Would acetazolamide inhibit progression of atheromatous vascular calcification?

Cochran, M.

doi:10.1016/j.mehy.2019.109354

Cited by 1 publication

(2 citation statements)

References 37 publications

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“…Previous studies have shown that acidosis can prevent and reduce soft tissue calcification by increasing the solubility of calcium phosphate deposits and/or suppressing the expression of various osteogenic transcription factors [59,61]. Additionally, mild acidosis decreases trivalent phosphate, which slows the rate of precipitation with calcium [60,62]. Acetazolamide inhibits the enzyme carbonic anhydrase reversibly [63].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, it decreases production of cerebrospinal fluid and aqueous humor and resulting in metabolic acidosis [63,64]. As a consequence of these mechanisms, acetazolamide is indicated for the treatment of high-altitude cerebral edema and acute angle-closure glaucoma and is also used offlabel in idiopathic intracranial hypertension and metabolic alkalosis [62][63][64]. In addition, acetazolamide induces phosphaturia, likely through the inhibitory effect of an altered tubular luminal fluid pH on Na-linked phosphate co-transporters [65].…”

Section: Discussionmentioning

confidence: 99%

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Venous Thrombosis in a Pseudohypoparathyroidism Patient with a Novel <i>GNAS</i> Frameshift Mutation and Complete Resolution of Vascular Calcifications with Acetazolamide Treatment

Seven Menevse,

Iwasaki,

Yavas Abali

et al. 2023

Horm Res Paediatr

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Introduction Pseudohypoparathyroidism type IA (PHP1A) is characterized by end-organ resistance to multiple hormones and Albright’s hereditary osteodystrophy (AHO). PHP1A is caused by inactivating mutations of the GNAS gene encoding the α-subunit of the stimulatory G protein (Gsα). In line with the underlying genetic defect, impaired inhibition of platelet aggregation has been demonstrated in some patients. However, no PHP1A case with thrombotic events has been described. Also, PHP1A cases typically have subcutaneous ossifications, but soft tissue calcifications are another common finding. Treatment options for those and other non-hormonal features of PHP1A are limited. Case Presentation A female patient presented with short stature, fatigue, and exercise-induced carpopedal spasms at age 117/12 years. Diagnosis of PHP1A was made based on hypocalcemia, hyperphosphatemia, elevated serum PTH, and AHO features, including short stature and brachydactyly. A novel frameshift variant was detected in the last exon of GNAS (c.1065_1068delGCGT, p.R356Tfs*47), showing complete loss of baseline and receptor-stimulated activity in transfected cells. The patient developed venous thrombosis and vascular and subcutaneous calcifications on both forearms after venous puncture on the right and extravasation of calcium gluconate during treatment on the left. The thrombosis and calcifications completely resolved following treatment with low molecular weight heparin and acetazolamide for 5 and 8 months, respectively. Conclusions This case represents the first PHP1A patient displaying thrombosis and the first successful use of acetazolamide for PHP1A-associated soft tissue calcifications, thus providing new insights into the treatment of non-endocrinological features in this disease.

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