Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The identification of marginal magnesium deficit, such as we have detected in a patient with anxiety, depression, and psychomatic complaints, is a difficult diagnostic problem. Electromyography of a limb, rendered acutely ischemic either just before or after hyperventilation, can elicit latent tetany in this condition, as well as in calcium deficiency. We have demonstrated iterative electrical activity in our patient, whose magnesium deficit is attributable to renal wasting of magnesium. We have elicited similar patterns in several other patients, who had marginally low serum magnesium and who also exhibited weakness, anxiety, and psychosomatic disorders. This preliminary report suggests the need for further consideration of the possibility that chronic magnesium-deficit may contribute to the syndrome of latent tetany, psychosomatic complaints, and weakness.
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PMID:Latent tetany and anxiety, marginal magnesium deficit, and normocalcemia. 116 68

The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.
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PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34

Mg deficiency is a frequent complication of inflammatory bowel disease (IBD) demonstrated in 13-88% of patients. Decreased oral intake, malabsorption and increased intestinal losses are the major causes of Mg deficiency. The complications of Mg deficiency include: cramps, bone pain, delirium, acute crises of tetany, fatigue, depression, cardiac abnormalities, urolithiasis, impaired healing and colonic motility disorders. Serum Mg is an insensitive index of Mg status in IBD. Twenty-four-hour urinary excretion of Mg is a sensitive index and should be monitored periodically. Parenteral Mg requirements in patients with IBD are at least 120 mg/day or more depending upon fecal or stomal losses. Oral requirements may be as great as 700 mg/day depending on the severity of malabsorption.
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PMID:Magnesium and inflammatory bowel disease. 329 19

During human hepatic transplantation, ionized calcium (ICa) measured in whole blood with an ion-selective electrode varied greatly from ICa predicted from total calcium (TCa), protein, albumin, and pH, by means of recently published nomograms. Measurement of ICa was necessary because the interaction of citrate in transfused blood and calcium chloride (administered to offset citrate binding) caused large variations in TCa. During hepatic transplantation, ICa and electrolyte measurements were obtained at approximately 15-minute intervals or more frequently if indicated by changing cardiac status. In one patient, hemodynamic instability was accompanied by a large decrease in ICa, which then was followed by cardiac arrest aggravated by myocardial depression from inadequate ICa. Cardiovascular phenomena associated with ionized hypocalcemia suggest that the critical value for ICa should be no more than 0.4 mmol/L (1.6 mg/dL) below the reference range mean. The authors propose critical limits for ICa and discuss their significance in clinical management of tetany, hypotension, arrythmias, and cardiac arrest.
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PMID:Monitoring of ionized calcium during human hepatic transplantation. Critical values and their relevance to cardiac and hemodynamic management. 352 94

We have observed a high frequency of chronic Candida albicans infection and of allergic sensitization to candida among patients with normocalcemic latent tetany (LT). Among 50 LT patients, 34% suffered from recurrent or chronic candida infection by history, 24% showed evidence of active infection and 48% demonstrated type I hypersensitivity to C. albicans extract on intradermal testing. Treatment with oral antifungal drugs and allergy desensitization to Candida produced complete relief of symptoms in 44% of the patients, with remission occurring for symptoms of depression, irritable bowel syndrome, fatigue, premenstrual tension, headache, anxiety and back pain. The complex relationship between candidiasis and Mg deficit is discussed. Patients with LT, refractory symptoms and a history of prolonged antibiotic exposure or recurrent candida infection should be considered for oral antifungal therapy and candida desensitization.
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PMID:Normocalcemic tetany and candidiasis. 391 83

Ten clinically healthy cats were allotted into 2 groups. Group A was given the low (60 ml), and group B was given the high (120 ml) recommended dose of a commercial hypertonic sodium phosphate enema. Enema retention was enforced. All cats developed clinical and/or laboratory abnormalities, with group B cats being more severely affected. Clinical signs that occurred rapidly included depression, ataxia, vomition, bloody diarrhea, mucous membrane pallor, and stupor; tetany was not seen. One cat in group B died. Laboratory abnormalities included hypernatremia, hyperphosphatemia, hypocalcemia, hyperglycemia, calculated hyperosmolality, and metabolic acidosis with high anion gap probably due to hyperlacticacidemia. There were no significant gross or microscopic lesions associated with enema administration. Therefore, the use of hypertonic sodium phosphate enema at recommended doses is potentially dangerous to cats.
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PMID:Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. 401 52

