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At least 613 records · Page 34Linked to original sources
PubMed1996

Diabetic ketoacidosis and hyperosmolar nonketotic state: gaining control over extreme hyperglycemic complications.

Decompensated hyperglycemia is a frequent, severe complication of diabetes mellitus. Ketoacidosis usually occurs in patients with insulin-dependent (type I) diabetes, and insulin therapy is required to correct their hyperglycemic derangement. Hyperosmolar nonketotic state is more common in patients with non-insulin-dependent (type II) diabetes, who usually present with severe dehydration and hyperosmolar plasma. They respond readily to aggressive volume expansion, and insulin has a lesser role in management. Some patients exhibit a mixture of ketoacidosis and hyperosmolarity, which suggests that the two conditions may represent variants of decompensated hyperglycemia that differ only by the magnitude of dehydration and the severity of acidosis. All diabetic patients with hyperglycemic decompensation should return to their usual hypoglycemic programs as soon as possible and receive close follow-up after hospitalization.

Diabetic Ketoacidosis↗
PubMed1994

[Diabetes prevalence in a school population of Avellaneda, Argentina].

An interview system was used to survey 56,199 students in Avellaneda between the ages of 3 and 20 years, representing 60.6% of the population of that age group in the census. The study covered 178 of the 201 pre-schools, grade schools, high schools and special schools in the area. Thirty three diabetic children were identified (18 girls, 15 boys), with a mean of 12.5 years of age. This represents a prevalence of diabetes in the school age population of 0.45/1000 in the 3-12 year old group, 1.25/1000 in the 13-20 year old group, with 0.59/1000 for the total of children surveyed. (93.82 of ascertainement, 95% CI 0.34 to 0.42/1000). Similar figures have resulted from studies in developed countries. The most frequent initial symptoms were the typical ones, with only 15% showing acidosis or diabetic coma as the initiation of the illness. Viral infections and stress appeared to be related to the onset of the disease. Diabetes was in the family history of 48.5% of the diabetic children, and 24.5% of the non-diabetics. The most common diabetic relative was the paternal grandfather. The maternal side showed a higher number of diabetic relatives with preponderance of males. No socio-economic differences were found between diabetics and non-diabetics.

Adolescent↗
PubMed2005

Improved obstetric outcomes and few maternal toxicities are associated with antiretroviral therapy, including highly active antiretroviral therapy during pregnancy.

Data from 2543 HIV-infected women were analyzed to correlate antiretroviral therapy (ART) used during pregnancy with maternal and pregnancy outcomes. ART was analyzed according to class of agents used and according to monotherapy versus combination ART containing neither protease inhibitors (PIs) nor nonnucleoside reverse transcriptase inhibitors versus highly active ART. Timing of ART was classified according to early (recorded at or before 25-week gestation study visit) and late (recorded at 32-week gestation or delivery visit) use. Maternal outcomes assessed included hematologic, gastrointestinal, neurologic, renal, and dermatologic complications; gestational diabetes; lactic acidosis; and death. Adverse pregnancy outcomes assessed included hypertensive complications; pre-term labor or rupture of membranes; preterm delivery (PTD); low birth weight; and stillbirth. Logistic regression analyses controlling for multiple covariates revealed ART to be independently associated with few maternal complications: ART use was associated with anemia (odds ratio [OR] = 1.6, 95% confidence interval [CI]: 1.1-2.4), and late use of ART was associated with gestational diabetes (OR = 3.5, 95% CI: 1.2-10.1). Logistic regression analyses revealed an increase in PTD at <37 weeks for 10 women with late use of ART not containing zidovudine (ZDV; OR = 7.9, 95% CI: 1.4-44.6) and a decrease in adverse pregnancy outcomes as follows: late use of ART containing ZDV was associated with decreased risk for stillbirth and PTD at <37 weeks (OR = 0.06, 95% CI: 0.02-0.18; OR = 0.5, 95% CI: 0.3-0.8, respectively), and ART containing nucleoside reverse transcriptase inhibitors but not ZDV during early and late pregnancy was associated with decreased risk for PTD at <32 weeks (OR = 0.3, 95% CI: 0.2-0.7). Benefits of ART continue to outweigh observed risks.

