Value of Serum Adenosine Deaminase (ADA) in Distinguishing between Tuberculous and Non-tuberculous Lymphadenopathies.

Persistent lymphadenopathy with or without fever is often a diagnostic challenge to the physician which are usually caused by infection like tuberculosis, hematological malignancy (lymphoma, leukemia), connective tissue diseases (SLE, RA, Sjogren's syndrome etc.), sarcoidosis, storage diseases, drugs (like phenytoin) in Bangladesh. To establish the cause of lymphadenopathy, we need to do a good number of investigations including invasive tests like FNAC or histopathology of the involved lymph node. In many instances these are not possible due to unavailability or cost. But for last few years the adenosine deaminase is an enzyme involved in purine catabolism and its significance in the diagnosis of tuberculosis has been demonstrated by many studies. In addition to tuberculosis, elevated serum adenosine deaminase has also been found in lymphoma, sarcoidosis and some connective tissue diseases. The study was intended to assess if there are any significant diagnostic difference in the level of elevated adenosine deaminase between tubercular and different types of non tubercular lymphadenopathy. It included 68 patients, equally divided into two groups, tuberculous lymphadenitis and non-tuberculous lymphadenopathy. Epitheloid granuloma with caseation necrosis in biopsy or FNAC was taken as case definition of tuberculous lymphadenitis. Causes of non-tuberculous lymphadenopathy were established on the basis of clinical findings, laboratory investigations and histopathological diagnosis of biopsy or FNAc materials. This cross-sectional observational study was done in Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh over a period of one year and participants of 18 years and above of both genders were included as per consecutive sampling technique. Serum ADA concentrations were estimated by enzymatic method. Mean serum ADA concentration was 25.52±7.11 in tuberculous lymphadenitis and in non-tuberculous lymphadenopathy patients it was 27.29±15.91U/L with no significant difference (p=0.480). The non-tuberculous lymphadenopathy group consisted of Hodgkin disease (n=9), non-Hodgkin lymphoma (n=10), sarcoidosis (n=2), reactive lymphadenitis (n=9) and other lymphadenopathy group (n=4) (that consisted one case of each of follicular hyperplasia, adult Still disease, sinus histiocytosis and Castleman's disease). The mean ADA of these groups was 32.77±13.14U/L, 46.40±46.10U/L, 13.94±2.81U/L and 21.75±3.17U/L respectively. Tuberculous lymphadenitis patients had significantly higher serum ADA than persistent reactive lymphadenitis. On the other hand, there were statistically significant elevation of serum ADA in non-Hodgkin lymphoma and sarcoidosis than in tuberculous lymphadenitis.