Adrenal Function in Chronic Pulmonary Tuberculosis

Abstract

The frequency, extent and importance of adrenal involvement in pulmonary tuberculosis, and the role of the adrenal in the clinical symptomatology of this disease have been the subject of widely divergent opinions for many years. This lack of unanimity has a variety of reasons, some of fundamental Importance. All too often, judgment as to the presence or absence of adrenal cortical hypo-function has been based solely on clinical criteria such as gastrointestinal disturbances, asthenia, hypotension, and so forth; these symptoms, though usually present in severe adrenal insufficiency, are by no means pathognomonic, and their significance is particularly difficult to interpret in a disease such as tuberculosis where intestinal lesions, malnutrition, and debility are so common. Thorn’ states, as a matter of fact, that the differential diagnosis of Addison’s disease may present great difficulty “in patients with established tuberculosis elsewhere (i.e., not in the adrenal) whose excessive weakness, gastrointestinal symptoms or pigmentation raises the question of adrenal involvement” unless detailed studies of adrenal function are performed. The small, globular heart which forms part of the clinical picture of the now discredited “habitus phthisicus” and which was thought to bear some relationship to the small heart commonly found in Addison’s disease has been shown by us to have no relation to adrenal function, as far as could be judged by available criteria.2 Even isolated biochemical data may be misleading in this problem, for low serum sodium values have been observed in patients with chronic pulmonary tuberculosis but without any evidence of adrenal failure.3 Other biochemical attempts to study adrenal function by highly roundabout means have served only to confuse the picture further. Trautwein,4 studying liver glycogen in tuberculous patients by indirect tests, found that depletion of liver glycogen exists in such patients, and that repletion could be induced by the administration of adrenal cortical substance. This and similar data were considered to be evidence of adrenal cortical insufficiency. Actually, they merely demonstrate well-known physiological effects of adrenal cortical hormones, and can be observed clinically as well as In starved nonadrenalectomized animals. Experiments of this type, then, cannot add to our knowledge of the adrenal status in tuberculosis. Abderhalden and Abderhalden5 claim that certain urinary proteases reflect adrenal cortical activity. On the basis of this measurement, they state that nearly all severe cases, as well as 36 per cent of “mild” cases of tuberculosis show disturbance of adrenal function.