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We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18-61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 +/- 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios delta anion gap/delta bicarbonate (delta AG/delta HCO3) and sodium/chloride (Na/Cl)). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status.
Diabetes Res Clin Pract 1996 Sep
PMID:Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis. 896 87

In adults with diabetes mellitus, hepatomegaly and abnormalities of liver enzymes occur as a consequence of hepatocellular glycogen accumulation, as has been well described in children. During periods of hyperglycemia glucose freely enters the hepatocytes driving glycogen synthesis, which is augmented further by administration of insulin to supraphysiologic levels. The accumulation of excessive amounts of glycogen in the hepatocytes is a function of intermittent episodes of hyperglycemia and hypoglycemia and the use of excessive insulin. Hepatic glycogenosis occurs in patients with poorly controlled insulin-dependent type I or type II diabetes. The clinical manifestations of this phenomenon may include abdominal pain and obstructive symptoms such as early satiety, nausea, and vomiting. Ascites has rarely been reported. The typical biochemical findings are mildly to moderately elevated aminotransferases, with or without mild elevations of alkaline phosphatase. Liver synthetic function is usually normal. All these abnormalities, including the hepatomegaly, are readily reversible with sustained euglycemic control. The other major cause of hepatomegaly in patients with diabetes is steatosis. This is a function of the body habitus and state of insulin resistance rather than glycemic control. However, the distinction between steatosis and glycogenosis is important: whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not, but reflects the need for better diabetic control. Glycogenosis and steatosis cannot be distinguished reliably on ultrasound examination. The histology, however, is definitive. In glycogenosis, as in primary glycogen storage diseases, there is excess glycogen in the cytoplasm, and often also in the nucleus, of hepatocytes. The hepatocytes throughout the lobule appear pale and swollen with clearly defined cell boundaries. Ultrastructural examination reveals cytoplasmic glycogen in clumps displacing organelles to the periphery of the cell, and there is little if any steatosis. We have shown that hepatomegaly due to glycogenosis in adults with diabetes is similar in all respects to the condition seen in children. As in children, liver enzyme abnormalities are unreliable in predicting the presence or the extent of glycogenosis. Hepatic glycogenosis can occur at any age, and therefore should be included in the differential diagnosis of hepatomegaly in all insulin-requiring diabetics.
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PMID:Hepatomegaly and abnormal liver tests due to glycogenosis in adults with diabetes. 898 49

A 41-year-old black woman with a history of well-controlled, insulin-dependent diabetes mellitus was in her usual state of relatively good health when she had acute onset of right upper quadrant and epigastric abdominal pain, nausea, and vomiting. Physical examination and laboratory evaluation revealed gastrointestinal hemorrhage, decreased mental status, and acidemia, and emergency exploratory laparotomy elucidated ischemic bowel, of which 90 cm was resected. Postoperatively, the patient had cardiac arrest and could not be resuscitated. Autopsy was remarkable for mesenteric venous thrombosis and pylethrombosis, with ischemic necrosis of bowel and passive hyperemia. The arterial side of the cardiovascular system was relatively unaffected. Although arterial vascular complications of diabetes mellitus are well known, venous complications are less well described.
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PMID:An unusual complication of diabetes mellitus: the zebra that became a horse. 900 34

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.
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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.
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PMID:Sudden death due to diabetic coma in insulin-department diabetes mellitus: an autopsy report. 918 21

The management of diabetes mellitus is often complicated in patients with advanced cancer. Anorexia and nausea or vomiting make caloric intake erratic. The use of diabetogenic medications such as glucocorticoids can produce profound hyperglycemia. Many malignant tumors cause derangement in intermediary metabolism and abnormal glucose tolerance in up to one-third of patients. Both hyperglycemia and hypoglycemia impair the quality of life of dying patients. Swings in blood sugar should be avoided wherever possible, but aggressive blood sugar monitoring also impairs quality of life. This paper discusses issues in the management of diabetes in patients with advanced cancer and suggests guidelines for maintaining glycemic control without excessive interventions.
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PMID:The management of diabetes in patients with advanced cancer. 956 14

A 41-year-old man died in 1995 during ketoacidotic coma. He suffered from chronic manic depression, used lithium carbonate, and consulted the psychiatrist and the general practitioner (GP) frequently. Diabetes had not been diagnosed. Late in 1994 the situation worsened, the patient complaining of general illness, fatigue, nausea, vomiting, diarrhoea, thirst and excessive drinking of soft drinks. The GP referred the patient to a neurologist who found no neurological disorder but who asked for determination of blood glucose and lithium levels, and of thyroid function. The day afterwards the neurologist went on holiday. The blood glucose level proved to be elevated (16.9 mmol/1) but nobody took any action and the GP was not informed. Six days after returning from his holiday, the neurologist who had an administration backlog, found the laboratory findings only after he had been informed that the patient had just died. The court gave the neurologist a warning. Lessons are that somatic problems should be treated as such, even in a psychiatric patient, and that a good administrative signalling system is a prerequisite for quality in medical practice.
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PMID:[Medical and administrative neglect of high blood glucose levels; comments on a decision by a medical disciplinary tribunal]. 954 47

