A 50-year-old woman, arriving directly from her village in the Kasai-province of the Democratic Republic of Congo was admitted in July 2010 to our department. She presented with painful abdominal distension that appeared 6 months before. Her past clinical history was unremarkable except for a Graves-Basedow disease discovered in 2008 and left untreated. She suffered from chronic weakness and severe dyspnea due to abdominal distention. She had neither ocular

complaint nor cutaneous itching. Physical examination was characterized by extreme cachexia (body weight: 33 kg; body mass index 12 kg/m2), clear lung auscultation, presence of ascites, and the absence of fever. Laboratory tests showed mild leukocytosis (11,490/µL) without peripheral eosinophilia (30/µL). She had moderate microcytic anemia (hemoglobin 10.8 g/dL; MCV 78 fL). C-reactive protein level was 9.3 mg/dL. The thyroid function tests demonstrated Graves’ disease [serum-free triiodothyronine BKM120 level, 9.4 pg/mL (reference range, 2.0–4.0 pg/mL); free thyroxine level, 3.3 ng/dL (reference range, 0.54–1.40 ng/dL); thyroid-stimulating hormone level, <0.003 microU/mL (reference range, 0.34–5.60 microU/mL); and thyrotropin receptor antibodies, 37.6 UI/L (reference value, <1 UI/L)] which was treated upon admission with thiamazol 10 mg b.i.d and levothyroxin 75 µg q.d. Biological liver and

kidney functions were normal. Albumin level was low (2.1 g/dL). Hepatitis B and C serology was not in favor of chronic infection and human immunodeficiency http://www.selleckchem.com/products/Cisplatin.html virus antibodies were absent. Initial cardiac ultrasound showed a mild reduction of the left ventricular ejection fraction (LVEF) at 40% which declined further during the hospital course (LVEF: 20%), despite adequate treatment of thyrotoxicosis. Metabolic and toxic liver disease was excluded (absence of alcoholism, diabetes, dyslipidemia, non-alcoholic steatohepatitis, alpha-1 antitrypsin deficiency, and absence of apparent autoimmune disease). Computed tomography of the abdomen failed to detect any intraperitoneal expansive process. However, large amounts of ascitic and pleural fluids were present. Positron

Emission Tomography did not show any pathological intraperitoneal Fludarabine datasheet activity. Abdominal and pleural paracentesis fluid was citreous and foamy with exudate parameters (protein levels were 39.9 and 42.2 g/L successively). No neoplastic cells were detected. Mycobacterium tuberculosis culture of peritoneal and pleural fluids remained negative beyond 6 weeks. Biopsy of peritoneal tissue showed chronic inflammation without granulomas. Polymerase chain reaction and culture of peritoneal fluid were both negative for M tuberculosis. Filarial serology using an enzyme-linked immunosorbent assay homemade assay (rat antibodies) was positive. Serologies for other helminths were negative. Smears of cytocentrifugated blood and pleural fluids showed the presence of L loa (Figure 1).