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Serum alcohol

Vitamin B12 depletion could be expected in chronic alcoholics since their diet is often low in animal protein, and, although many alcoholic beverages are the result of bacterial fermentation, they have nevertheless been found to be essentially free of vitamin B12 (L9). Reduced levels of serum vitamin B12 have been reported in alcoholics by some workers (H16.L9) while others have found the concentration to be normal or elevated (Dll). Because of the liver damage often associated with alcoholism, serum levels of the vitamin may be normal or elevated even though liver stores of the vitamin are reduced (RIO, S15). An elevated level of serum vitamin B12 binding protein may also serve to increase the vitamin B12 level. The interpretation of serum vitamin B12 levels in alcoholics is of very limited importance since a clinically significant deficiency of the vitamin very rarely occurs. [Pg.184]

Calcium-channel blockers Nifedipine and verapamil can increase alcohol serum levels by about 15-50%. The mechanism is speculated to be via inhibition of hepatic alcohol metabolism. Some data suggest that alcohol might also inhibit the metabolism of nifedipine, thus raising its serum levels with consequent effects. [Pg.201]

TABLE 2 Average blood alcohol, serum lactate plasma uric acid levels, urate clearance... [Pg.329]

Older adults are particularly susceptible to a potentially fatal hepatitis when taking isoniazd, especially if they consume alcohol on a regular basis. Two other antitubercular drugs rifampin and pyrazinamide, can cause liver dysfunction in the older adult. Careful observation and monitoring for signs of liver impairment are necessary (eg, increased serum aspartate transaminase, increased serum alanine transferase, increased serum bilirubin, and jaundice). [Pg.114]

If die nitrates are administered witii the antihypertensives, alcohol, calcium channel blockers, or the phe-notiiiazines, there may be an increased hypotensive effect. When nitroglycerin is administered intravenously (IV), die effects of heparin may be decreased. Increased nitrate serum concentrations may occur when the nitrates are administered witii aspirin. [Pg.384]

Another common liver disease, alcoholic liver damage produced by moderate to heavy alcoholic intake, is also reflected by an elevation of the serum GOT and GPT activities. The serim glutamyl transferase activity is reported to be a sensitive index of alcoholic intake and can serve to monitor persons on alcoholic withdrawal programs (60). The LD-5 isoenzyme arises mainly from liver tissue, but has a short half-life (61), which is about 1/5 and 1/2 of the half life of the transaminases, GPT and GOT respectively. Some authors consider that a normal LD-5 isoenzyme activity in a jaundiced patient is sufficient evidence to exclude primary liver disease and that obstruction is probably responsible for the jaundice (62). In hemolytic jaundice the LDH-1 and 2 isoenzymes are elevated. [Pg.208]

Rosalki. S. B. Rau, D. Serum Y"giutamyl-transpeptidase activity in alcoholism. Clin. Chim. Acta (1972), 39, 41-47. [Pg.222]

Ratnasinghe, D. et al., Serum carotenoids are associated with increased lung cancer risk among alcohol drinkers, but not among non-drinkers in a cohort of tin miners, Alcohol, 35, 355, 2000. [Pg.141]

Albanes, D. et al., Effect of supplemental P-carotene, cigarette smoking and alcohol consumption on serum carotenoids in alpha-tocopherol, P-carotene cancer prevention study, Am. J. Clin. Nutn, 66, 366, 1976. [Pg.423]

Determination of molecular mass of pectic enzymes The molecular mass were determined by gel filtration in a Sepharose CL-6B column (1,8 x 88cm) equilibrated and eluted with Tris-HCl 50 mM, pH 7,5 buffer, plus 100 mM KCl. Fractions (3,3 ml) were collected at a flow rate of 10 ml/h. Molecular mass markers were tyroglobulin (660 kDa) apoferritin (440 kDa) P-amylase (200 kDa) alcohol dehydrogenase (150 kDa) bovine serum albumin (66 kDa) and carbonic anhydrase (29 kDa). Urea-SDS-PAGE (7%) was carried out according to Swank and Munkres [12]. Molecular mass markers were myosin (205 kDa) p-galactosidase (116 kDa) phosphorylase b (97 kDa) bovine serum albumin (66 kDa), ovalbumin (45 kDa) and carbonic anhydrase (29 kDa). [Pg.788]

