Liver function in pulmonary heart disease.

It is well recognized that some liver function tests are abnormal in heart failure (Jolliffe, 1930; Felder, Mund, and Parker, 1950; Sherlock, 1951; White et al., 1955; Cantarow and Trumper, 1962). Richman, Delman, and Grob (1961) described alterations in indices of liver function in congestive heart failure with particular reference to serum enzymes and drew attention to the increased frequency of abnormal patterns of the tests in episodes of acute heart failure as against chronic heart failure. They and others have found the alkaline phosphatase, thymol turbidity, thymol flocculation, serum proteins, bilirubin, and cholesterol levels relatively insensitive in chronic heart failure (Felder et al., 1950). Richman et al. found the SGOT increased in 33 per cent of patients with increases limited almost entirely to those with acute failure. El-Shaboury, Thomas, and Williams (1964) found increases in SGOT levels in many patients with acute exacerbation of asthma, but without evidence of heart failure. Refsum (1963) showed a close correlation between SGOT and SGPT levels and severity of arterial hypoxaemia in severe pulmonary insufficiency. He remarked on the lack of correlation between the enzymatic changes and clinical signs of right heart failure. In most work the bromsulphthalein (BSP) retention was the most sensitive index of hepatic disorder in heart failure (Sherlock, 1951; Richman et al., 1961; Cantarow and Trumper, 1962). Maclagan and Rundle (1940) described the place of the galactose tolerance test in thyrotoxicosis and suggested that when the galactose index was high structural liver damage was present. It has been suggested that more rapid and complete intestinal absorption of galactose may play a part in this test in thyrotoxicosis, but apart from this, the galactose tolerance test is a test of structural liver damage (Cantarow and Trumper, 1962). The galactose may be given orally or intravenously and the measurements made either in the blood over a period of time up to two hours or in urine collected for five hours. Long experience of the oral galactose test with estimations made on blood samples as described by Maclagan and Rundle (1940) has satisfied us of its reliability and value. The present investigation was undertaken because of the observation that necropsy of the liver in many cases of pulmonary heart disease showed chronic passive venous congestion when right heart failure had not been noted during life. The galactose tolerance test was particularly studied but other indices of liver function were also recorded.