Should We Use Adenosine Deaminase Assay for the Differential Diagnosis of Tuberculous Peritonitis in CAPD Patients?

Abstract

Editor: We read the recent International Society for Peritoneal Dialysis (ISPD) peritonitis guidelines and recommendations (1). In the guideline, only Löwenstein-Jensen culture of peritoneal fluid, mycobacterial DNA PCR (polymerase chain reaction), and laparoscopic peritoneal biopsy are advised as a diagnostic work-up in tuberculous (TB) peritonitis. The principle of the adenosine deaminase (ADA) assay is to detect either hydrogen peroxide or ammonia after enzymatic deamination of adenosine to inosine. Production of the enzyme ADA in bodily fluids reflects the presence of activated T lymphocytes and monocytes (2). Many studies have investigated the usefulness of ADA in ascites for the diagnosis of TB peritonitis (3,4,5). Two metaanalyses suggested that ADA in the ascites can be a sensitive and specific target and a critical criterion for the diagnosis of TB ascites (6,7). Riquelme et al. reported a meta-analysis which included 12 prospective studies. They investigated 264 patients, of whom 50 (18.9%) had peritoneal tuberculosis. Adenosine deaminase levels showed high sensitivity (100%) and specificity (97%) using cut-off values from 36 to 40 IU/L (8). Some studies have shown that ADA assay sensitivity is substantially lower in patients with cirrhosis due to poor humoral and T-cell mediated response (9). A question that arises here is whether the ADA assay is reliable in immunocompromised patients, such as those with chronic kidney and liver diseases. We would therefore like to discuss using the ADA assay for diagnosis of TB peritonitis in peritoneal dialysis (PD) patients. In the literature, there are limited data for using ADA assay in continuous ambulatory PD (CAPD) patients. In one case report, patients with end-stage renal failure were tested for ADA levels in the peritoneal fluid, allowing an early presumptive treatment and a favorable outcome with a 3-year follow-up (10). On the other hand, in a study by Nakav et al., bacterial peritonitis was induced in mice by intraperitoneal injection of Escherichia coli. Following inoculation, ADA mRNA levels and activity in the lavage fluid significantly increased at 48 hours in the late phase of bacterial peritonitis (11). In conclusion, the ADA assay is inexpensive, quick, and simple to perform and has great value for the immediate diagnosis of tuberculous serositis while culture results are pending. It is clear that large-scale studies on the diagnostic value of the ADA assay in chronic renal failure and CAPD patients are needed. In the next guideline, the usefulness of ADA assay should be evaluated in CAPD patients.