Functional hepatic impairment in pulmonary tuberculosis.

The work presented in this paper has been prompted by the dearth of material on the subject. In a preliminary report of 18 cases by Hurst, Maier and ‘Lough’ the following observations have been made: That in a study of far advanced pulmonary tuberculosis using Hanger’s cephalin cholesterol flocculation test, the Hippuric acid synthesis and the 5 mg. serial Bromsulphaleln test as tests of hepatic function, where the NPN, Serum Protein, Cholesterol and Esters, Prothrombin Time, Bilirubin and Urobilinogen were within normal limits, hepatic dysfunction was demonstrated in a large percentage of cases. Bromsulphalein showed the greatest number of positive results-47 per cent. It will be our object to limit study to what we believe to be two of the most reliable tests of liver function and critically examine the values obtained in the light of the stage of the disease, the chronicity, the amount of inanition present and the character of the pulmonary lesion, always considering other etiological factors which might tend to distort results. The fact has long been established that hepatic parenchymal damage is a frequent finding at necropsy in the tuberculous. Conflicting opinions have been voiced as to the pathogenesis and the micropathology of the process. Florentin, et al,2 reviewed 35 cases of chronic pulmonary tuberculosis that came to autopsy and only reported three cases with fatty livers. However, twothirds of his cases gave evidence of typical inflammatory process without evidence of fatty degeneration. Periportal sclerosis was observed only rarely, but massive proliferation of Kupfer’s cells was an almost constant feature. He points out that fat deposition in the liver cells usually starts at the periphery of the hepatic lobule. In order that fat may be deposited, the body must have sufficient reserves in lipids and glucosides, and the endocrine system must be intact. He further reasons that since fatty livers