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Urinary excretion of sodium, calcium, and magnesium has been measured after single oral doses of hydrochlorothiazide (100 mg) and acetazolamide (500 mg) in unselected patients with calcareous renal stone formation and in normal control subjects. With hydrochlorothiazide, 36 stone formers had significantly greater increments in sodium (P less than 0.01), calcium (P less than 0.05), and magnesium (P less than 0.05) excretion than 20 normal subjects. With acetazolamide, 13 stone formers had a smaller increment in sodium excretion (P less than 0.05) than 10 normal subjects. The abnormal responses to both diuretics were most marked in the patients with hypercalciuria during fasting. These data suggest that the tubular handling of sodium, magnesium, and calcium may be abnormal in patients with calcareous renal stones and are consistent with the presence of a defect in proximal-tubular reabsorption of fluid and electrolytes that may be partly offset by increased reabsorption in the distal nephron.
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We reviewed cerebral blood flow (CBF)-related data obtained by xenon CT imaging (XeCT) in six patients with ischemic-type or asymptomatic moyamoya disease. The data were obtained as volume data using a 320-row CT, and applied to the automated region-of-interest-determining software (3DSRT) and converted to standardized images. Eight CBF-related parameters, including CBF value, cerebrovascular reserve capacity (CVRC), and hemodynamic distribution (hdSD), were compared between asymptomatic hemispheres and ischemic symptomatic hemispheres. A significant difference was determined by a two-sample t test. A difference with p<0.05 was considered significant. When statistically significant differences between parameters of asymptomatic hemispheres and ischemic symptomatic hemispheres were identified, cut-off points were calculated with receiver operating characteristic (ROC) curves. Change in the parameters before and after bypass surgery was also assessed.
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Drug-related blood dyscrasias as reported in Sweden during a 10-yr period have been analysed in relation to sales and prescription data. The number of cases reported were as follows: agranulocytosis 390, thrombocytopenia 391, pancytopenia 50 and aplastic anaemia 36. The annual incidence rates per 10(6) inhabitants were: agranulocytosis 4.8, thrombocytopenia 5.6, pancytopenia 1.1 and aplastic anaemia 0.5. Incidences in the elderly were higher for all dyscrasias except aplastic anaemia. The most commonly reported drugs for all dyscrasias were sulphonamides and diuretics, but when related to sales data the risk of agranulocytosis was high for clozapine, dapsone, mianserin and sulphasalazine, while the risk did not seem to be increased for furosemide. For thrombocytopenia, furosemide, co-trimoxazole and the measles, mumps and rubella vaccine were most commonly reported. The risk for pancytopenia and aplastic anaemia was increased for acetazolamide and co-trimoxazole. As spontaneous reporting systems are primarily set up for signalling purposes, such data must always be interpreted with utmost care.
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Exogenous prostaglandins have specific protective effects on the gastric mucosa called cytoprotection which is proposed to be connected to the stimulatory effects of prostaglandins on the gastric nonparietal secretions. The protection by oral prostaglandin E2 (PGE2) against indomethacin-induced gastric erosions was studied in the rat, as was the effect on the protection of blocking the gastric alkaline secretion by acetazolamide. PGE2 reduced dose-dependently the indomethacin gastric erosion formation, confirming previous results from others. Acetazolamide caused very little damage when given alone but potentiated the indomethacin erosion formation in a dose-related way. PGE2 was less protective or without effect against lesions caused by indomethacin when given together with acetazolamide, but protection could be obtained by increasing the doses of PGE2. Indomethacin and acetazolamide are both blockers of the gastric bicarbonate secretion, which is stimulated by PGE2. The potentiation of indomethacin induced lesions by acetazolamide and the antagonistic actions between acetazolamide and PGE2 on mucosal protection are compatible with the hypothesis that stimulation of the alkaline secretion is one mechanism of cytoprotection of the gastric mucosa by PGE2.
ACZ-enhanced SPECT scans, by assessing cerebral perfusion and vascular reactivity, may help to identify patients at risk of stroke should perfusion further diminish. Postoperative studies confirm improvement in vascular reactivity. ACZ-enhanced SPECT scans may provide objective evidence for the selection of patients with a high-grade asymptomatic carotid stenosis for CEA.
