Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report 12 cases of neurological syndromes due to folic acid deficiency, due in 8 cases to chronic alcoholism. In 5 cases there was polyneuritis, 3 cases had cerebellar atrophy, whilst 4 patients had subacute combined degeneration of the cord. Folic acid deficiency occurred alone in five cases out of twelve, as in 3 cases vitamin B1 deficiency was associated, and in four cases there was malabsorption of vitamin B12. A neuropathological study of these cases showed: 1) moderate involvement of the mamillary tubercles as observed in deficiency encephalopathies. 2) severe peripheral nerve involvement especially of axonal type. 3) involvement of the anterior horns of the spinal cord with appearances of central chromatolysis and a few atrophic neurones.
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PMID:[Role of folic-acid deficiency in deficiency diseases of the nervous system. Apropos of 12 cases including an anatomo-clinical case]. 19 44

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

Patients undergoing radical surgical treatment of head and neck neoplasms often are seen with a history of cirrhotic liver disease, electrolyte abnormalities, and other stigma of chronic disease. Despite skillful thyroid surgical technique performed as an isolated procedure or in combination with other procedures such as laryngectomy, hypocalcemia can occur. Common causes of lowered serum calcium levels secondary to removal of parathyroid glands, blood transfusions, hypoalbuminemia, gastrointestinal malabsorption, and renal insufficiency are well known. Less well known is the recently elucidated role of dependence of calcium metabolism on magnesium. Recently, it has been well documented that alcoholism directly lowers serum magnesium levels in both human and animal models without prior liver disease or malabsorption. The fact that three mechanisms are needed to explain calcium homeostasis implies that the magnesium-calcium interdependence is not clearly understood.
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PMID:Thyroid surgery: surgical and metabolic causes of hypocalcemia. 64 19

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Ten patients, aged 39-61 years, with hypomagnesaemia due to chronic alcoholism (7 cases) or malabsorption (3 cases), have been investigated by assessing the maximum isometric voluntary contraction force (MVC) of the quadriceps femoris muscle (7 cases), laboratory screening (9 cases) and estimating the electrolyte and metabolite content of biopsy specimens from the quadriceps femoris muscle. The MVC ranged from 0.5 to 34 kp and was significantly lower than in 12 apparently healthy normomagnesaemic controls (p is less than 0.001). The results of the laboratory screening, apart from a significant lowering of the serum magnesium concentration (p is less than 0.01), were mainly within the range of normal values, apart from signs of liver damage, such as an elevated activity of S-OCT (3 cases), alkaline phosphatease(3 cases), S-ALAT (1 case) and an elevation of bilirubin and blood ammonia (2 cases). Low serum iron-binding capacity occurred in 4 cases, a finding reported in protein-calorie malnutrition. Muscle magnesium content was significantly lower than in healthy controls (p is less than 0.001). Muslce sodium and chloride contents were significantly increased (p is less than 0.05). Total H2O content and the extracellular H2O content were both significantly increased (p is less than 0.05). Pyruvate and lactate values were within the normal range. The apparent equilibrium constant for creatine kinase differed significantly ( is less than 0.01). ATP values were within the normal range, but there were slight decreases for ADP (p is less than 0.05) and creatine phosphate ( is less than 0.01), whcih is of interest in view of the lowering of the MVC and the diminished capacity for sustained muscular effort in hypomagnesaemic patients reported earlier.
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PMID:Hypomagnesaemia and muscle electrolytes and metabolites. 85 Oct 37

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

In a collection of 3,571 patient's files admitted in the University Teaching Hospital and the Yaounde General Hospital, we studied 27 patients suspected of chronic pancreatitis. 20 patients with calcified chronic pancreatitis benefited from a detailed history, physical examination and a complete paraclinical work-up. From the data collected, chronic alcoholism seemed to have been the main aetiology. Industrial beer from barley alone and/or associated with other traditional liquors was most consumed. The majority of patients were heavy alcoholics and daily consumption varied from 75 to 124 g of pure alcohol. The natural history of the disease and physical examination were identical to that observed in the western countries. Associated pathology was observed in 10% of the patients. This included peptic ulcer disease, cirrhosis and bile stones. Complications included diabetics, obstructive jaundice, and malabsorption syndrome. As a conclusion, chronic pancreatitis is a pathology whose prevalence seems to be progressing constantly.
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PMID:[Chronic pancreatitis in Cameroon. Analysis of etiological and clinical aspects]. 151 63

The importance of zinc for human health was first documented in 1963. During the past 25 y, deficiency of zinc in humans due to nutritional factors and several disease states has now been recognized. The high phytate content of cereal proteins is known to decrease the availability of zinc, thus the prevalence of zinc deficiency is likely to be high in a population consuming large quantities of cereal proteins. Alcoholism, malabsorption, sickle cell anemia, chronic renal disease, and chronically debilitating diseases are now known to be predisposing factors for zinc deficiency. A spectrum of clinical manifestations ranging from mild to severe degree have now been recognized in human zinc-deficiency states. Zinc is required for many biological functions including DNA synthesis, cell division, and gene expression. It is required for the activity of many enzymes in biological systems. Recent studies indicate that zinc is needed for cell-mediated immunity.
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PMID:Discovery of human zinc deficiency and studies in an experimental human model. 198 5

We used the miniature pig to evaluate the effect of ethanol ingestion on the hydrolysis of pteroylpolyglutamate and on the uptake of pteroylmonoglutamate (PteGlu) by the intestinal brush border membrane, processes that are required for folate absorption. After feeding ethanol or sucrose at 60% of calories for 11 mo, the uptake of PteGlu by jejunal brush-border-membrane vesicles was similar in both groups of animals. Jejunal brush border pteroylpolyglutamate hydrolase was decreased by one-half in the ethanol-fed group. Jejunal brush-border-membrane fluidity, measured by fluorescence polarization, was similar in both groups. Acute exposure of the jejunal vesicles to ethanol increased membrane fluidity and decreased hydrolase activity but had no effect on PteGlu transport. Inhibition of jejunal folate hydrolase by chronic exposure to ethanol may be an early effect in the pathogenesis of folate malabsorption and deficiency in chronic alcoholism.
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PMID:Folate absorption in alcoholic pigs: in vitro hydrolysis and transport at the intestinal brush border membrane. 259 33

Dietary folates exist as pteroylpolyglutamates (PteGlun) that undergo hydrolysis to pteroylmonoglutamate (PteGlu) forms during the process of intestinal absorption. Using the technique of jejunal perfusion of separately labeled folates, our laboratory has demonstrated that hydrolysis of PteGlun occurs on the surface of the jejunum and is a prerequisite for folate absorption. An intestinal brush border pteroylpolyglutamate hydrolase (BB-PPH) has been identified in human and pig jejunum with characteristics that are distinct from those of an intracellular hydrolase (IC-PPH). Functional parallels of BB-PPH with in vivo hydrolysis of PteGlun in human and pig intestine and the clinical responsiveness of BB-PPH to different disease states indicate that this enzyme plays the major physiological role in folate absorption. Folate malabsorption is found in diseases which affect the jejunal mucosa and in response to various drugs. In most of these clinical conditions, folate malabsorption results from suppression of both of the processes of hydrolysis of PteGlun and jejunal uptake of PteGlu. Ongoing studies in miniature pigs are aimed at definition of the sequence of development of folate malabsorption in chronic alcoholism.
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PMID:The intestinal absorption of dietary folates in health and disease. 269 55


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