Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
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A case of chlorpropamide-induced, symptomatic hyponatremia in a diabetic patient is reported. The hyponatremia was associated with loss of appetite, nausea, and vomiting. These symptoms caused reduced food intake which provoked severe hypoglycemia with disturbed consciousness. The hyponatremia developed when the chlorpropamide doses were increased from 400 to 600 mg/day. Withdrawal of chlorpropamide was followed by remission of hyponatremia. Chlorpropamide-induced hyponatremia is a rare complication and is due to an antidiuretic effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of adiuretin in the tubuli of the kidney. This case report and the analysis of 18 published cases in the literature show the following characteristics for chlorpropamide-induced hyponatremia: (1) Hyponatremia is a rare complication in the treatment of diabetics with chlorpropamide. The patients typically are female and over sixty. The dosage of chlorpropamide usually was 500 mg daily or even more. (2) Hyponatremia is often unrecognized for a long time because the symptoms are not specific. The characteristic symptoms include loss of appetite, nausea, vomiting, abdominal pain, confusional state and, rarely, convulsions and coma. Recovery occurs spontaneously after withdrawal of the drug. (3) The incidence of this type of hyponatremia is increased in cases of preexisting tendency to water retention such as heart failure and renal failure, and in cases of diuretic therapy. In the light of these findings, the authors believe that chlorpropamide is no longer a drug of choice in the treatment of diabetic women, especially in cases of preexisting tendency to water retention and in diuretic therapy. In such cases, a sulfonylurea without antidiuretic effect is to be preferred.
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PMID:[Hyponatremia and hypoglycemia after treatment with chlorpropamide. Case histories with review of the literature on 18 cases of chlorpropamide induced hyponatremia]. 66 98

A 24-year-old woman was found comatose after 2 days of cephalalgia and vomiting. An immediate diagnosis of carbon monoxyde poisoning was disclaimed when blood carbon monoxyde was found to be 1.75 ml/100. A diagnosis of acute intracranial hypertension led to trephination with ventricular punction and brain biopsy on the third day. The patient died on the eleventh day. Ultrastructural study of biopsy tissue showed nearly normal cortex, and injured white matter, with disrupted or destroyed myelin and pycnotic oligodendroglia in contrast with nearly normal axons, astrocytes, and capillaries. Autopsy showed a typical semioval center myelinopathy. After discussion of the histotoxic, vascular, and edema theories for myelinopathy pathogenesis, primary oligodendrogial lesion is considered, and correlated with the diphasic evolution often observed in the course of carbon monoxyde myelinopathy.
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PMID:[Myelinopathy due to carbon monoxyde poisoning. A study in ultrastructural neuropathology (author's transl)]. 67 80

In 4 out of 9711 (= 1:2400) patients, lactice acidosis due to biguanides was diagnosed. Serum lactate concentration averaged 18.2 mmol/l and the pH value 6.87. All patients showed signs of renal insufficiency and three had congestive heart disease. In addition to treatment with biguanides, other factors might have contributed to the lactice acidosis in these patients: prolonged fasting, severe dehydration due to persistent vomiting, acute bronchopneumonia, and acute pyelonephritis. On addmission, two patients were in shock and all patients were semi-conscious or comatose. All patients were treated with bicarbonate and glucose/insulin. One patient was hemodialysed. Two of our four patients died. Oour four patients are compared with 179 patients in the literature with respect to mortality and prognosis of lactic acidosis due to biguanides.
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PMID:[Lactacidosis in biguanide therapy: diagnosis and therapy. 4 cases compared to 179 cases in the world literature]. 71 23

An analysis has been made of 2144 consecutive cases of latrodectism (envenomation by the red-back spider, Latrodectus mactans hasselti) reported to the Commonwealth Serum Laboratories. In the last eight years, notifications have averaged 240 cases per annum. Bites, usually on the extremities (74%), occurred most frequently in the summer months, and in the afternoon or evening. Most victims (79%) were aged between 18 and 50 years and 64.4% of them were males. Males are still often bitten on the genitals or buttocks (9.7% of cases). Local pain, redness and swelling were the most common symptoms, although significant pain was felt at other sites in 39% of the cases. The regional lymph nodes often became swollen and tender within 30 minutes. General effects included nausea, vomiting and sweating, but coma and respiratory failure were very uncommon, probably because of use of specific antivenom. This was administered within 24 hours of the bite in 92% of cases, and within two hours in 70%. Although 11 anaphylactic reactions (0.54%) were reported, no deaths resulted either from the venom or from reactions to the antivenom. Few delayed serum reactions (1.7%) were recorded. The action of the venom is described and the management of red-back spider bite is outlined.
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PMID:Survey of 2144 cases of red-back spider bites: Australia and New Zealand, 1963--1976. 73 70