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The Na-K-2Cl inhibitor bumetanide was highly effective in preventing attacks of weakness in the NaV1.4-R669H mouse model of HypoPP and should be considered for management of patients with HypoPP due to sodium channel mutations. Dehydration may aggravate HypoPP by stimulating the Na-K-2Cl transporter.
Acetazolamide, a carbonic anhydrase inhibitor, prevents acute gastric hemorrhagic lesions induced by ethanol. We used acetazolamide and other carbonic anhydrase inhibitors to correlate their gastroprotective effects with the degree of inhibition of carbonic anhydrase. Since acetazolamide is a thiadiazole, we also investigated structurally related thiadiazoles that contain sulfhydryls to test the hypothesis that the protection against ethanol-induced gastric erosions is related to the presence of sulfhydryls. Dose-response studies with acetazolamide revealed that the protection did not correlate with the inhibition of carbonic anhydrase in the rat gastric mucosa. The carbonic anhydrase inhibitors sulfanilamide and ethoxzolamide, did not offer protection. Bismuthiol I, a thiadiazole with two sulfhydryls, was twice as protective as 2-amino-5-mercapto-1,3,4-thiadiazole with only one sulfhydryl group. We conclude that the protection by acetazolamide against ethanol-induced lesions is not related to the inhibition of carbonic anhydrase in the gastric mucosa. The gastroprotective effect of acetazolamide and its derivatives may be related to their content of sulfhydryls in an oxidized or reduced state.
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Subjects referred to the glaucoma clinic that had a documented IOP of over 28 mm Hg, on no treatment, in one or both eyes were included. Tonometry, pachymetry, and scanning laser ophthalmoscopy were performed before and after lowering IOP with topical apraclonidine and oral acetazolamide. The significance of change in outcome variables was assessed using a paired t test allowing for dependence within subjects and, for sensitivity, with a nonparametric Wilcoxon signed-rank test.
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The authors studied the intraocular pressure (IOP) changes after phacoemulsification with two different kinds of foldable silicone lens implantation using Healon GV as viscoelastic substance. One hundred patients undergoing cataract surgery were enrolled in this study. Inclusion criteria were: absence of ocular hypertension or glaucoma. Patients were randomly assigned to plate haptic (Silens PH, Domilens Chiron Vision, Lyon, France) or three-piece (CeeOntrade mark& ;920, Pharmacia spa, Milano, Italia) silicone intraocular lens (IOL) implantation. Following phacoemulsification and cortical aspiration, the capsular bag was reinflated with Healon GV. After foldable silicone IOL insertion residual Healon GV was removed from the anterior chamber. IOP was measured preoperatively and at 6, 24 h and 1 week postoperatively. Six hours postoperatively IOP was higher in the Silens PH group than in the CeeOn group (20. 85+/-5.42 vs. 18.88+/-2.95 mm Hg, p= 0.026). The difference was confirmed after 24 h (21.02+/-5.18 vs. 17.34+/-3.18 mm Hg, p < 0.01). Despite the medical treatment (acetazolamide 250 mg orally every 6 h), at the 24-hour control 2 eyes with plate haptic silicone lens showed IOP values higher than 30 mm Hg. Slitlamp examination showed in both eyes a shallowing of the anterior chamber together with the evidence of capsular bag hyperdistension and capsular block resulting from the occlusion of the circular anterior capsule opening by the plate haptic IOL. Residual Healon GV removal from the anterior chamber was performed. At 1-week control both eyes showed normalization of IOP. The use of a plate haptic silicone lens may be associated with a more consistent retention of Healon GV in the eye with trapping in the capsular bag. Retained viscoelastic may cause either trabecular meshwork blockage by viscoelastic substance or postoperative capsular bag hyperdistension, anteroplacement of the IOL optic and capsular block from occlusion of the circular anterior opening by the IOL optic.
Patients were randomly assigned to 2 groups: group 1 (n=10) received 250mg of acetazolamide and 50mg of hydrochlorothiazide daily and group 2 (n=10) received 40mg of furosemide and 50mg of hydrochlorothiazide daily for 1 week in phase 1. In phase 2, both groups received 40mg of furosemide daily for 2 weeks.