The Effectiveness of Topical Cerium Nitrate-Silver Sulfadiazine Application on Overall Outcome in Patients with Calciphylaxis

Dermatology ◽  
2019 ◽  
Vol 235 (2) ◽  
pp. 120-129 ◽  
Author(s):  
Amandine Darres ◽  
Ronan Delaval ◽  
Alain Fournier ◽  
Emilie Tournier ◽  
Olivier Cointault ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Vitamin K ◽  
Vitamin K Antagonists ◽  
Sodium Thiosulfate ◽  
Comparative Trial ◽  
Skin Lesions ◽  
French Polynesia ◽  
Silver Sulfadiazine ◽  
Cerium Nitrate ◽  
South West

Background: Calciphylaxis (CPX) is a rare and life-threatening disease characterized by vascular calcification and development of painful and necrotizing skin lesions with a challenging management. Mechanisms of CPX are complex and include an imbalance between vascular calcification promoters and inhibitors, and frequently vitamin K deficiency. Objectives: To describe the various presentations and identify predictive factors of death in patients with CPX. Methods: In this multicenter retrospective study, we included 71 CPX patients followed in South-West France (n = 26) and in French Polynesia (n = 45), and who all received sodium thiosulfate (25 g thrice weekly for a median of 61 days). Results: Characteristics at presentation significantly differed between metropolitan and Polynesian French patients. Polynesians were less frequently on regular dialysis at the onset of CPX, had a higher incidence of diabetes mellitus and obesity, more disturbances of calcium-phosphorus metabolism, and received vitamin K antagonists less frequently than patients from South-West France. Despite intensive management, the 1-year mortality rate was 66% and median time to death was 200 days (IQR, 40; 514). The number of body areas involved (i.e., three: OR 2.70 [1.09; 6.65], p = 0.031; four: OR 8.79 [1.54; 50.29], p = 0.015) was the only predictive factor for death, whereas application of topical cerium nitrate-silver sulfadiazine was protective (OR 0.44 [0.20; 0.99], p = 0.046). Surgical debridement, hyperbaric oxygenation therapy, and geographical origin were not associated with overall outcomes. Conclusions: Cerium nitrate may lead to vascular decalcification and chelation of reactive oxygen species, and prevent infection. Cerium nitrate-silver sulfadiazine was associated with better outcomes and should be tested in a prospective comparative trial in CPX patients.

Role of vitamin K-dependent proteins in the arterial vessel wall

2011 ◽  
Vol 31 (04) ◽  
pp. 251-257 ◽  
Author(s):  
M. L. L. Chatrou ◽  
C. P. Reutelingsperger ◽  
L. J. Schurgers
Keyword(s):  
Vascular Calcification ◽  
Vitamin K ◽  
Independent Predictor ◽  
Vitamin K Antagonists ◽  
Venous Blood ◽  
Coagulation Factors ◽  
Coagulation Cascade ◽  
High Intake ◽  
Smooth Muscle Cell Migration

SummaryVitamin K was discovered early last century at the same time as the vitamin K-antagonists. For many years the role of vitamin K was solely ascribed to coagulation and coagulation was thought to be involved only at the venous blood side. This view has dramatically changed with the discovery of vitamin K-dependent proteins outside the coagulation cascade and the role of coagulation factors at the arterial side. Vitamin K-dependent proteins are involved in the regulation of vascular smooth muscle cell migration, apoptosis, and calcification. Vascular calcification has become an important independent predictor of cardiovascular disease. Vitamin K-antagonists induce inactivity of inhibitors of vascular calcification, leading to accelerated calcification. The involvement of vitamin K-dependent proteins such as MGP in vascular calcification make that calcification is amendable for intervention with high intake of vitamin K. This review focuses on the effect of vitamin K-dependent proteins in vascular disease.

