[EFFICACY OF CYTOFLAVIN IN COMPLEX TREATMENT OF DIABETIC FOOT SYNDROME].

The study involved 97 patients with severe diabetic foot syndrome (DFS) subcompensated type 2 diabetes. All patients were available mediacalcification foot and lower leg arteries of different severity. Depending on the treatment, all patients were divided into 2 groups by stratified randomization. The І group received standard therapy, which is indicated for the DFS. A ІІ group of patients additionally received basic therapy drug Cytoflavin 10 ml 0,9% NaCl 200 ml for 10 days, followed by transfer to tablet form Cytoflavin 2 tablets 2 times per day orally for one month. We noted a positive trend of treatment of patients who, in addition to standard therapy received the drug Cytoflavin. Thus, the use of complex surgical treatment of patients with mixed form of DFS Cytoflavin reduces the severity of distal polyneuropathy, improves oxygenation of tissues and restores the enzyme activity of antioxidant system, that manifested neuroprotective, antioxidant and anti-hypoxic effects of drugs, which substantiates the indications for its use in the this pathology.

Role of sodium thiosulfate therapy in the treatment of digital necrosis due to Mönckeberg sclerosis.

Accelerated vascular calcification is a well-described complication of chronic kidney disease often affecting large and small vessels alike through a variety of mechanisms. Accordingly, dysregulation of calcium and phosphate balance, vitamin D metabolism, hyperparathyroidism, and endothelial injury can lead to both macrovascular and microvascular complications. We describe a 56-year-old Hispanic male with a history of end-stage renal disease, diabetes mellitus type 2, and medical noncompliance who developed sequential digital ischemia and necrosis involving both hands as well as right foot as a result of Mönckeberg sclerosis. An extensive metabolic and serologic workup was unrevealing but radiographic studies and histopathology revealed the diagnosis. A multifaceted approach was instituted including wound debridement and amputations along with intensive medical support. In addition to improving hypertensive control and striving for improved calcium and phosphate balance, sodium thiosulfate solution was administered for more than 1 year. This aggressive approach allowed his wounds to heal and has arrested further digital ischemia from occurring.

A case of ochronosis with gout and Monckeberg arteries.

Alkaptonuria is an inborn error of amino acid metabolism. A defect in tyrosine metabolism that results in accumulation of homogentisic acid in connective tissue, especially cartilage, has long been known. Degenerative arthropathy, especially of the knee and spine, develops at a relatively early age in adults. Accumulation also occurs in heart valves, and there may be a predisposition to atherosclerosis. We describe a 72-year-old man with ochronosis, gouty arthritis of both hands, and monckeberg arteries.

Accelerated atherosclerotic calcification and Monckeberg's sclerosis: a continuum of advanced vascular pathology in chronic kidney disease.

Autopsy studies have demonstrated the near universal presence of fatty streaks and fibroatheromas in the general population from which patients with chronic kidney disease (CKD) arise. The vast majority of patients with CKD have multiple conventional cardiovascular risk factors. Vascular atherosclerotic calcification develops in most patients as they transition from the general population to significant CKD as part of cholesterol crystallization within atherosclerotic lesions. Once present, however, atherosclerotic medial calcification can become prominent and has been previously identified as Mönckeberg's sclerosis. A unifying concept supported by the preponderance of pathologic evidence contends that Mönckeberg's sclerosis is a manifestation of accelerated atherosclerosis in patients with CKD. The term has also been used in rare cases to describe vascular calcinosis not related to CKD. This clarification is critical to advance the field in terms of pathologic diagnosis and treatment of CKD bone and mineral disorder. Factors that seem to promote the osteoblastic transformation of vascular smooth muscle cells and enhance deposition of calcium hydroxyapatite crystals include phosphorus activation of the Pit-1 receptor, bone morphogenic proteins 2 and 4, leptin, endogenous 1,25 dihydroxyvitamin D, vascular calcification activating factor, and measures of oxidative stress. These entities work to accelerate the atherosclerotic process in patients with CKD and may be future targets for diagnosis and treatment because randomized trials with hydroxymethylglutaryl-CoA reductase inhibitors have failed to attenuate the rate of progressive vascular calcification.