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PubMedDate not supplied

Trends in liver disease prevalence in Mexico from 2005 to 2050 through mortality data.

BACKGROUND AND AIMS: The epidemiology of liver cirrhosis differs across sex, ethnic groups, and geographic regions. In 2000, chronic liver disease was the fifth leading cause of death in Mexico. Accurate knowledge of the demographics of liver disease is essential in formulating health-care policies. Our main aim was to project the trends in liver disease prevalence in Mexico from 2005 to 2050 based on mortality data. METHODS: Data on national mortality reported for the year 2002 in Mexico were analyzed. Specific-cause mortality rates were calculated for a selected age population (> 25 years old) and classified by sex and projected year (2005-2050). The following codes of the International Classification of Diseases for liver diseases were included: non-alcoholic chronic liver disease and cirrhosis, alcoholic liver disease, liver cancer, and acute and chronic hepatitis B and C infection. The projected prevalence of a chronic liver disease was estimated using the following equation: P = (ID x T) / [(ID xT) + 1], where P = prevalence, ID = incidence density (mortality rate multiplied by 2), T = median survival with the disease (= 20 years). RESULTS: Nearly two million cases of chronic liver disease are expected. Alcohol-related liver diseases remain the most important causes of chronic liver disease, accounting for 996,255 cases in 2050. An emergent syndrome is non-alcoholic liver disease, which will be more important that infectious liver diseases (823,366 vs 46,992 expected cases, respectively). Hepatocellular carcinoma will be the third leading cause of liver disease. CONCLUSIONS: Chronic liver disease will be an important cause of morbidity and mortality in the future. Preventive strategies are necessary, particularly those related to obesity and alcohol consumption, to avoid catastrophic consequences.

Adult↗
PubMed1995

Changes in laminin content in livers of patients with alcoholic liver disease.

An increase in serum laminin levels has been reported in patients with liver disease; however, the mechanisms for this increase have not yet been clarified. In the present study, the laminin content of liver biopsy specimens obtained from patients with alcoholic liver disease and non-alcoholic liver disease was determined with a one-step sandwich enzyme-immunoassay system, using monoclonal antibodies for human placental laminin. Hepatic laminin content was significantly higher in patients with liver disease than in normal controls. In alcoholic liver disease, the content in patients with mild fibrosis was lower than in patients with advanced types of alcoholic liver disease. In non-alcoholic liver disease, the hepatic laminin content tended to increase in parallel with the progression of fibrosis. The laminin content in alcoholic liver disease was significantly higher than in the corresponding type of non-alcoholic liver disease. The ratio of laminin to total collagen content was highest in alcoholic liver disease showing mild fibrosis and decreased in parallel with the progression of fibrosis. In contrast, the ratio was low in all types of nonalcoholic liver disease. The ratio in patients with alcoholic liver disease was significantly higher than these with the corresponding non-alcoholic liver disease. Hepatic laminin content increased in parallel with the increase in hepatic type IV collagen in alcoholic liver disease, and the correlation was statistically significant. However, similar correlation was not found in non-alcoholic liver disease. These results indicate that the response to laminin synthesis to alcoholic liver disease is strong in mild fibrosis and reached a plateau at a relatively early stage of fibrosis. The stimulation for laminin synthesis in non-alcoholic liver disease is different from that in alcoholic liver disease.

Adult↗
PubMed2000

Drug-induced liver disease.

Drug-induced liver disease may account for between 10% and 50% of adult patients with elevated enzymes, especially in patients over age 50 years. It accounts for nearly 25% of patients with fulminant hepatic failure. Liver injury can be cytotoxic, cholestatic, or mixed. A variety of systemic manifestations can accompany drug-induced hepatotoxicity. Drug-induced liver disease can mimic autoimmune hepatitis or it can evolve to cirrhosis. It can also mimic veno-occulusive disorders. The plethora of herbal and traditional agents currently ingested by many people should always be considered in any patient with abnormal hepatic biochemistry.

Chemical and Drug Induced Liver Injury↗
PubMed1982

Cellular and humoral immune reactions in chronic active liver disease. I. Lymphocyte subsets in liver biopsies of patients with untreated idiopathic autoimmune hepatitis, chronic active hepatitis B and primary biliary cirrhosis.