Figure 3. (A) Determination of molecular mass of pectic enzymes by gel filtration in Sepharose 6B. Molecular mass markers - tyroglobulin, 2- apoferritin, 3- p-amylase, 4-alcohol dehydrogenase, 5- bovine serum albumin, 6- carbonic anhydrase. (B) SDS-PAGE of pectolytic activities. Molecular mass markers 1- myosin, 2- p-galactosidase, 3- phosphorylase b, 4- bovine serum albumin, 5- ovalbumin, 6- carbonic anhydrase. Figure 3. (A) Determination of molecular mass of pectic enzymes by gel filtration in Sepharose 6B. Molecular mass markers - tyroglobulin, 2- apoferritin, 3- p-amylase, 4-alcohol dehydrogenase, 5- bovine serum albumin, 6- carbonic anhydrase. (B) SDS-PAGE of pectolytic activities. Molecular mass markers 1- myosin, 2- p-galactosidase, 3- phosphorylase b, 4- bovine serum albumin, 5- ovalbumin, 6- carbonic anhydrase.
Gerli, G., Locatelli, G.F., Mongiat, R., Zenoni, L., Agostoni, A., Moschini, G., Zafiropoulos, D., Bruno, S., Rossi, S., Vignati, A. Tarolo, G. and Podda, M. (1992). Erythrocyte antioxidant activity, serum caeruloplasmin, and trace element levels in subjects with alcoholic liver disease. Am. J. Clin. Pathol. 97, 614-618. [Pg.164]

Korpela, H., Kumpulainen, J., Luoma, P.V., Arranto, A.J. and Sotaniemi, E.A. (1985). Decreased serum selenium in alcoholics as related to liver structure and function. Am. J. Clin. Nutr. 42, 147-151. [Pg.166]

Valimaki, M.J., Harju, K.J. and Ylikahri, R.H. (1983). Decreased serum selenium in alcoholics - a consequence of liver dysfunction. Clin. Chim. Acta 130, 291-296. [Pg.173]

If the test is positive, the urine is examined microscopically for red blood cells. If no red blood cells are found, a tentative diagnosis of myoglobinuria is made, serum chemistries are obtained, and the patient is held to rule out rhabdomyolysis. If the uric acid and creatinine kinase (CK) values are normal, and the patient is asymptomatic, he/she is discharged from the hospital. Routine toxicology tests include urinary PCP, serum alcohol, and hypnotic screen. [Pg.228]

Hepatocellular damage manifests as elevated serum aminotransferases [alanine aminotransferase (ALT) and aspartate aminotransferase (AST)]. The degree of transaminase elevation does not correlate with the remaining functional metabolic capacity of the liver. An AST level two-fold higher than ALT is indicative of alcoholic liver damage. [Pg.328]

Pulse oximeter Check blood glucose Check laboratory tests complete blood count serum chemistries liver function tests arterial blood gas blood cultures serum anticonvulsant levels urine drug/alcohol screen... [Pg.467]


See other pages where Serum alcohol is mentioned: [Pg.193]    [Pg.201]    [Pg.67]    [Pg.145]    [Pg.193]    [Pg.201]    [Pg.67]    [Pg.145]    [Pg.222]    [Pg.261]    [Pg.218]    [Pg.18]    [Pg.139]    [Pg.111]    [Pg.299]    [Pg.593]    [Pg.38]    [Pg.105]    [Pg.129]    [Pg.196]    [Pg.185]    [Pg.32]    [Pg.132]    [Pg.189]    [Pg.169]    [Pg.154]    [Pg.236]    [Pg.247]    [Pg.26]    [Pg.408]    [Pg.413]    [Pg.414]    [Pg.415]    [Pg.463]    [Pg.544]   
See also in sourсe #XX -- [ Pg.541 ]




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