Human atrial natriuretic factor and renin-aldosterone in paracetamol induced fulminant hepatic failure

Article Abstract:

Blood volume is a physiological parameter that is ordinarily tightly controlled by a variety of homeostatic mechanisms. In patients with liver failure, there is a breakdown in these controls, and severe fluid retention is often a complication of hepatic (liver) dysfunction. It has been postulated that the body may develop either a deficiency in the secretion of, or a resistance to the actions of, a circulating natriuretic (causing urinary excretion of sodium) factor that might be partially responsible for the fluid retention. Atrial natriuretic factor (ANF) may be such a factor; it is released from the atria of the heart in response to atrial stretch (as would occur with increased blood volume) and induces diuresis (urination) and sodium excretion, resulting in a decrease in blood volume. To investigate the possible role of alterations in secretion of or sensitivity to ANF during hepatic failure, 33 patients with drug-induced liver failure and 12 healthy control subjects were studied. Blood levels of ANF were increased only in patients with evidence that kidney failure led to the increases in blood volume. Blood levels of renin and aldosterone (two other hormones involved in the regulation of fluid balance) were also increased in this group of patients. Hemodialysis (a technique for cleansing the blood of toxins) reduced ANF levels to an extent predicted by the decrease in blood volume. In a subset (six) of the patients that had no evidence of kidney failure, infusion of a protein solution (human albumin) induced an increase in ANF levels with no increase in urinary excretion of water or sodium. These results suggest that release of ANF is not impaired during hepatic failure, but the target tissues for this substance may develop an insensitivity to its actions. (Consumer Summary produced by Reliance Medical Information, Inc.)

Liver failure, Natriuretic peptides

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Amenorrhoea in women with non-alcoholic chronic liver disease

Article Abstract:

One of the consequences of prolonged excessive alcohol intake is liver damage. Gonadal dysfunction and feminization are well documented side effects of alcoholic cirrhosis in men; gonadal dysfunction is less well documented in women, but may occur. Questions have arisen concerning to what extent these changes are a direct result of alcohol or a consequence of the liver damage. To further investigate this, 12 young women with non-alcoholic liver disease were compared with 11 healthy age-matched controls studied in the follicular phase of their menstrual cycle. All 12 patients were amenorrheic (they did not menstruate); none of the patients had elevated levels of follicle-stimulating hormone, which would have suggested a primary disturbance of the ovaries. Seven of the 12 patients (58 percent) had decreased blood levels of luteinizing hormone, estradiol, and testosterone. Amenorrhea was not related to the duration or the severity of the liver disease. Bone density, as measured by metacarpal cortical bone area, was decreased in liver patients with low estrogen levels, and the extent of the change was proportional to the duration of amenorrhea. These results suggest that amenorrhea in women with non-alcoholic liver disease is the result of a dysfunction of the hypothalamic-pituitary system, and may occur at several points within that pathway. In cases where there is prolonged estrogen deficiency, adverse effects (such as the development of osteoporosis) may be predicted. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Complications and side effects, Amenorrhea, Menstruation disorders, Hormones, Sex, Sex hormones

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Immune mechanisms in tienilic acid associated hepatotoxicity

Article Abstract:

To identify the mechanisms underlying the destructive or poisonous effect (hepatotoxicity) upon liver cells of tienilic acid (Ticrynafen) ingestion, the authors looked for evidence of drug-altered liver cells using an indirect antibody-dependent, cell mediated cytotoxicity test (ADCC). (Ticrynafen, a diuretic drug, was withdrawn because of its destructive or poisonous effect upon liver cells.) Blood from 16 of 36 patients with presumed tienilic acid hepatotoxicity induced significant cytotoxicity to liver cells isolated from rabbits treated with tienilic acid. These results suggest that this drug reaction is associated with sensitization to drug-altered liver cell antigens and autoantigens. If the liver cell toxicity caused by ticrynafen is mediated by the immune system, then one possible mechanism is that the antigens formed by the drug attack normal liver cell components.

Evaluation, Drug therapy, Liver cells, Hepatocytes, Phenobarbital, Antibody-dependent cell cytotoxicity, Toxic hepatitis

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