Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety patients with chronic diffuse liver disease were evaluated with free hepatic venography, wedge hepatic venography, hepatic vein pressure measurements, and liver biopsy. Free hepatic venograms were normal and minimally pruned in patients with hepatic sarcoidosis and fatty liver due to alcohol, and their biopsies showed little or no fibrosis. Pruning of hepatic vein branches on free hepatic venography correlated well with the corrected wedged hepatic vein pressure and with the degree of fibrosis in patients with alcoholic hepatitis, alcoholic cirrhosis, and postnecrotic cirrhosis. Free hepatic venography correlated better with hemodynamic measurements and fibrosis than did wedge hepatic venography. Free hepatic venography is a reliable predictor of the presence and degree of hepatic fibrosis and may be a useful alternative to liver biopsy in patients with clotting disorders.
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PMID:Hepatic venography and wedge hepatic vein pressure measurements in diffuse liver disease. 40 97

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

Advances in imaging technology and development of liver-specific contrast agents have significantly increased the role of radiology in the detection and characterization of processes diffusely involving the liver. Tailored magnetic resonance imaging (MRI) sequences allow an accurate detection of many storage and metabolic diseases, such as iron overload disorders and steatosis (fatty liver). Faster scanning techniques available with both computed tomography (CT) and MRI provide, by assessing contrast dynamics, sufficient information for the characterization of diffuse neoplastic and vascular disorders. Characteristic changes in attenuation on CT, signal intensity on MRI, and enhancing features can be used to diagnose specific diffuse diseases such as candidiasis, diffuse/multifocal hepatocellular carcinoma, and schistosomiasis. Although an overlap in imaging findings still exists, familiarity with the imaging features of uncommon disorders such as Wilson's disease, amyloidosis, and sarcoidosis may be diagnostic in the proper clinical setting. This review focuses on the current role of imaging in the detection and characterization of diffuse liver disorders. Recent developments that have amplified the role of noninvasive diagnostic evaluation of these conditions are especially highlighted.
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PMID:Imaging of diffuse liver disease. 1143 72

The utility of protocol liver allograft biopsies remains controversial, particularly in patients with normal liver function tests (LFTs). However, histologic evaluation of these biopsies provides an opportunity to examine the types and severity of liver diseases that can occur in livers with normal clinical and biochemical function. We studied 165 protocol allograft biopsies taken from 100 liver transplant patients at the time of normal LFTs and normal clinical function at 3 to 8 months (n=36), 1 year (n=52), 2 to 3 years (n=54), and 4 to 5 years (n=23). Biopsies were classified as normal, minimal changes (eg, nonaggressive portal or lobular mononuclear inflammation, steatosis <10%), fatty liver disease, recurrent primary liver disease, and transplant-related disease (portal-based rejection or central venulitis, an inflammatory pattern that encompasses perivenular hepatocyte dropout, mononuclear inflammation, pigment-laden macrophages, and variable zone 3 fibrosis). Among these 100 patients, a total of 394 protocol biopsies were performed, and 165 (42%) were taken at the time of normal LFTs and normal clinical function. One hundred twenty-one (73%) were normal or showed minimal/nonspecific changes. Forty-four (27%) showed histologic abnormalities that included fatty liver disease (n=19, nonalcoholic in 18 cases; 13 with mild steatosis, 6 with moderate steatosis, 7 with grade 1/3 steatohepatitic activity, and 2 with stage 1/4 steatohepatitic fibrosis), recurrent primary biliary cirrhosis (n=9; all stage 1/4), recurrent hepatitis C infection (n=6; grade 0/4 in 1, grade 1/4 in 5, stage 0/4 in 4, stage 1/4 in 1, and stage 2/4 in 1), recurrent sarcoidosis (n=1), Ito cell hyperplasia (n=4; marked in 2 and mild in 2), central venulitis (n=10; 5 with mild zone 3 fibrosis or central vein obliteration and 1 with central-portal bridging fibrosis), and mild acute portal rejection (n=2). We judged the histologic changes to be of clinical significance in 19 (11.5%) cases. These results indicate that even at the time of normal clinical and laboratory function, a significant fraction of protocol allograft biopsies harbor histologic (27%) and clinically significant (11.5%) abnormalities. These most commonly include fatty liver disease, low-grade/low-stage recurrent hepatitis C and primary biliary cirrhosis, and central venulitis (including some cases with subsequent fibrosis progression). The data support performance of protocol biopsies to assess allograft status, and provide insight into the types and severity of liver diseases that can smolder in transplanted (and by extension, probably also in native) livers with apparent normal function.
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PMID:Histologic abnormalities are common in protocol liver allograft biopsies from patients with normal liver function tests. 1846 Sep 80

A 57-year-old white woman had serum ferritin 793 ng/mL, HFE C282Y homozygosity, elevated serum angiotensin-converting enzyme (ACE) levels, 3+ hepatocyte iron, cirrhosis, hepatic granulomas, and portal hypertension. Her 37-year-old son had ferritin 869 ng/mL, C282Y/wt, elevated ACE levels, 2+ hepatocyte iron, bridging fibrosis, and hepatic granulomas. Her daughters had HFE C282Y/H63D and C282Y/wt, respectively; neither had a hemochromatosis phenotype, sarcoid, or severe liver disease. All 4 subjects had nonalcoholic hepatic steatosis. Sarcoid did not segregate with the human leukocyte antigen-A and -B haplotype shared by the proband, her son, and 1 daughter. Phlebotomy to achieve iron depletion in the proband and her son yielded 1.6 and 1.5 g iron, respectively; their ACE levels remained elevated. We reviewed previous reports of 4 patients with hemochromatosis and sarcoid. We conclude that a combination of sarcoid, steatosis, and excessive hepatocyte iron caused cirrhosis or hepatic fibrosis in the proband and her son.
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PMID:HFE hemochromatosis and hepatic sarcoid. 1944 63

