Gene/Protein Disease Symptom Drug Enzyme Compound
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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Functional hepatic reserve was determined in 32 patients with known liver or biliary tract disease employing kinetic analysis of hepatic removal of indocyanine green (ICG). The initial removal rates of incremental doses of ICG (0.5, 1.0 and 5.0 mg/kg body weight) were plotted as a reciprocal against the inverse of dose (Lineweaver-Burk plot) to provide a means of determining maximal removal rate from submaximal doses (Rmax). This function equalled 3.40 mg/kg/min in ten patients with normal livers, but was only .24 mg/kg/min in eight patients with alcoholic cirrhosis. Portasystemic shunting did not further influence Rmax. Infiltrative liver disease had only a mild depressive effect on this function. The results show that hepatic function can be precisely quantitated by classical enzyme kinetics (Michaelis-Menten). If Rmax is an estimate of protein receptor mass for organic anions, then the technique may allow an indirect means for quantitating hepatocytes even in the presence of changes in blood flow or hepatic function. The profound depression in R(max) observed in patients with alcoholic cirrhosis is consistent with the progressive loss in hepatic mass associated with this disease.
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PMID:Estimation of the functional reserve of human liver. 441 86

The present status of oral contraceptive steroids and the IUD, the 2 most effective and increasingly popular contraceptive methods (used by 41.6% of all U.S. married couples practicing contraception in 1970), is presented. Oral steroid contraceptives with varying quantity and activity of estrogen (ethinyl estradiol or mestranol) and progestogen (norethindrone, norethynodrel, ethynodiol diacetate, or norgestrel), are of 3 types: combination, sequential, and minidose progestogen alone. The most effective contraceptive available is the combined oral pill with a pregnancy rate of less than .2 % per 100 women after 1 year. Contraceptive action is exerted primarily through inhibition of ovulation and secondarily by alterations in cervical mucus, endometrial glands, the ovary, and in the oviduct and uterine muscle. In comparison, sequential oral contraceptives are less effective with greater side effects, and should only be used in women with amenorrhea. Effects of oral contraceptives other than contraception include those on the (1) the primary targets of the female reproductive system, (2) on other endocrine oragans and (3) on the remainder of the body. In the first group, changes may include transitory stromal fibrosis in the ovary, enlarged fibromyomata, intermenstrual bleeding or amenorrhea, increased amount of cervical mucus, polypoid hyperplasia of the endocervical glands, breast tenderness, and changes in lactation. Changes in the second category which may occur affect the adrenal glands, hypothalamus, the thyroid (increased thyroid-binding globulin), and pancreas (alterations in glucose metabolism). Effects on the rest of the body may include increase in serum lipids and changed atherogenic index, abnormalities in liver function, thromboembolism (incidence in oral contraceptive users 4.4 times that in non-users), melasma, alterations in the central nervous system with increased incidence of cerebral vascular accidents, hypertension, and increased body weight. Absolute contraindications to oral contraceptive therapy include cancer of the breast and uterus, pregnancy, active liver disease, hyperlipidemia, and history of gestational diabetes, thromboembolic phenomena or coronary artery disease. Relative contraindications include depression, migraine, myomata of the uterus, hypertension, epilipsy, oligomenorrhea and amenorrhea. Reliable epidemiologic data on IUDs from the Cooperative Statistical Program indicated first year pregnancy rate of 2.5%. Problems with the IUD include: 1) pregnancy with device in situ, which is associated with a higher incidence of spontaneous abortion; 2) ectopic pregnancy, which is prevented at a rate of only 90% compared with intrauterine pregnancies prevented in 97-98%; and 3) expulsions (20% of which are unnoticed), the expulsion rate being higher with decreasing age and parity, higher in the first than second year of use, and higher with smaller than larger devices. A major problem is discontinuation for medical reasons (15% rate in the first year), mainly bleeding and pain. Perforation, another serious complication, occurs initially at time of insertion with an incidence of 1 per 2500 insertions for the loop. IUDs were found to produce a sterile inflammatory tissue reaction, which is postulated as the primary causative factor for their contraceptive effect in humans.
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PMID:Current status of contraceptive steroids and the intrauterine device. 459 80

Coagulation studies were carried out on 30 patients with chronic liver disease. The clotting defect was complex and involved factors V, VII, IX (Christmas factor), and prothrombin. Some patients showed a significant depression of factor IX in the presence of a normal one-stage prothrombin time. Thrombotest was found to be a good indicator of factor IX deficiency in this group of patients and may be of use as an additional liver function test. The screening of patients with liver disease for surgery or liver biopsy should assess the coagulation factors involved in both intrinsic and extrinsic thromboplastin generation.
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PMID:Coagulation factors in chronic liver disease. 577 51