Since severe obesity is frequently associated with serious metabolic, cardiovascular and psychological co-morbid conditions, and given the usually unsuccessful results of conservative therapeutic approaches, surgical treatment based on gastric restriction procedures is increasingly recognized as a treatment of choice for morbidly obese persons. Among several surgical approaches designed to promote a substantial loss of weight, two gastric restriction procedures, i.e. the vertical banded gastroplasty and the gastric bypass, have been increasingly used during the past years. Both techniques induce an impressive loss of weight, and are surprisingly well tolerated, even by severely obese persons. The usual 50-75% reduction of initial weight excess, is followed by a clear-cut reduction, or even disappearance of, obesity-related co-morbidity, such as hypertension, diabetes mellitus or sleep apnea syndrome. While serious peri- and postoperative risks are very limited, the intractable vomiting occurring after gastroplasty, and potential sequelae related to iron and calcium malabsorption after the gastric bypass, represent much more frequent complications of the surgical treatment of obesity. There is also a tendency towards a late regain of weight, but the benefit in terms of improvement in the obesity-associated co-morbidity is in general maintained despite this partial increase in weight. Gastric procedures are, therefore, an effective treatment of severe obesity and of its co-morbid conditions. However, careful medical and nutritional supervision is necessary during the follow-up after surgery, to prevent potential nutritional or digestive complications.
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PMID:Surgical treatment for morbid obesity. 924 44

Two cases of fatal strongyloidiasis associated with diabetes mellitus and malnutrition are reported. The patients presented with repeated vomiting and upper gastrointestinal bleeding respectively. Unusual findings in these two patients included: unexplained peripheral leukocytosis, pulmonary infiltrates, gastric aspirate leukocytosis, progression of gastrointestinal symptoms and concurrent presence of adult worms, eggs, filariform and rhabditiform larvae of Strongyloides stercoralis in alimentary canal specimens. Both patients succumbed while receiving treatment with mebendazole. The present report illustrates that unexplained gastrointestinal symptoms with extensive scratch marks below the umbilicus can be important clues to early diagnosis of the disease. In addition, the various presentations of S. stercoralis infestation are discussed with reference to predisposing factors. Current trends in laboratory diagnosis and therapeutic considerations are also delineated.
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PMID:Two cases of fatal strongyloidiasis in Hong Kong. 927 Oct 28

This study describes the medical practice among a sample of indigenous healers from Thaba Nchu, Ganyesa, Kurumane, Mankwe, and Molopo regions of the North West province of South Africa. Data were obtained from interviews conducted among 35 indigenous healers recommended by heads from a sample of 40 villages. Findings indicate that 60% were Botswanan. 51% were female. 85.7% were aged 30-59 years. 77% were married, and 5.7% were divorced. 31% had a lower primary education, and 25.7% finished high primary schooling. 22.4% had no formal schooling. 60% were bone throwers, and 34.2% were bone throwers and sangomas. 54% received their training "by their ancestors through dreams." 31% received formal training in indigenous healing. 14% served an apprenticeship with an experienced healer. 94% had a period of training from 2-5 years. 57% were registered with an association for indigenous healers. 77% relied on bone throwing for diagnosis of health problems. Other treatment methods included scarification, enema, induced vomiting, ritual performance, and prevention of witchcraft. Healers treated infertility, septic sores, impotence, sexually transmitted diseases, deliveries, makgome or boswagade, asthma, mental illness, high blood pressure, palpitations, tuberculosis, alcoholism, diabetes, and cancer. Pediatric diseases that were treated included tlhogwana, ditantanyane, measles, Kwashiorkor, and whooping cough. Healers relied on the following methods for disease prevention and health promotion: home fortifying, home cleansing, personal cleansing, scarification, and cultural education in taboos. 74% made referrals to either a western trained physician (17 out of 26) or other healers. All were generalists. Clients included professionals, such as nurses, teachers, and religious ministers. Although there is potential danger in some treatment methods, healers serve an important role in health prevention and treatment.
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PMID:Indigenous healers in the North West Province: a survey of their clinical activities in health care in the rural areas. 928 40


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