In addition to focal liver lesions, diffuse and vascular disorders of the liver represent a wide spectrum of liver diseases which are from the radiological point of view often difficult or nearly impossible to diagnose. Classical diagnostic methods are computed tomography and magnetic resonance imaging in addition to ultrasound. Diffuse parenchymal damage caused by diseases of various etiologies is therefore difficult to evaluate because it often lacks characteristic morphological features. For hepatic steatosis, hemochromatosis/siderosis as an example of a diffuse storage disease and sarcoidosis and candidiasis as infectious/inflammatory diseases, an image-based diagnosis is appropriate in some cases. For most diffuse liver diseases, however only nonspecific changes are visualized. Vascular pathologies of the liver, such as the Budd-Chiari syndrome and portal vein thrombosis, however, can usually be diagnosed very clearly using radiology and there is also a very effective interventional radiological treatment. Chronic diseases very often culminate in liver cirrhosis which is highly associated with an increased risk of liver cancer.
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PMID:[Diffuse and vascular hepatic diseases]. 2180 55

A retrospective study was carried out on 100 randomly selected medico-legal autopsies of victims who had committed suicide by hanging. All cases had undergone full police and coronial investigation. Complete external and internal examinations had been carried out including routine histological examination of organs. The age range of victims was 15-94 years (average, 41.7 years) with a male-to-female ratio of 7:1. External and internal injuries were consistent with the reported events. Diagnoses based purely on histology included hepatic steatosis (n = 16), asthma (n = 3), lymphocytic thyroiditis (n = 2), and pulmonary and cardiac sarcoidosis (n = 1). A large cell carcinoma of the lung and a rectal adenocarcinoma were confirmed. Histological evaluation was, however, of limited usefulness in contributing to the medico-legal evaluation of cases, with careful scene, external and internal examinations providing the most relevant information. The results of histological examination of tissues were all incidental to the cause, mechanism, and manner of death.
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PMID:An assessment of the usefulness of routine histological examination in hanging deaths. 2295 Jun 88

Diffuse liver disease, including all causes of chronic liver disease, affects tens of millions of people worldwide. There is a growing need for diagnostic evaluation as treatments become more readily available, particularly for viral liver disease. Magnetic resonance imaging (MRI) provides unique capabilities for noninvasive characterization of liver tissue that rival or surpass the diagnostic utility of liver biopsies. There has been incremental improvement in the use of standardized MRI sequences, acquired before and after administration of contrast for the evaluation of diffuse liver disease, and this includes study of the liver parenchyma and blood supply. More recent developments have led to methods for quantifying important liver metabolites, including fat and iron, and liver fibrosis, which is the hallmark for chronic liver disease. In this study, we review the MRI techniques and diagnostic features associated with common and uncommon etiologies of diffuse liver diseases, including processes that lead to abnormal perfusion (e.g. Budd-Chiari syndrome, congestive hepatomegaly), deposition diseases (e.g. fatty liver, hemochromatosis, Wilson's disease), and abnormalities that are related to inflammation and fibrosis (e.g. primary sclerosing cholangitis, sarcoidosis).
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PMID:MRI of diffuse liver disease: the common and uncommon etiologies. 2392 Dec 68

Environmental pollutants (such as diesel exhaust particles and silica) cause disorders ranging from bronchial asthma to malignant tumors. In recent years, it has been reported that some of the signaling pathways in which environmental contaminants act in vivo are associated with innate immunity. Innate immunity recognizes ligands and induces inflammation. Those ligands are pathogen-associated molecular patterns (PAMPs: e.g., lipopolysaccharide) and danger-associated molecular patterns (DAMPs: e.g., cholesterol crystallization or uric acid crystal). Activation of innate immunity stimulates the acquired immunity system. Therefore, innate immunity regulates the strength of the general immune system. Furthermore, crystal silica, which is an environmental pollutant, activates innate immunity as a ligand. Innate immunity involves the membrane-bound Toll-like receptors (TLR) and cytoplasm-localized nucleotide-binding oligomerization domain (NOD)-like receptors (NLR). We reported the innate immunity-system-related diseases such as Crohn's disease, Blau syndrome, myelogenous leukemia, and sarcoidosis. An inflammasome complex containing NLR has attracted attention owing to its correlation with the onset of several diseases. It is reported that the inflammasome activation is related to the development of lifestyle-related diseases such as myocardial infarction and fatty liver. It is also reported that the mechanism by which crystal silica and asbestos cause inflammation involves the inflammasome activation. Analyzing the genes of innate immunity contributes to the clarification of the mechanism of disease onset caused by environmental pollutants.
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PMID:[Immune System Reaction against Environmental Pollutants]. 2599 42

Conjunctival involvement in sarcoidosis is commonly characterized by epibulbar nodules or follicular conjunctivitis. The authors describe an apparently healthy woman who developed extensive monocular cicatricial conjunctivitis with symblepharon. The array of conditions presenting with cicatricial conjunctivitis was considered, with mucous membrane pemphigoid leading the diagnostic possibilities. Conjunctival biopsy disclosed the non-infectious, non-caseating granulomas of sarcoidosis and a systemic evaluation disclosed pulmonary nodules and hilar lymphadenopathy. As the patient had no respiratory symptoms and an old history of hepatic steatosis, oral hydroxychloroquine and topical cyclosporin were chosen for therapy rather than systemic corticosteroids.
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PMID:Pseudopemphigoid: Sarcoidosis presenting as cicatricial conjunctivitis with symblepharon. 3313 88


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