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Liver disease diabetes mellitus

Nephrotic syndrome Hepatic synthesis Liver disease Diabetes mellitus Estrogens/pregnancy Childhood Neural tube defects Ataxia telangiectasia Down s syndrome... [Pg.5286]

The 23-valent pneumococcal polysaccharide vaccine is recommended for use in all adults 65 years of age or older and adults less than 65 years who have medical comorbidities that increase the risk for serious complications from S. pneumoniae infection, such as chronic pulmonary disorders, cardiovascular disease, diabetes mellitus, chronic liver disease, chronic renal failure, functional or anatomic asplenia, and immunosuppressive disorders. Alaskan natives and certain Native American populations are also at increased risk. Children over the age of 2 years may be vaccinated with the 23-valent pneumococcal polysaccharide vaccine if they are at increased risk for invasive S. pneumoniae infections, such as children with sickle cell anemia or those receiving cochlear implants. [Pg.1245]

Chemical, biological, and pharmacological properties of lipoic acid as well as its therapeutic effects in several diseases (diabetes mellitus, liver cirrhosis, polyneuritis, etc.) are reviewed [198,199], It is evident from the chemical structures of LA and DHLA that only DHLA may be an efficient scavenger of all oxygen radicals, while LA should be active only in the reactions with highly reactive hydroxyl radicals. On the other hand, DHLA must be easily... [Pg.873]

Medical indications Chronic pulmonary disease (excluding asthma) chronic cardiovascular diseases, diabetes mellitus chronic liver diseases, including liver disease as a result of alcohol abuse (e.g., cirrhosis) chronic alcoholism, chronic renal failure or nephrotic syndrome functional or anatomic asplenia (e.g, sickle cell disease or splenectomy [if elective splenectomy is planned, vaccinate at least 2 weeks before surgery]) immunosuppressive conditions and cochlear implants and cerebrospinal fluid leaks. Vaccinate as close to HIV diagnosis as possible. [Pg.1067]

An elevation of ChE activity can be detected in fatty liver, obesity, diabetes mellitus, exudative enteropathy, nephrotic syndrome, hyperthyroidism, Meulengracht s icterus, chronic obstructive jaundice, etc. Specificity in liver diseases is 61%, and sensitivity is 49%. In cirrhosis, however, sensitivity is 88% normal ChE therefore widely excludes cirrhosis. In connection with other hepatobiliary enzymes, ChE can be useful in the diagnosis and assessment of the course of liver disease. There is a very good correlation of ChE activity with coagulation factors in liver diseases however, the correlation is less significant with albumin synthesis. [Pg.103]

Concomitant illness chronic liver, cardiac, pulmonary or kidney disease diabetes mellitus etc. [Pg.350]

Fatty acids are synthesized by an extramitochondrial system, which is responsible for the complete synthesis of palmitate from acetyl-CoA in the cytosol. In the rat, the pathway is well represented in adipose tissue and liver, whereas in humans adipose tissue may not be an important site, and liver has only low activity. In birds, lipogenesis is confined to the liver, where it is particularly important in providing lipids for egg formation. In most mammals, glucose is the primary substrate for lipogenesis, but in ruminants it is acetate, the main fuel molecule produced by the diet. Critical diseases of the pathway have not been reported in humans. However, inhibition of lipogenesis occurs in type 1 (insulin-de-pendent) diabetes mellitus, and variations in its activity may affect the nature and extent of obesity. [Pg.173]

Acute leukemia, acute lymphoma, short-bowel syndrome, liver disease (decreased clearance), diabetes mellitus, mitochondrial disease, and congenital enzyme deficiencies... [Pg.177]

Non-alcoholic fatty liver disease begins with asymptomatic fatty liver but may progress to cirrhosis. This is a disease of exclusion elimination of any possible viral, genetic, or environmental causes must be made prior to making this diagnosis. Non-alcoholic fatty liver disease is related to numerous metabolic abnormalities. Risk factors include diabetes mellitus, dyslipidemia, obesity, and other conditions associated with increased hepatic fat.26... [Pg.329]

