Author: Rassa Shahidzadeh, MDSeries Editor: Richard Goodgame, MD

Disclosures

April 25, 2003

Case Presentation

This 29-year-old man developed new-onset ascites while in hospital.

The patient has HIV infection, first diagnosed in 1994. He has been poorly compliant with his highly active antiretroviral therapy (HAART) medications, which were started 3 years ago. He was also previously prescribed prophylaxis for Pneumocystis carinii pneumonia (PCP) and Mycobacterium avium complex (MAC) infections. These latter medications were not taken regularly. A recent CD4+ cell count was 42 cells/mcL and HIV viral load was > 500,000 copies/mL.

Two weeks before admission the patient developed progressive shortness of breath associated with fever, dry cough, and loss of appetite. He presented to hospital and underwent evaluation. Findings on chest radiograph and sputum smear were diagnostic of PCP. He was treated with high-dose trimethoprim-sulfamethoxazole and prednisone. His respiratory status improved slowly. However, by the end of the 10th hospital day, he had developed significant ascites; gastroenterology consultation was requested.

The patient had no prior episodes of ascites or abdominal distension. He had no prior liver, cardiac, or renal disease. There was no nausea, vomiting, abdominal pain, or change in bowel habits. PPD (response to purified protein derivative tuberculin) 1 year ago was negative. He denied alcoholism, but drank 2-3 glasses of gin per day. His last use of crack cocaine and marijuana was about 6 months ago. There was no history of intravenous-drug use.

His pulse was 90 beats per minute; blood pressure, 121/70 mm Hg; respirations, 18 breaths per minute; and temperature, 102° F. There was no palmar erythema, spider angiomata, or scleral icterus. The peripheral pulses were normal. The lungs had persistent rales, but these were reported improved since admission. The cardiac examination was normal. The abdomen was mildly distended, mildly tense, without mass or tenderness. The flanks were bulging. The liver was felt 3 cm below the right costal margin in the midclavicular line; there was no hepatic mass or tenderness. The spleen was not palpable. Paracentesis had been performed and fluid of unusual color was oozing from the puncture site (Figure 1).

Laboratory data on admission were compatible with his acute respiratory illness and PCP. At the time of consultation, results of laboratory studies were as follows:

Hemoglobin: 11.6 g/dL
White blood cell count: 6.3 x 10 cells/mm3
Blood urea nitrogen: 15 mg/dL
Creatinine: 0.8 mg/dL
Total protein: 3.4 g/dL
Albumen: 1.4 g/dL
Total bilirubin: 0.3 mg/dL
Direct bilirubin: 0.1 mg/dL
Alkaline phosphatase: 157 U/L
Alanine aminotransferase: 81 U/L
Aspartate aminotransferase: 65 U/L
Hepatitis viral serologies: all negative

Iron studies and serum levels of ceruloplasmin, alpha-1-antitrypsin, and antinuclear antibody were all normal or negative. Results of sputum microscopy were positive for Pneumocystis carinii and negative for acid-fast bacilli (AFB).

Ascites laboratory results:

White blood cell count: 81 cells/mm3, all lymphocytes
Albumin: < 1 g/dL
Amylase: 32 U/L
Glucose: 105 mg/dL
Lactate dehydrogenase (LDH): 29 U/L
Triglycerides: 1540 mg/dL

No bacteria or mycobacteria were found on stain or culture; cytology was negative for malignancy.

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