Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperglycaemic, hyperosmolar coma developing in diabetes mellitus-with or without ketoacidosis-is a perilous metabolic catastrophe, preserving its clinical importance even nowadays. The features of the two basic forms of diabetic coma, the development and characteristics of clinical symptoms and laboratory alterations caused by absolute or relative lack of insulin are reported by the author. The importance of early diagnosis and up-to-date intensive treatment is emphasized, regarding the need of decreasing of the still now considerable mortality rate. Fundamental principles of the therapeutic interventions are the following: improvement of the microcirculation through appropriate compensation of fluid and elektrolytes, intravenous or intramuscular administration of low-dose insulin, prevention of hypokalemic condition, and correction of acidosis under pH 7,1 value. Moreover, the well-planned supportive treatment is also essential: prevention of thromboembolism, averting the occasional development of shock caused usually by infections, and prophylaxis of the often fatal cerebral oedema. The estimation and follow-up of osmolality and the prevention of rapid changes in serum glucose and electrolyte levels are of particular importance in every cases. Careful observation of the patients regarding the cardiorespiratory and renal functions is of great significance in both (first and second) phases of the treatment. Improvement of patients' education, controlled care of diabetic patients, reduction of the number of recidive cases and increasing knowledge regarding diabetes among the general practitioners are determined by the author as the future possibilities for the prevention of this severe metabolic disorder.
 ...
PMID:[Diabetic coma and bases of proper treatment]. 826 22

The author presents a practical guide for diagnosis and management of some common emergencies. The most common are hypoglycaemia in persons with diabetes, diabetic ketoacidosis and non-ketotic hyperosmolar diabetic coma. Acute adrenocortical failure is also quite common. These three conditions can be presented in persons with diagnosed disease. Therefore prevention should be possible with proper education. In rare cases the emergency situation is the presenting symptom. Thyreotoxic crisis, myxoedema coma and hypercalcemic crisis are less common. A high level of suspicion is important for early diagnosis and successful treatment of these conditions.
 ...
PMID:[Acute endocrinology]. 833 69

The artificial endocrine pancreas (AEP) is a controlled glucose and/or insulin infusion system in which continuously monitored blood sugar values are fed to a computerised analyser that uses predetermined algorithms to establish the doses to be administered. Since its first appearance in clinical practice and diabetological research during the Sixties, the AEP has been modified in various ways to overcome technical problems associated with the gluco-sensor and algorithms so as to make better use of the glucose-insulin feedback mechanism, and hence obtain a closer correspondence to physiological islet cell activity. As a result of these changes, the AEP can be employed in accordance with the physiopathological principles of insulin secretion in a variety of clinical conditions to secure the short-term control of metabolic alterations in the diabetic. Surgery is one field in which the AEP is used to great advantage, since this and its accompanying anaesthetics are the source of stress, which in turn may result in a rapid and sometimes serious postoperative metabolic derangement, including an increased secretion of anti-insulin hormones. The AEP has also been proposed for diabetic pregnancy and for the treatment of subjects in diabetic coma. It has proved useful in the diagnosis and management of hypoglycaemia due to organic hyperinsulinism, in diabetics with renal failure, in the honeymoon period, and in cases of unstable diabetes. The versatility of its application and its underlying physiopathological principles have enabled the AEP to be predominantly employed in research.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The artificial endocrine pancreas in clinical practice and research. The present position and future perspectives. 841 26

The discovery of insulin by Banting and Best in 1992 is the subject of many papers and one authoritative book (Bliss M. The Discovery of Insulin. Chicago: University of Chicago Press, 1982. See also Bliss M. Rewriting medical history: Charles Best and the Banting and Best myth. J Med Hist 1993; 48: 253-274.). This paper charts the introduction of insulin in England and examines its effects on medical practice. Before 1922 there were few effective drugs and only one (thyroid extract) which had to be taken continuously. Insulin was radically different; it restored weight and vigour and allowed survival in diabetic coma and after surgery but was potentially dangerous because of the possibility of hypoglycaemia, had to be given by injection, and the dose varied with the amount of food and exercise. The immediate questions to be answered after the supply of insulin was assured were how could such a powerful drug be kept out of the hands of ignorant people (a phrase used by The Times), who would administer it, and who would supervise the treatment? Within a year further problems were identified. Should the aims of treatment be the same as those in the starvation era? Could the diet be liberalized? How much biochemical monitoring was necessary? I set the scene by describing how, from Minkowski's announcement (1889) that pancreatectomy caused severe diabetes, most clinicians and physiologists believed that the pancreas (and specifically the islets of Langerhans) produced an internal secretion which controlled carbohydrate metabolism. After Murray's (1891) demonstration that myxoedema could be cured by thyroid extract, it was assumed that diabetes would soon yield in the same way. Yet by the beginning of the First World War most experts were pessimistic about isolating the hypothetical internal secretion and had pinned their hopes on starvation treatment. In the decade before the introduction of insulin the management of diabetes was grim; patients were kept in hospital for weeks or months, while their calorie intake and glucose excretion was meticulously recorded. They were in the wards of physicians with a strong interest in biochemistry whose forte was analysing urine not looking after patients. When the Medical Research Council set up a multicentre trial of insulin in late 1922 they enrolled the physician biochemists who produced the early publications and became the experts. The narrow views and innate conservatism of these doctors with the inflexibility of the system in (London) teaching hospitals meant that insulin treatment became a straightjacket for many patients.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:A force of magical activity: the introduction of insulin treatment in Britain 1922-1926. 854 34

