Dapsone-induced sulfone syndrome.

OBJECTIVE: To report a patient with dapsone-induced sulfone syndrome. CASE SUMMARY: A 42-year-old HIV-infected African American man developed fever, lymphadenopathy, exfoliative dermatitis, hepatitis, and methemoglobinemia 4 weeks after starting dapsone. Complete resolution of symptoms and laboratory abnormalities occurred with cessation of dapsone therapy. DISCUSSION: Sulfone syndrome is not a well-known sequela of dapsone therapy. It is not dose-related, usually occurs in doses of 50-300 mg/d, all cases occur within 2 months of starting dapsone, all patients have fever, and most patients will develop rash and evidence of hepatic injury. The temporal relationship between dapsone therapy and onset of clinical symptoms and objective data led us to believe that dapsone caused sulfone syndrome in our patient. An objective causality assessment revealed that the adverse drug event was probable. CONCLUSIONS: Although sulfone syndrome appears to be relatively uncommon, healthcare practitioners must be aware of the potentially fatal syndrome associated with dapsone use.

Regional left ventricular deafferentation increases baroreflex sensitivity following myocardial infarction.

OBJECTIVE: Depressed baroreflex sensitivity (BRS) has been observed following MI and has adverse prognostic implications. The mechanism for this finding is unknown. We tested the hypothesis that depressed BRS following myocardial infarction (MI) is related to augmented input from afferent receptors in the left ventricle. METHODS: Conscious, chronically-instrumented dogs were trained to undergo BRS testing. This testing was performed before and 4 weeks after creation of experimental anterior MI. Animals were then randomized to undergo regional deafferentation or sham thoracotomy. One week later, BRS testing was repeated. RESULTS: Animals with reduced BRS post-MI showed slight increases in sensitivity values after regional deafferentation. Following sham thoracotomy, animals with reduced BRS post-MI exhibited further decreases in sensitivity values. The differences in mean BRS values measured after regional or sham deafferentation were significant (17.4+/-2.0 ms/mmHg vs. 11.7+/-1.4 ms/mmHg; P<0.05). CONCLUSIONS: In animals with reduced BRS post-MI, deafferentation of the infarcted region prevented the progressive decline in sensitivity values that was noted in the control group. These data suggest that depressed BRS following MI is related to augmented afferent input from left ventricular receptors.