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Results for “Methazolamide”

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At least 19 recordsLinked to original sources

PubMed1994

Effect of methazolamide on chronic macular edema in patients with retinitis pigmentosa.

PURPOSE: To determine the effectiveness of methazolamide for improving visual acuity and macular edema in patients with retinitis pigmentosa. METHODS: Seventeen subjects with retinitis pigmentosa and chronic macular edema participated in a prospective, placebo-controlled, double-masked, crossover design study in which either methazolamide or a placebo was taken for 3 weeks. Visual acuity, fluorescein angiograms, and subjective impressions were obtained at baseline and after 3 weeks of treatment with each substance. A subgroup of subjects were enrolled in a more extended period of methazolamide treatment for an additional 3 months. RESULTS: Methazolamide resulted in the improvement of angiographic macular edema in 9 of 17 subjects. As a group, visual acuity statistically improved with methazolamide. However, improvement in at least one eye, of between two and four lines more than while taking placebo, occurred in only three (undilated pupils) or four (dilated pupils) subjects. Subjective improvement during treatment with methazolamide but not placebo occurred in only one subject. An extended period of methazolamide treatment for an additional 3 months in a subgroup of patients did not result in additional beneficial effects on visual acuity. In fact, a partial rebound in the extent of macular edema was found. CONCLUSIONS: Although angiographic improvement of macular edema can occur in patients with retinitis pigmentosa treated with methazolamide, notable (between 3 and 4 lines) or even moderate (between 2 and 3 lines) visual acuity improvement was seen in relatively few patients. When methazolamide was administered in a placebo-controlled fashion, subjective improvement in visual function also was not readily apparent. A more substantial subjective improvement in visual function had occurred with the use of acetazolamide in five of six subjects who also had participated in a previous treatment trial with the use of acetazolamide.

Adolescent↗

PubMed1987

Ocular pharmacology of methazolamide analogs: distribution in the eye and effects on pressure after topical application.

The authors studied the relation between physicochemical properties and lowering of intraocular pressure (IOP) after topical application to rabbit in a series of 5-acylimino- and related imino-substituted analogs of methazolamide (Compound 4). All had Ki vs. carbonic anhydrase C of about 10(-8) M. The parent, methazolamide (5-acetyl) does not lower IOP, in contrast to the 5-CF3 acetyl compound (Compound 28). The 5-propionyl compound (6) unexpectedly was 3 times more water soluble than methazolamide and had 10 times greater CHCl3-buffer partition. The in vivo transcorneal permeability constant was 6 times greater than methazolamide. One hour after 1 drop of a 2% suspension of Compound 6, anterior aqueous concentration (in micromolar) was 69 (for methazolamide, 8), posterior aqueous was 19 and ciliary process was 17. IOP dropped 2.2 mm Hg and returned to normal in 4 hr. Other compounds in the series showed varying degrees of activity, ranging from Compound 28, which elicited an IOP fall of 3.5 mm Hg, to Compound 7, (n-pentyryl), for which the fall was 1.3 mm Hg. Also studied are substitutions for CH3 on the ring N at position 4. There are multiple criteria for in vivo activity; a major factor is the balance between water and lipid solubility. The methazolamide analogs are compared with benzothiazole-2-sulfonamides, another class under investigation as topical carbonic anhydrase inhibitors designed to treat glaucoma.

Administration, Topical↗

PubMed1978

A repeated dose-response study of methazolamide in glaucoma.

Twenty-two patients with open-angle glaucoma were given weekly courses of methazolamide at different dosages. Mean intraocular pressure reductions of 3.3, 4.3, and 5.6 mm Hg were achieved at dosages of 25 mg, 50 mg, and 100 mg of methazolamide every eight hours, respectively. Maximal intraocular pressure lowering was still present nine to ten hours after administration. The mean reduction in outflow pressure for all eyes receiving a daily dosage of 300 mg was only 31%, but this included eyes (17% of the total) that demonstrated less than 13% reduction in outflow pressure, despite similar methazolamide serum levels. Eight patients subsequently received acetazolamide, 250 mg four times a day for a week. The effect of this dosage of acetazolamide on pressure was between the effects of 50 and 100 mg of methazolamide three times daily.

