Prolactin is a polypeptide hormone that is well known for its role in reproductive physiology. Recent studies highlight its role in neurohormonal appetite regulation and metabolism. Elevated prolactin levels are widely associated with worsening metabolic disease, but it appears that low prolactin levels could also be metabolically unfavorable. This review discusses the pathophysiology of prolactin related metabolic changes, and the less commonly recognized effects of prolactin on adipose tissue, pancreas, liver, and small bowel. Furthermore, the effect of dopamine agonists on the metabolic profiles of patients with hyperprolactinemia are discussed as well.

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We present a patient with mitochondrial myopathy who developed rhabdomyolysis following treatment with clindamycin. While clindamycin is not yet linked to drug-induced rhabdomyolysis in the literature, other drugs with mechanisms of action similar to clindamycin have been shown to damage human host mitochondria. Given this, we contend that clindamycin may also be capable of causing mitochondrial injury, and that while in otherwise healthy patients it may not produce any negative clinical outcome, it can precipitate rhabdomyolysis in certain patients whose mitochondria are already vulnerable.