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Genetics alcohol abuse

Cluster headache disorders are the most uncommon and severe primary headache syndromes.9 The estimated point prevalence is less than 1%. Unlike migraine and TTH, cluster headaches occur more frequently in men. Onset commonly occurs prior to age 30.6 A genetic predisposition seems apparent, although affected individuals often provide a history of tobacco use and alcohol abuse.6 Attacks consist of debilitating, unilateral head pains that occur in series lasting up to months at a time, but that remit over months to years between occurrences. In rare instances, cluster headache can be a chronic disorder without remissions.4... [Pg.502]

Hwu, H. G., and Chen, C. H. (2000) Association of 5HT2A receptor gene polymorphism and alcohol abuse with behavior problems. Am. J. Med. Genet. 96, 797-800. [Pg.174]

People who continue to drink alcohol in spite of adverse medical or social consequences related directly to their alcohol consumption suffer from alcoholism, a complex disorder that appears to have genetic as well as environmental determinants. The societal and medical costs of alcohol abuse are staggering. It is estimated that about 30% of all people admitted to hospitals have coexisting alcohol problems. Once in the hospital, people with chronic alcoholism generally have poorer outcomes. In addition, each year thousands of children are born in the USA with morphologic and functional defects resulting from prenatal exposure to ethanol. Despite the investment of many resources and much basic research, alcoholism remains a common chronic disease that is difficult to treat. [Pg.532]

Ferguson RA, Goldberg DM. Genetic markers of alcohol abuse. Clin Chim Acta 1997 257 199-250. [Pg.241]

To date, proteomic investigations into human heart disease have centered on dilated cardiomyopathy (DCM). DCM is a disease of unknown etiology, characterized by impaired systolic function resulting in heart failure. Known contributory factors of DCM are viral infections, cardiac-specific autoantibodies, toxic agents, genetic factors, and sustained alcohol abuse. As many as 100 cardiac proteins... [Pg.300]

The clinical course can be unfavourably affected by various risk factors (e.g. race, gender, advanced age, immune status, genetics) as well as by alcohol abuse (275, 337, 363), toxins, coinfections and chemicals. Conversely, the course and prognosis of HBV, HDV and HIV infections as well as of metabolic diseases (e.g. porphyria cutanea tarda, ai-antitrypsin deficiency) can deteriorate as a result of hepatitis C. [Pg.443]

Agarwal, D.P. Goedde, H.W. Medicohiological and genetic studies on alcoholism. Role of metabolic variation and ethnicity on drinking habits, alcohol abuse and alcohol-related mortality. Chn. Invest. 1992 70 465-477... [Pg.537]

In rural sub-Saharan Africa, there is a kind of beer which is traditionally brewed in iron vats. The daily iron overload can amount to as much as 200 mg with markedly increased iron absorption (T.H. Bothwell et at, 1965). Such a condition is also observed in South Africa among the black population. Their diet consists of porridge fermented in iron pots with an acid pH value (V.R. Gordeuk et al., 1986). In both conditions, absorption of iron is facilitated by various factors, e. g. protein or vitamin C deficiency, alcohol abuse, acidic diet. It has been suggested that such iron overload is triggered by genetic factors. (437)... [Pg.627]

Alcohol abuse Alcohol abuse is the most common cause of cirrhosis. Nevertheless, no more than 40-60% of alcoholics contract the disease. Thus genetic factors must also be involved in the development of alcoholic cirrhosis. Alcohol itself can be a facilitative factor or cofactor. Moreover, so-called additives contained in various alcoholic beverages in widely different quantities may also be of greater importance than has hitherto been assmned. (100, 171, 186) (s. pp 528, 532) (s. fig. 28.13, 28.14)... [Pg.721]

A classical example is alcoholic cirrhosis, which in the case of chronic alcohol abuse, leads to multiple, polyclonal areas of liver cell hyperplasia and an increased risk for development of hepatocellular neoplasia. In both preneoplasia and certain forms of hyperplasia, the antecedent lesions typically have a higher rate of cell proliferation than the surrounding normal cells and, thus, these cells are at increased risk to sustain additional genetic damage and progress to the next stage in the carcinogenic process. [Pg.450]

CDT is also assayed extensively, especially in Europe, for detection of alcohol abuse. Other proteins, such as tti-acid glycoprotein, are carbohydrate deficient in this case as well. The gold standard for assessment is HPLC, although both capillary electrophoresis and immunoassays are more commonly used in clinical settings. Immunoassays in particular are poorly standardized, both qualitatively and quantitatively positive tests should be confirmed by an alternative method." Genetic variants of Tf may also complicate interpretation of results. [Pg.562]

Porphyria cutanea tarda, characterized by fluid-filled vesicles and bullae on sun-exposed areas, can be either genetic or associated with alcohol abuse or hepatitis C. Although the associated iron overload is treated with phlebotomy, the dermatologic manifestations sometimes are treated with antimalarial agents. These patients require reduced doses because of the potential for hepatotoxic-ity, as manifested by elevated transaminase levels, and the rapid excretion of large amounts of uroporphyrins in the urine that can occur with usual doses. Low-dose twice-weekly administration is effective and avoids these side effects. [Pg.1086]

The first studies dealing with the quantitative determination of CDT in sera from alcohol abusers were performed by conventional lEF with immunological detection. This method can easily detect genetic variants and has the power to resolve individual isoforms. However, it is laborious and time consuming [178,184]. Since then, a number of CDT methods of analysis, such as anion-exchange chromatography, chromatofocusing, HPLC, and CZE have been developed [176,184]. [Pg.679]

A deficiency of biotin in humans may result from an unbalanced diet, alcohol abuse, side-effects of medication (e.g. with sulfonamides, antiepileptics), or genetic defects. In babies, this deficiency may appear after prolonged breastfeeding (> 4 months), as the biotin content of the mother s milk decreases. There has... [Pg.655]

Sokol, R.J., Martier, S. and Emhart, C.B. (1985). Identification of alcohol abuse in the prenatal clinic. In Early Identification of Alcohol Abuse. NIAAA Research Monograph-17, NIAAA Wesenberg, R.L. (1978). Neonatal thick blood" syndrome. Hosp. Pract., May, 137-145 Wibberley, D.G., Khera, A.K., Edwards, J.H. and Rushton, D.I. (1977). Lead levels in human placentae from normal and malformed births. ]. Med. Genet., 14, 339-345 Wirth, F.H., Goldberg, K.E. and Lubchenco, L.O. (1979). Neonatal hyperviscosity I. Incidence. Pediatrics, 63, 833-836... [Pg.370]


See other pages where Genetics alcohol abuse is mentioned: [Pg.88]    [Pg.136]    [Pg.137]    [Pg.313]    [Pg.417]    [Pg.418]    [Pg.435]    [Pg.36]    [Pg.209]    [Pg.244]    [Pg.499]    [Pg.288]    [Pg.541]    [Pg.619]    [Pg.88]    [Pg.108]    [Pg.355]    [Pg.48]    [Pg.97]    [Pg.1194]    [Pg.323]    [Pg.52]    [Pg.199]    [Pg.85]    [Pg.92]    [Pg.679]    [Pg.679]    [Pg.684]    [Pg.206]    [Pg.42]    [Pg.68]   
See also in sourсe #XX -- [ Pg.72 , Pg.73 , Pg.74 ]




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