calcification inhibitor whose function depends on vitamin K.
Warfarin use or vitamin-K deficient patients suppress matrix Gla
protein function causing vascular calcification [8].
A wide range of treatment options are proposed for CUA,
but none of them is based on prospective randomized trials.
The aim is to provide adequate wound care, pain control,
prevent infection and correct calcium, phosphorus and PTH
abnormalities. Intensifying hemodialysis dose is another option
proposed. Geurra et al. [9] reported successful treatment of severe
calciphylaxis with a combination of daily continuous venovenous
hemofiltration (CVVH) and intravenous sodium thiosulfate in an
attempt to mobilize and remove deposited vascular calcium [9].
Sodium thiosulfate administration is a promising therapeutic
strategy with increasing publications of its use in case reports and
case series [10,11]. Sodium thiosulfate is a chelating agent used for
cyanide intoxication with a documented efficacy for the treatment
of recurrent urolithiasis [12]. Its use for calciphylaxis treatment
was initially reported in 2004 [13]. Although it is believed that
sodium thiosulfate interferes with calcium phosphate crystal
formation, how this compound acts on vascular calcification is
largely unknown [14]. We are still in the dark with regard to the
optimal dose of sodium thiosulfate and the duration of treatment.
Parathyroidectomy is another widely discussed topic and an
option for severe hyperparathyroidism, but the role of surgical
intervention is unclear in borderline cases and if it is superior
to treatment with calcimimetics. Cinacalcet might also have
a preventive effect for the development of calciphylaxis when
compared to placebo [15]. Many other treatment options have
been reported, as a part of a multilevel approach such as, vitamin
K supplementation, use of bisphosphonates, hyperbaric oxygen
therapy etc and it’s up to the attending physician to evaluate their
appropriateness in specific cases.