Serum laminin and N-terminal type III procollagen in chronic alcoholic liver disease.
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Biomedical subjects
Publications and source records attributed to N Batista-López.
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Liver fibrogenesis involves the synthesis of collagen fibrils and proteoglycans by various types of liver cells, including Ito cells, transitional cells, myofibroblasts and hepatocytes. Synthesis of collagen fibrils follows a complex metabolic pathway with intermediate products such as type III procollagen (III-PC). Serum levels of III-PC may reflect the activity of the fibrogenetic process. We analysed the relationship between the serum levels of III-PC (N-terminal peptide) and diverse clinical, biochemical and histological parameters of 77 alcoholic patients (27 cirrhotics), comparing them with those of 15 age- and sex-matched controls. A highly significant difference was obtained between controls and patients (P less than 0.0001), but no differences were observed between cirrhotics and non-cirrhotics. Serum III-PC significantly correlated with clinical and biochemical data of liver function derangement (prothrombin activity, serum albumin, bilirubin, gynecomastia, ascites, encephalopathy, edema, splenomegaly); with the duration of ethanol addiction and with MCV. Sixty patients were followed up for a period ranging between 3 and 1056 days (mean = 356 days); 9 of them died. Patients with III-PC levels above 38 ng/ml had a significantly higher mortality (P = 0.006) than those with levels under 38 (log rank test). Thus, serum III-PC may be a useful tool in the clinical evaluation and prognostic assessment of patients with chronic alcoholic liver disease.
The aim of the present study is to analyze whether the addition of propylthiouracil reverts the influence of ethanol on the development of periportal and pericentral hepatocytes and their nuclei in male albino mice. Propylthiouracil-treated animals showed decreased cellular and nuclear areas when compared with the control animals, except for the 180-day-old animals, whose pericentral cells and nuclei were greater than those of the controls and exhibited fatty infiltration. Pericentral hepatocytes and nuclei of the ethanol-fed animals showed an increase of their sizes, especially in 180-day-old animals. In contrast, hepatocyte and nuclear sizes of the animals treated with both propylthiouracil and ethanol were similar to those of the control group, suggesting a protective effect of propylthiouracil against the ethanol-induced alterations.
Serum testosterone, FSH, LH and prolactin levels have been determined in a group of 32 non-cirrhotic heavy drinkers at 9 and 21 h of the 1st, 3rd, 6th, 11th and 15th days after the onset of a florid ethanol withdrawal syndrome. In addition, serum steroid hormone binding globulin (SHBG) levels were determined at the 1st and 15th days. Serum levels of all these hormones were also determined in a control group of 15 healthy male volunteers. Serum testosterone levels, significantly lower in alcoholics at the beginning of the study, progressively increased along the observation period, recovering the circadian rhythm at the end of it. A significant increase was also observed in serum prolactin levels, in the low and upper limits of the normal range at the beginning and at the end of the study respectively. Serum FSH and LH levels were significantly higher in the alcoholics at the beginning of the study, with no significant variations during the observation period. There was a strong relationship between FSH and LH levels, but not between these hormones and testosterone. Thus, our data suggest that ethanol-induced hypogonadism is primary in origin, functional in nature and transient in its evolution.
Ethanol consumption and/or liver damage may alter liver content of several trace elements, as iron, zinc, copper, and manganese. This alteration may play a role on ongoing liver fibrogenesis. Based on these facts we have determined liver, serum, and urinary Mn, Cu, Zn, and Fe levels in a group of alcoholic cirrhotics and noncirrhotics with normal renal function, comparing them with those of controls. We have observed low liver zinc and high liver copper--this last in relation with histomorphometrically determined total amount of liver fibrosis--and manganese contents in cirrhotics, together with increased excretion of zinc and iron and decreased excretion of manganese. Zinc, iron, and copper excretion kept a relation with data of severity of cirrhosis, including mortality in the case of urinary copper, independently of the use of diuretics. Thus, liver copper and urinary iron, zinc, and copper excretion seem to be related with data of severity of chronic alcoholic liver disease. Low urinary manganese excretion may play a role on liver manganese overload.
We analyzed the relations between nutritional status and several measures of the ability to perform the normal activities of daily living (ADL) in a long-term institutionalized geriatric population and also studied whether changes in this ability, as found ten months later, were associated with changes in the nutritional status. Nutritional status was assessed using objective anthropometric measurements (triceps skinfold, mid upper-arm circumference, midarm muscle area [AMA], midarm fat area [AFA]) and subjective clinical features (temporal muscle atrophy [TMA] and Bichat's fat atrophy [BFA]). The capacity to perform ADL was analyzed considering ability to eat and to walk, dental status, and mental performance status. Patients with total absence or loss of more than 50% of the teeth showed less AMA and AFA and greater degrees of TMA and BFA; the same happened with regard to deterioration of mental performance status. Those patients fed through a nasogastric tube showed less AFA and serum albumin and also a greater degree of TMA and BFA. Patients unable to walk without aid showed less AMA and AFA. Patients whose capacity to walk improved or whose mental performance status ameliorated showed an increase of their AMA, whereas AFA slightly decreased in those patients whose abilities to eat and to walk deteriorated. Long-term hospitalization in our center led to improvement and to deterioration of ADL in approximately the same number of patients, and similar changes were seen in the nutritional measures.