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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Since his birth, we have been monitoring a 12-year-old boy suffering from selective severe magnesium malabsorption. Our essential problem is to prepare a form of galena with acceptable taste, tolerated by the digestive tract and well absorbed; also, the carrier compound must not cause short- or long-term side effects. An additional factor is the steadily increasing need for magnesium from 1 mmol/kg.d at 1 year to 14 mmol/kg.d at present age (345 mg/kg.d). The galena forms currently on sale were, with the exception of lactate and pyrollidone carboxylate, immediately rejected since they contain insufficient Mg2+. Following short trials resulting in diarrhoea, the other two preparations were also rejected. We then constituted - and also abandoned - our own galena compounds: aspartate (bitterness), aspartate + glycerophosphate (GLP) (bitterness), glutamate + GLP ('Chinese restaurant syndrome' and fear of the long term toxic effect of the glutamate), gluconate (excessive volume: 11/1 proportion with Mg2+). A recent test featuring GLP of Mg 40 g + cocoa butter 40 g + cocoa 10 g, brought about vomiting and diarrhoea, and was not adequately absorbed. The best tolerated formula is: Mg GLP 21.33 g; saccharose 6 g; aspartam 1 g; gelatin 0.5 g; citric acid, conserving agent, fruity aroma; water: qs 100 g. Such composition yields a caramel cream absorbed in five small portions, at a daily quantity of 375 g (80 g GLP Mg, 10 g Mg2+). Vitamin B6, which promotes intestinal absorption of magnesium, must be given separately in tablet form at a dose of 1 g/d, since it causes nausea if it is included in the Mg preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Severe selective magnesium malabsorption: tests of tolerance of oral magnesium supplements. 213 77

A number of factors affect the concentration and distribution of magnesium in patients with chronic renal failure (CRF). Poor nutritional intake, impaired absorption from the intestine, vomiting, diarrhea, the use of diuretics and acidosis may result in a negative balance. More commonly, accumulation of magnesium may be the consequence of reduced renal excretion. Magnesium concentrations are increased in serum and red cells in CRF patients. Bone concentrations and total body magnesium also appear to be increased; muscle magnesium does not appear to be increased. Use of magnesium hydroxide-containing antacids as phosphate binders in patients with CRF was largely discontinued 2 decades ago after reports described increases in serum magnesium concentrations to toxic levels. More recently, the undesirable effects of aluminum-containing phosphate binders (encephalopathy, osteomalacia) have led several investigators to report favorable experiences using low concentrations of magnesium in dialysate and a combination of magnesium and aluminum-containing antacids, as phosphate binders, while closely monitoring serum magnesium concentrations.
Magnesium 1986
PMID:Chronic renal failure and magnesium metabolism. 380 22

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.
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PMID:Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. 784 87

The effect of carmoxirole, a presynaptic dopamine (DA2) receptor agonist, on blood pressure, plasma catecholamines, renin-aldosterone and atrial natriuretic peptide and the intracellular concentration and transmembrane fluxes of Na+ and K+, in erythrocytes and platelets was studied in 24 normal men, using a double-blind, parallel study design. After a run-in period of 1 week, the subjects were treated with either placebo (n = 8) or 0.5 mg carmoxirole (n = 16) once daily for 1 week. Blood pressure and heart rate were not changed during carmoxirole administration in these normal men. Surprisingly, no significant effect of carmoxirole was found on the circulating plasma concentration of noradrenaline, adrenaline or dopamine. Other hormones such as renin, aldosterone and atrial natriuretic peptide were also not changed during carmoxirole administration. No significant effect of carmoxirole could be demonstrated on the intracellular concentration of Na+, K+, Mg2+ and Ca2+ and on the transmembrane fluxes of Na+ and K+ in erythrocytes and platelets. In the carmoxirole-treated subjects (n = 16), 6 subjects reported spontaneously adverse events such as syncope, dizziness and vomiting tendencies and/or fatigue.
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PMID:Erythrocyte and platelet cationic concentrations and transport systems in normal volunteers treated with carmoxirole. 790 90

Hypermagnesemia is a well-known cause of hypotension and cardiac dysfunction but not well recognized is the induction of paralytic ileus. This report details the second and third adult patients reported with hypermagnesemia-induced paralytic ileus. The first patient was a 65-year-old white woman with normal renal function, who had consumed large amounts of magnesium citrate and milk of magnesia. As magnesium blood level fell from 5.1 mg/dl on admission to 2.4 mg/dl on day 3, the vomiting, obstipation, and abdominal distension resolved. The second patient was a 67-year-old woman with mild renal insufficiency, who consumed a large amount of Epsom salts containing magnesium sulfate to treat her constipation. Magnesium levels of 8.1 mg/dl on admission fell to below 3.1 mg/dl on the third hospital day and the paralytic ileus resolved. Mechanical obstruction was ruled out by colonoscopy, gastrographin enema, and barium small bowel series in both patients. Although the clinical findings of muscle weakness, flaccid paralysis, respiratory muscle paralysis or cardiac arrest due to hypermagnesemia are well described in the literature, intestinal smooth muscle dysfunction leading to paralytic ileus has only been reported in one other adult patient. The laboratory and clinical course of these two patients strongly suggest a causal relationship between hypermagnesemia and paralytic ileus.
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PMID:Hypermagnesemia-induced paralytic ileus. 817 29

