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Glucocorticoid regulation of muscle branched-chain amino acid metabolism.

Branched-chain alpha-keto acid dehydrogenase (BCKAD) is a multisubunit complex regulated by phosphorylation and is considered to be rate-limiting for branched-chain amino acid (BCAA) metabolism in skeletal muscle. Glucocorticoids increase net protein degradation in muscle; associated with this increased breakdown of muscle protein is an elevated rate of BCAA oxidation. The effects of glucocorticoids on skeletal muscle BCKAD were investigated in different rat models. BCKAD was activated after glucocorticoid treatment (both acutely, within 2 h, and chronically). The amount of enzyme per muscle cell increased after 5 d of cortisone acetate treatment. Insulin administration partially blocked the acute effects of glucocorticoids on muscle BCKAD. Activation was also observed during metabolic acidosis, insulinopenic diabetes mellitus, and endotoxic shock, three conditions characterized by elevated circulating glucocorticoids, increased BCAA oxidation, and increased net protein breakdown. Activation of BCKAD may account for the increased oxidation of BCAA observed during hypercortisolemia. The sequelae of this accelerated catabolism may include increased glutamine and alanine production for gluconeogenesis and provision of ATP for muscle work.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

Hyperkalemia as a complication of drug therapy.

A wide array of drugs in common use can produce hyperkalemia. We reviewed our experience with severe hyperkalemia (potassium levels greater than 5.9 mEq/L [greater than 5.9 mmol/L]) in adult inpatients during a one-year period, to evaluate the extent to which drugs could be implicated in this electrolyte disorder. Excluding hemolyzed samples, single unexplained values, and measurements obtained during cardiopulmonary bypass or resuscitation, drug therapy was a probable contributing factor in more than 60% of the hyperkalemic episodes; in 25%, drugs were temporally linked to the onset of the hyperkalemia. In declining order of frequency, the drugs associated with hyperkalemia were potassium chloride, captopril, nonsteroidal anti-inflammatory agents, and potassium-sparing diuretics. In more than 80% of the drug-related hyperkalemic episodes, potassium regulation was compromised by underlying disease states. The most common was renal insufficiency, followed by diabetes mellitus and metabolic acidosis. This review underscores the dictum that caution should be exercised when drugs with hyperkalemic potential are used in patients with impaired potassium homeostasis.

Acidosis↗

[Panorama of mycoses in otorhinolaryngology].

Three classes of important mycoses in O.R.L. field can be recognized according to the responsible fungi and to thier physiopathology: 1) mycoses due to cosmopolite, opportunistic fungi, yeast-like fungi (Candida albicans, Cryptococcus neoformans, Torulopsis glabrata) or filamentous fungi (Aspergillaceae, Mucoraceae, Penicillia, etc...) invading a compromised host by antibiotics, immunosuppressors, radiotherapy or by severe diseases (hemopathia, diabetes with acidosis). The oropharyngolaryngeal candidosis, the black tongue (a polyfungal syndrome), the sinusal aspergillosis, the otomycoses, the nasalorbital cerebral form of mucormycosis are reviewed and the allergic accompanying symptoms described. 2) deep, systemic mycoses of tropical origin with respiratory entry and oral pharyngeal laryngeal metastatic localizations (histoplasmosis, blastomycosis, paracoccidioidomycosis, coccidioimycosis); the histoplasmosis represent actually the principal imported systemic mycosis with O.R.L. localization. 3) tropical and african mycosis localized exclusively in O.R.L. area (rhino-enthomophtoromycosis and rhinosporidosis).

Diagnosis, Differential↗

Poisoning with N-3-pyridylmethyl-N'-p-nitrophenylurea (Vacor). Immunoperoxidase demonstration of beta-cell destruction.

A 49-year-old woman ate N-3-pyridylmethyl-N'-p'nitrophenylurea (PNU; Vacor) and was admitted to the hospital 12 hours later with a blood glucose level of 940 mg/dl and an anion-gap metabolic acidosis. Her diabetes was successfully treated, but she contained to manifest severe orthostatic hypotension. A painless ileus developed, followed by cecal perforation and death. Immunoperoxidase staining of paraffin-embedded pancreatic tissue obtained during postmortem examination clearly demonstrated the pancreatic beta-cell destruction. Results of this same staining technique also suggested that fewer alpha cells were present.

Brain↗

[Tubulointerstitial nephritis in chronic viral diseases of the liver].

The paper reports 4 cases of tubulointerstitial nephritis (TIN) in chronic diffuse diseases of the liver (CDDL). The latter comprised such conditions of virus etiology as chronic active hepatitis, chronic lobular hepatitis. TIN presented with pronounced renal tubular affections: defects of concentration capacity, distal renal tubular acidosis, renal diabetes insipidus. In 3 cases renal lesions occurred 1 and 6 years prior to CDDL detection. TIN pathogenesis in CDDL of viral etiology is discussed.

Adolescent↗