[DRAMATIC INCIDENTS DURING THE TREATMENT WITH ORAL ANTIDIABETICS].
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Acidosis↗
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LACTIC ACID ACIDEMIA AND PHENFORMIN.
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Acidosis↗
[Experiences with low-dose insulin therapy in diabetic precoma/coma in basic hospital care].
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Acidosis↗
Pulmonary mucormycosis as a complication of chronic salicylate poisoning.
Mucormycosis is an often-fatal opportunistic fungal infection caused by members of the class Zygomycetes (Phycomycetes), order Mucorales. Most cases are diagnosed by histologic examination, through the identification of mucormycotic hyphae in infected tissues. Chronic debilitating conditions accompanied by acidosis such as diabetes mellitus, as well as leukemia, lymphoma, and immunodeficient states, predispose to the development of this type of opportunistic infection. This report describes a hitherto undescribed finding, the presence of structures consistent with sporangia in tissue sections, in a case of pulmonary mucormycosis occurring in a nondiabetic patient with metabolic acidosis secondary to chronic salicylate poisoning.
Acidosis↗
[Rhinocerebral mycoses caused by Mucoraceae species (mucormycosis). Case report and literature review].
According to the literature and on the basis of the case reported in this paper of rhinocerebral mucoraceae mycosis we summarize the characteristic features as follows: mucoraceae--mycoses--common, but wrong term: "mucormycoses"--are a group of infections caused by members of the family mucoraceae (Mucor, Rhizomucor, Rhizopus, Absidia species)--most frequently by Rhizopus species. Primarily the fungi enter the pharynx or nose, local infections or trauma being a prerequisite. The most important predisposing factor is diabetes mellitus. Invading the tissue and causing vascular thrombosis the infection frequently takes an acute, often fulminating and fatal course. Acute sinusitis accompanied by swelling of the cheek and protrusion of the eye in a diabetic, particularly with acidosis, are pathognomonic. Diagnosis is confirmed by microscopic examination of infected tissue (unstained smear or histologically). Since systemically administered antifungals have not proved very effective in these myoses, mainly because an adequate tissue level can hardly be achieved, the most effective and curative treatment is surgical removal of infected tissue, simultaneous control of diabetes being mandatory.
Antifungal Agents↗
[Diagnosis of diabetes mellitus in children].
Diabetes in childhood is essentially represented by the type 1 or insulin-dependent diabetes mellitus (IDDM). Classical symptoms (polyuria, polydipsia, asthenia, weight loss) are usually present at the first consultation and allow an immediate diagnosis at the physician's office by performing capillary (finger-prick) blood glucose measurement (> or = 200 mg/dL) and urine-stripe test (detection of glucosuria and ketonuria). A diagnosis performed at this stage of the disease leads to the admission of the child at hospital, in order to institute the insulintherapy without delay. This attitude should permit to avoid the rapid development of diabetic keto-acidosis, which is at present too much frequent at diagnosis (50% of the cases) and which is associated with potential risks of severe complications in children. In case of incidental detection of hyperglycemia without ketonuria in childhood, the differential diagnoses of early IDDM are the rare form of familial non insulin-dependent diabetes with onset in childhood (MODY: maturity-onset diabetes of the young) and the transient hyperglycemia in childhood. Finally, diabetes could also develop in the course of an other chronic disease (i.e. cystic fibrosis) or as part of genetical syndroms.
Adolescent↗
Rhinocerebral mucormycosis in a pregnant woman with diabetic ketoacidosis.
Rhinocerebral mucormycosis (RCM) is a rare but often fatal condition characterized by aggressive necrotizing infection originating from nose and spreading to paranasal sinuses, orbit and central nervous system. Although Fungi and spores of mucorales show minimal intrinsic pathogenicity towards normal persons, they can initiate fulminant infections in patients with underlying debilitating conditions. A case of RCM in a pregnant woman with diabetic keto-acidosis successfully treated by supportive care, amphotericin B and surgery is reported.
Adult↗
Lithium and the kidney.
Three middle-aged women treated with lithium carbonate for a manic-depressive illness have had complicating nephrogenic diabetes insipidus, renal tubular acidosis, acute reversible renal functional impairment in association with hypercalcaemia, or irreversible chronic renal damage. Renal toxicity developed in the presence of normal levels of lithium in the serum. The possibility of permanent renal damage as a result of long-term lithium therapy is of major concern.
Acidosis, Renal Tubular↗
Management of diabetic ketoacidosis.
Diabetic ketoacidosis is a common acute complication of insulin-dependent diabetes mellitus. It is defined as the triad of hyperglycemia, acidosis and ketosis. Once diabetic ketoacidosis is suspected, the diagnosis should be established rapidly and treatment initiated. Fluid administration, insulin therapy and correction of metabolic abnormalities are the cornerstones of therapy. Treatment of any underlying illnesses, particularly infection, is also essential to ensure the best possible outcome. Appropriate patient monitoring allows the clinician to assess therapy and make necessary adjustments.