Aged↗

PubMed1993

Rebound of macular edema with continued use of methazolamide in patients with retinitis pigmentosa.

PURPOSE: To assess the effect of methazolamide on chronic macular edema in patients with retinitis pigmentosa in a double-masked, placebo-controlled, crossover study. Three subjects who had an initial improvement in their macular edema as demonstrated on fluorescein angiography received a continued course of methazolamide to assess its effect on macular edema. METHODS: Seventeen subjects were enrolled in the initial study. On angiography, nine subjects demonstrated improvement in their macular edema with the use of methazolamide for 3 weeks; three of these continued receiving the drug at a dosage of 50 mg twice daily for either an additional 6 (one subject) or 12 (two subjects) weeks. All subjects were assessed at each visit with fluorescein angiography and on best corrected visual acuity, both undilated and dilated; a subjective impression was also documented. RESULTS: After 6 and 12 weeks of treatment, all three subjects experienced a rebound of angiographic macular edema to some extent. The visual acuity varied only slightly (up to 7 letters) from both the baseline and most recent examinations after 6 and 12 weeks of treatment. CONCLUSION: Results from these few subjects suggest that at least a partial rebound of macular edema seen angiographically may occur with the continued use of methazolamide in patients with retinitis pigmentosa and chronic macular edema. Further study is required to determine if this rebound effect also occurs in treatment of other ocular disorders with chronic macular edema.

Adult↗

PubMed1991

Treatment of essential tremor with methazolamide.

We treated 28 patients (16 women and 12 men) who had essential tremor with methazolamide. Their median age was 69 years (range, 34 to 89 years), and the median duration of tremor was 16 years (range, less than 1 to 69 years). Fifteen cases were familial and 13 were sporadic. Improvement in 10 patients who continued taking the drug ranged from moderate to complete relief. In addition, four patients had marked improvement and two had moderate improvement but discontinued use of the drug because of side effects. Five patients with a mild response and seven with no response also discontinued methazolamide therapy. The maximal mean daily dose was 203 mg for all patients and 129 mg (maintenance dose) for the patients who continued taking the drug. Side effects consisted primarily of somnolence, nausea, epigastric discomfort, anorexia, paresthesias, and numbness. No aplastic anemia was noted in any of the patients. The median duration of follow-up was 6 months (range, 10 weeks to 29 months). The therapeutic effect seemed unrelated to a family history of tremor, the effect of alcohol, or the responsiveness to propranolol or primidone. Methazolamide may be an effective drug in the treatment of some patients with essential tremor, particularly those with head and voice tremor.

Adult↗

PubMed1980

Blood dyscrasias in patients using methazolamide (neptazane) for glaucoma.

Carbonic anhydrase inhibitors used in the treatment of glaucoma are rarely associated with blood dyscrasias. Several case reports of aplastic anemia with use of acetazolamide, and two cases with use of methazolamide, have appeared in the literature. This report documents two cases of aplastic anemia, at least one of which was almost certainly induced by the use of methazolamide, one case of agranulocytosis, and two cases of neutropenia related to the use of methazolamide. In each case several weeks to months elapsed between initiation of therapy and onset of reaction. This suggests that changes in patients' general medical condition should be continually monitored when using these drugs.

Adolescent↗

PubMed1980

[Effect of methazolamide on the intraocular pressure of patients with open-angle glaucoma (author's transl)].

The ocular hypotensive effects of different oral doses of methazolamide, a carbonic anhydrase inhibitor with similar properties to acetazolamide, were compared in a double-blind trial with 11 patients with glaucoma. In low doses methazolamide offers the possibility of treating glaucoma without side effects or acidosis, but acetazolamide remains the oral medication of choice for glaucoma, because it lowers intraocular pressure more effectively than methazolamide.