In liver biopsies of 37 patients with chronic active liver disease (CALD) the inflammatory infiltrate was studied with monoclonal antibodies to the surface antigens on helper/inducer (OKT4+), suppressor/cytotoxic (OKT8+), killer/natural killer (OKM1,2+) cells and common T cell antigens (OKT1+, OKT3+). Furthermore OKT11 antibody was applied, which defines the E rosette receptor. Special emphasis was given to areas with piece-meal necrosis (PMN). In areas with PMN in idiopathic autoimmune CALD (IA-CALD, n = 15) OKT8+ and OKM+ lymphocytes and IgG plasma cells were present, whereas in hepatitis B-CALD (HB-CALD, n = 12) almost exclusively OKT8+ cells were found. In PBC (n = 10) OKT4+ cells in central parts of portal tracts and OKT8+ cells in areas with PMN predominated. These findings indicate that in IA-CALD antibody-dependent cell-mediated cytotoxicity (ADCC), as well as T cell cytotoxicity may be responsible for liver cell damage, while in HB-CALD T cell cytotoxicity seems to be the only mechanism. In PBC liver cell damage also predominantly is the result of T cell cytotoxicity. In addition, helper T lymphocytes seem to play a role since these are found in central areas of the portal tracts.

Adolescent↗
PubMed2006

Risk factors and ultrasound can predict chronic hepatitis caused by nonalcoholic fatty liver disease.

The diagnosis of nonalcoholic fatty liver disease (NAFLD) is under-recognized. The aim of this study was to develop a scoring system that separates NAFLD diagnosis as a cause of chronic hepatitis from controls by using clinical features and liver ultrasound. A retrospective review of consecutive NAFLD cases and other liver disease controls was undertaken selecting patients from an abnormal liver function test code. To qualify for analysis all patients had to have elevated liver injury tests for more then 6 months, a biopsy-confirmed diagnosis, and an ultrasound as part of the evaluation. There were 84 cases of NAFLD and 75 liver disease controls. The NAFLD group had a larger body mass index (BMI) (34.9 versus 26.1; P < or = 0.0001), a larger liver span (9.8 versus 8.1 cm; P < or = 0.0001), and higher triglycerides (252 versus 142.6; P < or = 0.0001). The ultrasound reports recorded features consistent with fatty infiltration in 65.5% of NAFLD cases, compared to 5.3% of other liver diseases (P < or = 0.0001). Diabetes mellitus was found in 35% of NAFLD and 6.7% of other cases (P < or = 0.0001). The BMI was >30 in 79.8% of NAFLD cases and 22.7% of other liver disease cases (P < or = 0.0001). The liver span was >8 cm in 78.6% of NAFLD cases and in only 16% of controls (P = 0.0001). On multivariate analysis using logistic regression, the odds ratio of having ultrasound report findings suggestive of fatty infiltration was 15.9 (CI, 4.1-60). The odds ratio was 9.4 (CI, 2.3-37.9) for diabetes, 5.0 (CI, 1.7-14.6) for BMI >30, and 2.3 for liver span >8 cm (CI, 1.36-3.90). A scoring system using clinical features and ultrasound was shown to reliably separate NAFLD from other cases of chronic hepatitis.

Biopsy↗
PubMed1983

Changes of hepatic microtubules and secretory proteins in human alcoholic liver disease.

It has been shown that alcohol consumption disrupts liver microtubules, impairs protein secretion and leads to ballooning of the hepatocytes in rats. Ethanol-induced hepatomegaly was accounted for by an increase of the hepatocytes volume. To study whether these changes occur in human alcoholic liver disease, hepatic tubular protein and export protein content were measured in 29 cases of alcoholic liver disease and were compared with those of 37 cases of non-alcoholic liver disease and 5 cases of non-hepatobiliary disease. Hepatic polymerized tubulin was significantly decreased in alcoholic liver disease compared to non-alcoholic liver disease (p less than 0.01), while free tubulin was increased in alcoholic liver disease. Hepatic transferrin (one of the export proteins) content was significantly higher (p less than 0.01) and serum transferrin level was significantly lower (p less than 0.05) in alcoholic liver disease than in non-alcoholic liver disease. These findings indicated that even in humans, chronic alcohol consumption decreased hepatic microtubules by impairing polymerization of tubular protein and increased hepatic export protein content. This decrease in hepatic microtubules by chronic alcohol consumption may play an important role in the development of human alcoholic liver disease.

Albumins↗
PubMed2000

Coagulopathy of Liver Disease.

Coagulopathy in patients with liver disease results from impairments in the clotting and fibrinolytic systems, as well as from reduced number and function of platelets. Parenteral vitamin K replacement corrects coagulopathy related to biliary obstruction, bacterial overgrowth, or malnutrition. Vitamin K is less effective for coagulopathy caused by severe parenchymal liver injury. Transfusion of fresh frozen plasma is the hallmark of treatment of significant coagulopathy in patients with liver disease and active bleeding. Transfusion of fresh frozen plasma also reverses moderate to severe coagulopathy of cirrhosis prior to invasive procedures. Cryoprecipitate is useful for severe coagulopathy with hypofibrinogenemia, especially when avoidance of volume overload is desired. Exchange plasmapheresis is useful in selected patients with coagulopathy due to liver disease, in whom fresh frozen plasma fails to correct coagulopathy or in patients who have coexistent severe fluid overload. Platelet transfusions, pooled or single donor, are useful in thrombocytopenic patients prior to performing invasive procedures or in the presence of significant bleeding, especially when the platelet count is below 50,000/mL. The use of recombinant factor VIIa and thrombopoietin therapy for correction of coagulopathy and thrombocytopenia, respectively, in patients with cirrhosis, is currently under investigation. Therapy with prothrombin complex concentrates, 1-deamino-8-d-arginine vasopressin and antithrombin III concentrates for the management of coagulopathy caused by liver disease can be hazardous and the use of these products is considered investigational at the present time.

