Alcoholism phosphate deficiency

Vitamin B Three substances are classed under the term pyridoxine or adermine pyridoxol, pyridoxal and pyridoxamine. Pyridoxine was isolated by various study groups in 1938. Its structure was described by Folkers and Kuhn in 1939. Pyridoxal and pyridoxamine were discovered by Snell in 1942. Pyridoxal phosphate and pyridoxamine phosphate are biologically active substances. Intestinal absorption of Bg is dose-dependent and not limited. In alcoholism, a deficiency of vitamin Bg is encountered in 20—30% of cases, whereas the respective percentage is 50—70% in alcoholic cirrhosis. Vitamin Bg is an important coenzyme for transaminases, which transfer amino groups from amino adds to keto acids. In this way, biochemical pathways between the dtiic acid cycle and carbohydrate and amino acid metabolisms are created. (104)... 

False-normal GPT values are often found - despite the presence of liver damage - in (7.) haemochroma-tosis, (2.) ileo-jejunal bypass, (2.) marked (e. g. alcohol-induced) deficiency of pyridoxal phosphate (Bg), 4.) severe loss of liver parenchyma, and (5.) during the terminal stages of liver disease with exhaustion and/or blockage of hepatocellular enzyme synthesis caused by toxins. (31) In healthy persons, slightly elevated GPT values were detected in 0.5% of cases. 

Dietary phtxsphate deficiency is relatively rare because the phosphate content in plant and animal foods is well above the requirement and b ause of the efficient absorption of phosphate (50-90%). Phosphate deficiency can occur in a number of situations. It can occur with the chronic intake of aluminum-based antacids, particularly with a low-phosphate diet. These antacids form a complex with dietary phosphate, preventing its absorption and resulting in the deficiency. Deficiency can occur with increased urinary excretion of phosphate that occurs w ith starvation and in diabetics experiencing ketoacidosis. Chronic alcoholics may be phosphate deficient because of decreased dietary intake, impaired absorption, and increased urinary excretion (Berner and Shike, Phosphate defi-... 

AST were significantly below those seen in acute viral hepatitis. In addition, the ratio of the absolute values for serum ALT and AST often differ in the two diseases, tending to be greater than 1 in acute viral hepatitis and less than 1 in chronic alcohol-induced cirrhosis. The reason for the difference in ratio of enzyme activities released is not understood, but a lower level of ALT in the serum may be attributable to an alcohol-induced deficiency of pyridoxal phosphate. In addition, serologic tests for viral hepatitis were nonreactive. Her serum folate, vitamin B12, and iron levels were also slightly suppressed, indicating impaired nutritional status. 

Figure 5 Model of phosphorus (P) deficiency-induced physiological changes associated with the release of P-mobilizing root exudates in cluster roots of white lupin. Solid lines indicate stimulation and dotted lines inhibition of biochemical reaction sequences or mclaholic pathways in response to P deliciency. For a detailed description see Sec. 4.1. Abbreviations SS = sucrose synthase FK = fructokinase PGM = phosphoglueomutase PEP = phosphoenol pyruvate PE PC = PEP-carboxylase MDH = malate dehydrogenase ME = malic enzyme CS = citrate synthase PDC = pyruvate decarboxylase ALDH — alcohol dehydrogenase E-4-P = erythrosc-4-phosphate DAMP = dihydraxyaceConephos-phate APase = acid phosphatase.

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

The dehydration of alcohols on stoichiometric and nonstoichiometric (calcium-deficient) hydroxyapatite (series 8 and 9 in Table II) gave results consistent with the above findings. Although there is a difference in the reaction temperature, it is evident that with the nonstoichiometric catalyst, which must be more acidic, the slope found is more negative than that with the stoichiometric calcium phosphate. 

Vitamin B deficiency is a rare condition, but it is prevalent in persons with chronic alcoholism due to low dietary Intake and impaired conversion ofpyridoxine to the active coenzyme pyridoxal phosphate. 