Vascular calcification: The price to pay for anticoagulation therapy with vitamin K-antagonists

Blood Reviews ◽  
2012 ◽  
Vol 26 (4) ◽  
pp. 155-166 ◽  
Author(s):  
Martijn L.L. Chatrou ◽  
Kristien Winckers ◽  
Tilman M. Hackeng ◽  
Chris P. Reutelingsperger ◽  
Leon J. Schurgers
Keyword(s):  
Vascular Calcification ◽  
Vitamin K ◽  
Vitamin K Antagonists ◽  
Anticoagulation Therapy

scholarly journals Vitamin K Antagonists, Non–Vitamin K Antagonist Oral Anticoagulants, and Vascular Calcification in Patients with Atrial Fibrillation

TH Open ◽  
2018 ◽  
Vol 02 (04) ◽  
pp. e391-e398 ◽  
Author(s):  
Frederique Peeters ◽  
Elton Dudink ◽  
Dorien Kimenai ◽  
Bob Weijs ◽  
Sibel Altintas ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Logistic Regression ◽  
Aortic Valve ◽  
Propensity Score ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Vitamin K Antagonist ◽  
Adjusted Logistic Regression

Background Vitamin K antagonists (VKAs) are associated with coronary artery calcification in low-risk populations, but their effect on calcification of large arteries remains uncertain. The effect of non–vitamin K antagonist oral anticoagulants (NOACs) on vascular calcification is unknown. We investigated the influence of use of VKA and NOAC on calcification of the aorta and aortic valve. Methods In patients with atrial fibrillation without a history of major adverse cardiac or cerebrovascular events who underwent computed tomographic angiography, the presence of ascending aorta calcification (AsAC), descending aorta calcification (DAC), and aortic valve calcification (AVC) was determined. Confounders for VKA/NOAC treatment were identified and propensity score adjusted logistic regression explored the association between treatment and calcification (Agatston score > 0). AsAC, DAC, and AVC differences were assessed in propensity score–matched groups. Results Of 236 patients (33% female, age: 58 ± 9 years), 71 (30%) used VKA (median duration: 122 weeks) and 79 (34%) used NOAC (median duration: 16 weeks). Propensity score–adjusted logistic regression revealed that use of VKA was significantly associated with AsAC (odds ratio [OR]: 2.31; 95% confidence interval [CI]: 1.16–4.59; p = 0.017) and DAC (OR: 2.38; 95% CI: 1.22–4.67; p = 0.012) and a trend in AVC (OR: 1.92; 95% CI: 0.98–3.80; p = 0.059) compared with non-anticoagulation. This association was absent in NOAC versus non-anticoagulant (AsAC OR: 0.51; 95% CI: 0.21–1.21; p = 0.127; DAC OR: 0.80; 95% CI: 0.36–1.76; p = 0.577; AVC OR: 0.62; 95% CI: 0.27–1.40; p = 0.248). A total of 178 patients were propensity score matched in three pairwise comparisons. Again, use of VKA was associated with DAC (p = 0.043) and a trend toward more AsAC (p = 0.059), while use of NOAC was not (AsAC p = 0.264; DAC p = 0.154; AVC p = 0.280). Conclusion This cross-sectional study shows that use of VKA seems to contribute to vascular calcification. The calcification effect was not observed in NOAC users.

scholarly journals Vitamin K antagonist use induces calcification and atherosclerotic plaque progression resulting in increased hypercoagulability

2021 ◽  
Author(s):  
Rick H van Gorp ◽  
Constance C F M J Baaten ◽  
Anxhela Habibi ◽  
Armand M G Jaminon ◽  
Frederique E C M Peeters ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Vitamin K ◽  
Atherosclerotic Plaque ◽  
Vitamin K Antagonists ◽  
Phenotypic Switching ◽  
Plaque Burden ◽  
Dependent Manner ◽  
Atherosclerotic Burden ◽  
Patients At Risk

