In October 2011, the authors visited a 46-year-old immigrant Moroccan for the first time.
The patient reported having suffered 4-6 months from a relentless hiccup, irregular dyspeptic illness, a lack of appetite, a tense (but not painful) abdomen, and weight loss. He did not report fever or sweating. The examination showed the presence of hard, non-painful, bilaterally enlarged lymph nodes in the inguinal and axillary sites, and abdominal distension that suggested an ascitic fluid collection. No cardiovascular signs or symptoms were present. An abdominal ultrasound examination (Figure 1) confirmed the presence of ascites, but there was no enlargement of the liver or the spleen. In summary, an ascitic fluid collection with no signs of portal hypertension was present. The patient was admitted to the hospital, where further diagnostic procedures were performed including: an esophagogastric-duodenoscopy (OGD-scopy) showing signs of Helicobacter pylori and erosive gastritis, and colonos-copy showing a villous adenoma with low-grade dysplasia. A chest and abdomen CT scan (Figure 2) revealed bilateral apical scarring of the lung parenchyma and absence of hilar and mediastinal lymphoadenomegaly, and confirming the presence of abundant ascitic fluid. No significant alterations were seen in the other organs. Blood tests showed normochromic and normocytic anaemia (Hgb 10.6 gr/dl), low iron, and normal ferritin. Transaminases were slightly high, and indexes of inflammation were consistently high, with CRP values between 3.4 and 4.3 mg/dl, D-Dimer 1187 ng/ml, and ESR 42. A Mantoux intradermal reaction was positive (8 mm), but an HIV test, tumor markers, and serologies for hepatitis were negative. The following test results were normal: rheumatoid test (anti-nuclear antibodies), antimitochondrial antibodies, anti-smooth muscle antibody, liver-kidney-microsome antibodies, and anti-neutrophil cytoplasmatic antibodies), antiphospholipid antibodies, and circulating immunocomplex and complement factors. Examination of the ascitic fluid was positive to alkaline reaction, and the Rivalta test showed a protein content of 65.3 g/l. Microscopic examination of the sediment revealed the presence of erythrocytes, leukocytes with predominantly mature lymphocytes (lymph: 80%), and a total amount of polymorphonuclear leukocytes of 1100 n /mmc. Direct bacterioscopy and cultures for mycobacteria were consistently negative. Cytological analysis for atypical cells was negative.
The average albumin in the ascitic fluid was 3.2 g/dL, and the average albumin in the serum was 2.8 g/dl; therefore, the serum ascitic albumin gradient (SAAG) was 0.4 g/dl.
M. tuberculosis PCR (Polymerase Chain Reaction), performed in a laboratory at another local hospital, was negative. A biopsy of 2 small lymph nodes in the left inguinal side showed only aspecific reactive inflammation. The patient was discharged from the hospital after 32 days, with a diagnosis of "ascites of uncertain nature and signs of inflammation". Radiographic examination of the small intestine was negative. A laparoscopy with directed peritoneal biopsy, which is thought to be the best diagnostic procedure for tuberculosis peritonitis, was subsequently performed at another hospital. Laparoscopy of the abdomen revealed large macro- and micro-nodular degeneration of the visceral and parietal peritoneum, and the presence of plaques and omental thickening, interpreted macroscopically to be similar to a massive peritoneal carcinomatosis.
Histological examination of the peritoneal biopsies showed epithelial granuloma with the presence of Langhans-type giant cells and a wide area of caseous necrosis, but without acid-fast bacilli Figure 3). Cytological examination of the ascitic fluid showed the presence of inflammatory cells, predominantly lymphocytes, monocytes, and a small number of polymorphonuclear cells, similar to Langhans cells (Figure 4). The patient was dismissed with a final diagnosis of massive peritoneal tuberculosis. During the short period (15 days) of hospitalization in the Infectious Disease Department, the patient was started on a 4-drug regimen of isoniazid, rifampicin, pyrazinamide, and streptomycin. During the final stay in the hospital, direct examination and cultures of urine, feces, and sputum for mycobacteria were performed, but all results were negative. After administration of the last treatment with streptomycin, the patient was dismissed in good general condition, with maintenance therapy and a follow-up protocol.