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K P Maier

Publications and source records attributed to K P Maier.

At least 19 recordsLinked to original sources
PubMed2006

[Non-alcoholic liver disease (NASH)].

NASH, an increasingly recognized condition resembles alcohol-induced liver disease, but occurs in patients who do not abuse alcohol. Obesity, insulin resistance and oxidative stress have critical roles in the pathogenesis of NASH. Liver biopsy remains the only modality that can reliably distinguish steatosis from steatohepatitis. Simple steatosis may have the best prognosis. In patients with NASH liver enzymes are insensitive and can not be used reliably to confirm the diagnosis or stage the extent of fibrosis. Currently no effective medical therapy is available. Weight reduction may improve the disease. Liver-transplantation in end-stage liver disease is a potential therapeutic option also in patients with NASH.

Biopsy↗
PubMed2006

[Risk-classification in liver cirrhosis].

Prognostic models are useful in estimating disease severity and survivial and are used to make decisions regarding specific medical interventions. These models are developed using analytical methods that involve determining the effects of variables of interest (eg, laboratory values) on specific outcomes such as death. There are two models that are used commonly in the care of patients witch chronic liver disease: the Child-Pugh score and the recently described Model for End-Stage Liver Disease (MELD). MELD score is a prospectively developed and validated chronic liver disease severity scoring system that uses a patient's laboratory values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. The score was proposed as a the most promising alternative to Child-Pugh score. Weather Child-Pugh score should definitely be abandoned for MELD score remains uncertain. The aims of this paper are to summarize and to compare the characteristics, applications and limitations of Child-Pugh and MELD scores.

Bilirubin↗
PubMed2005

[The patient with slightly increased liver function tests].

The availability of serum blood chemistries for screening both symptomatic and asymptomatic patients has resulted in a marked increase in the number of abnormal liver chemistry tests that must be interpreted by physicians. Usually the first step in the evaluation of a patient with elevated liver enzymes is to repeat the test to confirm the result. If the result is still abnormal, it seems wise to differentiate between a predominant "necrotic pattern" of liver chemistry, as indicated by an elevation of ALT- or AST-activity or a predominant "cholestatic pattern", as indicated by elevated activities of g-GT and alkaline phosphatase. In patients with elevated serum amino transferases hepatic diseases should be excluded primarily with non-invasive serologic tests. The most common causes of elevated amino transferase levels are chronic hepatitis B and C, autoimmunhepatitis, non-alcoholic steatohepatitis, hemochromatosis, Wilson-disease and (only recently recognized) celiac sprue. In the case of a dominant "cholestatic pattern", primary biliary cirrhosis, primary sclerosing cholangitis, but also drugs and granulomatose hepatitis must be excluded. If non-invasive serologic studies remain inconclusive, ultrasound, mini-laparoscopy and liver biopsy will help to establish the final diagnoses.

Alkaline Phosphatase↗
PubMed2003

[Phenprocoumon-induced liver failure].

HISTORY: A 61-year-old woman was referred because of painless jaundice, laboratory tests having indicated hepatitis with impaired liver functions. For the past two years she had been taking phenprocoumon because she had atrial fibrillation. INVESTIGATIONS: Serological tests largely excluded infectious, autoimmune or metabolic etiology, so that the diagnosis of drug-induced hepatic disease was made. Liver biopsy showed necrotic liver cells and mild inflammatory reaction. TREATMENT AND COURSE: A perforating duodenal ulcer required urgent surgical intervention, after which liver functions further deteriorated. The patient having refused liver transplantation she was treated symptomatically (oral vitamin K. lactulose, diuretics), phenprocoumon was discontinued and her condition slowly improved. She was discharged after two months. At subsequent examination she was symptom-free, the INR was 1.41, transaminases were normal and ultrasound merely showed a slightly inhomogeneous internal structure. CONCLUSION: Phenprocoumon can cause liver damage even when the drug has been taken for prolonged periods without any problems. A careful history about previously administered drugs should be taken in any case of hepatitis of uncertain etiology.

