Abstract
Peritoneal tuberculosis arises from hematogenous spread of pulmonary foci or from direct spread from an adjacent structure. Diagnosis of peritoneal tuberculosis can be challenging due to nonspecific symptoms, insidious onset, and variable imaging findings. Herein, we report a patient presenting with ascites who was eventually diagnosed with peritoneal tuberculosis.
Keywords: Ascites, peritonitis, tuberculosis
Peritoneal tuberculosis (PT) arises from hematogenous spread of pulmonary foci or from direct spread of Mycobacteria from adjacent structures. PT is the most common type of abdominal tuberculosis (TB), whose prevalence ranges from 5% to 16.6% of extrapulmonary TB.1,2 It is projected that PT accounts for more than two-thirds of abdominal TB, while less common types of abdominal TB include intestinal, luminal, and abdominal-nodal TB.1,3 Herein we present a case of PT in an immunocompetent patient.
CASE REPORT
A 48-year-old man presented with complaints of increased abdominal girth, weight loss, low-grade fever, and night sweats for 3 months. Physical exam revealed a soft and distended abdomen with shifting dullness. He was not on any medications and had no comorbidities. He denied alcohol consumption or tobacco smoking. He had no sick close contacts or any recent travel history.
Laboratory tests showed a mild anemia, with a hemoglobin of 13.0 g/dL (reference range, 13.1–17.2 g/dL), erythrocyte sedimentation rate of 34 mm/h (0–15 mm/h), and C-reactive protein of 34.46 mg/L (<5 mg/L). Abdominal ultrasound revealed the presence of free abdominal fluid and diffuse heterogeneous granular liver parenchyma, supporting the diagnosis of chronic liver disease. Liver tests were within normal limits, and tests for hepatitis A, B, and C and HIV were negative. A diagnostic paracentesis showed a serum ascites albumin gradient (SAAG) of 0.2 g/dL and ascitic fluid white blood cells of 1.70 × 103 cells/dL (91.8% lymphocytes). Ascitic fluid cytology was negative for malignant cells. An ascitic fluid acid-fast bacilli (AFB) test and mycobacterial culture were negative. The adenosine deaminase (ADA) level in ascitic fluid was elevated at 108.5 U/L (0–40 U/L). The Quantiferon test was positive.
Contrast-enhanced computed tomography (CT) of the abdomen and pelvis revealed diffuse thickening and nodularity of the peritoneum, stranding and thickening of the omentum with omental cake appearance, and normal liver parenchymal findings (Figure 1a). CT was suggestive of peritoneal carcinomatosis, with a differential diagnosis of PT. Esophagogastroduodenoscopy and colonoscopy were unremarkable. Serum levels of carcinoembryonic antigen: 1.31 ug/L (<5 ug/dL), alpha fetoprotein: 3.64 ug/dL (0–8.04 ug/dL), and CA-19-9: 9.04 U/mL (0–37 U/mL) were within normal ranges. Thorax CT revealed pleural effusion in the left hemithorax with no signs of pulmonary TB.
Figure 1.
Axial contrast-enhanced CT. (a) Before treatment, showing moderate ascites and diffuse thickening and nodularity of peritoneum. Imaging is suggestive of peritoneal carcinomatosis. (b) After treatment, showing resolution of ascites and peritoneal findings.
With the clinical history, SAAG < 1.1, predominant lymphocytic white blood cells in the ascitic fluid, elevated ADA levels, and a positive Quantiferon test, a diagnosis of PT was made. Anti-TB treatment was initiated for 6 months. With the initiation of treatment, the patient’s clinical symptoms improved. A CT scan at the end of treatment showed resolution of ascites and peritoneal findings (Figure 1b).
DISCUSSION
Diagnosis of abdominal TB can be difficult given the nonspecific and variable clinical presentation. Most cases have symptoms persisting for weeks or months and present with ascites, abdominal pain, loss of appetite, weight loss, and fever.4,5 Ascites is the most common presenting symptom of PT, and it is present in approximately 90% of cases. High suspicion of PT is important in the setting of ascites of unknown origin. Although the ultrasound findings were suggestive of chronic liver disease in our patient, CT scan revealed normal liver findings, and the patient did not have any significant risk factors or any peripheral/laboratory findings of chronic liver disease. CT revealed normal liver imaging and was suggestive of peritoneal carcinomatosis. Peritoneal carcinomatosis, Budd-Chiari syndrome, malignancies causing carcinomatosis ascites (e.g., ovarian cancer, gastric cancer), and peritoneal lymphomatosis should be differentiated from PT, although that might be challenging due to overlapping findings on imaging. The absence of findings of chronic liver disease (palmar erythema, spider angiomata, dilated veins on abdomen, gynecomastia) increases the suspicion for PT.6
Ascitic fluid analysis with SAAG < 1.1, high ADA levels, and a positive Quantiferon test should lead toward the diagnosis of PT, even in the setting of no pulmonary foci and negative mycobacterial culture and AFB of ascitic fluid. AFB and mycobacterial culture of the ascitic fluid often has a low diagnostic yield in PT and can be repeatedly negative.
Early diagnosis, treatment, and follow-up are important, as delayed initiation of anti-TB treatment and a delay in the diagnosis of PT have been shown to be the most important factors in mortality.4,7 Clinical symptoms and ascites usually resolve within a few weeks of treatment initiation.8 Empirical treatment in countries with a high prevalence of TB can be considered in cases with clinical and radiologic findings compatible with PT after excluding other causes.
Disclosure statement/Funding
The authors report no funding or conflict of interest. The patient consented to publication of the case.
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