Sideroblastic anemia is characterized by excessive iron in the cells that cannot be incorporated into porphyrin to form heme. Although it is rare, the most common cause of sideroblastic anemia is alcoholism and pyridoxine deficiency. Pyridoxine is required for the formation of pyri-doxal phosphate, a coenzyme in porphyrin synthesis. 

Isoniazid (isonicotinic acid hydrazide), a drug frequently used to treat tuberculosis, can induce a B6 deficiency by forming an iiactive derivative with pyridoxal phosphate. Dietary supplementation with B is, thus, an adjunct to isoniazide treatment. Otherwise, cletary deficiencies in pyridoxine are rare but have been observed in newborn infants fed formulas low in vitamin B6, in women taking oral contraceptives, and in alcoholics. 

Vitamin B1 (thiamine) has the active form, thiamine pyrophosphate. It is a cofactor of enzymes catalyzing the conversion of pyruvate to acetyl CoA, a-ketoglutarate to succinyl CoA, and the transketolase reactions in the pentose phosphate pathway. A deficiency of thiamine causes beriberi, with symptoms of tachycardia, vomiting, and convulsions. In Wernicke-Korsakoff syndrome (most common in alcoholics), individuals suffer from apa thy, loss of memory, and eye movements. There is no known toxicity for this vitamin. 

The most important prophylactic measures for preventing the development of hepatic osteopathy are (i.) avoidance of harmful noxae (alcohol, nicotine), (2.) avoidance of risk factors (e. g. overweight calcium, phosphate or vitamin D deficiency use of glucocorticoids, cholestyramine and antacids containing aluminium), (2.) administration of vitamin K2 (menatetrenone) in women with risk factors, and (4.) routine physical exercise. (s. p. 650) We have instructed our chronic liver patients to carry out the following exercises on a regular basis ... 

Calcium absorption is reduced by high pH complex-ing agents such as oxalate, phytate, free fatty acids, and phosphate and shortened transit times. These factors are probably of clinical importance only when associated with vitamin D deficiency, marginal calcium intake, or malabsorption disorders. Absorption is also reduced by increased intake of protein, fat, and plant fiber increasing age stress chronic alcoholism immobilization (e.g., prolonged hospitalization) and drugs such as tetracycline, thyroid extract, diuretics, and aluminum-containing antacids. 

Many alcoholics such as Al Martini develop thiamine deficiency because alcohol inhibits the transport of thiamine through the intestinal mucosal cells. In the body, thiamine is converted to thiamine pyrophosphate (TPP). TPP acts as a coenzyme in the decarboxylation of a-keto acids such as pyruvate and a-ketoglutarate (see Fig. 8.11) and in the utilization of pentose phosphates in the pentose phosphate pathway. As a result of thiamine deficiency, the oxidation of a-keto acids is impaired. Dysfunction occurs in the central and peripheral nervous system, the cardiovascular system, and other organs. 

Antacids are used in die treatment of hyperacidity, such as heartburn, gastroesoph eal reflux, sour stomach, acid indigestion, and in the medical treatment of peptic ulcer. Many antacid preparations contain more than one ingredient. An additional use for aluminum carbonate is in die treatment of hyiDeqihosphatemia or for use widi a low phosphate diet to prevent formation of phosphate urinaiy ston. Clalcium carbonate may be used in treating calcium deficiency states such as menopausal osteoporosis. M nesium oxide may be used in the treatment of m nesium deficiencies or m nesium depletion from malnutrition, restricted diet, or alcoholism. 

When NADP (a phosphate ester of NAD) oxidizes an alcohol to a carbonyl compound, the pyridine ring in the nicotinamide part of the coenzyme is reduced to a dihydropyridine, giving NADPH. The reverse process occurs when NADPH reduces a carbonyl compound to an alcohol. Nicotinic acid is a B vitamin needed for synthesis of this coenzyme. Its deficiency causes the chronic disease pellagra. 

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