In patients with type 1 insulin-dependent diabetes mellitus not adequately treated with insulin, fatty add release from adipose tissue and ketone synthesis in the liver exceed the ability of other tissues to metabolize them, and a profound, life-threatening ketoaddosis may ocxnir. An infection or trauma (causing an increase in cortisol or epinephrine) may predpitate an episode of ketoaddosis. Patients with type 2 non-insulin-dependent diabetes meUitus (NIDDM) are much less likely to show ketoaddosis. The basis for this observation is not completely understood, although type 2 disease has a much slower, insidious onset, and insulin resistance in the periphery is usually not complete. Type 2 diabetics can develop ketoacidosis after an infection or trauma. In certain populations with NIDDM, ketoaddosis is much more common than previously appredated. [Pg.232]

Contributing diseases Prior to initiating therapy, investigate and treat diseases contributing to increased blood cholesterol (eg, alcoholism, diabetes mellitus, dysproteinemias, hypothyroidism, nephrotic syndrome, obstructive liver disease, other drug therapy). [Pg.607]

The measurement of serum cholesterol is one of the most common tests performed in the clinical laboratory. Hypercholesterolemia (high blood cholesterol levels) can be the result of a variety of medical conditions. Among the conditions implicated are diabetes mellitus, atherosclerosis, and diseases of the endocrine system, liver, or kidney. High blood cholesterol levels do not point to a specific disease determination of cholesterol is used in conjunction with other clinical measurements mainly for confirmation of a particular diseased condition, rather than for diagnosis of a specific ailment. [Pg.373]

Abnormally high systemic iron levels can lead to cirrhosis of the liver, diabetes mellitus, and heart failure. Although a number of disease processes can lead to iron overload, this chapter focuses on hereditary hemochromatosis, the prototypical disease of iron overload. [Pg.335]

Plasma zinc levels are commonly decreased in the elderly (Gil). These authors reported mean ( SD) plasma levels in normal young adults at 12.7 ( 1.4) mmol/liter versus 10.5 ( 4.7) mmol/liter in the elderly intracellular levels (neutrophils) were 1.26 ( 0.28) and 0.95 ( 0.26) nmol/mg protein, respectively. This deficiency is most often due to lack of dietary lean meat, poultry, and fish. As a result, zinc intake is frequently less than the minimum recommended intake of 15 mg/day. Moreover, Zn deficiency is particularly common in individuals with diabetes mellitus, liver and renal diseases, malabsorption, alcohol abuse, and those taking diuretic medications (K13). Interestingly, many of the signs and symptoms of Zn deficiency are the same as those often attributed to the aging process (Table 3). [Pg.23]

Diabetes mellitus ( sweet urine ) involves relative over-production of glucose by the liver and under-utilization by other organs. Diabetes is the most serious metabolic disease in terms of its social impact. Obesity and the indulgent Western diet correlates with mature age diabetes. Type 1 diabetes (juvenile diabetes) typically manifests at less than 20 years from autoimmune destruction of the insulin-producing pancreatic (3 cells. Type 1 diabetes is insulin-dependent diabetes mellitus (IDDM) and is fatal without exogenous insulin. Type 2 diabetes mellitus (mature age diabetes) occurs later in life and typically involves both deficient insulin production and insulin resistance , that is, the target cells are less responsive to insulin. Type 2 diabetes is initially non-insulin-dependent diabetes (NIDDM) but insulin therapy (in addition to oral antidiabetics) may eventually be required. Hyperglycaemia due... [Pg.599]

Q8 In type 1 diabetes, because of a lack of insulin, a high level of triglyceride is stored in the liver and can subsequently be converted to phospholipids and cholesterol. Hepatocytes synthesize VLDLs, which can be converted to other types of lipoproteins. These lipoproteins are major sources of cholesterol and triglycerides for most other tissues. They leave the liver, enter the blood and can result in rapid development of vascular atherosclerosis. Increased levels of atherogenic oxidized low-density lipoproteins (LDLs) are seen in hyperglycaemic individuals and contribute to macrovascular disease, which is a complication of diabetes mellitus. [Pg.160]

A 77-year-old woman was found dead in her bathtub. She had a history of depression, liver disease, spinal stenosis, and diabetes mellitus. An empty bottle of triazolam was found in the bin. At autopsy there was no injury or evidence of drowning. There was triazolam 0.12 mg/1 in the heart blood. [Pg.431]

Liver disease is now recognised as a major complication of type 2 diabetes. Diabetes mellitus can lead to metabolic changes that alter normal hepatic and biliary function and structure. Type 2 diabetes is associated with an increased risk of a range of hepatobiliary diseases, including non-alcoholic fatty liver disease, cirrhosis, acute liver failure, hepatocellular carcinoma and cholelithiasis [22]. [Pg.69]

