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

The aim of this article is to describe the fat-soluble vitamin status in patients with hepatobiliary and pancreatic diseases, and the contribution of these vitamin deficiency or excess to hepatic injury. A considerable number of patients with advanced liver disease and cholestasis might actually be fat-soluble vitamin deficient, although clinical signs of deficiency are uncommonly seen in patients with vitamin A and E deficiency. Increased bone resorption may be the predominant cause of hepatic osteodystrophy. On the other hand, the possible causes of vitamin K deficiency seen in patients with hepatobiliary disease are the decrease of vitamin K absorption from intestine, the disturbance of vitamin K cycle and the decrease of pool area for vitamin K storage. The intake of vitamin A may be associated with the risk of liver cirrhosis in lifetime teetotalers, although the retinyl palmitate reduces hepatic fibrosis in rats.
 ...
PMID:[Hepatobiliary and pancreatic disorders as risk factors for fat-soluble vitamin deficiencies]. 1054 Aug 89

This study investigated the incidence and severity of hepatic osteodystrophy in patients with posthepatitic liver cirrhosis, and the role of hepatocellular injury in bone loss. Twenty-four patients (15 females and 9 males, mean age 49 +/- 13 years) with posthepatitic cirrhosis were enrolled in this study. The control group consisted of 22 healthy age and sex matched adults. The bone mineral density (BMD) was evaluated by dual energy x-ray absorptiometry of the L1-L4 vertebral bodies. A detailed questionnaire was used to assess the epidemiological findings. A statistically significant decrease in BMD of the patients was observed. There were no significant differences in the alkaline phosphatase, parathyroid hormone, calcitonin, 25-hydroxyvitamin D, osteocalcin, free testosterone, luteinizing hormone, follicle stimulating hormone, and estradiol levels, oral calcium intake, urinary calcium, phosphorus and hydroxypyroline excretion between patients and controls. The control group smoked more cigarettes, consumed more coffee and meat, and were exposed the sun light for a longer period than the study group. Multiple regression analysis showed that osteopenia depends significantly on the extent of liver disease. The data shows that the patients with posthepatitic cirrhosis had osteopenia, and that cirrhosis was a direct and independent risk factor.
 ...
PMID:Osteodystrophy in posthepatitic cirrhosis. 1167 84

Primary biliary cirrhosis is a chronic liver disease of unknown etiology, characterized by inflammation and destruction of the intrahepatic biliary ducts, resulting in chronic cholestasis and eventually cirrhosis. The main clinical manifestations consists of pruritus, jaundice, xanthomas, and the consequences of intestinal malabsorption, including vitamin deficiencies and osteodystrophy. Treatment of PBC is addressed at preventing or relieving the symptoms and clinical consequences of chronic cholestasis, and also at correcting the bile duct abnormalities by specific treatments. Pruritus is treated with cholestyramine, but in some cases other drugs, such as rifampicin or opioid antagonists are needed. Bisphosphanates are effective for increasing bone mass in osteopenic patients. Vitamin D and cAlcium supplements are also recommended, particularly in patients with severe cholestasis. Ursodeoxycholic acid (UDCA) has become the standard treatment (13-15 mg/kg/day), resulting in marked relieving of cholestasis. UDCA also prevents the histological progression of the disease, although the effects on survival are less apparent. Small trials of combination therapy using UDCA with methotrexate, colchicine, or prednisone, have been reported but have not shown any increased efficacy over UDCA therapy. Liver transplantation is the only treatment available when cholestasis progresses, with very good survival rates.
 ...
PMID:Treatment of primary biliary cirrhosis. 1649 78