Pretreatment with ammonium acetate (NH4Ac) (6 mmol/kg s.c.) approximately doubled the time morphine-treated mice remained on a hot surface and similarly increased muscular incoordination by diazepam, but NH4Ac treatment alone had no effect. Thus, hyperammonemia is capable of altering drug action and must be considered along with impaired drug metabolism in enhanced drug responses associated with liver disease. Experiments in vitro showed that acetylcholine-induced catecholamine release from bovine adrenal medulla is depressed as much as 50% by 0.3 mM NH4Ac and KCl-induced contractions of guinea-pig ileum were inhibited 20% by 5 mM NH4Ac. Addition of excess calcium reversed the depression in both tissues, but calcium-independent catecholamine release by acetaldehyde was not blocked by NH4Ac. These results suggested that ammonia blocks calcium channels. Parallels in the actions of NH4Ac and the calcium channel blocker verapamil support this concept. Both verapamil (10 mg/kg i.p.) and NH4Ac pretreatment enhanced morphine analgesia- and diazepam-induced muscular incoordination and antagonized amphetamine-induced motor activity, and neither verapamil nor NH4Ac affected the convulsant action of metrazol. The data suggest that hyperammonemia exerts a calcium channel blocking action which enhances the effects of central nervous system depressants and certain opioid analgesics.
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PMID:Modification of drug action by hyperammonemia. 632 92

Plasma amino acid abnormalities are frequently reported in alcoholics, with the most common abnormalities being those of depressed branched chain amino acids (BCAA) and increased aromatic amino acids. The depression in branched chain amino acids is due to multiple factors including portal-systemic shunting, hyperinsulinemia, hyperglucagonemia (all due to advanced liver disease) as well as dietary deficiency. alpha-Amino-n-butyric acid is a nonessential amino acid derived primarily from the catabolism of methionine, threonine, and serine. Increased levels due to chronic alcohol consumption may reflect altered glutathione metabolism and lipid peroxidation due to alcohol and may be used empirically as a biochemical marker of heavy drinking. The high levels of aromatic amino acids such as tyrosine and tryptophan as well as their breakdown products may be due to impaired hepatic metabolism and appear to play a role in the pathogenesis of hepatic encephalopathy. The effects of high levels of aromatic amino acids may be potentiated by depressed BCAA; these normally compete with each other for CNS transport. Alterations in these amino acids may have implications for nutritional requirements for amino acids in these patients as well as therapeutic approaches.
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PMID:Plasma amino acids in the alcoholic: nutritional aspects. 634 43

We conducted formal psychiatric evaluations and extensive chart reviews in a series of 34 patients surviving an average of 5 1/4 years after hepatic transplantation. Seven of 14 children and 19 of 20 adults exhibited obvious psychiatric disturbances before the operation. (There was not time to evaluate another 5 children and a sixth was an infant; one adult arrived in hepatic coma.) All patients experienced psychiatric problems postoperatively. Organic brain syndromes and apprehensiveness were the most common preoperative problems in pediatric patients, and problems in relationships with family members, anxiety, regression, and helplessness were most common after surgery. In adults, organic brain syndromes, anxiety, and depression were the most common preoperative and postoperative problems. While psychosocial disturbances in liver transplant recipients were similar in many respects to those of the more well-studied kidney homograft patients, a number of important differences emerged: organic brain syndromes, fear of death, severe regression (psychological functioning appropriate to a younger age), worries that a suitable donor would not be found in time, and insomnia were more common, and concerns about the origin of the homograft and about changes in body image were relatively rare postoperatively. These differences seem to be related to the severity of liver disease requiring transplantation, the effects of the illness on the brain, the lack of an alternative means of life support resulting in greater prominence of concerns about survival, the exclusive use of cadaver rather than living donors, and the greater effect of the illness than of its treatment on physical appearance.
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PMID:Psychiatric aspects of hepatic transplantation. 634 38

The literature on the causes of neuropsychological deficits (NDs) in alcoholics is reviewed. It is asserted that NDs are caused not simply by the neurotoxicity of alcohol but by the interrelationships of various factors. NDs might thus reflect problems antecedent to or concomitant with alcoholism and not just the consequences of alcohol use. The family histories of alcoholics have shown that a differential susceptibility to NDs might have a genetic basis. NDs might also be due to the fetal alcohol syndrome. Children who eventually become alcoholics have been shown to be more impulsive and hyperactive than other children, factors related to NDs. There seem to be multiple pathways leading to NDs--two ND syndromes, an acceleration of the normal aging process and an amnesic syndrome, seem to be a consequence of alcoholism. Depression and sociopathy are independently related to both alcoholism and NDs, so causal attributions are difficult to determine. The contribution of head injury to NDs in alcoholics might also be important. NDs in alcoholics suffering from liver disease seem to be caused in part by the liver disease and not the alcoholism per se. Liver disease is also associated with nutritional deficiencies which, in turn, can produce certain NDs. Dysfunction in several neurological mechanisms has been shown to be related to alcohol consumption. However, neuronal metabolism, metabolizing enzymes, membrane permeability, neurotransmitters, endocrine function, cerebrovascular pathology and cerebrospinal pathology have not been found to be related to NDs. The effect of congeners has not been investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuropsychological deficits in alcoholics: etiological considerations. 636 76