Administration, Oral↗

PubMed1995

Carbonic anhydrase and control of breathing: different effects of benzolamide and methazolamide in the anaesthetized cat.

1. The effect of inhibition of erythrocyte carbonic anhydrase on the ventilatory response to CO2 was studied by administering benzolamide (70 mg kg-1, i.v.), an inhibitor which does not cross the blood-brain barrier, to carotid body denervated cats which were anaesthetized with chloralose-urethane. 2. In the same animals the effect on the ventilatory response to CO2 of subsequent inhibition of central nervous system (CNS) carbonic anhydrase was studied by infusing methazolamide (20 mg kg-1), an inhibitor which rapidly penetrates into brain tissue. 3. The results show that inhibition of erythrocyte carbonic anhydrase by benzolamide leads to a decrease in the slope of the normoxic CO2 response curve, and a decrease of the extrapolated arterial PCO2 at zero ventilation. 4. Inhibition of CNS carbonic anhydrase by methazolamide results in an increase in slope and alpha-intercept of the ventilatory CO2 response curve. 5. Using a mass balance equation for CO2 of a brain compartment, it is argued that inhibition of erythrocyte carbonic anhydrase results in a decrease in slope of the in vivo CO2 dissociation curve, which can explain the effects of benzolamide. 6. The changes in slope and intercept induced by methazolamide are discussed in relation to effects on neurones containing carbonic anhydrase, which may include central chemoreceptors.

Acidosis↗

PubMed1993

Double-blind controlled study of methazolamide in the treatment of essential tremor.

We studied the effect of the carbonic anhydrase inhibitor methazolamide in 25 patients with essential tremor (ET) in a double-blind, placebo-controlled trial. Tremor assessment included patient self-reporting of functional disability, clinical rating of motor tasks and tremor severity, and accelerometric measurements. There was no significant difference between methazolamide and placebo in any of the assessments. Side effects, paresthesias, sedation, headaches, and gastrointestinal symptoms were common. Only two patients elected to remain on the drug after the study. Methazolamide has only limited efficacy in the treatment of essential tremor.

Analysis of Variance↗

PubMed1996

Methazolamide for essential voice tremor.

We studied the safety and efficacy of methazolamide (average dose 168 mg/day) in a placebo-controlled blinded investigation in nine patients with essential voice tremor. There were no significant differences for physician or patient clinical rating scores. Digital audio tape recordings showed no difference for amplitude modulation, but frequency modulation was significantly altered by methazolamide. Side effects were common with the drug. We conclude that methazolamide has limited usefulness in the treatment of essential voice tremor.

Aged↗

PubMed1979

Aplastic anemia and agranulocytosis in patients using methazolamide for glaucoma.

Carbonic anhydrase inhibitors used in the treatment of glaucoma, seizure disorders, and hypertension are rarely associated with blood dyscrasias. Several case reports of aplastic anemia with use of acetazolamide, and two cases with use of methazolamide, have appeared in the literature. This article describes two cases of aplastic anemia, at least one of which was almost certainly induced by the use of methazolamide, and one case of agranulocytosis related to the use of methazolamide.

Aged↗

PubMed1981

Time course and disposition of methazolamide in human plasma and red blood cells.

Methazolamide was determined in plasma, whole blood, and urine by a GLC-mass spectrometric method. Temporal patterns of methazolamide concentrations in plasma and red blood cells were obtained following single- and multiple-dose oral administration of the drug. The nonlinearity in the binding of the drug to the red blood cell carbonic anhydrase was evident from a comparison of plasma and red blood cells concentrations. The drug was cleared slowly from the red blood cells. The binding constants to the two isoenzymes of carbonic anhydrase were determined from the plasma and red blood cell concentrations and were in agreement with those determined by previous measurements. The half-life of elimination was 7.5 hr. The urinary recovery of unchanged drug was approximately 25% of the administered dose.

Carbonic Anhydrases↗

PubMed1990

Glutathione conjugation of methazolamide and subsequent reactions in the ciliary body in vitro.