Journal Article↗
PubMed1993

Endstage liver disease associated with nitrofurantoin requiring liver transplantation.

OBJECTIVE: To report the apparent development of endstage liver disease secondary to nitrofurantoin administration. PATIENT: A 40-year-old woman developed hepatic failure after receiving nitrofurantoin 200 mg po bid for one month for prophylaxis against urinary-tract infections. Symptoms first occurred after two weeks of nitrofurantoin therapy. Other causes of hepatic failure (e.g., viral infection, autoimmune disorder, concomitant medications, cancer, Wilson's disease, ethanol abuse, pregnancy) were ruled out. CONCLUSIONS: Acute and chronic hepatic injury has previously been reported with the use of nitrofurantoin. The proposed mechanism may be immunoallergic or metabolic in origin. On evaluating concomitant diseases and medications in our patient as well as the temporal sequence of her signs and symptoms, it appears that she developed hepatic failure secondary to the use of nitrofurantoin, ultimately necessitating orthotopic liver transplantation. The potential for the development of such a severe adverse reaction warrants careful evaluation of symptoms that may potentially be caused by hepatic damage as well as immediate discontinuation of nitrofurantoin in patients presenting with jaundice.

Adult↗
PubMed1989

In vitro evidence for B cell dysfunction in patients with chronic liver disease.

Patients with chronic liver disease have been reported to have multiple immunologic abnormalities. We evaluated immune function in 40 such patients. The patient group had a decreased proportion of CD3 positive cells compared to controls (54.2 +/- 13.2 vs 67.9 +/- 5.7, p less than 0.01), CD4 positive cells (38.4 +/- 10.0 vs 44.3 +/- 4.9, p less than 0.01) and CD8 positive cells (17.7 +/- 8.2 vs 26.3 +/- 3.9, p less than 0.05). B cells were increased over controls (8.3 +/- 4.0 vs 6.0 +/- 1.9, p less than 0.01). In vitro immunoglobulin synthesis studies demonstrated decreased production in both IgM (632 +/- 482 ng/ml vs 2,050 +/- 1,720 ng/ml, p less than 0.01) and IgG synthesis (726 +/- 640 ng/ml vs 1,117 +/- 1,012 ng/ml, p less than 0.05) by patients as compared to controls. Coculture of fractionated populations of lymphocytes indicated that the patients had adequate T helper cell activity and no evidence for enhanced T suppressor cell activity. B cells of patients with chronic liver disease appear to have an impaired capacity to produce immunoglobulin in vitro.

Adult↗
PubMed2002

[Cholestatic liver disease in children].

Cholestatic liver disease constitutes a large part of chronic liver diseases during infancy. It is caused either by extrahepatic disorders (obstruction) or by intrahepatic cholestasis (functional). The differential diagnosis should be done as early as possible because the delayed surgical therapy in extrahepatic cholestasis has a very bad prognosis. Intrahepatic cholestasis may be caused by a broad spectrum of different disorders such as congenital infection, endocrine, chromosomal abnormalities or inborn errors of metabolism. Familial clustering is typical for the Byler's disease, Alagille's syndrome, PFIC, errors of bile acid synthesis or alpha-1-ATD. The established diagnosis allows to start etiological treatment: dietary--in metabolic diseases, antibiotics--in bacterial infections, antiviral--in viral infections etc. To lower bile acids level pharmacological treatment (UDCA) or surgical procedures (hepatoportoenterostomy, partial biliary diversion) should be performed. In progressive cholestasis the only effective therapy is liver transplantation.

Age Factors↗
PubMed1991

Alcoholic liver disease: pathologic, pathogenetic and clinical aspects.

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.

Diagnosis, Differential↗
PubMed1986

Gastrointestinal hormones in alcoholic patients with and without liver disease.