Adult↗
Hyperosmolar non-ketotic diabetic coma as a cause of emergency hyperglycaemic admission to Baragwanath Hospital.
There were 136 emergency hyperglycaemic admissions to Baragwanath Hospital over a 6-month period during 1992-1993, representing 1.2% of the total number of medical admissions; 24 (18%) patients died. Diabetic keto-acidosis (DKA) accounted for 88 (65%) admissions (mortality rate 9%) while 16 admissions (12%) were as a result of hyperosmolar non-ketotic coma (HNKC), defined as hyperglycaemia, dehydration and an altered level of consciousness with a plasma osmolality > or = 330 and an arterial pH > or = 7.30, with absent or minimal ketonuria. Of these 16 patients, 9 (56%) were known to have diabetes mellitus. Patients with HNKC were significantly older than those with DKA (P < 0.001) and other patients with nonketotic hyperglycaemia (P < 0.05). The overall mortality rate was 44%; prophylactic low-molecular-weight heparin appeared of benefit (P < 0.05).
Adult↗
[New data in the domain of insulin resistance].
Insulin resistance may occur to a variable degree in various disease conditions. Obesity is frequently accompanied by insulin resistance. The anti-insulin antibodies in patients treated with insulin are a classical cause, but in fact rare. Insulin resistance of variable degree may accompany certain metabolic disorders, e.g. diabetic ketosis and acidosis, and endocrine disorders, e.g. Cushing's syndrome, acromegaly. The measurement of insulin receptors brings a new dimension to the investigation of insulin resistance. Insulin receptors are reduced in number during obesity. The abnormality, partly responsible for insulin resistance, is reducible by reduction in calory intake. Circulating insulin anti-receptor antibodies appear to be responsible for insulin resistance which is particularly marked although exeptional, in nonobese diabetics with acanthosis nigrans and auto-immune symptoms.
Diabetes Mellitus↗
[Coma and praecoma diabeticum. Physiopathology, clinical aspects and therapy].
The diabetic coma is characterized by fundamental metabolic changes. Apart from the hyperglycaemia, exsiccosis and the disturbed electrolyte metabolism are considerable factors contributing to the coma. The treatment of diabetic coma puts great demands on the doctors, since the prognosis can only be improved by systematic and correct intervention. A fast filling up of the volume and a specific electrolyte (potassium) substitution are very important. In cases of ketoacidotic diabetic coma the acidosis must be carefully balanced, whereby the "rest-acidosis" up to pH 7.1 can be tolerated. The administration of insulin can only begin, when the volume and electrolyte substitution is guaranteed, otherwise dangerous insulin-induced hypokalaemia is unavoidable. By no means may the first treatment for the insulinisation be carried out ambulatory.
Bicarbonates↗
[MELAS syndrome (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes].
BACKGROUND: The MELAS syndrome (Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes) belongs to the category of mitochondrial disorders. The most common molecular etiology of the syndrome is a mutation A to G transition at base pair 3243 in the mitochondrial genome. The phenotype is varied and depends on the proportion of DNA muted and which organ on aerobic metabolism suffers most. CASE-REPORT: An 17 year-old woman had successively neurosensory hearing loss, renal disease, cardiomyopathy, diabetes mellitus, lactic acidosis and stroke-like episodes that evoked a MELAS syndrome. DISCUSSION: The skin manifestations of patients with MELAS syndrome are scaly, pruritic, diffuse erythema, reticular pigmentation, moderate hypertrichosis, seborrheic eczema, atopy and vitiligo. Our patient presented severe hirsutism and reticular pigmentation of the limbs. No abnormal histologic and electron microscopic findings were noted in the skin or the follicles involved.
Adolescent↗
Heparin-induced hyperkalemia: a prospective study.
Heparin is frequently used for the prophylaxis and treatment of deep venous thromboembolism and it induces hypoaldosteronism leading to hyperkalemia, an uncommon adverse effect. In an intensive prospective drug monitoring study, 154 inpatients at the Internal Medicine Unit of Hospital Sotero del Río, Santiago, Chile, received heparin in the period between March and November 1990. Mean age of the patients was 65.8 +/- 12.9 years and 56.5% were female. Twenty-one (13.6%) patients developed heparin-induced adverse reactions. Thirteen events were hyperkalemia, 7 ecchymoses and 1 hematuria. The monitoring team and attending physicians have agreed to classify 9 heparin-induced hyperkalemia cases as probable and the other 4 as possible. No adverse reaction was fatal but 8 of the patients had severe hyperkalemia. Almost all reactions were dose-related. Hyperkalemia was more frequent in patients with diabetes mellitus, metabolic acidosis and long-term heparin therapy. The frequency of hyperkalemia did not correlate with age, sex, renal impairment or with previous use of anti-inflammatory drugs, heparin or aspirin.