Conjugation reaction of methazolamide with glutathione and its subsequent reactions were studied in vitro. Glutathione, cysteinylglycine, and cysteine conjugates of methazolamide were chemically synthesized. All of the three compounds showed absorbance below 330 nm, with maximal absorbance at approximately 300 nm. At the wavelengths below 220 nm, absorbance was proportional to the number of the amino acids each compound had. Amino acid analysis of the glutathione conjugate showed that the conjugation reaction involved the cysteine residue of glutathione. In order to identify the chemical structure of the reaction product, cysteine conjugate was subjected to infrared, proton nuclear magnetic resonance, and mass spectral analyses. These studies indicated that the cysteine conjugate was S-(5-acetylimino-4-methyl-delta 2-1,3,4-thiadiazolinyl)cysteine. The reaction with glutathione was not catalyzed by glutathione S-transferases, but proceeded in the absence of the enzyme. The glutathione conjugate was degraded by bovine ciliary body homogenate to the cysteinylglycine conjugate and then to the cysteine conjugate.

Animals↗

PubMed1979

The intraocular pressure responses of low-dose bupranolol (Ophtorenin) and methazolamide (Neptazane) in glaucomatous eyes. A controlled clinical study.

In a single-dose, double-blind study, the minimum effective doses of bupranolol and methazolamide were established. The beta-blocker bupranolol (Ophtorenin, Dr. Winzer, Konstanz) in an oily solution reduced IOP significantly in a concentration of 0.05%. The carboanhydrase inhibitor Methazolamide (Neptazane) did not change IOP in a peroral dose of 50 mg, while 100 mg p.o. gave a significant IOP decrease. Both drugs exhibited an additive effect in this low regimen. It is concluded that the combined application of both drugs will postpone or avoid side effects and prolong the time and the field of clinical usefulness. It appears possible that both have a different mechanism of action.

Bupranolol↗

PubMed1976

Urinary calculus during methazolamide therapy.

A 68-year-old white man with Paget's disease and open-angle glaucoma was treated with methazolamide, 50 to 100 mg three times daily. Ten months after the medication was initiated he developed ureteral colic and a calcium oxalate stone was surgically removed. Three months after the drug was reinstituted the patient passed three calcium phosphate stones. This suggested a casual relationship between methazolamide and stone formation, although renal calculi also complicate Paget's disease and acetazolamide had been administered briefly.

Acetazolamide↗

PubMed1977

Low-dose methazolamide and intraocular pressure.

Sixteen patients with increased intraocular pressure (over 20 mm Hg) received 25 and 50 mg of oral methazolamide, twice daily, during consecutive weeks and then 500 mg (Sequels) of acetazolamide. The two methazolamide regimens produced significant decreases in intraocular pressure. Acetazolamide treatment resulted in a greater decrease in intraocular pressure but more systemic acidosis and side effects.

Acetazolamide↗

PubMed1978

Nonfatal methazolamide-induced aplastic anemia.

An 83-year-old man developed nonfatal aplastic anemia after taking methazolamide for three months. We made a diagnosis of methazolamide-induced aplastic anemia, discontinued all medication, gave the patient platelet and red blood cell transfusions, and treated him with oxymetholone. Approximately four months after initiation of treatment, the patient felt well, and he is currently receiving packed red blood cell transfusions every three weeks.

Acetazolamide↗

PubMed1977

The anticonvulsant action of methazolamide in mice: antagonism by various inhibitors of dopamine beta-hydroxylase.

The dopamine beta-hydroxylase inhibitors, FLA-63 and picolinic acid, antagonized the anticonvulsant action of methazolamine in mice; disulfiram and pyrimidinethiol were inactive. FLA-63 and picolinic acid, but not disulfiram or pyrimidinethiol prevented pheniprazine restoration of the anticonvulsant action of methazolamide in reserpinized mice. The present findings clearly demonstrate that differences exist among inhibitors of dopamine beta-hydroxylase regarding their ability to antagonize the anticonvulsant action of methazolamide under various test conditions.

Animals↗