Gene/Protein Disease Symptom Drug Enzyme Compound
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 23,468 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

Aspirin (acetylsalicylic acid) and its salicylate derivatives are effective antipyretic, analgesic, and anti-inflammatory agents that are still very widely used by the elderly despite the advent of newer, potentially safer nonsteroidal anti-inflammatory drugs (NSAIDs). However, none of the new NSAIDs have been proven to be more effective than aspirin or salicylic acid. Chronic salicylate intoxication which is most common in the elderly, may occur with therapeutic doses. Increased toxicity in older patients often appears due to inadvertent overdosage. Dual prescribing or additional use of nonprescription salicylates are some causes of unwitting long term toxicity. According to some studies, systemic clearance of salicylate (mainly by hepatic metabolism) is reduced with age, as is renal elimination. These changes are of increased importance in the elderly using high therapeutic doses of salicylates when metabolism is saturated and more unchanged drug is available for renal excretion. In the face of renal impairment, the risk of toxicity is increased. The diagnosis of acute salicylate intoxication generally does not pose diagnostic problems. Patients often present with a history of intentional overdose, with hyperventilation, fever, and nausea. The diagnosis can be confirmed by measuring serum salicylate concentrations. Chronic intoxication often poses a diagnostic dilemma with atypical presentations mimicking other disease states such as diabetic ketoacidosis, delirium, cerebrovascular accident, myocardial infarction or cardiac failure. The diagnosis of salicylate intoxication should be borne in mind when an older patient presents with recent deterioration in activities of daily living with no known cause. Plasma salicylate concentrations should be measured if salicylate intoxication is suspected, even if there is no documented history of salicylate ingestion. The risk of salicylate nephrotoxicity is also increased with age, and upper gastrointestinal haemorrhage is associated with increased mortality in older age groups. Treatment of acute toxicity consists of prompt recognition of salicylate intoxication, use of activated charcoal, correction of acid-base abnormalities, general supportive measures, and if concentrations are extremely high, dialysis can be effectively used. Chronic toxicity, which can occur even with marginally high salicylate concentrations, is treated with drug withdrawal and supportive therapy. Chronic salicylate toxicity can be averted by prescription of conservative doses of drug, avoidance of concomitant use of different salicylate preparations, and therapeutic monitoring to guide dosage. Renal function should be monitored to detect nephrotoxicity from chronic salicylate therapy. Patients should be regularly screened for evidence of gastrointestinal bleeding.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Salicylate intoxication in the elderly. Recognition and recommendations on how to prevent it. 155 71

A 41-year-old male with a 25-year history of diabetes mellitus requiring 25 to 30 units of neutral protamine hagedorn (NPH) insulin daily was found dead at home. Recent history revealed that he was well until the last four days of life when he had the onset of nausea, vomiting, and anorexia coinciding with procurement of a new bottle of insulin from his pharmacist. Pertinent autopsy findings included coronary and aortic atherosclerosis, a peptic ulcer, and diabetic glomerulopathy. Chemical analysis of the vitreous humor, including glucose (813 mg/dL) and acetone (40 mg/dL), revealed that he died of diabetic ketoacidosis. Further investigation revealed that the pharmacist had accidentally substituted regular insulin, with a duration of action of up to 6 h as opposed to 24 to 28 h, for NPH. Cultures of blood and of the regular insulin yielded no growth. Analysis of this case emphasizes the importance of obtaining a careful medical and medication history and the usefulness of vitreous electrolytes when investigating a sudden death in a diabetic.
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PMID:Pharmaceutical error resulting in fatal diabetic ketoacidosis. 308 89

The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA. Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3-4 units protamine-zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11.4 pmol/l compared with 1.6 pmol/l; P less than 0.05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, beta-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P less than 0.05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = + 0.75; P less than 0.01), and plasma ketone bodies and plasma AVP (r = +0.60; P less than 0.05) were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible mechanisms responsible for the rise in plasma vasopressin associated with diabetic ketoacidosis in the rat. 312 19

The evaluation of gastrointestinal symptoms in patients with diabetic acidosis frequently challenges the physician's clinical acumen. Faced with a seriously ill patient, he must judge whether the abdominal pain, nausea, or vomiting are a consequence of the metabolic decompensation, and hence likely to resolve with correction of the ketoacidosis, or if these symptoms signal a serious underlying intra-abdominal process (e.g., cholecystitis, appendicitis, etc.) which may have precipitated the development of ketoacidosis. The pathogenesis of the reversible gastrointestinal symptoms which frequently accompany diabetic acidosis has not been rigorously defined and may be multifactorial, involving metabolic, humoral, and neural processes. Careful attention to the medical history and abdominal examination greatly facilitates distinguishing patients with intra-abdominal pathology from those with reversible symptoms secondary to ketoacidosis. Similarly, the judicious use of laboratory tests (electrocardiography, blood counts, urinalysis, serum enzyme profile, and abdominal roentgenograms) materially aids in differential diagnosis. Finally, clinical suspicion of an acute abdominal process should prompt early surgical consultation and, if required, surgical intervention as the acidosis is being brought under control.
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PMID:Gastrointestinal manifestations of diabetic ketoacidosis. 641 81

