acetazolamide has been researched along with Caffey Disease in 2 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)
| 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) |
| "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 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) |
| "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) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 1 (50.00) | 24.3611 |
| 2020's | 1 (50.00) | 2.80 |
| Authors | Studies |
|---|---|
| Döneray, H | 1 |
| Özden, A | 1 |
| Gürbüz, K | 1 |
| Finer, G | 1 |
| Price, HE | 1 |
| Shore, RM | 1 |
| White, KE | 1 |
| Langman, CB | 1 |
2 other studies available for acetazolamide and Caffey Disease
| 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 |
Hyperphosphatemic familial tumoral calcinosis: response to acetazolamide and postulated mechanisms.
Topics: Acetazolamide; Acidosis; Black or African American; Calcinosis; Carbonic Anhydrase Inhibitors; Chela | 2014 |