In addition to asking their patients about recent foreign travel, Canadian doctors need to be aware of what features to ask about in considering imported illnesses. Of these illnesses, malaria is one of the most common and serious. Because of its cerebral renal, pulmonary and intestinal complications, falciparum malaria must be distinguished from non-falciparum forms. Anyone with a fever who has arrived recently from an endemic area should be tested for malaria. In addition, headache, malaise, myalgias, arthralgias, low back pain, nausea, vomiting, diarrhea or cough should raise suspicion. Malaria should be remembered as a cause of coma. Persons taking any form of drug prophylaxis for malaria are not protected absolutely and those who are semi-immune can become severely ill occasionally.
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PMID:Symptoms and signs of malaria. 78 78

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

Two siblings who were repeatedly admitted to hospital with acute episodes of vomiting, dehydration and coma were found to be suffering from isovaleric acidaemia. This condition is a rare inherited abnormality of leucine metabolism, which is frequently fatal in the early weeks of life and leads to mental retardation in a high proportion of those who survive early attacts. However, both our patients were of normal intelligence. The clinical presentation, biochemical defect, diagnosis and suggested therapies are reviewed.
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PMID:Isovaleric acidaemia in two South African children. 88 34

Hyperosmolar nonketotic coma is characterized by hyperglycemia, hyperosmolarity and dehydration in the absence of ketoacidosis. Two cases of hyperosmolar nonketotic coma, in which both the patients recovered, were presented. One of the cases was a 59-year-old female who had suffered from a metastatic brain tumor. After removal of the tumor, the patient's condition improved for a period. This was followed by a period of frequent vomiting, subsequently followed by coma. The laboratory data showed the absence of ketoacidosis in the blood sugar measured at 672 mg/dl and serum osmolarity at 343.1 mOsm./kg. The other case was a 74-year-old female who was admitted to the clinic because of cerebral thrombosis. Her caloric in-take was restricted and insulin was administered because of a mild diabetes mellitus which occured after admission. Then she entered a hyperosmolar non-ketotic coma. The laboratory data revealed blood sugar to be 1068 mg/dl and serum osmolarity to be 418 mOsm./kg. Immediately after large amounts of intravenous drip infusion and insulin were administerd, she recovered from the syndrome. The clinical observations and the pathogenesis of this syndrome were discussed.
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PMID:[Two cases of nonketotic hyperosmolar coma in neurosurgery (author's transl)]. 91 16

Acute subdural hematoma in infants is characterized by convulsive seizure, disturbance of consciousness, vomiting and irritability soon after mild head injury. The majority of cases have tence or bulged anterior fontanel and preretinal hemorrhage. Eleven cases, all traumatic in etiology and male under the age of one year were reported. Nine of them were treated by percutaneous subdural tapping alone, i.e., "Tapping Only Method". For the first several days, tappings were carried out daily. The subdural content was liquefied old dark blood or liquefied fresh-appearing blood in most cases. After that taps were performed only in the presence of intracranial hypertension. Vomiting and irritability were fairly reliable indicaters of intracranial hypertension but the most consistent signs were the fontanel tension to palpation and the measurement of head circumference. As soon as it could be determined that increased pressure did not recur within ten days after the last tap or that dry tap was confirmed the infant was discharged and follow as an outpatient. Follow-up studies on this series by cerebral angiography, EEG, skull measurement and Denver developmental screening test revealed normal physical and mental development in nine cases, although three out of nine cases showed mild but persistent avascular area. The remaining two cases showed more or less physically and mentally retarded developments: the initial treatment for both of them was delayed more than ten days. Acute infantile subdural hematoma due to mild head injury should be divided into the following two types: "Fulminant type", which rapidly falls in coma and may be fatal. The another, "Mild type" manifests only signs and symptoms of mild intracranial hypertension. This mild type should be treated by tapping only method without delay. There is a possibility that some mild type cases are overlooked and later progress to chronic infantile subdural hematoma. For comparison, thirteen cases of acute infantile subdural hematoma treated by trephination and/or craniotomy were reviewed. Pathological study revealed that early formation of capsular membrane is one of the characteristic findings.
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PMID:[Treatment of acute subdural hematoma in infancy-tapping only method and a follow-up study (author's transl)]. 94 81

An 18-year-old mentally and physically retarded boy, suffering from episodes of anorexia, vomiting, coma and convulsion which have been severer with advance in age, had periodic hyperammonemia, hyperlysinemia and homocitrullinuria. Blood cell arginase activity of the patient on normal diet was markedly reduced after an oral load of L-lysine. The oral loading tests of L-lysine revealed hyperammonemia, hyperlysinemia, hyperargininemia, hypercitrullinemia and homocitrullinuria. Etiology of metabolic error of our patient was discussed in reference to lysine-urea cycle.
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PMID:Clinical and biochemical studies on periodic hyperammonemia with hyperlysinemia and homocitrullinuria. 98 31


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