Subject(s)
Hematologic Diseases/blood , Hematologic Diseases/epidemiology , Hospitalization/statistics & numerical data , Adult , Aged , Blood Sedimentation , Comorbidity , Female , Humans , Infections/blood , Infections/epidemiology , Inflammation/blood , Inflammation/epidemiology , Kidney Diseases/blood , Kidney Diseases/epidemiology , Male , Middle Aged , Neoplasms/blood , Neoplasms/epidemiology , Prospective Studies , South Africa/epidemiologyABSTRACT
Adenosine deaminase (ADA) activity is increased in effusions caused by certain clinical conditions including tuberculosis and bacterial infections. In this study, the ADA isoenzyme patterns in tuberculous and parainfective effusions were investigated to determine the isoenzyme responsible for this increase in activity. Fifty-one tuberculous effusions and six parainfective effusions were investigated. All effusions had increased ADA activity (median values of 126 and 127 units/L, respectively). In the tuberculous effusions, ADA2 isoenzyme was found to be primarily responsible for total activity, with a median contribution of 88 percent. The ADA1 (both ADA1m and ADA1c isoenzymes) was the major isoenzyme in the parainfective effusions with a median contribution of 70 percent. The ADA2 isoenzyme activity most likely reflects monocyte-macrophage turnover or activity, while ADA1 probably originates from lymphocytes or neutrophils. It is therefore essential to determine the isoenzyme profile when interpreting ADA activity levels in effusions. The measurement of the individual isoenzymes will enhance the diagnostic utility of ADA activity determinations in pleural effusions.
Subject(s)
Adenosine Deaminase/analysis , Isoenzymes/analysis , Pleural Effusion/enzymology , Tuberculosis, Pulmonary/enzymology , Adult , Aged , Aged, 80 and over , Ascites/enzymology , Ascites/etiology , Biomarkers/analysis , Electrophoresis, Polyacrylamide Gel , Female , Humans , Male , Middle Aged , Pleural Effusion/etiology , Spectrophotometry , Tuberculosis, Pulmonary/complications , Tuberculosis, Pulmonary/diagnosisABSTRACT
A patient presented with typical features of ankylosing spondylitis, as well as some of the biochemical abnormalities expected in this disease. In addition the patient had symptoms and signs of biventricular heart failure (dilated cardiomyopathy) with conduction defect. No valve lesions were demonstrated. A non-reducible head tilt, seldom described in ankylosing spondylitis, was also present. A short review of the possible mechanisms in the development of dilated cardiomyopathy in ankylosing spondylitis is given.
