Monckeberg Medial Calcific Sclerosis
Multiple Sclerosis
Novel conformation-specific antibodies against matrix gamma-carboxyglutamic acid (Gla) protein: undercarboxylated matrix Gla protein as marker for vascular calcification. (1/5)
OBJECTIVE: Matrix gamma-carboxyglutamic acid (Gla) protein (MGP), a vitamin K-dependent protein, is a potent in vivo inhibitor of arterial calcification. We hypothesized that low endogenous production of MGP and impaired carboxylation of MGP may contribute to the development or the progression of vascular disease. METHODS AND RESULTS: Novel conformation-specific antibodies against MGP were used for immunohistochemistry of healthy and sclerotic arteries. In healthy arteries, MGP was mainly displayed around the elastin fibers in the tunica media. The staining colocalized with that for carboxylated MGP, whereas undercarboxylated MGP (ucMGP) was not detected. In atherosclerotic arteries, ucMGP was found in the intima, where it was associated with vesicular structures. In Monckeberg's sclerosis of the media, ucMGP was localized around all areas of calcification. The results indicate that ucMGP is strongly associated with vascular calcification of different etiologies. In a separate study, serum MGP concentrations in a cohort of 172 subjects who had undergone percutaneous coronary intervention were significantly reduced compared with an apparently healthy population. CONCLUSIONS: These data show that impaired carboxylation of MGP is associated with intimal and medial vascular calcification and suggest the essentiality of the vitamin K modification to the function of MGP as an inhibitor of ectopic calcification. (+info)Monckeberg's sclerosis - is the artery the only target of calcification? (2/5)
BACKGROUND: Since its first description, Monckeberg's sclerosis has only been related to arterial media calcification, being listed among the primary diseases of the vessels. CASE PRESENTATION: We report here a clinically and histologically confirmed case of Monckeberg's sclerosis in which the patient presented with massive areas of soft tissue calcifications in the pharynx and larynx. Polysomnographic parameters showed severe obstructive apnea refractory to nasal continuous positive airway pressure. Clinical and laboratory findings excluded concomitant endocrine or rheumatological diseases. CONCLUSION: Our data provide a new insight about Monckeberg's sclerosis, i.e., the fact that the etiopathogenic process involved in the phenomenon of calcification may not be restricted only to the arteries, but may occur in the entire organism. Further studies of the etiopathogenesis of this disease are needed. (+info)Accelerated atherosclerotic calcification and Monckeberg's sclerosis: a continuum of advanced vascular pathology in chronic kidney disease. (3/5)
(+info)Media calcification and intima calcification are distinct entities in chronic kidney disease. (4/5)
(+info)Clinical decision-making for vitamin K-1 and K-2 deficiency and coronary artery calcification with warfarin therapy: are diet, factor Xa inhibitors or both the answer? (5/5)
Coronary artery calcification is a recognised risk factor for ischaemic heart disease and mortality. Evidence is now strong that Monckeberg's arteriosclerosis, a form of vascular calcification, can be attributable to vitamin K deficiency, but that vitamin K-2, especially the MK-4 form from foods like cheese can be protective. Warfarin blocks the recycling of hepatic and peripheral vitamin K leading to secondary vitamin K deficiency with adverse effects on vasculature, bone, kidneys, brain and other tissues and systems (inflammatory, immune function and neoplasia at least). There is individual susceptibility to vitamin K deficiency and warfarin sensitivity, partly explicable in terms of genetic polymorphisms, epigenetics, diet and pharmacotherapy. The emergence of extensive coronary calcification in a man with atrial fibrillation treated for a decade with warfarin is described by way of illustration and to raise the present clinical management conundrums. Finally, a putative set of recommendations is provided. (+info)Monckeberg medial calcific sclerosis is a medical condition that affects the muscular layer (media) of medium-sized and large arteries, most commonly the muscular arteries of the legs. It is characterized by calcium deposits in the media of the artery wall, resulting in stiffening and hardening of the arteries, which can lead to decreased blood flow and oxygen supply to the affected tissues.
The condition was first described by a German pathologist named Johann Georg Monckeberg in 1903. It is often asymptomatic and found incidentally during imaging studies or at autopsy. However, in some cases, it can lead to complications such as peripheral artery disease, claudication (pain in the legs with exercise), or even tissue necrosis (tissue death) due to insufficient blood supply.
It is important to note that Monckeberg medial calcific sclerosis is different from atherosclerosis, which is a more common condition characterized by plaque buildup in the inner lining of the arteries. While both conditions can lead to hardening and narrowing of the arteries, they have different underlying causes and risk factors.
Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system mistakenly attacks the protective covering of nerve fibers, called myelin, leading to damage and scarring (sclerosis). This results in disrupted communication between the brain and the rest of the body, causing a variety of neurological symptoms that can vary widely from person to person.
The term "multiple" refers to the numerous areas of scarring that occur throughout the CNS in this condition. The progression, severity, and specific symptoms of MS are unpredictable and may include vision problems, muscle weakness, numbness or tingling, difficulty with balance and coordination, cognitive impairment, and mood changes. There is currently no cure for MS, but various treatments can help manage symptoms, modify the course of the disease, and improve quality of life for those affected.