Type 4 phosphodiesterases (PDE4) inhibitors are emerging therapeutics in the treatment of a number of chronic disorders including asthma, chronic obstructive pulmonary disease (COPD) and cognitive disorders. This study delineates the preclinical profile of L-454,560, which is a potent, competitive and preferential inhibitor of PDE4A, 4B, and 4D with IC50 values of 1.6, 0.5 and 1.2 nM, respectively. In contrast to the exclusive binding of cilomilast and the preferential binding of roflumilast to the PDE4 holoenzyme state (Mg2+-bound form), L-454,560 binds to both the apo-(Mg2+-free) and holoenzyme states of PDE4. The intrinsic enzyme potency for PDE4 inhibition by L-454,560 also results in an effective blockade of LPS-induced TNFalpha formation in whole blood (IC50 = 161 nM) and is comparable to the human whole blood potency of roflumilast. The cytokine profile of inhibition of L-454,560 is mainly a Th1 profile with significant inhibition of IFNgamma and no detectable inhibition of IL-13 formation up to 1 microM. L-454,560 was also found to be efficacious in two models of airway hyper-reactivity, the ovalbumin (OVA) sensitized and challenged guinea pig and the ascaris sensitized sheep model. Furthermore, L-454560 was also effective in improving performance in the delayed matching to position (DMTP) version of the Morris watermaze, at a dose removed from that associated with potential emesis. Therefore, L-454,560 is a novel PDE4 inhibitor with an overall in vivo efficacy profile at least comparable to roflumilast and clearly superior to cilomilast.
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PMID:L-454,560, a potent and selective PDE4 inhibitor with in vivo efficacy in animal models of asthma and cognition. 1742 47

Magnesium fructose-1,6-diphosphate is a novel agent of antimyocardial ischaemia. In the present study, the subchronic toxicity of magnesium fructose-1,6-diphosphate was investigated after 13-week repeated intravenous administration in beagle dogs. The animals received doses of 0, 75, 150 and 300 mg/kg/day (three males and three females for each dose). During the study period, clinical signs, mortality, body weights, food consumption, electrocardiogram, urinalysis, haematology, clinical biochemistry, macroscopic findings, organ weights and histopathology were examined. The administration of magnesium fructose-1,6-diphosphate resulted in increased incidence of clinical signs, including salivation and emesis. These effects were transient and were noted in almost all dogs given 300 mg/kg/day and occasionally noted in the 150 mg/kg/day dose-treated animals. Serum magnesium in the 150 mg/kg/day and 300 mg/kg/day dose-treated animals was significantly increased after 6- and 13-week administration, but recovered at the end of a 2-week recovery period. At 6 weeks, a statistically significant decrease in serum electrolytes, including sodium and potassium, was observed in the treatment groups. There were no other treatment-related findings. Under the conditions of the present study, magnesium fructose-1,6-diphosphate did not show any evidence of target organ toxicity. The no-observed-adverse-effect level for 13-week intravenous administration of magnesium fructose-1,6-diphosphate to beagle dogs was considered 75 mg/kg/day based on observations of clinical signs and serum electrolytes.
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PMID:A subchronic intravenous toxicity study of magnesium fructose-1,6-diphosphate in beagle dogs. 1905 93

Inherited classic Bartter syndrome (cBS) is an autosomal recessive renal tubular disorder resulting from inactivating mutations in the asolateral chloride channel (C1C-Kb) and usually presents in early infancy or childhood with mild to moderate hypokalemia. Profound hypokalemic paralysis in patients with cBS is extremely rare, especially in middle age. A 45-year-old Chinese female patient was referred for evaluation of chronic severe hypokalemia despite regular K+ supplementation (1 mmol/kg/d). She had had two episodes of muscle paralysis due to severe hypokalemia (K+ 1.9 - 2.1 mmol/l) in the past 3 years. She denied vomiting, diarrhea, or the use of laxatives or diuretics. Her blood pressure was normal. Biochemical studies showed hypokalemia (K+ 2.5 mmol/l) with renal potassium wasting, metabolic alkalosis (HCO3- 32 mmol/l), normomagnesemia (Mg2+ 0.8 mmol/l), hypercalciuria (calcium to creatinine ratio 0.5 mmol/mmol; normal < 0.22 mmol/mol), high plasma renin activity, but normal plasma aldosterone concentration. Abdominal sonography revealed neither renal stones nor nephrocalcinosis. Acquired causes of cBS such as autoimmune disease and drugs were all excluded. Molecular analysis of the CLCNKB gene, encoding ClC-Kb, and SLC12A3, encoding the thiazide-sensitive sodium chloride cotransporter (NCC), revealed compound heterozygous mutations in CLCNKB (L335P and G470E) inherited from her parents; her SLC12A3 was normal. These two mutations were not identified in 100 healthy subjects. Her plasma K+ concentration rose to 3 - 3.5 mmol/l after the addition of spironolactone. Inherited cBS may present with hypokalemic paralysis and should be considered in adult patients with hypokalemia and metabolic alkalosis.
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PMID:Hypokalemic paralysis in a middle-aged female with classic Bartter syndrome. 2285 65

Preeclampsia is characterized by hypertension, peripheral edema and proteinuria, but very often also includes neurologic complications. Neurologic complications of severe preeclampsia are indentical to those of hypertensive encephalopathy. The most common neurologic symptoms are headache, vomiting, mental disorders, visual disturbances, sensorimotor deficits and seizures. Endothelial cell dysfunction is the main cause of multiorgan failure. It is of utmost importance to recognize these symptoms and initiate apropriate therapy. Systemic blood presure must not exceed the cerebrovascular autoregulatory capacity. Serum magnesium level is significantly decreased in pregnant women with severe preeclampsia and cerebral edema. Magnesium has been shown to be effective in reducing the occurrence of seizures in preeclampsia by decreasing neuronal excitability, protecting the endothelium against free radicals and reducing cerebral perfusion.
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PMID:[Neurological disorders in pregnancy]. 2308 92


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