Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen female patients with primary biliary cirrhosis were evaluated for vitamin D status and evidence of metabolic bone disease. Full-thickness iliac crest bone biopsy specimens with histomorphometric analysis after double tetracycline labeling were performed before and after 1 yr of treatment with oral 25-hydroxyvitamin D (100 micrograms/day). Initially, serum 25-hydroxyvitamin D levels were low (less than 15 ng/ml) in 11 of the 15 patients and were increased to normal (greater than 25 ng/ml) in all patients within 3 mo. Serum parathyroid hormone levels were low normal or not detectable in all patients and did not change with therapy. No patient had a fracture during the treatment. No evidence of osteomalacia was found initially or in follow-up study in any patient. Follow-up histomorphometric analysis at the end of the 1-yr treatment showed that bone volume decreased during the study interval despite therapy (p less than 0.001). Photon beam densitometry confirmed the loss in trabecular density of the radius over the study interval (p less than 0.03). The mean fractional osteoid surface was not increased initially and did not change with therapy. The mean linear bone appositional rate as measured by double tetracycline labeling was not decreased initially and did not change with therapy. It was concluded that in moderate to severe primary ciliary cirrhosis, initial 25-hydroxyvitamin D levels are low and are rapidly corrected by oral 25-hydroxyvitamin D. These patients have significant osteoporosis which progresses despite 25-hydroxyvitamin D.
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PMID:Bone disease in primary biliary cirrhosis: histologic features and response to 25-hydroxyvitamin D. 697 27

In the last decade our knowledge on vitamin D has grown considerably due to the identification of numerous steps of the vitamin D metabolism and to the isolation and synthesis of active metabolites. Therefore a lot of progress had been made in the understanding of the physiological mechanism of regulating blood calcium homeostasis and of the pathogenesis of many related diseases. The diseases connected to the calcium-phosphate metabolism requiring treatment with vitamin D and its metabolites are numerous. The basis for a rational therapeutic approach is provided by the new concepts on the pathogensis of the various diseases and on the pharmacology of vitamin D metabolites. Pure vitamin D depletion may be controlled with physiological doses of vitamin D. Administration of 25-OHD3 is advisable in chronic hepatitis or cirrhosis accompanied by a defect of 25-hydroxylation and/or intestinal loss of the metabolite. A defect in the synthesis of 1,25-(OH)2D3, the metabolite of renal origin, is present in an interesting and wide group of diseases. These are: chronic renal insufficiency, hypoparathyroidism, hypocalcemic D-resistant rickets and senile or post-menopausal osteoporosis. In the treatment of this group of diseases, which sometimes is of a preventive nature, it is preferable to administer the dihydroxylated metabolites of vitamin D. The results of treatments and prevention in a few selected conditions are reported.
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PMID:[Physiopathological and therapeutic aspects of vitamin D (author's transl)]. 724 90

The mechanisms of vitamin D deficiency already described are triggered off by a variety of causes. Confinement indoors leads to defective photosynthesis and dietary restrictions to insufficient intake. Malabsorption results from digestive tract diseases: mainly adult coeliac disease, but also sequelae of gastrectomy, exocrine pancreatic insufficiency, chronic biliary obstruction and all other causes of steatorrhoea. Practically, osteomalacia of digestive origin usually results from multifactorial hypovitaminosis D. The same applies to primary or nutritional biliary cirrhosis, which frequently entails low vitamin D blood levels despite subnormal 25-hydroxylation. Osteomalacia is also found in renal osteodystrophy, where it is partly due to inhibition of 1,25-hydroxylase and subsequent deficiency of 1,25-dihydrocholecalciferol, though other, non vitaminic substances may also be involved. Two misleading forms of the disease must be borne in mind: one with renal tubular lsions, the other associated with functional pseudo-hypoparathyroidism. The aetiology of most cases of osteomalacia due to vitamin D deficiency can be elucidated by a few simple tests.
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PMID:[Osteomalacia due to vitamin D deficiency. Part two: Aetiology (author's transl)]. 742 86

In 46 patients with decompensated posthepatitis cirrhosis, various clinical manifestations resulted from changes of bone density were noted. The relation between the changes of bone density and the level of blood calcium, blood phosphorus and alkaline phosphatase (AKP) as well as the metabolism of vitamin D was studied. It is shown that: (1) Bone mineral content (BMC) in the cirrhosis group decreased as compared with that in a control group (P < 0.05). (2) Blood calcium and phosphorus level decreased, whereas AKP level increased significantly (P < 0.01) in the cirrhosis group. (3) When BMC decreased, blood calcium and phosphorus level also decreased significantly (P < 0.01). When the condition of cirrhosis deteriorated, these changes became more obvious. The reasons may be: (1) Disorder of vitamin D metabolism in cirrhosis. (2) Decrease of calcium absorption by intestine. (3) Nutritional disturbance. It is suggested that the occurrence of bone rarefaction in cirrhosis was due to multiple factors.
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PMID:[A clinical analysis on the variance of bone density in patients with cirrhosis]. 776 39