Anticoagulants↗
PubMed2003

[Hepatitis: associated diseases. Risk groups -- prevention -- treatment].

Active vaccination against HBV-infection results in a very high protection rate. Therefore, all persons at risk should be vaccinated. Acute HBV-infection seems to progress to chronicity in a minority of adults. Unfortunately, treatment of chronic HBV-infection with interferon and Lamivudine is effective only in about 40% of patients, leading to a complete virus elimination. However, relapse-rates are high. Additionally, mutant viruses arise in the case of Lamivudine treatment (YMDD-mutants). Interestingly, Adefovir, a new nucleoside analogue, seems not to induce virus-mutants, at least after a therapy of 48 weeks. HBV-DNA declines rapidly, transaminases normalize in more than 2/3 of the patients, liver histology improves. As mentioned, active vaccination against HBV is very effective in preventing the infection. Unfortunately, this is not the case in HCV-infection. So far, the development of an HCV-vaccine is mainly hampered due to the variability of the HCV (RNA) virus. Untreated, more than 2/3 of the HCV-infected patients with acute HCV-positive hepatitis develop chronicity. Chronic hepatitis C can be treated preferably with a combination therapy (pegylated interferons + Ribavirin). Sustained response rates average 50 per cent (and more). However, treatment of non-responders as well as the treatment of relapsers remain an unresolved problem.

Adenine↗
PubMed2003

[Pantoprazole-induced hepatitis].

HISTORY: A 46-year-old woman presented for an emergency admission because of colic-like upper abdominal pain and markedly impaired general condition. Eight days before admission she had started and continued to take pantoprazole because of symptoms of gastroesophageal reflux. INVESTIGATIONS: Clinical examination and laboratory tests indicated abnormal liver functions suggesting hepatitis. Serology largely excluded an infectious, autoimmunological or metabolic cause. Duplex sonography gave no evidence of bile obstruction or Budd-Chiari syndrome. DIAGNOSIS AND COURSE: The patient's condition and laboratory tests after the drug had been discontinued gradually improved on symptomatic treatment, indicating pantoprazole-induced hepatitis. CONCLUSION: Intake of proton pump inhibitors is a rare cause but should be considered in the differential diagnosis of hepatitis of uncertain etiology.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2002

[Rare, but important chronic liver diseases].

The presence of steatosis and inflammatory infiltrate in liver biopsies is essential for the diagnosis of non-alcoholic steatohepatitis (NASH). These findings are similar to those with alcoholic liver disease. However, in the NASH-situation alcohol doesn't play an important role. Risk factors for the development of NASH are obesity and diabetes. Most of the patients are clinically asymptomatic. This means, that a diagnosis of NASH is a diagnosis of exclusion: Viral induced, autoimmune, metabolic and toxic liver disease have to be excluded. The disease has a benign clinical course. The risk of cirrhosis is low. So far, there is no established treatment. Preliminary reports suggest a positive effect of weight-loss and ursodeoxycholic acid. Wilson's disease, a copper storage disorder, in which biliary copper excretion is reduced, is inherited as an autosomal recessive trait. Most patients with Wilson disease become symptomatic between the ages of 6 and 15. In about 90% of patients serum ceruloplasmin levels and serum copper concentrations are reduced. Copper excreation is increased. Histologic examination of liver biopsy specimens reveals fatty infiltration, Mallory bodies and ballooned glycogen nuclei, abnormalities which are also found in alcoholic liver disease. The definitive diagnostic parameter is the quantitative determination of liver copper content (> 250 micrograms/g dryweight). Untreated Wilson disease is always fatal. Lifelong treatment with anti-copper drugs are essential, D-penicillamine being the firstline therapy. Hereditary hemochromatosis (HH) is an iron overload disease inherited as an autosomal recessive trait. The frequency of the disease is high. The first symptoms usually can be found at the age of 20-50 years. Arthralgia develops in up to 50% of the patients. Many organs are involved, most often the liver. The organ is usually enlarged, transaminases are always moderately elevated. Laboratory findings disclose a marked elevation in serum ferritin and transferrin saturation. More than 80% of HH-patients are homozygous for the C282Y-mutation in the HFE-gene. The firstline treatment of HH is phlebotomy. Treatment is lifelong. When serum ferritin drops below 50 micrograms/l, the frequency of phlebotomy should be reduced (4-12 per year). If the patient already has cirrhosis, the risk of HCC is very high.

