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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hereditary hemochromatosis is the most common cause of iron overload in adults and is probably the second most common cause of iron overload in children in the United States next to transfusional overload. Serious morbidity from this disorder of iron absorption can occur in early as well as in middle and advanced age, iron overload having been reported in children with hereditary hemochromatosis as early as 2 years of age. Younger persons differ from older persons in that the risk for iron loading in females appears to be equal to the risk for males, in contrast to a preponderance of males among older patients. Also, younger patients frequently demonstrate cardiac and gonadal involvement, with cardiac failure commonly leading to death, whereas older patients are more likely to have liver involvement and diabetes mellitus, with liver failure and hepatoma commonly leading to death. Because early diagnosis and treatment can prevent the toxicities of iron overload, appropriate screening can be lifesaving. Transferrin saturation is the most reliable screening test. Liver biopsy with objective measurement of hepatic iron stores is the most important diagnostic criterion at present, although reliable noninvasive methods for quantitating body iron are being developed. Young individuals who should be screened for iron overload include patients with cardiac myopathies, hypogonadism, amenorrhea, loss of libido, diabetes mellitus, other endocrine disorders, cirrhosis of the liver, and arthritis, as well as the siblings, parents, and children of patients with hereditary hemochromatosis or iron loading of unknown cause.
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PMID:Hereditary hemochromatosis in children, adolescents, and young adults. 305 60

Hemochromatosis is a disease in which the inappropriate absorption of iron over 30-40 yr results in tissue iron overload and the development of cirrhosis of the liver, diabetes, hypogonadism, arthropathy, and skin pigmentation. We present an infant who died at 2 days of age, and who was found to have massive iron overload in the liver. This case is consistent with a rare condition that has been called neonatal hemochromatosis. This disease is discussed in the context of an overview of iron metabolism and adult hemochromatosis.
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PMID:Neonatal hemochromatosis: a case and review of the literature. 327 60

To investigate the relationship between hypogonadism and altered amino acid metabolism in patients with liver cirrhosis, we measured the basal levels of plasma testosterone, estradiol, and free amino acids, plus urinary 3-methylhistidine excretion, in 16 control and 19 cirrhotic patients. The concentration of plasma testosterone correlated significantly with that of plasma branched-chain amino acids, and inversely with urinary 3-methylhistidine excretion. This suggests that hypogonadism causes a disturbance in amino acid metabolism at least partly related to an augmented muscle protein turnover.
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PMID:Hypogonadism in liver cirrhosis: implication in altered amino acid metabolism in muscle. 337 5

Seven males with liver cirrhosis associated with hepatitis and one with schistosomal liver fibrosis were studied for hypophyseal gonadal dysfunction and compared to six age matched controls. Cirrhotics as a group had higher serum 17 beta estradiol levels (22.1 +/- 6.3 vs 7.8 +/- 0.8 pg/ml, p less than 0.05) which did not rise after four days of human chorionic gonadotropin (hCG) stimulation. Conversely, there was an adequate rise in serum testosterone level after hCG stimulation (332.8 +/- 99.7 ng/dl baseline to 887.6 +/- 67.1 ng/dl, p less than 0.01). Compared to the controls, cirrhotics had lower baseline serum follicle stimulating hormone (FSH) (3.6 +/- 1.7 vs. 10.2 +/- 1.5 mIu/ml, p less than 0.02) and higher serum prolactin (13.5 +/- 2.5 vs. 6.8 +/- 1.0 ng/ml, p less than 0.05). Pituitary dynamic function testing in cirrhotics revealed blunted response of luteinizing hormone (LH) and FSH, to luteinizing hormone releasing hormone (LHRH) in four out of eight subjects tested. We conclude that the mechanism of hypogonadism in non-alcoholic cirrhosis is mostly hypogonadotropic in origin rather than primary gonadal injury which is common in alcoholic cirrhosis.
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PMID:Hypophyseal-gonadal dysfunction in men with non-alcoholic liver cirrhosis. 392 49

Zinc sulfate was administered in a double-blind manner for 6-8 months to cirrhotic outpatients with impotence and/or hypogonadism. Seven placebo and six zinc-treated patients showed mild symptomatic improvement; however, there was no significant clinical difference between the two groups. Serum zinc levels rose significantly in the zinc-treated group but urinary gonadotropin and serum testosterone levels did not change in either group. Zinc sulfate does not appear to be an effective treatment for sexual dysfunction associated with alcohol-induced hepatic cirrhosis.
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PMID:Effect of the administration of zinc sulfate on hypogonadism and impotence in patients with chronic stable hepatic cirrhosis. 635 Apr 4

During the past two decades, the essentiality of zinc for man has been established. Deficiency of zinc in man due to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in a population subsisting mainly on cereal proteins. Alcoholism is known to cause hyperzincuria and thus may play a role in producing zinc deficiency in man. Malabsorption, cirrhosis of the liver, chronic renal disease and other chronically debilitating diseases may similarly induce zinc deficiency in human subjects. A severe deficiency of zinc has recently been recognized to occur in patients with sickle cell anemia and a beneficial effect of zinc therapy in such patients has been reported. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. Taste abnormalities, correctable with zinc supplementation, have been observed in uremic subjects. Recently, abnormal dark adaptation related to zinc deficiency in patients with cirrhosis of the liver and sickle cell disease has been reported. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate and if untreated the condition becomes fatal. Zinc deficiency is known to affect testicular functions adversely in man and animals. This effect of zinc is at the end organ level and it appears that zinc is essential for spermatogenesis and testosterone steroidogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. Thymidine kinase, RNA polymerase, DNA-polymerase from various sources and RNA-dependent DNA polymerase from viruses have been shown to be zinc-dependent enzymes. Zinc also regulates the activity of RNase; thus the catabolism of RNA appears to be zinc-dependent. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Three enzymes, alkaline phosphatase, carboxypeptidase and thymidine kinase, appear to be most sensitive to zinc restriction in that their activities are affected adversely within three to six days of institution of a zinc-deficient diet to experimental animals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Zinc deficiency in human subjects. 636 78