This article reviews osteoporosis (OP) in adults with chronic liver disease. OP in this setting is characterized in general by low bone turnover. The pathogenesis is unclear but is probably not related to vitamin D abnormalities. Patients at high risk of OP include those with evidence of cirrhosis, hypogonadism, overt calcium malabsorption, steroid therapy and choleostatic liver disease (particularly primary biliary cirrhosis). OP is best managed by adequate calcium intake, regular weight bearing exercise, and the avoidance of alcohol and tobacco smoking. There is probably no reason for vitamin D supplementation. Hormonal replacement therapy when necessary is indicated in males and should be considered in females. Finally, liver transplantation has the potential to improve or stabilize OP in the median term, although it is associated with significant short-term deterioration.
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PMID:Osteoporosis in chronic liver disease: pathogenesis, risk factors, and management. 785 Oct 1

Liver cirrhosis may be accompanied by osteoporosis and, rarely, osteomalacia. Normal liver function is required for normal digestion and absorption of calcium-containing nutrients. The liver plays an important role for the metabolisation of vitamin D: the 25-hydroxylation takes place in the liver. However, the respective enzymatic capacity is not limited by liver diseases except for almost complete liver insufficiency. Therefore, true hypovitaminosis D only rarely plays a role in hepatic osteopenia, but direct toxic effects on bone forming cells (osteoblasts) are discussed: e.g. by bile salts. Coexisting hypogonadism leads to further bone loss. Patients with primary biliary cirrhosis in part present with osteoporosis and fractures. Bone histology reveals normal resorption, but decreased formation. Calcitropic hormones are generally normal. Chronic alcoholism induces the same histologic picture in bone, i.e. normal resorption and diminished formation. These changes are reversible after abstinence and as long as of cirrhosis has not yet developed. Patients undergoing liver transplantation due to end stage liver insufficiency including cirrhosis present with diminished bone mass before receiving a new liver, and they show further bone loss after the transplantation due to immunosuppressive treatment including glucocorticoids. There is no specific treatment of bone loss or osteoporosis due to liver cirrhosis. Preventive efforts should be devoted to the avoidance of suboptimal calcium and vitamin D supply, immobilization, and hypogonadism. Fluorides may increase bone mass after liver transplantation--perhaps they are also useful in liver cirrhosis. Antiresorption agents like calcitonins or bisphosphonates may be cautiously tried.
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PMID:[Osteoporosis]. 793 67

Nutritional assessment and adequacy of spontaneous dietary intake was evaluated in thirty-seven clinically stable hospitalized patients with alcoholic liver cirrhosis. About two-thirds of the patients had ascites or oedema, or both, and, therefore, body weight could not be used for assessment of nutritional status. Lean body mass (LBM; measured by three consecutive 24 h creatinine excretions) was 62 (range 40-95)% of reference values, mid-arm-muscle area (MAMA) was 70 (range 43-115)% and triceps skinfold (TSF) was 45 (range 20-113)% of reference values (all median values). In patients without ascites or oedema, or both, there was a rectilinear correlation between body weight and LBM and between body weight and MAMA (r 0.93 and 0.85 respectively). In patients with ascites or oedema, or both, the correlation between body weight and LBM was poor as could be expected. We suggest that LBM is a useful measure of nutritional status when body weight is unreliable because of ascites or oedema, or both. Energy balance for the group was calculated from energy intake recorded by a 24 h dietary recall and energy expenditure calculated by the factorial method. Median intake was 102 (range 34-176)% of expenditure. N loss was calculated from the average of three 24 h urea excretions. Protein intake was calculated from the 24 h dietary recall. The N balance was positive in the patients as a group (median intake was 120 (range 26-183)% of output). The most malnourished patients tended to have the most positive N balance which was due to a significantly lower N excretion. The protein requirement for N balance was 0.83 (SE 0.05) g/kg per d and only at an intake above 1.20 g/kg per d were all patients in positive N balance. The median intakes of thiamin, folacin, vitamin D, vitamin E, Mg, and Zn were judged to be insufficient. It is concluded that impaired nutritional status is common among patients with liver cirrhosis, even in a stable clinical condition. It is suggested that nutritional status in these patients is evaluated by dietary recalls, in combination with measurement of body weight in patients without ascites or oedema, or both, or in combination with determination of LBM by three 24 h creatinine excretions in patients with ascites or oedema, or both. Criteria for selection of patients that might benefit from nutritional therapy are discussed.
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PMID:Nutritional assessment and adequacy of dietary intake in hospitalized patients with alcoholic liver cirrhosis. 832 43