Adolescent↗
PubMed2002

[Hepatocellular carcinoma: risk groups--screening].

Cirrhosis of the liver has to be regarded as a premalignant condition independent of its etiology. The annual risk of developing HCC in cirrhosis is between 1% and 6%. Surveillance-programs have been introduced to detect early stages of HCC in order to improve mortality. However, only controlled trials will answer the question of the efficacy of such programs. Studies on the potential benefit of surveillance-programs comparing survival in surveilled and unsurveilled patients are so far lacking. It seems clear, however, that surveillance-programs can detect small tumors, often unfocal and potentially treatable by a curative approach. Moreover, the etiology (HBV, HCV, genetic hemochromatosis) and activity of liver cirrhosis as measured by serum-transaminases, liver histology (small-cell dysplasia and atypical regenerative nodules), Child-Pugh-stage and the concentration of alpha-fetoprotein at the beginning of a surveillance-program--all these factors reflect a high risk of developing HCC in an individual patient. Until programs are introduced on the basis of randomized, controlled trials of surveillance vs. usual care (with liver-related, specific deaths and all-cause-mortality as end-points) it seems reasonable to screen high-risk patients semi-annually by liver ultrasound and determination of AFP-concentration in the serum.

Carcinoma, Hepatocellular↗
PubMed1999

Oral budesonide and ursodeoxycholic acid for treatment of primary biliary cirrhosis: results of a prospective double-blind trial.

BACKGROUND & AIMS: Ursodeoxycholic acid (UDCA) is used for treatment of primary biliary cirrhosis. Previous studies showed that, compared with UDCA monotherapy, bile salts plus prednisolone had no further effect on laboratory data but improved liver histology. Thirty percent of these patients had prednisolone-related side effects. Budesonide is a glucocorticoid with a high receptor affinity and a high first-pass metabolism. In this study we investigated whether budesonide and UDCA are superior to UDCA monotherapy. METHODS: A 2-year prospective, controlled double-blind trial was performed. Twenty patients (mainly with early-stage disease) were treated with UDCA at a dose of 10-15 mg/kg daily in addition to 3 mg budesonide 3 times daily (group A), and 19 patients (1 dropped out for personal reasons) were treated with UDCA plus placebo (group B). Liver biopsy specimens were taken before, after 12 months, and at the end of study. Glucose tolerance tests, serum cortisol levels, and adrenocorticotropin-stimulated cortisol secretion were assessed at regular intervals. Bone mass density was measured by dual-energy photon absorptiometry. RESULTS: Compared with pretreatment values, liver enzyme and immunoglobulin M and G levels decreased significantly in both groups. Improvement in group A was significantly more pronounced (P < 0.05) than in group B. Titers of antimitochondrial antibodies did not change. In group A, the point score of liver histology improved by 30.3%; in group B, it deteriorated by 3.5% (P < 0.001). Changes in bone mineral density after 2 years were -1.747% in group A and -0.983% in group B (P = 0.43). Budesonide had little influence on the hypothalamic-pituitary-adrenal axis. One patient in group A had budesonide-related side effects; in 3 patients in group B, complications of liver disease developed. CONCLUSIONS: Combination therapy with UDCA and budesonide is superior to UDCA and placebo.

Administration, Oral↗