Adult↗
PubMed1991

Persistent normal anion gap acidosis in the recovery phase of diabetic ketoacidosis.

Diabetic ketoacidosis is associated with an increased anion gap but its recovery phase may be complicated by hyperchloraemic acidosis with a normal anion gap. We report a case where this complication developed. There was a delayed return to normal acid-balance, possibly aggravated by administration of hyperchloraemic fluids, and the true diagnosis was overlooked. Measurement of the anion gap remains an important part of the assessment of diabetic acid-base disturbances.

Acid-Base Equilibrium↗
PubMed1959

The development of the acute inflammatory response to experimental cutaneous mucormycosis in normal and diabetic rabbits.

The histologic changes associated with the development of the acute inflammatory response to experimental cutaneous mucormycosis were studied at various times from 5 minutes to 24 hours after inoculation into normal rabbits and in rabbits with acute alloxan diabetes and acidosis. In normal animals the response by polymorphonuclear leukocytes began within a few minutes after inoculation, increased rapidly in extent and intensity and reached its peak within 6 to 12 hours. By that time there was also early proliferation of fibroblasts and of large mononuclear cells and these cellular reactions, together with the accumulated granulocytes, began to produce a demarcation of the lesions. Beginning 4 to 6 hours after inoculation the fungus showed some growth but this remained confined to the necrotic center of the lesions. In the diabetic rabbits the onset of the response by polymorphonuclear leukocytes was delayed by several hours, reduced in intensity and was apparently less effective. There was no proliferation of fibroblasts and the lesions were spreading rather than circumscribed. Fungus growth in the tissues began shortly after inoculation, was marked, progressed rapidly, and soon extended beyond the site of inoculation. The large mononuclear cells, however, appeared at about the same time and in equal number in the lesions of both diabetic and non-diabetic animals and showed no morphologic changes. It is concluded that a significant delay and impaired effectiveness of the response by polymorphonuclear leukocytes, a lack of fibroblastic proliferation and an enhanced growth of the fungus lower host resistance to infection with it and are directly consequent on severe alterations in host metabolism.

Animals↗
PubMed1998

[Urologic complications of pancreas-kidney simultaneous transplantation].

Pancreas Transplantation (PT) is the only available therapy today for diabetes that allows an insulin-independent euglycemic state with complete normalization of glycosilated haemoglobin levels. Survival of patient, pancreatic graft and renal graft is 93%, 86% and 90% respectively at one year and 90%, 84% and 85% at three years. The most accepted method for exocrine drainage in most centres where simultaneous pancreas-kidney transplantation is being performed is vesical drainage. In spite of the improvements achieved in graft and patient survival, it is evident that a most frequent use of this type of technique involves a greater number of urological complications (repeat infections, haematuria, fistulae or leakage, reflux pancreatitis, urethral stenosis and disruption, dehydration and acidosis, previous diabetic bladder) and the familiarization of the urologist with this type of disease in immunodepressed patients. This paper reviews the current situation and illustrates the general approach regimes in our Pancreas-Kidney Transplantation Unit with regard to each complication.

Hematuria↗
PubMed1981

Phenytoin-induced hyperglycemia.

A case of diabetic ketoacidosis in a 64-year-old black woman with maturity-onset diabetes receiving phenytoin for a seizure disorder is reported. The woman was admitted to the hospital with a one-day history of polyuria and polydipsia. For the 10 months before admission, her diabetes was controlled with isophane insulin suspension 27 units daily. She also took phenytoin 100 mg orally three times a day. This was prescribed approximately six weeks earlier for right-sided focal seizures that were detected by electroencephalogram during a previous hospitalization for nonketotic hyperosmolar coma. No other medications were taken. The patient was treated with i.v. fluids and intermittent doses of i.v. insulin. Her condition rapidly improved and insulin zinc suspension 35 units daily was prescribed on discharge. Phenytoin was discontinued because the seizure disorder was considered secondary to the previous episode of hyperosmolar coma. A literature review of phenytoin-induced hyperglycemia is presented, including previous case reports, possible mechanisms of action, monitoring guidelines, and potential therapeutic uses. If hyperglycemia occurs in a patient taking phenytoin, especially after starting phenytoin therapy or increasing the dose, drug-induced hyperglycemia should be considered in the differential diagnosis.

