Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five serious cases of diabetic ketoacidosis, representing 23 patients, with ages ranging from 4 to 15 years are reported. School agers and adolescents were the groups most affected without existing significant predilection for sex. In 40% there was no success in finding the precipitating cause of the crisis; 32% was attributed to infectious processes, specially of the respiratory ducts and the rest, due to negligence in the application of insulin. The clinical signs showed: vomiting, dehydration, Kussamaul's respiration, sopor, stupor and in 5 cases a state of coma. Determinations of glucose, were integrated in 88% within the range of 451 to 750 mg % and the rest in lower figures. The pH in most was reported below 7.10 and CO2 lower than 10 mEq/l. Electrolytes in blood were generally evaluated within normal limits. Potassium in 20% was reported high, but we consider this was due to dehydration and because of its influence we recommend an electrocardiographic evaluation. Our classification which attempts to correlate the clinic and the laboratory is reported and our therapeutic scheme is discussed as well as the possible causes in two patients who died.
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PMID:[Diabetic ketoacidosis in children and adolescents. Clinical and therapeutical considerations in 25 severe cases]. 2 Sep 2

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
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PMID:Mixed acid-base abnormalities in diabetes. 10 96

Acute digoxin poisoning, its recognition and management, are reviewed. The uses of syrup of ipecac, gastric lavage, activated charcoal, cholestyramine, colestipol, edetate sodium and cathartics as measures to terminate the drug exposure are discussed. Measures to hasten digoxin elimination, such as the use of furosemide, hemodialysis and digoxin-specific antibodies are reviewed. Supportive management may include treatment with atropine, phenytoin, lidocaine, propranolol, glucose, insulin and sodium polystyrene sulfonate. Proper management of digoxin poisoning involves the use of standard decontamination procedures (emesis or gastric lavage). Activated charcoal is strongly recommended, followed by rapidly acting cathartics. Antiarrhythmic therapy usually involves atropine sulfate and phenytoin sodium.
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PMID:Acute digoxin poisonings: review of therapy. 34 83

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

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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PMID:[Alcoholic ketoacidosis (author's transl)]. 53 15

Hypoglycin A(0.01--1.0 mmol/l) stimulated insulin release from pieces of rabbit pancreas in vitro in the presence or absence of extracellular glucose. The relevance of this finding to the hypoglycaemia of Jamaican vomiting sickness is discussed.
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PMID:Hypoglycin stimulates insulin secretion. 59 Jun 55

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

The urgent admission to hospital of diabetic patients is often precipitated by hypoglycaemia, by vomiting or by ketoacidosis following cessation insulin therapy. By the use of simple agents, such as glucagon, lemonade and quick-acting insulin, such episodes can usually be averted in the early stages by the diabetic, his family and his doctor. These preventive measures keep the diabetic at work or at school and out of hospital, but require the provision of a simple emergency kit.
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PMID:The emergency management of the diabetic at home. 81 86

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

Successful treatment of the diabetic patient is possible only if the patient himself takes an interest in his disease and also an active part in treating it, i.e. by adherence to diet, testing of urinary sugar and insulin administration. The precondition for cooperation is intensive medical advice covering the following three aspects: 1. education, 2. motivation to put the acquired knowledge into practice, 3. practicability of the advice given. Our program covers 5 points: 1. basic education on the nature of diabetes, 2. diet instructions, 3. testing of urinary sugar, 4. instruction on insulin administration, 5. oral hypoglycemic agents. Special instructions must be given to motorists and all other types of driver, and also for emergency situations (vomiting, fever etc.). An instruction sheet carrying the key points in helpful. The results of this educational scheme are regularly checked by questionnaire. Refresher courses have been found to be necessary at regular intervals. The permanent educational efforts of regional Diabetic Associations and appropriate literature (D-Journal) are also recommended. The time-consuming effort of achieving the goals associated with education of the diabetic calls for teamwork between general practitioner and teaching center, e.g. the hospital with its facilities (audiovisual program, dieteticians etc.). However, the crucial factor remains the physician's commitment to his patient and his disease, since education and treatment must be geared to the needs of the individual patient.
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PMID:[How do we counsel our diabetic patients?]. 99 29


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