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Hyperglycemic nonketotic coma in insulin-dependent diabetes mellitus.
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[Therapy of diabetic coma in childhood].
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Lithium nephrotoxicity: a review.
Lithium, a group I alkali metal, is widely used for treatment of manic-depressive psychosis. A number of toxic side effects have been reported, among which the most common ones are nephrogenic diabetes insipidus, distal tubular acidosis, and impairment of renal concentrating ability. The proposed mechanisms in the literature of these renal complications of lithium salt therapy are reviewed. None of the proposed mechanisms can be definitively established. Recently reported observations contradict the causative role of lithium in the pathogenesis of renal complications. More careful selection of control subjects is required for further investigation of the nephrotoxic effects of lithium.
Hypophosphataemia with intravascular haemolysis: A case report.
Severe hypophosphataemia in an alcoholic patient during active treatment for acute pancreatitis and diabetic keto-acidosis was associated with a transient intravascular haemolytic anaemia, thrombocytopenia and some evidence of muscular disorder. The mechanism of the clinical changes is briefly discussed, and it is stressed that such complications could easily be overlooked in a patient with other serious disorders.
Reorganization of ambulatory health care in an urban municipal hospital. Primary care and its impact on hospitalization.
Ambulatory care services have been reorganized in a New York City hospital. A newly developed Neighborhood Family Care Center (NFCC) replaced the outpatient clinics. The NFCC and both inpatient and emergency services are totally integrated so as to overcome many of the deficiencies that previously existed in ambulatory care, such as inferior quality of care, minimal academic involvement, fragmentation of services, overspecialization, and unresponsiveness to patients' needs. A review of all patients admitted to the Adult Medical Service has shown a statistically significant decrease in admission rates for diabetic coma-acidosis, severe hypertension, congestive heart failure, cerebrovascular accidents, and severe asthma during the 18 months following the reorganization of ambulatory care. Analysis of cost effectiveness of these changes on the utilization of hospital beds indicates the potential for reduced expenditures of limited health care dollars.
Acute diabetic complications.
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[Biguanide-induced lactate acidoses in diabetic patients].
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Lactic acidosis with therapeutic metformin blood level in a low-risk diabetic patient.
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Metformin-associated nonketotic metabolic acidosis.
OBJECTIVE: To document a case of anion gap, nonketotic metabolic acidosis occurring in a patient with acute renal failure who was receiving metformin. CASE SUMMARY: A 67-year-old white man presented with a 9-day history of weakness, nausea, dizziness, and difficulty moving; he had also not eaten during the previous 2 days. The patient had numerous abnormalities on his serum chemistry panel and arterial blood gases, including a pH of 7.1 and an anion gap of 21 mEq/L No ketones were detected in the urine. The patient was treated with intravenous fluids, sodium bicarbonate, insulin, and hemodialysis. All medications were discontinued. The acidosis resolved shortly after hemodialysis. The hospital course was complicated by the onset of atrial fibrillation occurring on day 2 that did not respond to chemical cardioversion. On day 6 the patient was discharged home with resolving acute renal failure and normal serum pH. CONCLUSIONS: The mortality rate of biguanide-induced lactic acidosis is approximately 50%; thus, early recognition and treatment are essential. Suspicion of lactic acidosis should be high when diabetic patients who are taking a biguanide present with acidosis. The majority of cases of metformin-induced lactic acidosis have occurred in patients with contraindications to the drug (i.e., renal dysfunction). Thus, it is important to maintain strict adherence to these contraindications and monitor patients for deteriorating renal function.
[THE INCIDENCE OF ABNORMALITIES IN CHILDREN OF DIABETIC MOTHERS].
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LACTATE ACIDOSIS ASSOCIATED WITH PHENFORMIN THERAPY AND LOCALIZED TISSUE HYPOXIA. REPORT OF A CASE TREATED BY HEMODIALYSIS.
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Intracellular protons inhibit transient outward K+ current in ventricular myocytes from diabetic rats.
This study examined the effects of protons on cardiac ion channel function in early stages of diabetes mellitus. Transient outward (I(to)) and inward rectifier K+ (IK1) currents were recorded by the whole cell, voltage-clamp technique in ventricular myocytes isolated from hearts of streptozotocin-induced diabetic and control rats. Proton concentration was controlled by independently varying the pH of buffered external or pipette (pHp) solutions. External acidification did not alter I(to) in diabetic rat myocytes when initiated after intracellular dialysis with standard pHp 7.2, but when these cells were dialyzed with acidic pHp (6.6 or 6.0), I(to) density was significantly reduced. Low pHp also reduced I(to) density more in cells from diabetic rats than in controls, whereas alkaline pHp had no effect on either group of cells compared with standard pHp 7.2. In control myocytes dialyzed with pHp 6.0, block of Na+/H+ exchange with 5-(N,N-dimethyl)-amiloride (DMA) or Na(+)-free external solution further reduced I(to) density compared with pHp 6.0 alone, whereas these treatments had less effect on acid-dialyzed cells from diabetic rats. Dialysis with pHp to 6.0 did not alter IK1 in either group of cells compared with standard pHp 7.2, but when done in the presence of DMA or Na(+)-free conditions, IK1 density in both groups was significantly reduced by nearly the same amount. We conclude that intracellular protons inhibit I(to) channels in ventricular myocytes from diabetic and control rats, but that for a given acid load, inhibition is markedly greater in diabetics. This difference may be explained by a diabetes-induced decrease in Na+/H+ exchange that limits proton extrusion during intracellular acidosis. Moreover, acidosis may differentially suppress I(to) and IK1, suggesting that these K+ channels exhibit dissimilar sensitivities to intracellular protons.
[WATER-SALT METABOLISM IN DIABETES MELLITUS IN CHILDREN].
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Lactic acidosis. Lactic acidosis associated with metformin use in treatment of type 2 diabetes mellitus.
Metformin, an antihyperglycemic, is widely used in the treatment of type 2 diabetes mellitus (DM). A rare, but important complication associated with this drug is the development of lactic acidosis: Overall mortality of lactic acidosis is approximately 50%. Certain subsets of patients taking metformin are at greater risk of developing lactic acidosis. This report discusses the development of metformin-associated lactic acidosis in four older adults admitted to an institution during a 2-month period, treatments, and outcomes. We recommend an aggressive treatment strategy of hemodialysis followed by peritoneal dialysis, continuous bicarbonate infusion, and tight glucose control. We review the cautions and contraindications of metformin use for the treatment of type 2 DM and report an educational plan for residents and staff instituted to improve drug complication awareness and reduce mortality.
[Diagnosis of diabetic coma and its therapy in a district hospital].
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