Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In order to determine the frequency of hypoxaemia and to evaluate the role of increased closing capacity in producing hypoxaemia in patients with
cirrhosis of the liver
, 13 patients with well-established
cirrhosis
were studied. Arterial blood gases, spirometry, lung volume, and closing capacity measurements were made with the patients in the seated and recumbent positions after exclusion of cardiopulmonary dysfunction. Four of 13 and six of 12 patients exhibited significant hypoxaemia in the seated and recumbent positions respectively. Five of 13 patients showed a closing capacity greater than predicted. This frequency of increased closing capacity was not higher than in a group of smokers of the same age. Unlike Ruff et al. (1971), we did not find a consistent relationship between hypoxaemia and closing capacity.
Thorax
1976 Jun
PMID:Hypoxaemia and cirrhosis of the liver. 94 Nov 16
The first reported case of pulmonary infection with Nocardia caviae in Britain occurred in a 67 year old woman, in whom diabetes mellitus and
liver cirrhosis
probably contributed to impaired cell mediated immunity. She was successfully treated with gentamicin 60 mg eight hourly and sulphadimidine 500 mg six hourly for six months and then with sulphadimidine 2 g/day for a further three months. When Nocardia caviae is isolated from the sputum of a patient with chronic respiratory infection and fever, effective treatment should be started promptly.
Thorax
1988 Nov
PMID:Pulmonary infection with Nocardia caviae in a patient with diabetes mellitus and liver cirrhosis. 322 67
Pulmonary arterial hypertension with severe pulmonary vascular disease is a rare association of portal hypertension in man, be it the result of
cirrhosis of the liver
or obstruction of the portal vein. We induced portal hypertension in 23 rats by partially ligating the portal vein or by totally occluding it in two stages. The rats were killed between one and 15 months after operation. A collateral circulation of varicose, anastomotic vessels was established, and in six animals well-marked oesophageal varices developed. Despite this evidence of sustained portal hypertension, hypertrophy did not develop in the right ventricle or in the media of the pulmonary trunk or muscular pulmonary arteries in any of the animals. This suggests that mechanical obstruction of the portal vein per se is not responsible for the development of pulmonary hypertension. Other factors, perhaps of a humoral nature, appear to be required to induce this rare association of portal hypertension but we have been unable to identify these. In particular, blood levels of oestrogen were not raised after ligation of the portal vein.
Thorax
1980 Dec
PMID:Observations on the rare association between portal and pulmonary hypertension. 726 72
Primary pulmonary hypertension with plexiform vascular changes in the lungs and
liver cirrhosis
is a rare combination of unclear pathogenesis. Until now, the real prevalence has not been known. The diagnosis of this association is usually made retrospectively. The criteria are morphological--that is, right ventricular hypertrophy and the characteristic pulmonary arterial lesions, as well as clinical--based on ECG and chest radiography. Between 1970 and 1977, two such cases have been found among a total of 11988 necropsies performed on adults. In the same necropsy series, 765 cases of
liver cirrhosis
were found. The prevalence of this combination is 0.26% of the
cirrhosis
and 0.016% of all necropsies of adults. This low prevalence raises serious doubts as to whether the association is more than coincidental.
Thorax
1980 Feb
PMID:Plexogenic pulmonary arteriopathy and liver cirrhosis. 737 17
Pulmonary complications of alpha 1-antitrypsin deficiency are most commonly manifested by panlobular emphysema. This report describes histologically proven bronchiectasis in a 21 year old man with massive haemoptysis and homozygous deficiency of alpha 1-antitrypsin. Neither panlobular emphysema nor
cirrhosis of the liver
were present. Bronchiectasis must be considered part of the spectrum of the pulmonary pathology that may be encountered in individuals with alpha 1-antitrypsin deficiency.
Thorax
1995 Apr
PMID:Bronchiectasis and homozygous (P1ZZ) alpha 1-antitrypsin deficiency in a young man. 871 67
A clear association has been described between numbers of pulmonary endocrine cells and the migration and/or proliferation of myofibroblasts which is thought to underlie the vascular changes seen in plexogenic pulmonary arteriopathy due to cardiac shunts and primary pulmonary hypertension. In contrast, the pulmonary endocrine system in a subject with florid pulmonary plexogenic arteriopathy associated with
cirrhosis
was entirely normal, suggesting possible differences in its pathogenesis.
Thorax
1995 Jan
PMID:Pulmonary endocrine cells in plexogenic pulmonary arteriopathy associated with cirrhosis. 788 60
A 37 year old patient with chronic active hepatitis progressing to
cirrhosis
presented with increasing breathlessness and was found to be hypoxic with finger clubbing. A progressive exercise study with measurement of oxygen saturation (SaO2) showed abnormally high ventilation and desaturation to 81% at 100 W. Serial studies over nearly two years showed, first, deterioration, then improvement with lower ventilation and higher saturation levels at all work loads. This could not be correlated with any change in treatment with azathioprine, prednisolone, or propranolol.
Thorax
1994 Jul
PMID:Spontaneous improvement in a patient with the hepatopulmonary syndrome assessed by serial exercise tests. 806 74