Zinc is essential for many metabolic and enzymatic functions in man. Deficiency of zinc in man has now been recognized to occur not only as a result of nutritional factors, but also in various disease states, including malabsorption syndromes, acrodermatitis enteropathica, Crohn's disease, alcoholism and cirrhosis of the liver. The deficiency state in human subjects exists as a spectrum extending from mild to severe degree. The clinical manifestations of mild zinc deficiency include oligospermia, weight loss and hyperammonaemia. Moderate zinc deficiency is characterized clinically by growth retardation, hypogonadism in males, skin changes, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In severe zinc deficiency states, bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorders, weight loss, intercurrent infections, hypogonadism in males and, if unrecognized, death have been observed. Zinc is needed for the functions of over 100 enzymes. It is essential for DNA, RNA and protein synthesis and, as such, is important for cell division. Zinc is an inducer of mRNA of metallothionein, a protein which may have an important role in the regulation of intestinal zinc absorption. Zinc has a specific effect on testes in animals and man. Recent reports indicate that in human subjects thymopoietin may be zinc dependent and in animal studies somatomedin may be affected adversely due to dietary zinc restriction. Zinc plays an important role in the protection of cell membrane integrity and may be protective against free radical injury. Zinc is known to compete with cadmium, lead, copper, iron and calcium for similar binding sites. In the future, a potential use of zinc may be to alleviate toxic effects of cadmium and lead in human subjects. Recent evidence suggests that thymic-dependent lymphocytes (T cells are zinc dependent. T-helper and suppressor cells, T-effector cells and T-natural killer cells appear to be zinc dependent. Zinc is also essential for some of the neutrophil functions. Thus, it appears that zinc may play an important role in immunity. One may suggest that some of the clinical features of cirrhosis of the liver, such as testicular atrophy, loss of body hair, night blindness, poor wound healing, poor appetite, susceptibility to infections and enhanced sensitivity to drugs, may be related to conditioned deficiency of zinc, future studies are required to determine whether or not zinc supplementation is beneficial to these patients.
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PMID:The role of zinc in gastrointestinal and liver disease. 661 39

In several gastroenterological diseases andrological anomalies have become known. From this point of view up to now the liver cirrhosis has been examined most frequently. In patients with cirrhosis apparently the two functions of the testicles are disturbed. On the one hand, a decreased or missing fertility is to be assumed, on the other hand, a cirrhosis does not always exclude the procreative capacity. The hormone analyses plead for the fact that the hypogonadism might rather be conditioned testicularly, in which case the direct toxicity of alcohol may be of importance. In haemochromatosis the hypogonadism develops by a combined mechanism. The cystic fibrosis of the pancreas is practically always associated with a male infertility. In Crohn's disease a disturbance of the spermatogenesis is observed. Even the salazo-sulphapyridine therapy is accompanied by unfavourable influences on the spermiogramme. Cimetidine used in the ulcer therapy shows a certain antiandrogenic effect and after a longer time may evoke impotence and other undesirable andrological side-effects which we, however, did not realize in 4 weeks treatment periods.
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PMID:[Andrologic anomalies in various gastrointestinal diseases]. 663 7

From the pharmacology of the therapeutically available androgen preparations and the clinical experience results that a highly dosed androgen long-term therapy is effectively possible only by testosterone esters which are to be injected intramuscularly (e.g. testosterone oenanthate). It is indicated in all forms of endocrine hypogonadism, certain aplastic anaemias and if necessary in extreme male high growth. In partial androgen deficiency (pubertas tarda, Klinefelter's syndrome, climacterium virile and others) orally applicable androgens such as testosterone-undecanoate (Andriol) and mesterolone (Vistimon) can be used. The latter is to be preferred when a hyperoestrogenism is present, e.g. in liver cirrhosis. When 17-alpha-alkylated oral androgens are used, their often not sufficiently confirmed anabolic effect and their potential liver toxicity should more be taken into consideration.
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PMID:[Recent aspects of therapy with androgenic and anabolic steroids]. 666 79

Anterior pituitary functions and sex steroid levels were measured in 12 patients with idiopathic haemochromatosis (eight males, four postmenopausal females) and age-matched controls, 12 with diabetes mellitus and five with hepatic cirrhosis. In idiopathic haemochromatosis gonadotrophin deficiency was present in seven of 12 patients including six of seven patients who had clinical evidence of hypogonadism. Basal prolactin levels were significantly lower in the patients with idiopathic haemochromatosis compared with either of the control groups (p less than 0.02). Nine patients with idiopathic haemochromatosis exhibited subnormal prolactin responses to thyrotrophin releasing hormone. Thyroid and adrenocortical functions were normal in all patients with idiopathic haemochromatosis. Testosterone values were subnormal in five of eight males with idiopathic haemochromatosis; females with idiopathic haemochromatosis had significantly lower testosterone values compared with the diabetic females (p less than 0.05). Oestradiol values in both sexes and sex hormone binding globulin values in the males were not significantly different in patients with idiopathic haemochromatosis compared with the controls. Sex hormone binding globulin levels were significantly higher in females with idiopathic haemochromatosis compared with either diabetic or cirrhotic females (p less than 0.05). Impairment of anterior pituitary function occurs in idiopathic haemochromatosis but is selective; gonadotrophin and prolactin deficiencies are common. Clinical hypogonadism is usually hypogonadotrophic in origin.
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PMID:Endocrine abnormalities in idiopathic haemochromatosis. 668 54


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