Two metabolism trials were conducted with 12 crossbred wether lambs, each surgically equipped with a ruminal catheter and abomasal and ileal cannulae, to study the effect of K infusion in different sites of the digestive tract on site of absorption and flow of minerals. The treatments consisted of the infusion of 33.6, 12.0 or 12.0 g K/d as bicarbonate into either the rumen, abomasum or ileum, respectively. Each trial consisted of a minimum 5-d preliminary period, five 3-d collection periods to determine mineral balance and a 6-d sampling period to determine mineral flow and site of absorption. Chromic oxide was incorporated into the diet for use as a marker. Magnesium was absorbed primarily from the preintestinal region. Ruminal infusion of K tended to decrease preintestinal Mg absorption. Absorption of Mg in the entire tract was decreased (P less than .05) 43% when K was infused into the rumen. There was a slight absorption of Mg in the small intestine, followed by a net secretion into the large intestine. Serum Mg levels tended to be depressed in lambs infused with K intraruminally. Calcium flow from the preintestinal region was decreased (P less than .05) by infusion of K into the rumen. Only lambs infused with K in the rumen had a net secretion of Na into the small intestine. The large intestine was the primary site of net Na absorption for ruminal-infused lambs. Phosphorus flow from the preintestinal region was decreased (P less than .05) by infusion of K into the rumen. Potassium flow from both the preintestine and small intestine was increased (P less than .05) by ruminal K infusion. The infusion of K into the rumen, abomasum or ileum increased (P less than .05) the total absorption of K, with the small intestine being the major absorptive site. The infusion of potassium bicarbonate into the rumen of sheep raised (P less than .05) the pH of the ruminal contents 15%. Ruminal infusion of K depresses Mg absorption, while the infusion of K into the abomasum or ileum does not affect Mg absorption. Therefore, the role of K in grass tetany may be via this depression of Mg absorption.
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PMID:Absorption of magnesium and other macrominerals in sheep infused with potassium in different parts of the digestive tract. 407 68

The present authors observed and treated a siblings case of normocalcemic tetany, which is considered as belonging to Bartter's syndrome. As far as we know, there are a number of familial cases of tetany in literature, but none of them spreads over more than two generations, so that the tetany appears to be recessive in hereditary characters including our patients. Both of them presented tetanic seizures in the course of Bartter's syndrome and they were regarded as one of various manifestations of the syndrome. In other words, the Bartter's syndrome or the hypopotassemia should be one of the fundamental disorders for developing tetanic symptom. The tetanic symptoms became extinct during the treatment with spironolactone against hypopotassemia. Of the two patients, younger sister had shown an agitated depression developed on her childish and over-sensitive personality, but the depression was improved in parallel to the recovery from tetany and hypopotassemia. Therefore, it appears to be certain that the patients would have some premorbid deviation of personality traits, where symptomatic psychoses could be attributed, in the case of Bartter's syndrome. Generally speaking the psychic disorders, such as personality deviation and psychotic episode, seem to by very important symptoms in patient with Bartter's syndrome as well as in patient with hypocalcemia or hypoparathyroidism.
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PMID:[Development of tetany in siblings suffered from Bartter's syndrome]. 649 22

Dimethyl sulfoxide (DMSO) is commonly used in studies of skeletal muscle as a selective antioxidant (DMSO preferentially scavenges hydroxyl radicals) or as a solvent for drugs. The present experiments tested DMSO for direct effects on diaphragm contractile properties. Fiber bundles were removed from anesthetized rats, mounted in vitro at optimal length (37 degrees C), curarized, and stimulated directly. Protocol 1 tested for contractile depression and dose dependence by comparing bundles treated with DMSO (0.6-640 mM) with time- and stimulus-matched controls. Protocol 2 tested reversibility of 220 mM DMSO effects by using each bundle as its own control. DMSO decreased the relative forces developed during twitch and submaximal tetanic (30- and 60-Hz) contractions, shifting the force-frequency relationship down and to the right. These effects were strongly dose dependent and were reversed by DMSO washout. DMSO had no detectable effect on the forces developed during maximal tetany (200 Hz). DMSO depresses contractile function of diaphragm fibers by reversible dose-dependent inhibition of excitation-contraction coupling.
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PMID:Dimethyl sulfoxide depresses skeletal muscle contractility. 806 85

Five of 24 cows pastured in a 40-acre field in east Tennessee died after they consumed leaves from a privet (Ligustrum amurease) hedge. Clinical findings included ataxia, recumbency with an inability to stand, depression, greenish nasal discharge, cessation of rumination, normal body temperature, and increased heart and respiratory rates. Differential diagnoses included grass tetany, nitrate toxicosis, and plant toxicosis. Privet toxicosis was confirmed by finding privet in ruminal contents, by the presence of a large quantity of privet in the field, by observing places where this privet had been eaten by the cows, by the immediate cessation of the problem when the cows were removed from the field, and by observing no recurrent problems after the privet was destroyed with a herbicide and the cows were returned to the field.
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PMID:Fatal privet (Ligustrum amurease) toxicosis in Tennessee cows. 1092 96


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