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Biomedical subjects

A Parés

Publications and source records attributed to A Parés.

At least 91 records · Page 5Linked to original sources
PubMed1987

Portal hypertension in primary biliary cirrhosis. Relationship with histological features.

The prevalence and type of portal hypertension (PH) in primary biliary cirrhosis (PBC) and their relationship with liver lesions have been investigated in 32 patients with the disease. Portal hypertension was considered when oesophageal or gastric varices were observed by endoscopy and/or when hepatic venous pressure gradient measured by hepatic vein catheterization was greater than 6 mmHg. Within 3 days of endoscopy, a liver biopsy was performed for histological staging and semiquantitative grading (0 to 3+) of portal and sinusoidal fibrosis, portal inflammation, piecemeal necrosis, lobular necrosis, cholestasis, as well as the presence of granulomas and Mallory's hyaline. Twenty patients (62.5%) had portal hypertension, five of them showing presinusoidal PH (15.5%) and the remaining 15 (47%) with sinusoidal component. The four patients in stage IV had sinusoidal PH and the only patient in stage I had no PH. The prevalence of portal hypertension was similar in patients in stage II (57%) and stage III (55%), but presinusoidal PH was only observed in patients in stage II. Patients with PH showed significantly higher portal inflammation and piecemeal necrosis than patients without PH. By contrast, there were no differences in portal and sinusoidal fibrosis, nor in the other histologic features. These results indicate that portal hypertension is common in PBC and it may be present in the early stages of the disease. The fact that presinusoidal PH was only observed in patients in stage II suggests that portal hypertension is initially of presinusoidal type, and then as the disease progresses is joined by a sinusoidal component.

Adult↗
PubMed1987

Hepatic alcohol and aldehyde dehydrogenases in liver disease.

To investigate the influence of liver injury on the activities of hepatic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), these enzymes have been measured in tissue from alcoholic and non alcoholic patients with different severity of liver damage. ADH and ALDH activities decreased proportionatelly with the progression of liver disease in alcoholics. By contrast, in non-alcoholics, there was a reduction of Low-Km ALDH related with the severity of liver injury but ADH was similar in patients with chronic hepatitis and non-alcoholic cirrhosis. Furthermore, ADH was significantly lower in alcoholic than in non-alcoholic cirrhotics. These results suggests that the decreased ADH and ALDH in alcoholics are not primary abnormalities predisposing to alcoholism and alcoholic liver disease. The diminution of ADH found only in alcoholics could be due to the loss of the enzyme produced by centrolobulillar cell necrosis, that is often observed in alcoholic liver disease.

Adult↗
PubMed1987

Cyanamide hepatotoxicity. Incidence and clinico-pathological features.

Ground-glass hepatocytes resembling those seen in HBsAg carriers on hematoxylin and eosin and on trichrome stained sections, but giving a negative reaction to orcein and a positive one to PAS, were found in liver biopsy specimens from nine asymptomatic former alcoholics who were on treatment with cyanamide, in one of four who had been treated with cyanamide several months before the liver biopsy procedure, in none of 15 treated with disulfiram, and in one of eight who had apparently not received aversive drugs. Portal and periportal inflammatory changes and fibrosis were more frequently observed in biopsy specimens containing PAS-positive ground-glass hepatocytes than in those without, but cirrhosis was found with a similar frequency. It is concluded that periportal PAS-positive ground-glass hepatocytes are a histological marker of cyanamide treatment.

Adult↗
PubMed1986

Serum procollagen type III peptide as a marker of hepatic fibrogenesis in alcoholic hepatitis.

