Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and eight patients with gastric ulcer subjected to planned and urgent surgery have been treated for postoperative gastric atonia and intestinal paresis using electroacupuncture stimulation (EAPS). The treatment was effective in 85% of cases, with the efficacy confirmed by clinical results and gastroenterologic findings. EAPS promoted a decrease in the initially high blood levels of cortisol, aldosterone and histamine, an increase in serotonin and a reduction in gastric juice histamine levels, which were indicative of the analgetic and antihistamine EAPS effect and attenuation of parasympathetic activity. EAPS introduction into a complex of postoperative rehabilitation procedures led to reduction of drug doses or total drug replacement, early activation of surgical patients and prompt recovery of normal gastrointestinal evacuation.
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PMID:[Electroacupuncture stimulation in the treatment of postoperative disorders of the motor-evacuatory function of the stomach and intestines]. 141 12

A 16-year-old woman was admitted to our hospital because of abdominal pain, paresis of extremities, and muscle weakness. Bartter's syndrome was suspected because of the features of the hypokalemia, hyperaldosteronism, hyperreninemia, increased concentration of plasma angiotensin I & II, the defect in distal fractional reabsorption of chloride and normotension. The concentrations of the plasma angiotensin II and aldosterone, however, were decreased to normal levels after admission probably due to a decrease in the salt intake because of the regular hospital diet. Furthermore, the hyperplasia of the juxtaglomerular apparatus was not found. Therefore, at first we thought we were dealing with another disease, that is pseudo-Bartter's syndrome, which is caused by different pathogenesis. Gill et al. reported that the defect in distal fractional reabsorption of chloride was a characteristic feature in the diagnosis of the Bartter's syndrome. Thus, we tried to explain the clinical symptoms and diagnosis of this case as the Bartter's syndrome according to the theory of Gill et al. If the defect of chloride reabsorption was the only pathogenesis of the Bartter's syndrome, other symptoms seen in our case could be thought of as secondary (or new) changes. Therefore, this case could be differentiated from the pseudo-Bartter's syndrome or the "true" Bartter's syndrome because of the clinical symptoms and the defect in chloride reabsorption.
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PMID:[A case of Bartter-like syndrome with abdominal pain, paresis of the extremities and muscle weakness]. 343 14

In recent years, there has been renewed interest in primary hyperaldosteronism, particularly because of its possible role in the progression of kidney disease. While most studies have concerned humans and experimental animal models, we here report on the occurrence of a spontaneous form of (non-tumorous) primary hyperaldosteronism in cats. At presentation, the main physical features of 11 elderly cats were hypokalemic paroxysmal flaccid paresis and loss of vision due to retinal detachment with hemorrhages. Primary hyperaldosteronism was diagnosed on the basis of plasma concentrations of aldosterone (PAC) and plasma renin activity (PRA), and the calculation of the PAC:PRA ratio. In all animals, PACs were at the upper end or higher than the reference range. The PRAs were at the lower end of the reference range, and the PAC:PRA ratios exceeded the reference range. Diagnostic imaging by ultrasonography and computed tomography revealed no or only very minor changes in the adrenals compatible with nodular hyperplasia. Adrenal gland histopathology revealed extensive micronodular hyperplasia extending from zona glomerulosa into the zona fasciculata and reticularis. In three cats, plasma urea and creatinine concentrations were normal when hyperaldosteronism was diagnosed but thereafter increased to above the upper limit of the respective reference range. In the other eight cats, urea and creatinine concentrations were raised at first examination and gradually further increased. Even in end-stage renal insufficiency, there was a tendency to hypophosphatemia rather than to hyperphosphatemia. The histopathological changes in the kidneys mimicked those of humans with hyperaldosteronism: hyaline arteriolar sclerosis, glomerular sclerosis, tubular atrophy and interstitial fibrosis. The non-tumorous form of primary hyperaldosteronism in cats has many similarities with "idiopathic" primary hyperaldosteronism in humans. The condition is associated with progressive renal disease, which may in part be due to the often incompletely suppressed plasma renin activity.
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PMID:Primary hyperaldosteronism, a mediator of progressive renal disease in cats. 1562 Aug 9

Generalised paresis, severe hypokalaemia and kaliuresis, metabolic alkalosis and hypertension, characteristic of mineralocorticoid excess, were identified in a dog with hyperadrenocorticism due to a functional adrenocortical carcinoma. Aldosterone concentration was decreased and deoxycorticosterone concentration increased in the presence of hypokalaemia. These metabolic abnormalities resolved with resection of the carcinoma. Mineralocorticoid excess in dogs with hyperadrenocorticism is generally considered to be of little clinical significance but resulted in the acute presentation of this patient. The possible pathogenesis of mineralocorticoid excess in this case of canine hyperadrenocorticism is discussed.
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PMID:Hypokalaemic paresis, hypertension, alkalosis and adrenal-dependent hyperadrenocorticism in a dog. 1836 88

Adrenocortical carcinoma (ACC) co-secreting aldosterone and cortisol is extremely rare. We report the case of a 37-yearold female who presented with paresis and facial puffiness. Evaluation revealed hypertension, hyperglycemia, severe hypokalemia and hyperaldosteronemia with elevated plasma aldosterone to renin ratio (ARR). Urinary free cortisol estimation showed elevated levels. Computed tomography scan revealed a right adrenal mass. Radical adrenalectomy specimen revealed ACC (T3N1). Post-operatively, the patient became normotensive and euglycemic with normalization of urinary cortisol and ARR. This case highlights the need for a complete evaluation in patients of hyperaldosteronism if overlapping symptoms of hypercortisolism are encountered, to avoid post-operative adrenal crisis.
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PMID:Aldosterone and cortisol co-secreting bifunctional adrenal cortical carcinoma: A rare event. 2509 23