Brunt EM. Nonalcoholic steatohepatitis. Semin Liver Dis 2004 24 3-20. Marchesini G, Bugianesi E, Forlani G, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 2003 37 917-923. Wanless IR, Lentz JS. Eatty liver hepatitis (steatohepatitis) and obesity an autopsy study with analysis of risk factors. Hepatology 1990 12 1106-1110. Zimmerman HJ. Hepatotoxicity. The adverse effects of drugs and other chemicals in the liver, 2nd edn. Philadelphia Lippincott Williams Wilkins, 1999. Mason P. Cystic fibrosis - the disease. Hosptal Pharmacist 2005 12 201-207. Tolman KG, Eonseca V, Tan MH, et al. Narrative review hepatobiliary disease in type 2 diabetes mellitus. Ann Intern Med 2004 141 946-956. [Pg.72]

GGT levels may also be raised in patients taking enzyme-inducing drugs such as phenytoin or rifampicin, where levels can be commonly measured at twice ULN and potentially up to five times. Those with concomitant diseases, such as diabetes mellitus, can have GGT levels up to three times ULN, which may be due to a fatty liver. [Pg.79]

Because ADRs are more likely to occur in the very young and the elderly, lower drug dosages may be indicated at these two extremes of the human life span. The elderly are more likely to have diseases such as cancer, coronary heart disease, dementia, diabetes mellitus, hypertension, and osteoporosis and may also have adverse nutritional reactions. Deficiencies in liver and kidney function can result in marked delay of drug detoxification and elimination. Constant review of established diagnoses and treatments is important to minimize the number of drugs administered, and care must be taken to determine whether other nutritional supplements and herbal products are being incorporated into self-treatment. [Pg.703]

Elevation of y-GT is found in cholestasis, liver cirrhosis, viral hepatitis, fatty liver, porphyria, toxic liver damage, pancreatitis and pancreatic cancer, myocardial infarction, nephrotic syndrome, diabetes mellitus, right heart failure, obesity, nicotine abuse, and brain tumours. There is a good correlation of y-GT with CEA in colon cancer, involving a metastatic spread to the liver - an increase in y-GT in neoplastic disease is likewise supportive of the diagnosis of hepatic metastases. [Pg.98]

Acute liver failure is a rare occurrence. It is estimated that approx. 5 cases are found out of 6,000 hospital admissions (in the USA a total of ca. 2000 patients per year, in Germany ca. 150). However, there can be wide variations in frequency due to the effect of regional differences on the individual aetiology of this disease. The causes of acute liver failure are numerous and multiform. Diabetes mellitus is an extremely high risk factor... [Pg.377]

The following factors are decisive in achieving a favourable prognosis for all forms of alcoholic liver disease (7.) total abstention from alcohol, (2.) extent of irreversible loss of liver parenchyma, (S.) exclusion of other risk factors (e. g. obesity, diabetes mellitus, malnutrition), 4.) additional effects of hepatotoxic substances (e.g. medication, chemical agents), and (5.) coexistence of further alcohol-induced organ damage. (5, 23, 37, 80, 81, 86, 99, 102, 108)... [Pg.535]

Aceruloplasminaemia is a very rare, autosomal recessive disease with diffuse iron overload. It is caused by a mutation of the ceruloplasmin gene. This leads to excessive iron storage, mainly in the brain, liver and pancreas. The principal symptoms are increased serum ferritin, decreased serum iron and transferrin saturation as well as extrapyramidal disturbances, retinal degeneration, cerebellar ataxia and diabetes mellitus. (486-488) (s. tab. 31.17)... [Pg.618]


See other pages where Liver disease diabetes mellitus is mentioned: [Pg.354]    [Pg.617]    [Pg.118]    [Pg.2253]    [Pg.5391]    [Pg.320]    [Pg.102]    [Pg.212]    [Pg.89]    [Pg.274]    [Pg.344]    [Pg.382]    [Pg.162]    [Pg.195]    [Pg.229]    [Pg.5391]    [Pg.1266]    [Pg.589]    [Pg.513]    [Pg.528]    [Pg.579]    [Pg.581]    [Pg.584]   
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