The clinical and biochemical data obtained in 85 patients with diabetic ketoacidosis (DKA) are presented. DKA is an acute exacerbation of diabetes, a characteristic clinico-biochemical syndrome including increasing thirst, polyuria, adynamia, dryness of the skin and mucous membranes, anorexia, nausea, vomiting, occasionally abdominal pain, Kussmaul's breath, acetone odour in the exhaled air, circulatory collapse, prerenal azotemia, stupor, coma. Glycemia level exceeds 19 mmol/l, blood pH over 7.3. The disease is marked by neutrophilic leukocytosis, blood count shift to the left, elevated blood content of creatinine and urea. It was established that the degree of consciousness abnormality does not always correlate with the degree of the clinico-biochemical manifestations of DKA. During DKA, coma occurs relatively seldom (5.9%). It is suggested to use the term "diabetic ketoacidosis", incipient or marked, indicating the degree of consciousness abnormality (stupor, coma).
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PMID:[Diabetic ketoacidosis (causes, clinico-biochemical correlations and terminology problems)]. 644 Dec 97

Zygomycosis is an uncommon, but frequently fatal, fungal infection caused by members of the class Zygomycetes. The risk factors include diabetes mellitus, uremia, leukemia and use of deferoxamine as an iron-chelating agent; healthy persons also are occasionally infected. Those fungi, spread by their ubiquitous spores, most frequently involve the respiratory system. Rhinocerebral zygomycosis occurs predominantly in patients with uncontrolled diabetic ketoacidosis. Pulmonary zygomycosis most frequently is observed in granulocytopenic and corticosteroid-treated patients. Other clinical manifestations are gastrointestinal, cutaneous, disseminated and miscellaneous. This report concerns a previously robust farmer who suffered from left upper lung abscess caused by Rhizopus spp.-one member of the order Mucorales. Initially, it was intended to administer amphotericin B to a total dose of 2,000 mg; however, the patient could not tolerate such side effects as nausea, vomiting and refused further management when the cumulative dose was 948 mg. However, he did recover without further fever and cough. Chest X-ray, followed every three months, disclosed satisfactory improvement.
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PMID:Zygomycotic lung abscess: a case report. 755 21

A 24-year-old previously healthy man presented with a 3-week history of progressively intensifying symptoms of diabetes mellitus. He had become increasingly unwell during the night preceding his admission to hospital and had developed central pleuritic chest pains with nausea; he had vomited once. On admission, he was clinically dehydrated and acidotic with Kussmaul's respiration. A diagnosis of diabetic ketoacidosis was confirmed by laboratory tests (arterial pH 7.21; bicarbonate 11.6 mmol l-1; blood glucose 40.5 mmol l-1, and heavy ketonuria). Subcutaneous emphysema was palpable in the neck tissues and a chest X-ray revealed mediastinal emphysema. There was no clinical or radiological evidence of acute or chronic pulmonary disease and a barium swallow confirmed the integrity of the oesophagus. He made an uneventful recovery from the ketoacidosis with conventional therapy. The subcutaneous emphysema and pneumomediastinum had completely resolved at review 4 weeks later.
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PMID:Pneumomediastinum complicating diabetic ketoacidosis. 879 65

The purpose of the present study was to examine the presentation and outcomes associated with diabetic ketoacidosis (DKA) in pregnancies complicated by diabetes. Eleven episodes (2%) of DKA were diagnosed during the 10-year study period. All patients were under close observation by the Diabetes-in-Pregnancy Service. Plasma glucose levels of less than 200 mg/dL were present in 4 of the 11 patients (36%), 10 (90%) of whom presented with nausea, vomiting, and decreased caloric intake. Two subsequently had fetal distress necessitating cesarean section. One fetal death occurred in a patient treated with subcutaneous insulin. Despite contemporary methods of diabetes care, near-normal plasma glucose levels are not enough to preclude diabetic ketoacidosis. Nausea, vomiting, and decreased caloric intake in an otherwise normal pregnant, diabetic woman requires evaluation to exclude ketosis.
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PMID:The changing presentations of diabetic ketoacidosis during pregnancy. 896 Jun 16

Emphysematous pyelonephritis is a rare life threatening infection in diabetes characterised by suppurative infection of renal parenchyma and perirenal tissues. It usually presents with fever, nausea, vomiting, abdominal pain, shock, lethargy, and confusion. Diabetic ketoacidosis is an uncommon presentation. In the present case, an elderly female presented with abdominal pain, fever, vomiting, and altered sensorium. She was diagnosed to have diabetic ketoacidosis with metabolic encephalopathy with right emphysematous pyelonephritis. She had an excellent response to medical treatment alone and was later discharged on oral hypoglycaemic agents.
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PMID:Emphysematous pyelonephritis: a rare presentation. 1085 76


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