A surprising cause of paresis following scoliosis correction.
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Paralysis following scoliosis correction is a catastrophic situation. We report an unusual metabolic cause of neurological deficit after anterior thoracic release. A 15-year-old female developed proximal leg paralysis 1 day after surgery. Investigations disclosed severe serum hypokalaemia (2.8 mmol/l). After intravenous potassium substitution the neurological status completely normalized within a few hours. We assume that the condition was a manifestation of hypokalaemic paralysis since no further abnormalities could be disclosed. Spinal surgeons should bear in mind hypokalaemia as a benign and easily correctable cause of paresis following surgical scoliosis correction. (+info)
Refeeding syndrome.
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CASE REPORT: An elderly woman with poor nutritional intake developed profound hypophosphataemia and hypokalaemia following the institution of nasogastric feeding. DISCUSSION: Refeeding syndrome is well recognized in certain undernourished groups of patients, but may not be so well known to physicians looking after elderly patients, whose nutritional status may be more deficient than is originally apparent. (+info)
Hypertension-related intermyocyte junction remodelling is associated with a higher incidence of low-K(+)-induced lethal arrhythmias in isolated rat heart.
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The aim of this study was to characterise the arrhythmogenic mechanisms involved in hypokalaemia-induced sustained ventricular fibrillation (SVF), in hypertensive rats. The hearts from rats with hypertension induced by the nitric oxide synthase inhibitor L-NAME, and age-matched normotensive controls, were perfused in Langendorff mode with oxygenated Krebs-Henseleit solution followed by a K(+)-deficient solution. In additional experiments, free intracellular Ca(2+) concentration ([Ca(2+)](i)) was measured using fura-2 in conjunction with an epicardial optical probe. The epicardial electrocardiogram was continuously monitored during all experiments. The gap junction protein connexin-43 and the ultrastructure of the cardiomyocytes were examined, and selected enzyme activities were measured in situ. There was a higher incidence of low-K(+)-induced SVF in the hearts of hypertensive compared to normotensive rats (83 % vs. 33 %, P < 0.05). Perfusion with a low-K(+)-containing solution lead to elevation of diastolic [Ca(2+)](i) that was accompanied by premature beats, bigeminy, ventricular tachycardia and transient ventricular fibrillation. These events occurred earlier with increased incidence and duration in the hearts of hypertensive rats (arrhythmia scores: hypertensive, 4.9 +/- 0.7; normotensive, 3.1 +/- 0.1; P < 0.05), which exhibited apparent remodelling accompanied by a significant decrease in the density of connexin-43-positive gap junctions. Moreover, low-K(+)-related myocardial changes, including local impairment of intermyocyte junctions, ultrastructural alterations due to Ca(2+) overload and intercellular uncoupling, and decreased enzyme activities were more pronounced and more dispersed in hypertensive than normotensive rats. In conclusion, nitric oxide-deficient hypertension is associated with decreased myocardial coupling at gap junctions. The further localised deterioration of junctional coupling, due to low-K(+)-induced Ca(2+) disturbances, as well as spatial heterogeneity of myocardial alterations including interstitial fibrosis, probably provide the mechanisms for re-entry and sustaining ventricular fibrillation. (+info)
Inhibition of 11beta-hydroxysteroid dehydrogenase in guinea pig kidney by three bioflavonoids and their interactions with gossypol.
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AIM: To study the effects of some bioflavonoids on the gossypol-induced hypokalemia. METHODS: The 11beta-hydroxysteroid dehydrogenase (11beta-OHSD) protein was prepared from guinea pig kidney. The activity of 11beta-OHSD with NAD as the coenzyme was measured by HPLC. The drug interaction was analysed by isobolographic method. RESULTS: The 11beta-OHSD can be inhibited by some bioflavonoids. The IC50 (95 % confidence limits) values were: quercetin 164 (79 - 341) micromol/L, morin 913 (385 - 2173) micromol/L, and naringenin 2193 (1114 - 4315) micromol/L. When the 11beta-OHSD was treated with quercetin, tangeretin, morin, naringenin plus gossypol, the combination index (CI) values were 0.92, 0.85, 0.98, and 1.01 respectively. CONCLUSION: The interaction of some bioflavonoids with gossypol might be one of the factors for gossypol-induced hypokalemia. (+info)
Hyponatremic-hypertensive syndrome associated with renovascular hypertension: a case report.