Abstract Aims Vascular calcification is a hallmark of atherosclerotic burden and can predict cardiovascular outcome. Vitamin K-antagonists (VKA) are widely used anticoagulant drugs to treat patients at risk of arterial and venous thrombosis, but are also associated with increase vascular calcification progression. We aim to unravel the paradox that VKA suppresses plasma coagulation but promotes vascular calcification and subsequent atherosclerosis-dependent coagulability of the vessel wall. Methods and results Apoe -/- mice were placed on western type diet enriched with the VKA warfarin for 18 weeks to measure atherosclerotic plaque burden, calcification and coagulation. Patients (n = 54) displaying paroxysmal atrial fibrillation with a low cardiovascular risk, who were treated with VKA were included to measure prethrombotic state. Finally, primary vascular smooth muscle cells (VSMC) derived from human tissue explants were used for in vitro experiments. In Apoe-/- mice, VKA increases both atherosclerotic plaque size and calcification. Higher plaque calcification was associated with increased plasma levels of thrombin-antithrombin and factor IXa-antithrombin complexes in mice and patients treated with VKA. Mechanistically, phenotypic switching of VSMC into synthetic VSMC promotes thrombin generation, which is enhanced in a tissue-factor (TF)-dependent manner by VSMC calcification. Moreover, calcified VSMC exposed to whole blood under flow significantly enhanced platelet deposition and TF-dependent fibrin formation. Conclusions Oral anticoagulation with VKA aggravates vascular calcification and atherosclerosis. VSMC phenotype differentiation impacts coagulation potential in a TF-dependent manner. VKA induced vascular calcification increases hypercoagulability and could thereby potentially positively affect atherothrombosis.

Chronic coumarin treatment is associated with increased extracoronary arterial calcification in humans

Blood ◽  
2010 ◽  
Vol 115 (24) ◽  
pp. 5121-5123 ◽  
Author(s):  
Roger J. M. W. Rennenberg ◽  
Bernard J. van Varik ◽  
Leon J. Schurgers ◽  
Karly Hamulyak ◽  
Hugo ten Cate ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Vitamin K Antagonists ◽  
Cross Sectional Study ◽  
Matrix Gla Protein ◽  
Arterial Calcification ◽  
Cross Sectional

Abstract Vascular calcification is a marker of increased cardiovascular risk. Vitamin K–dependent matrix Gla protein (MGP) is important in inhibiting calcification. Because MGP activation is vitamin K dependent, we performed a cross-sectional study investigating the relationship between the use of vitamin K antagonists and extracoronary vascular calcification. From the Dutch thrombosis services we selected 19 patients younger than 55 years who had no other cardiovascular risk factors and who had used coumarins for more than 10 years, and compared these to 18 matched healthy controls. MGP was measured, and a plain x-ray of the thighs was taken to assess femoral arterial calcifications. The odds ratio for calcification in patients versus controls was 8.5 (95% confidence interval [CI] 2.01-35.95). Coumarin use and MGP were associated with calcification, even after adjusting for other risk factors. We conclude that long-term use of coumarins is associated with enhanced extracoronary vascular calcification, possibly through the inhibition of MGP carboxylation.

Idiopathic venous thrombosis

2006 ◽  
Vol 26 (01) ◽  
pp. 52-54 ◽  
Author(s):  
P. A. Kyrle
Keyword(s):  
Chronic Disease ◽  
Venous Thrombosis ◽  
Vitamin K ◽  
Clinical Benefit ◽  
Plasma Levels ◽  
Vitamin K Antagonists ◽  
Antithrombin Deficiency ◽  
Optimal Duration ◽  
Risk Of Treatment

SummaryVenous thrombosis is a chronic disease with a recurrence rate of approximately 30% within 5-8 years. The optimal duration of secondary thromboprophylaxis in these patients entails balancing the risk of recurrence against the risk of treatment-associated bleeding. There is agreement that patients with a first idiopathic venous thrombosis should receive vitamin K antagonists for at least 3-6 months. Convincing trials showing a clinical benefit in terms of morbidity or mortality with respect to expansion of anticoagulation beyond 6 months are lacking. Nevertheless, some subgroups of patients with venous thrombosis may benefit from indefinite anticoagulation. Thus, patients with antithrombin deficiency, combined or homozygous defects, more than one unprovoked episode of thrombosis, the lupus anticoagulant or high factor VIII plasma levels are good candidates for long-term prevention.