Adolescent↗
[Measurement of insulin sensitivity in obese or diabetic children in vivo. A comparison of three methods (author's transl)].
Three groups of ten similar obese children were infused with one of three protocols. Protocol I glucose only (1.15 mM/min/m2). protocol II, glucose, insulin (42 mM/min/m2). Protocol III, glucose insulin, propanolol (0.04 mg/min/m2) adrenalin (3 micrograms/min/m2). Eighteen newly diagnosed diabetic children without acidosis received glucose according to protocol II. Thirteen normal adults (controls) received glucose infusion according to protocol I. Protocols I and II were well tolerated and gave consistent results but Protocol III was not well tolerated and did not give interpretable results. In obese children steady state blood glucose levels are significantly higher than in controls but this difference was only moderate (8.8 + 0.7 mM, against 6.6 +/- 0.4 mM for protocol I). There was no difference in insulin levels. In diabetic children the steady state was more rarely obtained after a 120 min infusion and blood glucose levels were higher than in the controls or in obese children.
Adolescent↗
In vivo bicarbonate deficiency and insulin dissolution.
Exogenous insulin exists primarily as the monomer in human plasma. However, in U100 regular insulin formulations, the concentrations of zinc and peptide are such that the insulin hexamer predominates. The biologic result is further disassociation to the monomer after subcutaneous or i.v. administration. Because of this, human plasma from seven normal controls dissolved 20-30 microm hexagonal insulin crystals in 3-8 min. This ability was inhibited by acid titration to a stable pH of 6.30, at which point bicarbonate depletion could be suggested. Repletion of bicarbonate remarkably restored the solvent effect, while back-titration to the initial pH without repleting bicarbonate had only a moderate result. To establish whether the in vivo reduction of bicarbonate in pathologic states had similar results, plasma from five Type I diabetics in severe acidosis (pH 7.06 +/- 0.04, HCO3 -7.3 +/- 0.6 mmol/l) was similarly studied after stabilization under 5% CO2 (pH, 6.97-7.17). In all cases, the dissolution of insulin crystals was inhibited (dissolution times greater than 25 min). When bicarbonate was replenished (HCO3- 24.1-26.7 mmol/l) and pH accordingly renormalized (pH 7.39-7.43), the dissolution of insulin crystals was completely restored. Because of these observations, we conclude that both plasma bicarbonate and pH markedly affect the dissolution of insulin and that reduced bicarbonate/pH in diabetic ketoacidosis may limit the availability of the biologically active monomer. These influences may play a role in the initial insensitivity to insulin frequently seen in severe insulin deficiency and ketoacidosis.
Adult↗
Short chain diol metabolism in human disease states.
Recent clinical studies have shown the presence of two short chain diols, meso-2,3-butanediol and D/L-2,3-butanediol, and in most cases 1,2-propanediol in either serum or urine collected from humans in several apparently unrelated disease states: congenital propionic and methylmalonic acidemia, premature infants, and alcoholics both in the presence and absence of ethanol. In addition 1,2-propanediol has been shown in patients during prolonged starvation, and in patients with diabetic keto-acidosis. No common defect is known to exist in these metabolic states. Understanding how these compounds are produced in clinically well-defined diseases such as methyl malonic and propionic aciduria, however, may help explain how and why these compounds are produced in alcoholics.
Acetoin↗
Elevated postmortem ethanol concentrations in an insulin-dependent diabetic.
A 54-year-old woman (165 cm, 37 kg) was found dead in her home during a welfare check after not having been seen for at least three days. The body showed clear evidence of decomposition. Her head was in what appeared to be a pool of blood. The residence was clean, neat, and showed no evidence of violence. Insulin was found in the refrigerator, and syringes were in the kitchen cabinet. In agreement with these physical findings, her clinical history indicated that she suffered insulin-dependent diabetes mellitus. Autolytic changes were noticed at autopsy, and no obvious cause of death was demonstrated. The autopsy heart blood sample screened negative for cocaine and/or metabolite (benzoylecgonine), phenethylamines, opiates, and barbiturates by radioimmunoassay. The alcohol concentration was 0.51 g/dL in the blood, 0.04 g/dL in the brain, 0.08 g/dL in the liver, and 0.05 g/dL in the urine, and acetone levels were 42 mg/dL, 53 mg/dL, 14 mg/dL, and 19 mg/dL, respectively. Isopropanol was also present in all samples analyzed. The cause of death was ruled as metabolic acidosis due to diabetes mellitus. Possible bacterial postmortem production of ethanol is considered as an explanation for the increased concentration of ethanol found in the postmortem heart blood.
Cause of Death↗