acetazolamide has been researched along with Hyperphosphatemia in 7 studies
Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)
Hyperphosphatemia: A condition of abnormally high level of PHOSPHATES in the blood, usually significantly above the normal range of 0.84-1.58 mmol per liter of serum.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Hyperphosphatemic familial tumoral calcinosis (HFTC) is a rare autosomal recessive disorder." | 5.72 | The Successful Treatment of Deep Soft-tissue Calcifications with Topical Sodium Thiosulphate and Acetazolamide in a Boy with Hyperphosphatemic Familial Tumoral Calcinosis due to a Novel Mutation in ( Döneray, H; Gürbüz, K; Özden, A, 2022) |
| "Familial hyperphosphatemic tumoral calcinosis is a rare disorder characterized by hyperphosphatemia with recurrent ectopic periarticular calcifications, in addition to other visceral and vascular manifestations, without any inflammatory or neoplastic disorder." | 5.62 | Familial hyperphosphatemic tumoral calcinosis in an unusual and usual sites and dramatic improvement with the treatment of acetazolamide, sevelamer and topical sodium thiosulfate. ( Aktasoglu, E; Emecen Sanli, M; Ezgu, F; Inci, A; Kilic, A; Okur, I; Tumer, L, 2021) |
| "Acetazolamide (ACM) treatment partially reversed the growth deficit of kl/kl mice." | 5.43 | Acetazolamide sensitive tissue calcification and aging of klotho-hypomorphic mice. ( Alesutan, I; Castor, T; Kohlhofer, U; Kübler, L; Kuro-o, M; Lang, F; Leibrock, CB; Mannheim, JG; Michael, D; Pichler, BJ; Quintanilla-Martinez, L; Rosenblatt, KP; Voelkl, J, 2016) |
| "Hyperphosphatemic familial tumoral calcinosis (HFTC) is characterized by enhanced renal phosphate absorption, hyperphosphatemia, and tumor-like extraosseous calcifications due to inactivating mutations in FGF23 or associated proteins." | 5.40 | Hyperphosphatemic familial tumoral calcinosis: response to acetazolamide and postulated mechanisms. ( Finer, G; Langman, CB; Price, HE; Shore, RM; White, KE, 2014) |
| "Hyperphosphatemic familial tumoral calcinosis (HFTC) is an uncommon disease characterized by periarticular calcifications produced by the deposition of amorphous extraosseous calcifications of hydroxyapatite." | 5.35 | Familial tumoral calcinosis caused by a novel FGF23 mutation: response to induction of tubular renal acidosis with acetazolamide and the non-calcium phosphate binder sevelamer. ( Lammoglia, JJ; Mericq, V, 2009) |
| "Hyperphosphatemic familial tumoral calcinosis (HFTC) is a rare autosomal recessive disorder." | 1.72 | The Successful Treatment of Deep Soft-tissue Calcifications with Topical Sodium Thiosulphate and Acetazolamide in a Boy with Hyperphosphatemic Familial Tumoral Calcinosis due to a Novel Mutation in ( Döneray, H; Gürbüz, K; Özden, A, 2022) |
| "Familial hyperphosphatemic tumoral calcinosis is a rare disorder characterized by hyperphosphatemia with recurrent ectopic periarticular calcifications, in addition to other visceral and vascular manifestations, without any inflammatory or neoplastic disorder." | 1.62 | Familial hyperphosphatemic tumoral calcinosis in an unusual and usual sites and dramatic improvement with the treatment of acetazolamide, sevelamer and topical sodium thiosulfate. ( Aktasoglu, E; Emecen Sanli, M; Ezgu, F; Inci, A; Kilic, A; Okur, I; Tumer, L, 2021) |
| "Acetazolamide (ACM) treatment partially reversed the growth deficit of kl/kl mice." | 1.43 | Acetazolamide sensitive tissue calcification and aging of klotho-hypomorphic mice. ( Alesutan, I; Castor, T; Kohlhofer, U; Kübler, L; Kuro-o, M; Lang, F; Leibrock, CB; Mannheim, JG; Michael, D; Pichler, BJ; Quintanilla-Martinez, L; Rosenblatt, KP; Voelkl, J, 2016) |
| "Hyperphosphatemic familial tumoral calcinosis (HFTC) is characterized by enhanced renal phosphate absorption, hyperphosphatemia, and tumor-like extraosseous calcifications due to inactivating mutations in FGF23 or associated proteins." | 1.40 | Hyperphosphatemic familial tumoral calcinosis: response to acetazolamide and postulated mechanisms. ( Finer, G; Langman, CB; Price, HE; Shore, RM; White, KE, 2014) |
