Reply to Angel-Moreno and Perez-Arellano

Le résumé fourni par la source

Sir—In response to the letter by Angel-Moreno and Perez-Arellano [1] regarding our recent article [2], we agree that our case represents an exceedingly uncommon and morbid chain of events after discontinuation of antiretroviral therapy (ART). However, we did, in fact, conduct an exhaustive search for other unifying diagnoses, although limitations on the length of the article made it impossible to report every negative study result that was noted during our patient's long, complex hospitalization. This patient never had significantly elevated lactate levels, although we, too, suspected mitochondrial toxicity caused by ART. He had transthoracic and transesophageal echocardiographs that did not show either signs of infective endocarditis or myocardial dysfunction consistent with infarction. We performed many blood cultures that revealed no growth of mycobacterial and fungal isolators. Several abdominal CTs showed no significant abnormalities and no evidence of hepatic steatosis; no signs of lymphoma or other malignancies were found either during cytological examination or during consultation with our oncology service. This patient had many concomitant medical problems, including hepatitis C virus infection and diabetes mellitus, and he was a cigarette smoker; these, as well as cumulative drug toxicity, may very well have played roles in the cascade of events that led to death. His hypercoagulability may have preceded retroviral rebound syndrome, or it may have been triggered by other circumstances, but he had never had clinically apparent thrombotic events before. It is true that the temporal relationship of his marked deterioration to his discontinuation of ART provides only circumstantial evidence of a causal connection; however, the striking time line of his hospital course and rapid viral rebound, as well as the plausible physiological mechanism, led us to report his case. This patient came to us sick, but his condition rapidly became dramatically worse when we discontinued ART, which corresponded with a striking decrease in his absolute CD4 count and a spike in his HIV load. None of our investigations could explain his condition, and he then improved once ART was resumed, which added support for a relationship between his rapid viral rebound and his symptoms. Our supposition is that, for this already debilitated patient with comorbidities, the discontinuation of ART and resulting rapid rebound of viremia set in motion a systemic process that included an increased predilection for thrombosis that eventually led to his death. Treatment interruptions may be necessary in order to manage drug toxicity, which was our intention regarding the care of this patient. The dramatic details of this case serve to illustrate an extreme form of retroviral rebound syndrome that, in this patient, who had several underlying disease processes, unfortunately resulted in a fatal outcome. Potential conflicts of interest. A.G. and P.S.: no conflicts.

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