Successful treatment of aggressive HIV-associated multicentric Castleman's disease: a case report.

BACKGROUND: Multicentric Castleman's disease (MCD) in human immunodeficiency virus (HIV)-infected patients is an aggressive form of lymphoproliferative disorder that usually has a rapidly fatal outcome. Overall mortality is 70%-85%, and median survival is only 8-14 months. No standard or optimal therapy for MCD has been established. CASE: A 49-year-old man with HIV infection presented with 1-week duration of low-grade fever, night sweats, left sided abdominal pain, and generalized weakness. Physical examination revealed a supraclavicular, anterior cervical and axillary lymphadenopathy, and splenomegaly. Excisional biopsy of the left axillary lymph node confirmed the diagnosis of an angiofollicular hyperplasia, or MCD, hyaline vascular type with CD20 positivity. Treatment included a combination of the chemotherapy regimen of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) with the monoclonal anti-CD20 antibody rituximab. The chemotherapy was administered in parallel with highly active antiretroviral therapy (HAART). At a 3-year follow-up, the patient remains in complete remission and his HIV parameters have normalized with continued HAART. CONCLUSION: This is the second publication describing the use of an aggressive combination of chemotherapy with rituximab in HIV-associated MCD. For an HIV patient with MCD, an aggressive treatment with full CHOP regimen combined with monoclonal anti-CD20 antibody rituximab should be considered, and the use of HAART does not need to be discontinued.

Alveolar proteinosis in a patient recovering from Pneumocystis carinii infection: a case report with a review of literature.

BACKGROUND: Pulmonary alveolar proteinosis is a rare lung disorder, which was first reported as idiopathic condition in 1958. The prevalence of acquired pulmonary alveolar proteinosis has been estimated to be 0.37 per 100,000 population. The cause of this condition is not entirely clear. We present alveolar proteinosis in a case recently treated for pulmonary Pneumocystis carinii infection. CASE PRESENTATION: A 25-year-old Caucasian female presented with shortness of breath during management of acute pancreatitis. She had a heart-transplant six years ago, a distal pancreatectomy secondary to pancreatitis two years ago, chronic renal failure secondary to Prograft taken for six years to suppress transplant rejection, and a more recent history of Pneumocystis carinii infection treated in the preceding 21 days with augmented doses of Bactrim (Trimethoprim, Sulfamethoxazole). She had bilateral pleural effusions with radiological and clinical features suspicious for interstitial lung disease. Cytopathologic evaluation of broncho-alveolar lavage (BAL) showed hyaline alveolar casts admixed with amorphous debris and scant chronic inflammatory cells, consistent with alveolar proteinosis. GMS and PAS stains were negative for P. carinii. Direct Fluorescent Antibody (DFA) test for P. carinii performed on the BAL specimen in our Microbiology Lab had been repeatedly negative. CONCLUSION: Cytopathological findings in bronchoalveolar lavage, with clinical differential diagnosis of interstitial lung disease, were diagnostic. Pulmonary alveolar proteinosis after recent treatment for P. carinii infection suggests a relationship of pulmonary alveolar proteinosis with P. carinii infection in the immunocompromised patient.