Non-uremic calciphylaxis associated with alcoholic hepatitis: A case report

Abstract

BACKGROUNDCalciphylaxis is a form of vascular calcification more commonly associated with renal disease. While the exact mechanism of calciphylaxis is poorly understood, most cases are due to end stage kidney disease. However, it can also be found in patients without kidney disease and in such cases is termed non-uremic calciphylaxis for which have multiple proposed etiologies.CASE SUMMARYWe describe a case of a thirty-year-old morbidly obese Caucasian female who had a positive history of alcoholic hepatitis and presented with painful calciphylaxis wounds of the abdomen, hips, and thighs. The hypercoagulability panel showed low levels of Protein C and normal Protein S, low Antithrombin III and positive lupus anticoagulant and negative anticardiolipin. Wound biopsy confirmed the diagnosis of non-uremic calciphylaxis in the setting of alcoholic liver disease. The calciphylaxis wounds did not improve when Sodium Thiosulfate was used alone. The patient underwent a series of bedside and surgical debridement. Broad spectrum antibiotics were also used for secondary wound bacterial infections. The patient passed away shortly after due to sepsis and multiorgan failure.CONCLUSIONNon-uremic Calciphylaxis can occur in the setting of alcoholic liver disease. The treatment of choice is still unknown.

Multiorgan failure with fatal outcome after stem cell tourism

“…Even chronic inflammatory states are possible risk factors since TNF-alpha was shown to induce osteogenic phenotype of human smooth muscle cells [9][10][11]. Although we have not found a complete explanation for the observed extensive and accelerated formation of small vessels' calcifications, we conclude that in the presented case, besides end-stage renal failure, hepatic impairment may certainly have played an important role [12].…”

Multiorgan failure with fatal outcome after stem cell tourism

“…Even chronic in ammatory states are possible risk factors since TNF-alpha was shown to induce osteogenic phenotype of human smooth muscle cells [9][10][11]. Although we have not found a complete explanation for the observed extensive and accelerated formation of small vessels' calci cations, we conclude that in the presented case, besides end-stage renal failure, hepatic impairment may certainly have played an important role [12].…”

Tender Nonhealing Lesion on the Leg

“…It is postulated that microvascular calcification occurs as an active cell-mediated process that depends on the balance between the promoters and inhibitors of calcification. 1 In our patient, liver disease likely predisposed formation of calcification through the creation of an environment susceptible to vascular injury via decreased synthesis of proteins C and S. 3 Synthesis of fetuin-A, a protein that acts as a circulating inhibitor of vascular ossification/calcification, also is decreased in calcification. Another inhibitor of calcification, matrix Gla protein, is unable to undergo activation through vitamin K-dependent carboxylation secondary to liver disease-induced vitamin K deficiency.…”