To evaluate if serum procollagen type III peptide levels reflect the extent of liver fibrosis and hepatic collagen synthesis, we have studied 19 patients with histologically proven alcoholic hepatitis and 9 chronic alcoholics with normal liver histology or minimal steatosis. Serum procollagen peptide type III was measured at the time of liver biopsy, and determination of hepatic prolyl-hydroxylase activity, as an index of collagen synthesis, was performed in all liver samples. Hepatic prolyl-hydroxylase activity and serum procollagen peptide levels were significantly higher in patients with alcoholic hepatitis (959 +/- 115 cpm/mg and 33.2 +/- 5.3 ng/ml, respectively) than in alcoholics from the control group (537 +/- 62 cpm/mg and 10.9 +/- 1.5 ng/ml, respectively) (p less than 0.05 and p less than 0.01, respectively). All patients with alcoholic hepatitis had fibrosis (10 mild and 9 severe). Prolyl-hydroxylase activity and procollagen peptide levels were significantly higher in alcoholic hepatitis patients with severe fibrosis than in those with mild fibrosis (1208 +/- 154 cpm/mg vs. 734 +/- 138 cpm/mg, p less than 0.05 and 49.1 +/- 8.8 ng/ml vs. 20.4 +/- 2.6 ng/ml, p less than 0.01). Furthermore, a close correlation was found between the hepatic prolyl-hydroxylase activity and the serum level of procollagen peptide (r = 0.76, p less than 0.001). We conclude that the serum procollagen peptide level is a good marker of hepatic fibrogenesis in alcoholic hepatitis; thus, its serial measurement could be useful in identifying patients in progress to cirrhosis and in assessing the therapeutic efficiency of antifibrogenic drugs.

Adult↗
PubMed1986

Histological course of alcoholic hepatitis. Influence of abstinence, sex and extent of hepatic damage.

The factors influencing the histological evolution of alcoholic hepatitis without cirrhosis have been evaluated in 26 patients (14 males and 12 females) submitted to repeated liver biopsies over a mean period of 1.7 years (1-3). Drinking habits during follow-up were checked by inquiries to patients and relatives and by serial determination of ethanol in urine. At the end of the follow-up, 9 patients (34.6%) had progressed to cirrhosis, 5 (19.2%) still had alcoholic hepatitis and 12 (46.1%) had normal liver or only minimal changes. Nine patients continued drinking heavily, 4 reduced their daily intake markedly and 13 stopped drinking. Improvement of liver lesions was observed in 9 of the abstainers and in 3 non-abstainers that had markedly reduced their alcohol consumption. Among the 9 patients with persistent heavy alcohol consumption, 5 developed cirrhosis and 4 still showed alcoholic hepatitis in their last biopsy. Cirrhosis also developed over 1-2 years in 4 females who had stopped drinking, indicating a marked influence of sex on the course of alcoholic hepatitis. Progression of the disease to cirrhosis despite abstinence occurred in a high proportion of women (4/7) but not in men (0/6). These observations indicate that discontinuation of heavy alcohol consumption often results in improvement of liver lesion in patients with alcoholic hepatitis. However, the risk of progression to cirrhosis remains elevated in women.

Adult↗
PubMed1985

Lymphocytotoxic antibodies in primary biliary cirrhosis.

Sera of 30 patients with primary biliary cirrhosis (PBC) and 72 normal subjects matched for age and sex were examined for the presence of lymphocytotoxic antibodies (LCAs) against B and T cells at 4 degrees C and 37 degrees C. Patients were prospectively screened for: Sjögren's syndrome, scleroderma, Hashimoto's thyroiditis, and rheumatoid arthritis, in which LCAs have been described. Seventeen patients with PBC (56.6%) had LCAs against B cells as compared with only 11 of the 72 normal subjects (P less than 0.001). Five PBC patients (16.6%) also reacted against T cells as compared with none in control group (P less than 0.01). Clinical and biochemical features and the histological stage of PBC were similar in patients with and without LCA. Sjögren's syndrome was present in 13 patients--two with scleroderma and another with Hashimoto's thyroiditis. No patient had rheumatoid arthritis. The prevalence of LCAs was similar in PBC patients with or without autoimmune associated disease (54% vs 59%). We conclude that in PBC a high incidence of LCA is unrelated to the presence of an associated disease. LCA in PBC might be a nonspecific marker of an immune disorder.

Adult↗
PubMed1982

Acute thallium poisoning: an evaluation of different forms of treatment.

Hemodialysis, forced potassium diuresis, chelating agents per os, and Dithiocarb given intravenously during short periods of time were used for the treatment of acute thallium poisoning (ingestion of 750 mg of thallium sulfate), and the effectiveness of these different therapeutic procedures was analyzed. Chelating agents per os (Prussian blue, Dithiocarb, and Dithiozone) were ineffective in our patient, since fecal excretion of thallium was very low and unmodified by them. Forced potassium diuresis and hemodialysis were very useful therapeutic measures, especially in the first 12 days following ingestion. Dithiocarb perfusion seems to be the most effective method for enhancing urinary thallium excretion. This method might be most useful in the treatment of thallium poisoning if its deleterious effects could be eliminated.

Acute Disease↗