnostic study was performed on patients with CK elevation above normal limits, complained of general weakness or muscle pains, and/or had abnormal clinically significant findings. In 13 patients (13.8%), abnormal CK levels were found. Six patients complained of some muscular weakness. In two patients, clinical assessment revealed mild general muscular weakness; one revealed decreased tendon reflexes and, in both, CK levels were above 1,750 IU/L. On electrophysiologic examinations performed in the six patients with abnormal neurologic findings, the motor and sensory nerve conduction velocity were within normal range in all but one patient, who exhibited some prolongation of distal latency in the lower limbs. In two patients, the electromyography demonstrated a myopathic pattern. In 2.1% of medically healthy patients with schizophrenia treated with clozapine on a long-term basis, signs of myotoxicity were found. It seems warranted to discontinue CLZ therapy in patients who exhibit abnormal CK levels and myopathic features during treatment. Further studies are needed to provide more objective data on the impact of CLZ treatment on muscle tissue.
Paraneoplastic neurologic syndromes may develop in Hodgkin's disease (HD). We describe three young female patients with neurological disorders, not explained by other causes, preceding diagnosis or relapse of HD. The lack of response of the paraneoplastic syndrome to successful treatment of HD among our three patients emphasizes the poor prognosis of longstanding paraneoplastic neurologic symptoms in HD.
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