| "Treatment with niacinamide and acetazolamide decreased TmP/GFR and serum phosphate, which was paralleled by a decrease in serum C-terminus FGF23." | 1.35 | A case of familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome due to a compound heterozygous mutation in GALNT3 demonstrating new phenotypic features. ( Brahim, J; Collins, MT; Dumitrescu, CE; Farrow, EG; Hart, TC; Kelly, MH; Khosravi, A; Murphey, MD; Nathan, MH; White, KE, 2009) |
| "Hyperphosphatemic familial tumoral calcinosis (HFTC) is an uncommon disease characterized by periarticular calcifications produced by the deposition of amorphous extraosseous calcifications of hydroxyapatite." | 1.35 | Familial tumoral calcinosis caused by a novel FGF23 mutation: response to induction of tubular renal acidosis with acetazolamide and the non-calcium phosphate binder sevelamer. ( Lammoglia, JJ; Mericq, V, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 2 (28.57) | 29.6817 |
| 2010's | 3 (42.86) | 24.3611 |
| 2020's | 2 (28.57) | 2.80 |
| Authors | Studies |
|---|---|
| Döneray, H | 1 |
| Özden, A | 1 |
| Gürbüz, K | 1 |
| Emecen Sanli, M | 1 |
| Kilic, A | 1 |
| Aktasoglu, E | 1 |
| Inci, A | 1 |
| Okur, I | 1 |
| Ezgu, F | 1 |
| Tumer, L | 1 |
| Finer, G | 1 |
| Price, HE | 1 |
| Shore, RM | 1 |
| White, KE | 2 |
| Langman, CB | 1 |
| Cheung, MS | 1 |
| Leibrock, CB | 1 |
| Alesutan, I | 1 |
| Voelkl, J | 1 |
| Michael, D | 1 |
| Castor, T | 1 |
| Kohlhofer, U | 1 |
| Quintanilla-Martinez, L | 1 |
| Kübler, L | 1 |
| Mannheim, JG | 1 |
| Pichler, BJ | 1 |
| Rosenblatt, KP | 1 |
| Kuro-o, M | 1 |
| Lang, F | 1 |
| Dumitrescu, CE | 1 |
| Kelly, MH | 1 |
| Khosravi, A | 1 |
| Hart, TC | 1 |
| Brahim, J | 1 |
| Farrow, EG | 1 |
| Nathan, MH | 1 |
| Murphey, MD | 1 |
| Collins, MT | 1 |
| Lammoglia, JJ | 1 |
| Mericq, V | 1 |
1 review available for acetazolamide and Hyperphosphatemia
| Article | Year |
|---|---|
Drugs Used in Paediatric Bone and Calcium Disorders.
Topics: Acetazolamide; Bone and Bones; Bone Density Conservation Agents; Bone Diseases, Metabolic; Calcitoni | 2015 |
6 other studies available for acetazolamide and Hyperphosphatemia
| Article | Year |
|---|---|
The Successful Treatment of Deep Soft-tissue Calcifications with Topical Sodium Thiosulphate and Acetazolamide in a Boy with Hyperphosphatemic Familial Tumoral Calcinosis due to a Novel Mutation in
Topics: Acetazolamide; Calcinosis; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Humans; Hyperosto | 2022 |
Familial hyperphosphatemic tumoral calcinosis in an unusual and usual sites and dramatic improvement with the treatment of acetazolamide, sevelamer and topical sodium thiosulfate.
Topics: Acetazolamide; Administration, Topical; Anticonvulsants; Antioxidants; Calcinosis; Chelating Agents; | 2021 |
Hyperphosphatemic familial tumoral calcinosis: response to acetazolamide and postulated mechanisms.
Topics: Acetazolamide; Acidosis; Black or African American; Calcinosis; Carbonic Anhydrase Inhibitors; Chela | 2014 |
Acetazolamide sensitive tissue calcification and aging of klotho-hypomorphic mice.
Topics: Acetazolamide; Acidosis; Aging; Alkaline Phosphatase; Animals; Calcitriol; Calcium; Carbonic Anhydra | 2016 |
A case of familial tumoral calcinosis/hyperostosis-hyperphosphatemia syndrome due to a compound heterozygous mutation in GALNT3 demonstrating new phenotypic features.
Topics: Acetazolamide; Adult; Calcinosis; Child; Diuretics; Female; Fibroblast Growth Factor-23; Fibroblast | 2009 |
Familial tumoral calcinosis caused by a novel FGF23 mutation: response to induction of tubular renal acidosis with acetazolamide and the non-calcium phosphate binder sevelamer.
Topics: Acetazolamide; Acidosis, Renal Tubular; Calcinosis; Chelating Agents; Child, Preschool; Diuretics; D | 2009 |