Hyperprolactinaemia: A guide for psychiatrists

SummaryMedications prescribed by psychiatrists are known to elevate serum prolactin levels, but hyperprolactinaemia remains underrecognised, as the adverse effects of an elevated prolactin are mostly not visible. Hyperprolactinaemia can lead to adverse health outcomes, so clinicians need not only to be alert to its symptoms, but to manage the consequences as well. In this article we provide a brief overview of prolactin physiology, regulation and function. We list various factors that can lead to elevated serum prolactin. We discuss the interpretation of blood results and the management of psychotropic-induced hyperprolactinaemia. We include a flow diagram to assist clinicians in decision-making in the clinical management of hyperprolactinaemia.Learning Objectives• Understand prolactin physiology and regulation• Understand hyperprolactinaemia and its causes• Know the consequences of hyperprolactinaemia and appropriately manage it in clinical practice

Brief oral stimulation, but especially oral fat exposure, elevates serum triglycerides in humans

Oral exposure to dietary fat results in an early initial spike, followed by a prolonged elevation, of serum triglycerides in humans. The physiological and pathophysiological implications remain unknown. This study sought to determine the incidence of the effect, the required fat exposure duration, and its reliability. Thirty-four healthy adults participated in four to six response-driven trials held at least a week apart. They reported to the laboratory after an overnight fast, a catheter was placed in an antecubital vein, and a blood sample was obtained. Participants then ingested 50 g of safflower oil in capsules with 500 ml of water within 15 min to mimic a high fat meal but without oral fat exposure. Blood was collected 0, 10, 20, 30, 40, 50, 60, 120, 240, 360, and 480 min after capsule ingestion with different forms (full fat, nonfat, none) and durations of oral fat exposures (10 s, 5 min, 20 min, and/or 2 h). A triglyceride response (increase of triglyceride >10 mg/dl within 30 min) was observed in 88.2%, 70.5%, and 50% of participants with full-fat, nonfat, and no oral exposure, respectively. Test-retest reliability was 75% with full-fat exposure but only 45.4% with nonfat exposure. Full-fat and nonfat exposures led to comparable significant elevations of triglyceride over no oral stimulation with 10-s exposures, but full fat led to a greater rise than nonfat with 20 min of exposure. These data indicate that nutritionally relevant oral fat exposures reliably elevate serum triglyceride concentrations in most people.

Cardiac Arrest Associated with Combination Cisapride and Itraconazole Therapy

We report a case of cardiac arrest associated with cisapride in combination with itraconazole and provide a brief review of pertinent literature. Cisapride (Propulsid; Janssen Pharmaceuticals, Titusville, NJ), a gastrointestinal prokinetic drug, has recently been reported to prolong the QT interval. Itraconazole, an oral antifungal agent, is an inhibitor of cytochrome P450 (CYP3A4) metabolism and may elevate serum drug levels of compounds metabolized by this pathway. A 31-year-old woman had a witnessed cardiac arrest while taking the combination of cisapride and itraconazole. Following resucitation, the prolonged QT interval returned to normal after withdrawal of both agents. Echocardiography and cardiac catheterization were within normal limits; electrophysiologic testing failed to induce ventricular tachycardia/ventricular fibrillation. She has had no documented arrhythmias since the arrest. This combination can now be added to a growing list of drugs that may cause torsades de pointes and sudden cardiac death.