Administration of vitamins or metals may cause severe side effects. Retinoids (derivatives of vitamin A) used for the treatment of various skin disorders are teratogenic, hepatotoxic and may induce a substantial increase in serum lipids. A case report demonstrates that vitamin D supplementation in a patient under total parenteral nutrition can cause hypercalcemia. The isolated administration of vitamin B1, without concomitant vitamin B6 and nicotinamide may precipitate potentially life-threatening pellagra encephalopathy. Repeat blood transfusions may produce clinically overt organ hemosiderosis, e.g. cirrhosis of the liver, diabetes mellitus or myocardiopathy. The literature contains reports on a few cases of sarcoma associated with orthopedic metal implants. The controversial issue of the potential dangers of dental amalgams is briefly mentioned.
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PMID:[Vitamins and metals: possible hazards for humans]. 866 74

Bone mineral density (BMD) of the lumber vertebrae and factors related to bone metabolism were determined in patients with chronic viral hepatitis and patients with liver cirrhosis to clarify correlations between hepatic dysfunction, considered to be one of the causes of hepatic osteodystrophy, and decrease in bone mass. BMD of the second to fourth lumbar vertebrae was determined with a Lunar (Madison, WI, USA) DPX, a dual-energy X-ray absorptiometry diagnostic system. BMD was significantly lowest in patients with liver cirrhosis, followed by patients with chronic hepatitis, and healthy subjects, in this order. There was a significantly positive but weak correlation between albumin and BMD. Levels of 25(OH)D and 1,25(OH)2D were significantly lower in patients with liver cirrhosis than in those with chronic hepatitis. BMD and vitamin D were decreased in all patients whose cholinesterase (ChE) was below 0.3 delta pH. Urinary pyridinoline (Upyr) was significantly higher in the patients with liver cirrhosis, in whom bone mass was decreased, than in the patients with chronic hepatitis, whereas serum osteocalcin levels were distributed in the upper normal range in patients with chronic hepatitis and those with liver cirrhosis. There was a positive correlation between 25(OH)D and serum osteocalcin levels in patients with liver cirrhosis. These results indicate that osteogenesis is decreased and suggest that the decrease in BMD which occurs in viral liver cirrhosis, probably related to decreased, bone formation and slight promotion of bone resorption, reflects deranged hepatic function. This is the first report of Upyr and urinary deoxypyridinoline (UDpyr) determination in patients with liver cirrhosis and patients with chronic hepatitis. The negative correlation of Upyr and UDpyr with ChE is a novel finding.
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PMID:Osteodystrophy in patients with chronic hepatitis and liver cirrhosis. 888 33

The characteristics of intestinal calcium transport in chronic cholestasis remain largely unknown. Using an experimental model of biliary cirrhosis in the rat, we aimed to investigate changes in calcium transport at the jejunal and ileal levels. Two methods were used: 1) uptake of 45Ca in brush border membrane vesicles and 2) measurements of transepithelial fluxes of calcium in Ussing chambers. Thirty days postsurgery, cholestatic rats presented biliary cirrhosis, with normal growth, normal daily energy, and calcium intakes, but had depressed circulating levels of 25-(OH)-vitamin D2 and 1,25-(OH)-vitamin D3. Compared with sham-operated controls, 45Ca uptake ([Ca2+] = 0.03 mmol) measured in vesicles from cholestatic rats was decreased by 3-fold in the duodenojejunum, in concordance with a lower content in brush border membrane calmodulin. Other changes in brush border membrane composition included decreases in structural proteins, microvillous enzymes, and in triglyceride content. Transepithelial fluxes of calcium measured in the ileum ([Ca2+] = 1.2 mmol) revealed in controls a net basal secretion flux (Jnet = -30.4 +/- 8.1 mmol.h-1.cm-2) that was reduced by 3-fold (p < 0.05) in vitamin D-deficient rats (Jnet = -10.4 +/- 4.8 mmol.h-1.cm-2). In response to 25-(OH)-vitamin D2 treatment, calcium uptake rates increased by 40% in the jejunum, whereas in the ileum, the secretion flux returned to basal control levels. Oral administration of taurocholate or tauroursodeoxycholate (50 mmol) depressed almost completely calcium uptake capacity in the duodenojejunum. By complexing free calcium, tauroconjugated bile acids inhibited in vitro calcium uptake proportionally to their concentration in the medium (0-40 mmol). Our data indicate that, in rat biliary cirrhosis, transport capacity of calcium in the duodenojejunum is markedly reduced in association with vitamin D deficiency and alterations in brush border membrane composition.
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PMID:Intestinal transport of calcium in rat biliary cirrhosis. 888 79


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