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Renovascular hypertension occasionally manifests clinically as electrolyte disorders and albuminuria in addition to elevated blood pressure. A 49-year-old man who had renovascular hypertension also had severe hypokalemia, hyponatremia, polyuria and polydipsia that were treated by an angiotensin-converting enzyme inhibitor and resection of an atrophic kidney with a compromised blood supply. This is a case of hyponatremic-hypertensive syndrome related to renovascular hypertension and occurring as an additional abnormality. (+info)
Hypercalcaemia and metabolic alkalosis with betel nut chewing: emphasis on its integrative pathophysiology.
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BACKGROUND: Events in the gastrointestinal tract that might contribute to a high absorption of calcium were simulated in vitro to evaluate why only a small proportion of individuals who ingest alkaline calcium salts develop hypercalcaemia, hypokalaemia and metabolic alkalosis. METHODS: A patient who chewed and swallowed around 40 betel nuts daily developed hypercalcaemia, metabolic alkalosis, hypokalaemia with renal potassium wasting, and renal insufficiency. The quantities of calcium and alkali per betel nut preparation were measured. Factors that might increase intestinal absorption of calcium were evaluated. RESULTS: Hypercalcaemia in the index case was accompanied by a high daily calcium excretion (248 mg, 6.2 mmol). Circulating levels of 1,25-dihydroxyvitamin D(3) and parathyroid hormone were low. Hypokalaemia with a high transtubular K(+) concentration gradient, metabolic alkalosis, a low excretion of phosphate and a very low glomerular filtration rate were prominent features. CONCLUSIONS: Possible explanations for the pathophysiology of metabolic alkalosis and hypokalaemia are provided. We speculate that a relatively greater availability of ionized calcium than inorganic phosphate in the lumen of the intestinal tract could have enhanced dietary calcium absorption. (+info)
Preclinical Cushing's syndrome due to ACTH-independent bilateral macronodular adrenocortical hyperplasia with excessive secretion of 18-hydroxydeoxycorticosterone and corticosterone.
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A 64-year-old woman developed hypertension and hypokalemia, due to ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH) with excessive secretion of 18-hydroxydeoxycorticosterone and corticosterone. Plasma cortisol did not show a diurnal rhythm, and was not suppressed by dexamethasone (8 mg). Plasma cortisol responded to ACTH and was increased by hypoglycemia without modifying ACTH levels. Radiological studies demonstrated that adrenal glands were enlarged with macronodules. Although the patient exhibited a low plasma renin activity and aldosterone levels, hypokalemia and hypertension were observed. Hormonal findings would support the hypothesis that the tumor of AIMAH originated from cells of the upper zona fasciculata. (+info)
Secretory-defect distal renal tubular acidosis is associated with transporter defect in H(+)-ATPase and anion exchanger-1.
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Recent progress in molecular physiology has permitted us to understand pathophysiology of various channelopathies at a molecular level. The secretion of H(+) from alpha-intercalated cells is mediated by apical plasma membrane H(+)-ATPase and basolateral plasma membrane anion exchanger-1 (AE1). Studies have demonstrated the lack of H(+)-ATPase immunostaining in the intercalated cells in a few patients with distal renal tubular acidosis (dRTA). Mutations in H(+)-ATPase and AE1 gene have recently been reported to cause dRTA. This study extends the investigation of the role of transporter defect in dRTA by using immunohistochemical methods. Eleven patients with hyperchloremic metabolic acidosis were diagnosed functionally to have secretory-defect dRTA: urine pH >5.5 during acidemia, normokalemia or hypokalemia, and urine-to-blood pCO(2) <25 mmHg during bicarbonaturia. Renal biopsy tissue was obtained from each patient, and immunohistochemistry was carried out using antibodies to H(+)-ATPase and AE1. For comparison, renal tissues from the patients who had no evidences of distal acidification defect by functional studies were used: four with glomerulopathy or tubulointerstitial nephritis (disease controls) and three from nephrectomized kidneys for renal cell carcinoma (normal controls). The H(+)-ATPase immunoreactivity in alpha-intercalated cells was almost absent in all of the 11 patients with secretory-defect dRTA. In addition, 7 of 11 patients with secretory-defect dRTA were accompanied by negative AE1 immunoreactivity. In both disease controls and normal controls, the immunoreactivity of H(+)-ATPase and AE1 was strong in alpha-intercalated cells. In conclusion, significant defect in acid-base transporters is the major cause of secretory-defect dRTA. (+info)