Spectrophotometric Assays of Prothrombin in Plasma of Patients Using Oral Anticoagulants

1979 ◽  
Vol 42 (04) ◽  
pp. 1296-1305 ◽  
Author(s):  
R M Bertina ◽  
W van der Marel-van Nieuwkoop ◽  
E A Loeliger
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Oral Anticoagulation ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Factor Xa ◽  
Factor V ◽  
Anticoagulant Treatment ◽  
Factor Ii ◽  
K Deficiency

SummaryTwo spectrophotometric assays for prothrombin have been developed and compared with a one stage coagulant and an immunological assay. One of these assays (called the XAPC assay) uses a combination of factor Xa, phospholipid, Ca2+ and factor V as activator of prothrombin, and measures only normal prothrombin. The second (the ECAR assay) uses Echis carinatus venom as activator. This assay measures both normal prothrombin and PIVKA II (protein induced by vitamin K antagonists/absence). Combination of the results obtained by the XAPC and ECAR assays provides rapid and reliable information on the degree of “subcarboxylation” of prothrombin (oral anticoagulation, vitamin K deficiency).For patients on long term anticoagulant treatment the prothrombin time (Thrombotest) shows better correlation with the ratio prothrombin/prothrombin plus PIVKA II (XAPC/ ECAR) than with the factor II concentration. For patients starting the anticoagulant treatment there is no correlation between the Thrombotest time and the XAPC/ECAR ratio.It seems doubtful that (a) spectrophotometric factor II assay(s) will be as useful as the prothrombin time in the control of oral anticoagulation.

New Drugs for Thromboembolic Prevention in Atrial Fibrillation

2010 ◽  
Vol 6 (4) ◽  
pp. 64
Author(s):  
Jose L Merino ◽  
Jose López-Sendón ◽  
◽  
Keyword(s):  
Atrial Fibrillation ◽  
Vitamin K ◽  
Negative Impact ◽  
Vitamin K Antagonists ◽  
Coagulation Factor ◽  
Developed Countries ◽  
New Drugs ◽  
Risk Scores ◽  
Bleeding Events ◽  
Risk Patients

Atrial fibrillation (AF) is the most frequent sustained arrhythmia and its prevalence is increasing in developed countries. This progressive increase and the negative impact of this arrhythmia on the patient’s prognosis make AF one of the main healthcare problems faced today. This has led to intense research into the main aspects of AF, one of them being thromboembolism prevention. AF patients have a four to five times higher risk of stroke than the general population. Several factors increase thromboembolic risk in patients with AF and the use of risk scores, such as the Congestive Heart Failure, Hypertension, Age Greater than 75, Diabetes, and Prior Stroke or Transient Ischemic Attack (CHADS2), have been used to identify the best candidates for anticoagulation. Antithrombotic drugs are the mainstay of therapy for embolic prevention. The clinical use of these drugs is based on the risk–benefit ratio, where benefit is the reduction of stroke and systemic embolic events and risk is mostly driven by the increase in bleeding events. Generally, antiplatelets are indicated for low-risk patients in light of the fact anticoagulants are the drug of choice for moderate- or high-risk patients. Vitamin K antagonists have been the only option for oral anticoagulation for the last 50 years. However, these drugs have many pharmacodynamic and pharmacokinetic problems. The problems of anticoagulation with vitamin K antagonists have led to the investigation of new drugs that can be administered orally and have a better dose–response relationship, a shorter half-life and, in particular, higher efficacy and safety without the need for frequent anticoagulation controls. The drugs that have been studied most thoroughly in patients with AF are inhibitors of the activated coagulation factor X and inhibitors of coagulation factor II (thrombin), including ximelagatran and dabigatran. In addition, non-pharmacological therapies have been developed to prevent recurrent embolism in certain patient populations.

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