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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary arterio-venous shunts represent a rare cause of hypoxia in cirrhosis. We present two cases, the first was an alcoholic cirrhotic with anthracosilicosis. This patient rapidly developed a picture of significant hypoxaemia with a raised alveolar-arterial oxygen gradient. The presence of this shunt was confirmed by a scintigraphic analysis. A porto-pulmonary localisation was excluded by a changing angiographic picture. Death supervened after refractory hypoxaemia. Post mortem microangiographic studies confirmed the pulmonary nature of the shunt and its pre-capillary localisation. The second patient was alcoholic, with a compensated cirrhosis and developed severe hypoxaemia which progressed to death in less than two months, when he was being treated effectively with corticosteroids for a diffuse interstitial pulmonary fibrosis confirmed histologically. The pulmonary localisation of the shunt was confirmed by an analysis of the angioscintigraphs. The different techniques for the investigation of intra-pulmonary shunt are discussed, as well as the patho-physiological mechanisms involved. The hormone levels measured (sex hormones, serotonin, prostaglandins, intestinal hormones) remained normal. The therapeutic trials tried out (oestrogen, CPD Choline, indomethacin) were ineffective.
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PMID:[Technics for the exploration of pulmonary arteriovenous shunts in liver cirrhosis. Apropos of 2 cases]. 374 86

Histological sections of the liver taken at the autopsy of 26 patients with anthracosilicosis of different degrees of severity were investigated retrospectively. Single macrophages containing dust were found in the portal fields, as well as dust storing Kupfer cells proliferating centroacinarity. Granuloma of the walls of central and sublobular veins could be observed, containing infiltrates of lymphocytes and plasma cells, proliferating fibroblasts including histiocytes, and fibrosis and hyalinisation in later stages. It may be assumed, that dust pigments are being transported by blood and taken up by Kupler cells in the first line, to be transmitted directly to the central vein and to a lesser degree by way of lymph drainage into the portal mesenchyma in a later stage. These morphological changes of the liver apparently did not cause any clinical symptoms; they could be found in a high percentage of all patients, which did not have cirrhosis of the liver, and they could be found in all degrees of severity of anthracosilicosis. Thus liver biopsy will yield valuable diagnostic results in this granulomatous disease of the liver as well.
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PMID:[Morphology of the liver in anthracosilicosis (author's transl)]. 741 61

352 hepatocirrhosis cases were among the 7139 autopsy cases of the years 1964--1973. It could be ascertained statistically: Together with the increasing scarred liver transformation the number of oesophageal piles and ascites increased. The greater the scarred transformation and cirrhosis activity the higher was the number of hepatocirrhoses known at lifetime. An increase of spleen weight due to scarred liver transformation could not be proved. The expected correlation between degree of fibrosis and liver weight could not be confirmed. According to expectation, hepatocirrhosis cases known at lifetime caused death more frequently than cases with unknown hepatocirrhosis. We want to point out, however, that 13 cases of death may be directly attributed to clinically unknown hepatocirrhosis. The medically unknown hepatocirrhosis cases in one group were frequently still "young" hepatocirrhosis cases without ascites and oesophageal piles, or the clinical features of advanced hepatocirrhosis were masked by other severe diseases (e.g., anthracosilicosis of the lung).
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PMID:[Comparative morphological-statistical investigations in deaths with clinically known and unknown hepatocirrhosis (author's transl)]. 744 95