To assess the effects of both alcoholism and liver disease on gastroentero-pancreatic hormones, fasting and post-prandial concentrations were analysed in the following four groups: (1) Alcoholic subjects with liver disease; (2) Alcoholic subjects without liver disease; (3) Control subjects with liver disease; (4) Control subjects without liver disease.Liver disease was associated with increased fasting serum glucose, plasma insulin, pancreatic polypeptide, gastrin and vasoactive intestinal polypeptide. Alcoholism in the absence of liver disease did not influence either the fasting or post-prandial concentrations of serum glucose, plasma gastrin, insulin, pancreatic polypeptide, gastric inhibitory polypeptide, N- and C-terminal glucagon or vasoactive intestinal polypeptide. Alcoholism with liver disease depressed plasma gastric inhibitory polypeptide concentrations. The results suggest that the abnormalities in gastroenteropancreatic hormone in alcoholics are likely to be related to liver disease which is often concurrent.

Adult↗
PubMed2002

Celiac disease in patients with severe liver disease: gluten-free diet may reverse hepatic failure.

BACKGROUND & AIMS: Mild liver abnormalities are common in patients with celiac disease and usually resolve with a gluten-free diet. We investigated the occurrence of celiac disease in patients with severe liver failure. METHODS: Four patients with untreated celiac disease and severe liver disease are described. Further, the occurrence of celiac disease was studied in 185 adults with previous liver transplantation using serum immunoglobulin A endomysial and tissue transglutaminase antibodies in screening. RESULTS: Of the 4 patients with severe liver disease and celiac disease, 1 had congenital liver fibrosis, 1 had massive hepatic steatosis, and 2 had progressive hepatitis without apparent origin. Three were even remitted for consideration of liver transplantation. Hepatic dysfunction reversed in all cases when a gluten-free diet was adopted. In the transplantation group, 8 patients (4.3%) had celiac disease. Six cases were detected before the operation: 3 had primary biliary cirrhosis, 1 had autoimmune hepatitis, 1 had primary sclerosing cholangitis, and 1 had congenital liver fibrosis. Only 1 patient had maintained a long-term strict gluten-free diet. Screening found 2 cases of celiac disease, 1 with autoimmune hepatitis and 1 with secondary sclerosing cholangitis. CONCLUSIONS: The possible presence of celiac disease should be investigated in patients with severe liver disease. Dietary treatment may prevent progression to hepatic failure, even in cases in which liver transplantation is considered.

Adolescent↗
PubMed1976

[Gamma-glutamyl-transpeptidase in alcoholic liver diseases].

In well defined liver diseases in 69 alcoholics and in 71 patients without history of alcoholism the enzymatic findings were compared. Also a group of 43 alcoholics with praedelirium or delirium tremens were examined. In steatosis due to alcohol, the average of GGTP (145 U/l) attains values two times higher than in comparable cases of non-alcoholic origin (73 U/l). In cirrhotics with alcoholism, the average GGTP levels (477 U/l) exceed those obtained in patients with cirrhosis of other origin (110 U/l), four times more. Similar or higher GGTP values were found only in primary biliary cirrhosis. After a period of at least 3 months of abstinence, GGTP values had decreased (to 68 U/l) in the average). The highest values of GGTP were found in acute alcoholic hepatitis and in chronic alcoholics with praedelirium or delirium tremens. GGTP accords diagnostic hints in comparison with other enzymes, as shown by a quotient of GGTP-GPT. GGTP is very helpful for differentiation and long time observation of alcoholic liver disease, especially with regards controlling abstinence of alcohol.

Alcoholism↗
PubMed1994

Cerebral dysfunction in chronic alcoholism: role of alcoholic liver disease.

Evidence suggests that liver disease per se may contribute to the cognitive and motor impairments encountered in chronic alcoholics. Neuropathologic studies reveal astrocytic changes (Alzheimer type II astrocytosis) in the brains of alcoholic cirrhotic patients who died in hepatic coma. Pathophysiologic mechanisms responsible for hepatic (portal-systemic) encephalopathy in alcoholics include the loss of neuron-astrocytic metabolic trafficking as well as selective alterations of serotoninergic and dopaminergic function. In addition, there is evidence to suggest that endogenous ligands for both central-type (GABA-related) and "peripheral-type" (astrocytic) benzodiazepine receptors are implicated in the pathogenesis of hepatic encephalopathy in these patients. Chronic liver disease may also interfere with brain thiamine homeostasis and thus contribute to the pathogenesis of the Wernicke-Korsakoff syndrome in chronic alcoholism.

Alcoholism↗
PubMed2002

Hepatic progenitor cells in human liver diseases.

The canals of Hering and bile ductules in human liver contain hepatic progenitor cells that can differentiate towards the biliary and hepatocytic lineage. Proliferation and differentiation of hepatic progenitor cells is referred to as 'activation' and this process occurs to a variable degree in almost all human liver diseases. Several studies indicate that hepatic progenitor cell activation in diseased liver is regulated by neural and neuroendocrine factors such as the vagal innervation. Analogous to oval cells in animal liver, there is evidence that human hepatic progenitor cells may be able to give rise to hepatocellular carcinoma and other liver tumors.

Animals↗