Centrilobular hypoxia has been postulated as a mechanism for the development of hepatocellular necrosis and fibrosis in alcoholic liver disease. Chronic ethanol ingestion in rodents results in increased hepatic oxygen consumption and in a steeper fall in oxygen tension between the periportal and the pericentral area of the lobule, rendering the pericentral area susceptible to hypoxia. Hepatocellular necrosis occurs when ethanol-fed animals are exposed to low atmospheric oxygen. In man, the existence of a hypermetabolic state is more tenuous, but suggested by an increased rate of ethanol elimination after chronic ethanol consumption that has been linked to increased oxygen consumption in animals. Also, decreases in hepatic blood flow and hepatic vein oxygen tension were found in alcoholics with histological evidence of liver-cell necrosis as compared to those without necrosis. It is postulated that in man, reduction in the availability of oxygen to the liver may be caused by miscellaneous conditions such as anemia, respiratory depression or infection, cigarette-smoking, or reduction of hepatic blood flow, but the contribution of one or more of these factors remains to be proven. Trials of the effect of propylthiouracil (PTU) on alcoholic hepatitis are based on the effect of this drug in decreasing the ethanol-induced hypermetabolic state and in preventing hepatocellular necrosis in animals exposed to low atmospheric oxygen. A tentative conclusion of the two small trials that have been completed is that PTU may be beneficial in moderately ill patients with a low mortality, but not useful in severely ill patients with a high mortality.
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PMID:Commentary on the hypermetabolic state and the role of oxygen in alcohol-induced liver injury. 637 79

This volume details the history of vitamin B6, its chemistry and biochemistry, methods for the assessment of vitamin B6 status, and the clinical chemistry of the vitamin. Since its discovery and synthesis over 40 years ago, vitamin B6 has been implicated in a number of disease states. All approaches to the assessment of vitamin B6 status--direct measurement of blood levels, measurement of the excretion rate of the vitamin, measurement of the metabolites or abnormal metabolic products resulting from a deficient state, or measurement of some other process dependent on the concentration of the vitamin in the body--have significant technical or physiological problems. Dietary allowances vary for different age groups and situations. In the US, the National Academy of Sciences has recommended a daily dietary allowance of 2.2 mg for young adult males and 2.0 mg for young adult females. Additional allowances have been suggested for women during pregnancy and lactation, but not for users of oral contraceptives (OCs). Vitamin B6 deficiency can be either exogenous (when intake falls below the recommended dietary allowance) or conditioned (in cases where the physiologic requirement for the vitamin is higher than the dietary allowance). Conditioned deficiency arises in the following situations: defective intestinal absorption, defective cellular and intercellular transport, and impaired oxidtion or phosphorylation mechanisms in vitamin B6 metabolism. Studies aimed at assessing the abnormal tryptophan metabolism observed in some OC users have produced conflicting results. It appears that severe depression and impairment of glucose tolerance are the only important abnormalities encountered in OC users related to vitamin B6 deficiency. Abnormalities of tryptophan metabolism have been noted in patients with rheumatoid arthritis, some malignant diseases, liver disease, diabetes mellitus, atherosclerosis, and hyperkinetic syndromes.
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PMID:Clinical chemistry of vitamin B6. 639 13

Liver disease may cause a variety of clinical signs, including depression, anorexia, weakness, weight loss, vomiting, diarrhea, fever, abdominal pain, jaundice, ascites and CNS signs. Treatment is aimed at eliminating the cause, providing supportive care, and preventing secondary complications. Rest facilitates liver regeneration. Hypokalemia, respiratory alkalosis and hypoglycemia may complicate liver disease. Fluids should be given IV rather than SC to severely dehydrated animals. Preferred solutions include Ringer's and half-strength saline with 2.5% dextrose. Solutions containing lactate should not be used. Dietary management includes feeding adequate amounts of protein of high biologic value, carbohydrates, fat, vitamins and minerals.
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PMID:Management of liver disease in dogs and cats. 672 30


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