Levetiracetam-Induced Rhabdomyolysis Reversed by Discontinuation: A Case Report.

Rhabdomyolysis has been reported as a rare side effect of levetiracetam, a first-line anti-epileptic medication. We report the case of a 64-year-old man who presented to the medical center after suffering an unwitnessed seizure. Following the initiation of levetiracetam, the patient's serum creatine kinase (CPK) levels rose rapidly and remained elevated for multiple days. However, the patient did not report any symptoms of acute rhabdomyolysis. Following discontinuation of the medication CPK levels normalized, suggesting that this is a reversible adverse effect of levetiracetam. The patient made a complete recovery and did not display any seizure activity after the initial presentation. This seemingly more common side effect could cause further damage, particularly to the kidneys, and should be monitored closely by prescribing clinicians.

Dietary iron restriction protects against vaso-occlusion and organ damage in murine sickle cell disease.

Sickle cell disease (SCD) is an inherited disorder resulting from a ß-globin gene mutation, and SCD patients experience erythrocyte sickling, vaso-occlusive episodes (VOE), and progressive organ damage. Chronic hemolysis, inflammation, and repeated red blood cell transfusions in SCD can disrupt iron homeostasis. Patients who receive multiple blood transfusions develop iron overload, and another subpopulation of SCD patients manifest iron deficiency. To elucidate connections between dietary iron, the microbiome, and SCD pathogenesis, we treated SCD mice with an iron-restricted diet (IRD). IRD treatment reduced iron availability and hemolysis, decreased acute VOE, and ameliorated chronic organ damage in SCD mice. Our results extend previous studies indicating that the gut microbiota regulate disease in SCD mice. IRD alters microbiota load and improves gut integrity, together preventing crosstalk between the gut microbiome and inflammatory factors such as aged neutrophils, dampening VOE, and organ damage. These findings provide strong evidence for the therapeutic potential of manipulating iron homeostasis and the gut microbiome to ameliorate SCD pathophysiology. Many treatments, which are under development, focus on lowering the systemic iron concentration to relieve disease complications, and our data suggest that iron-induced changes in microbiota load and gut integrity are related- and novel-therapeutic targets.