Acidosis↗
PubMed1982

The role of catecholamines in metabolic acidosis.

Catecholamines (noradrenaline and adrenaline) are catabolic hormones secreted during stress. They initiate many metabolic processes including increased production of both ketoacids and lactic acid. Support for a direct participation of these hormones in the development and/or maintenance of ketoacidosis includes: (1) the high incidence of stress (approx. 70%) as a precipitating factor for ketoacidosis; (2) the elevated plasma levels of noradrenaline (norepinephrine) in patients with ketoacidosis; (3) the rise in plasma concentrations of ketone bodies during catecholamine infusion; and (4) the reduction in the incidence of ketoacidosis with beta-adrenergic pharmacological blockade. Support for a direct participation of catecholamines in the development and/or maintenance of lactic acidosis includes: (1) the common association of stress and lactic acidosis; (2) the rise in plasma lactate concentration during adrenaline (epinephrine) infusion; (3) the precipitation of lactic acidosis by adrenaline intoxication and phaeochromocytoma; and (4) the vasoconstrictor effects of catecholamines leading to tissue anoxia and lactic acid production. Thus, in susceptible patients, catecholamines may be principal determinants of whether ketoacidosis and/or lactic acidosis develops.

Acidosis↗
PubMed2000

[Mitochondrial medicine for internists].

Human mitochondrial DNA (mtDNA) is a small, circular molecule, encoding for the translational machinery of the mitochondrion, as well as for 13 structural proteins that are all subunits of the respiratory chain. Point mutations, deletions, and copy-number variations are now functionally and genetically linked to human disease. Despite the fact that mtDNA is solely transmitted from the mother to the offspring, e.g. is maternally inherited, some mutations may occur spontaneously or may be acquired due to defects in nuclear DNA, e.g. are inherited in a mendelian fashion. The internist encounters predominantly myopathies, cardiomyopathies, lactic acidosis or diabetes mellitus but mtDNA-changes are also present with neurologic, hematologic and renal symptoms. Acquired mtDNA alterations are responsible for important drug side effects, such as ifosfamide, carboplatin, doxorubicin or nucleoside-analog reverse-transcriptase inhibitors. A specific mtDNA point-mutation predisposes to aminoglycoside-induced sensorineural deafness.

DNA Mutational Analysis↗
PubMed2006

Role of kidney chloride channels in health and disease.

Chloride channels are expressed along the entire mammalian nephron. They participate in transepithelial chloride transport, cell volume regulation and acidification of intracellular vesicles. Some chloride channels are constitutively active and others are regulated by either second messengers such as cAMP or Ca(++) or secondary to changes in membrane potential. The molecular identities of a number of chloride channels within the kidney are still unknown. Abnormalities in chloride channel expression and function in the kidney can cause a range of disorders such as autosomal recessive Dent's disease, Bartter's syndrome, renal tubular acidosis and diabetes insipidus. The purpose of this review is to give an overview of the chloride channels in the kidney and to focus on the function of renal chloride channels as revealed by diseases associated with channel dysfunction.

Animals↗
PubMed1986

Amyloidosis in subcutaneous heroin abusers ("skin poppers' amyloidosis").

Systemic amyloidosis has recently emerged as a major cause of nephropathy among heroin abusers in New York City. Although focal glomerulosclerosis is typically seen in intravenous drug abusers who present with the nephrotic syndrome, those who escape this complication are at risk for the later development of amyloidosis related to their use of the subcutaneous route. Twenty such addicts identified between 1981 and 1984 are described. Patients typically present with chronic suppurative skin infections, edema, the nephrotic syndrome, benign urinary sediment, and normal-sized or enlarged kidneys. Tubular dysfunction, particularly renal tubular acidosis and diabetes insipidus, is frequent. Progression of renal insufficiency is characteristically rapid. Prolonged survival of heroin abusers and exhaustion of intravenous access requiring recourse to the subcutaneous route underlie the occurrence of amyloidosis in the addict population. Chronic suppurative skin infection consequent to repeated subcutaneous injection appears to be the underlying cause.

Adult↗