Metabolic bone disease, mainly osteopenia/osteoporosis and occasionally osteomalacia, is a major extrahepatic manifestation of chronic cholestatic liver disease (synonym: hepatic osteodystrophy). Reduced bone mineral density is found in up to 60% and atraumatic fractures in about 20% of patients with chronic liver disease. Hepatic osteodystrophy is characterized by reduced formation and increased resorption of bone; major risk factors are chronic cholestasis and advanced cirrhosis. Pathogenetic mechanisms include genetic factors, abnormalities of calcium, vitamin D, vitamin K and bilirubin metabolism, IGF-1 deficiency, the RANKL/OPG-system, hypogonadism, drugs harmful to bone, lifestyle factors (smoking, alcoholism, immobility), malnutrition and low body mass index. Screening for osteopenia should be performed and reversible risk factors must be corrected. At present, bisphosphonates are the predominantly used specific drugs for the treatment of osteoporosis in chronic liver disease. After orthotopic liver transplantation bone mineral density improves in long-term follow-up. Studies are needed for fracture prevention in chronic liver disease.
 ...
PMID:Cholestasis and metabolic bone disease - a clinical review. 1899 71

Primary sclerosing cholangitis (PSC) is a chronic cholestatic disease of the liver and that is characterized by progressive inflammation, fibrosis, and stricturing of the intrahepatic and extrahepatic bile ducts. It is progressive in most patients and leads to cirrhosis. It is a rare disease, mostly affecting people of northern European descent, males greater than females. The diagnosis is best established by contrast cholangiography, which reveals a characteristic picture of diffuse, multifocal strictures and focal dilation of the bile ducts, leading to a beaded appearance. Inflammatory bowel disease (IBD) is present in ~75% of the patients with PSC, mostly ulcerative colitis (~85% of the cases). In addition to biliary cirrhosis, complications of PSC include dominant strictures of the bile ducts, cholangitis, cholangiocarcinoma, colon dysplasia and cancer in patients with IBD, gallbladder polyps and cancer, and hepatic osteodystrophy. The etiology of PSC is not clear, but studies are ongoing. The median survival without liver transplantation is 12 to 15 years after diagnosis. Currently there are no effective treatments except liver transplantation. Immunosuppressive medications have not been shown to be effective but antibiotics and anti-fibrotic agents seem promising.
 ...
PMID:Diagnosis and classification of primary sclerosing cholangitis. 2442 80

Metabolic disturbances of bone are frequent in patients with chronic liver disease. The prevalence of osteoporosis among patients with advanced chronic liver disease is reported between 12% and 55%; it is higher in primary biliary cirrhosis. All patients with advanced liver disease should be screened for osteoporosis with a densitometry, especially if the etiology is cholestatic and in the presence of other risk factors. Clinical relevance of hepatic osteodystrophy increases after liver transplantation. After liver transplant, a rapid loss of bone mineral density can be detected in the first 6 months, followed by stabilization and slight improvement of the values. At the time of transplantation, bone density values are very important prognostic factors. Therapy of hepatic osteodystrophy is based primarily on the control of risk factors: cessation of tobacco and alcohol assumption, reduction of caffeine ingestion, exercise, supplementation of calcium and vitamin D, limitation of drugs such as loop diuretics, corticosteroids, cholestyramine. Bisphosphonates have been proposed for the therapy of osteoporosis in patients with liver disease, particularly after liver transplantation. The possible side effects of oral administration of bisphosphonates, such as the occurrence of esophageal ulcerations, are of particular concern in patients with liver cirrhosis and portal hypertension, due to the risk of gastrointestinal hemorrhage from ruptured esophageal varices, although this risk is probably overestimated.
...
PMID:Hepatic osteodystrophy. 2556 51

Chronic liver diseases, including liver cirrhosis, are caused by various pathogenesis, such as viral hepatitis, primary biliary cirrhosis, autoimmune hepatitis and steatohepatitis. There have not been enough clinical evidence about the treatment of hepatic osteodystrophy at the present time. Several reports suggested that bisphosphonates, such as alendronate, are effective for an increase in bone mineral density in patients with chronic liver disease. Vitamin D treatment might be useful for the frequent prevalence of vitamin D deficiency in the pathogenesis of hepatic oseodystrophy. The use of estrogens will be limited for the risk of liver dysfunction and hepatocellular carcinoma.
...
PMID:[Treatment for hepatic osteodystrophy]. 2650 75

