ABSTRACT
BACKGROUND: Kaposi's sarcoma is a low-grade mesenchymal angioproliferative tumor, most commonly observed in immunocompromised individuals, such as HIV-infected patients. Iatrogenic Kaposi's sarcoma occurs in patients undergoing immunosuppressive therapies. Rituximab is a chimeric monoclonal antibody targeted against the pan B cell marker CD20. Because of its immunosuppressive effects through reduction of mature B-cells, it may exacerbate Kaposi's sarcoma in HIV-positive patients. Rituximab-related Kaposi's sarcomas have been previously reported in only two HIV-negative patients and were treated surgically. CASE PRESENTATION: Here, we report on a Kaposi's sarcoma that developed under rituximab treatment in a HIV-negative 55-year-old patient treated for follicular lymphoma. The lesion developed during the maintenance rituximab therapy at the rectal level with an aspect of apparent ulcerative colitis, without any cutaneous lesion. The premature stop of rituximab led to the complete regression of Kaposi's sarcoma, without any additional specific treatment. CONCLUSIONS: To our knowledge, this is the third case of Kaposi's sarcoma diagnosed under rituximab in a HIV-negative patient, the first one at the rectal level and the first one that completely regresses after stop of rituximab. This case raises awareness of iatrogenic Kaposi's sarcoma in HIV-negative patients treated with rituximab, and further highlights the importance of immunosuppression in the pathophysiology of disease.
ABSTRACT
BACKGROUND & AIMS: Severe alcoholic hepatitis (AH) has a poor short-term prognosis. Although infections are frequent complications of AH, the incidence of invasive aspergillosis (IA) and its impact on outcome remain unknown. METHODS: We prospectively followed 94 biopsy-proven severe AH episodes for 3 months. We retrospectively reviewed our diagnosis of IA based on EORTC/MSG and AspICU criteria, except for host factors. RESULTS: Fifteen IA (6 proven, 8 probable, and 1 possible) were diagnosed after a median delay of 26 days following diagnosis of AH. The sites of infection were the lungs (n=11) and central nervous system (n=2), while IA was disseminated in 2 cases. Baseline MELD score ≥24 and ICU admission were independent risk factors for IA. Thirteen IA occurred in the context of corticosteroids, and 2 had received no specific treatment for AH. Non-response to corticosteroids at day 7 was not a risk factor for IA, but IA was associated with absence of liver improvement at day 28. Despite antifungal treatment, 3-month transplant-free survival of patients with IA was 0% compared to 53% in those without IA. IA, Lille score ≥0.45, and overt encephalopathy were independent predictors of transplant-free mortality. CONCLUSIONS: IA is a frequent complication of severe AH and carries a very high risk of mortality. Systematic screening for IA should be recommended in these patients. Further studies are needed to identify high-risk populations requiring antifungal prophylactic treatment.