ContextQuizalofop-p-ethyl is an often applied, slightly toxic herbicide for which no severe toxicity has been reported in humans.Case presentationWe present the case of a farmer exposed to quizalofop-p-ethyl who presented with obstructive cholestasis. A complete workup disclosed no other cause of liver pathology, but liver biopsy established drug-induced hepatotoxicity. The patient was treated with ursodeoxycholic acid and prednisolone, and was recovered fully 70 days after his exposure to the herbicide. The patient was followed for the next 9 months.ConclusionQuizalofop-p-ethyl can induce a mixed cholestatic/hepatocellular liver injury. We discuss possible mechanisms implicated in liver injury after exposure to quizalofop-p-ethyl.Relevance to clinical or professional practiceIn patients presenting with mixed cholestatic/ hepatocellular liver injury, occupational exposure to quizalofop-p-ethyl in the course of agricultural use should be investigated.

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Background:To evaluate if splenectomy results in severely impaired immune responses against primary cytomegalovirus (CMV) infection compared to the general immunocompetent population.Methods:We performed a systemic literature review to study CMV infections in splenectomized individuals, a special population group presently considered immunocompetent to viral infections. We retrieved 30 cases with established CMV infection post-splenectomy and we recorded their disease manifestations, laboratory findings, immunological studies, and histopathology reports. In addition, we retrieved numerous multidisciplinary articles in view of post-splenectomy immunology defects, as well as of immune responses to primary invading CMV in the absence of the spleen. Two clinical studies directly comparing splenectomized with nonsplenectomized individuals under severe iatrogenic immunosuppression as well as the numerically largest review articles of CMV infections in immunocompetent were retained.Results:Splenectomy results in the loss of spleen's ability to fend-off blood-borne pathogens and impairs the link between innate and adaptive immunity. The major post-splenectomy immune-defects against CMV are: weakened, delayed or absent anti-CMV IgM, and compensatory marked IgG response; severely impaired B-cell and CD4+, CD8+ T-cells function responses; and post-splenectomy, bone marrow compensates for the absence of spleen's immune responses against CMV, mimicking a monoclonal T-cell lymphoproliferative process.Conclusion:The puzzled diagnosis of the CMV syndrome post-splenectomy is of the most challenging and misleading, resulting in risky and costly interventions and a subsequent prolonged hospitalization (2 months). The mounting multi-disciplinary literature evidence renders us to suggest that splenectomized individuals are not only prone to encapsulated bacteria but also behave as immunocompromised to CMV.

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We present an unusual onset of meningoencephalitis due to VZV reactivation, with increased intrathecal production of IgG VZV antibodies and negative PCR, in a young, immunocompetent adult. Herpes zoster erupted 5 d later. Rare complication of VZV-related rhabdomyolysis occurred, with subsequent ARF, in combination with acyclovir and ceftriaxone. The patient recovered fully and remained healthy.