Musculoskeletal problems in patients with liver disease are common; however, they are not so well described in the literature. Therefore, there is a need to collate information on these disorders, as their incidence is on a constant rise and some of these pathologies can severely debilitate the patient's quality of life. These disorders are parietal wall varices with or without bleeding, spontaneous intramuscular haematoma (e.g. rectus sheath), abdominal wall hernia, anasarca, hepatic osteodystrophy, septic arthritis, osteomyelitis, necrotizing fasciitis, osseous metastases from hepatocellular carcinoma etc. While portal hypertension plays a key role in disorders, in others, dysregulation of the coagulation system or a compromised immune system are responsible. Imaging plays an essential role in the assessment of these complications and awareness of these musculoskeletal manifestations is vital for establishing a timely diagnosis and planning of appropriate therapy, as these disorders can significantly impact the morbidity and mortality and also influence candidacy for liver transplantation. We herein comprehensively appraise various musculoskeletal complications associated with chronic liver disease/liver cirrhosis especially from an imaging perspective which, to the best of our knowledge, have not been collectively described in English literature.
...
PMID:Cirrhosis-related musculoskeletal disease: radiological review. 2735 9

An 8-yr-old, captive, female golden lion tamarin ( Leontopithecus rosalia ) with a 6-yr history of hyperbilirubinemia was examined for inappetence and weight loss. Physical examination and blood pressure monitoring under anesthesia revealed hypothermia and hypotension, and blood work revealed hypoglycemia, markedly elevated liver enzymes, including serum alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase, and confirmed the hyperbilirubinemia. A complete blood count suggested chronic lymphoid leukemia. The animal's condition deteriorated during recovery, and the animal died despite aggressive treatment. Grossly, there was micronodular cirrhosis of the liver, severe icterus, and diffuse osteopenia of all examined bones. Microscopic examination of the liver confirmed the micronodular cirrhosis and bone lesions were compatible with diffuse osteopenia and osteomalacia. This brief communication presents a case of chronic liver disease and lesions indicative of metabolic bone disease, also known as hepatic osteodystrophy. To the authors' knowledge, this is the first documented case of hepatic osteodystrophy in the veterinary literature.
 ...
PMID:HEPATIC OSTEODYSTROPHY IN A GOLDEN LION TAMARIN (LEONTOPITHECUS ROSALIA). 2769 75

Primary Biliary Cholangitis is a progressive, autoimmune cholestatic liver disorder. Cholestasis with disease progression may lead to dyslipidemia, osteodystrophy and fat-soluble vitamin deficiency. Portal hypertension may develop prior to advanced stages of fibrosis. Untreated disease may lead to cirrhosis, hepatocellular cancer and need for orthotopic liver transplantation. Classically, diagnosis is made with elevation of alkaline phosphatase, demonstration of circulating antimitochondrial antibody, and if performed: asymmetric destruction/nonsupperative cholangitis of intralobular bile ducts on biopsy. Disease pathogenesis is complex and results from innate and adaptive (cell-mediated and humoral) responses that lead to inflammation of biliary duct epithelium. Ongoing damage is amplified and sustained through bile acid toxicity. Use of weight based (13-15mg/kg) ursodeoxycholic acid is well established in retarding disease progression and improving survival; however, is ineffective in achieving complete biochemical remission in many. Recently, a Farnesoid X Receptor agonist, obeticholic acid, has been approved for use. A number of ongoing clinical studies are underway to evaluate utility of fibric acid derivatives, biologics, antifibrotics, and stem cells as monotherapy or in combination with ursodeoxycholic acid for primary biliary cholangitis. The aim of this review is to discuss disease pathogenesis and highlight rationale/implications for both established and novel therapeutics.
 ...
PMID:Primary Biliary Cholangitis: Disease Pathogenesis and Implications for Established and Novel Therapeutics. 2800 21


<< Previous 1 2 3 Next >>