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.
 ...
PMID:[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function]. 882 59

Mortality in insulin-dependent diabetes is markedly increased compared to the general population. Although strong associations have been found between renal disease and the risk of cardiovascular disease (CVD) the interaction between these two factors is not well understood. This study, which addresses risk factors for mortality in IDDM with a particular focus on the renal-CVD link, is based on the prospective Epidemiology of Diabetes Complications study. Thirty-seven (mean age 36 years, mean duration of IDDM 28 years at baseline) of the 658 IDDM individuals (mean age 28 years, mean duration of IDDM 20 years at baseline) have died in the first 4 years of follow up. A nested case-control study was performed, matching on sex and duration of diabetes. Twenty-two (59%) of the deaths were attributed to coronary heart disease, with an additional 16% attributed to diabetic coma. Only nine (41%) of the 22 individuals who died from cardiovascular disease had clinical evidence of coronary heart disease when seen for their last biennial exam. However, 54% of those who died of CVD without prior evidence did have evidence of lower extremity arterial disease. A strong link with renal disease was confirmed, with 81% of those with a coronary artery disease death having renal disease. Multivariate analyses suggest that smoking history, triglycerides and total platelet count are independent predictors of mortality, while LDL cholesterol best predicted CVD mortality. These results suggest a need for more intensive screening for cardiovascular disease, and correction of cardiovascular risk factors, in order to reduce the increased rate of mortality in this population. Efforts to prevent or delay the onset of renal disease may also be of benefit.
Diabetes Res Clin Pract 1995 Dec
PMID:High mortality from unidentified CVD in IDDM: time to start screening? 886 62

Malignant hyperthermia (MH) in humans is usually triggered by volatile anaesthetics and depolarizing muscle relaxants. However, other factors or drugs (e.g. cresol) are thought to induce MH. We report a case of fulminant MH associated with a ketoacidotic diabetic coma. After therapy for diabetic coma with insulin (containing the preservative cresol) and electrolyte solutions was started, the patient complained of increasing myalgia, developed a high fever and respiratory and metabolic acidosis and lost consciousness. MH was treated immediately with dantrolene; the patient recovered within 14 days. Five months later the patient was diagnosed as MH-susceptible by the in vitro caffeine and halothane contracture test. This case supports the assessment that MH and diabetes are associated diseases and that cresol could possibly trigger MH. Furthermore, therapy with dantrolene has been demonstrated to be beneficial in the treatment of MH associated with diabetic coma.
 ...
PMID:Fulminant malignant hyperthermia associated with ketoacidotic diabetic coma. 888 Feb 51

Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.
 ...
PMID:[Diabetic emergencies]. 914 92

Sudden death caused by the acute onset of diabetic coma is reported. A 15-year-old female had been suffering from insulin-dependent diabetes mellitus for the prior 8 years and had a fever and vomiting for the past few days. On the 4th day, after the onset of fever and vomiting, she died suddenly, and was autopsied to clarify the cause of death. Macroscopic examination revealed that the pancreas was atrophic (40 g) whereas the liver was markedly enlarged (2,740 g). Histological findings were: 1) The islets of Langerhans were decreased in size and number. They were not positive for aldehyde-fuchsin staining, 2) There were severe fatty changes in the liver cells. The retained blood in the left ventricle was analyzed: glucose, 1,016 mg/dl; acetone, 345 mg/l; acetoacetate, 5.91 mmol/l: D-3-hydroxybutyrate, 4.17 mmol/l; hemoglobin A1c, 10.2%; fructosamine, 416 mumol/l; total serum cholesterol, 220 mg/dl; triglycerides, 205 mg/dl; free fatty acid, 8.0 mEq/l; urea nitrogen, 40 mg/dl. Although the biochemical estimation of the glucose and ketone levels in post-mortem body fluids was recognized as being unreliable, many of these values were far elevated in comparison with those of normal individuals. Thus, we concluded that the cause of death was diabetic ketoacidosis. We also discuss the diagnostic problems of postmortem blood chemistry.
 ...
PMID:Sudden death due to diabetic coma in insulin-department diabetes mellitus: an autopsy report. 918 21

It has been reported that there is an inverse relationship between serum sodium (Na) and potassium (K) levels in patients with diabetic coma. The present study was undertaken to determine whether such an inverse relation depends upon plasma glucose levels in diabetic patients for their glycemic control. We examined two hundred and fifty-two patients with diabetes mellitus admitted to our hospital during the one-year period to control their plasma glucose levels, except for those having nephropathy or liver dysfunction. Serum Na and K, plasma glucose, and serum and urinary C-peptide levels were determined. There was a negative correlation between serum Na levels and fasting plasma glucose (FPG), and, conversely, a positive correlation between serum K levels and FPG. The changes were more evident in the patients with insulin-dependent diabetes mellitus than those with non-insulin-dependent diabetes mellitus. There was an inverse relation between serum Na and K levels and it was profoundly dependent upon plasma glucose levels in all the diabetic patients before tight control of their glycemic levels. The disorder may be based on the movement of electrolytes between intra- and extracellular spaces, dependent on the impaired insulin action as well as hyperosmolality.
 ...
PMID:Inverse distribution of serum sodium and potassium in uncontrolled inpatients with diabetes mellitus. 1042 70


<< Previous 1 2 3 4 5 6 7 8 9 Next >>