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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of chronic inflammation causing metabolic and vascular disorders is increasingly recognized. It is hypothesized that proinflammatory cytokines contribute to atherogenesis, peripheral insulin resistance, and the development of hypertension and type II diabetes. Psoriasis as a chronic inflammatory skin disorder is characterized by a variety of immunologic and inflammatory changes and may similarly predispose for those disorders. The objective of this study was to elucidate the association of psoriasis with chronic vascular and metabolic disorders. We investigated a total of 581 adult patients hospitalised for plaque type psoriasis as compared to 1,044 hospital-based controls. A distinct pattern of chronic disorders was found to be significantly associated with psoriasis, including diabetes mellitus type II [odds ratio (OR)=2.48], arterial hypertension (OR = 3.27), hyperlipidemia (OR = 2.09), and coronary heart disease (OR = 1.95). The combined presence of these conditions together with obesity, known as the metabolic syndrome, was clearly more prevalent in psoriasis patients (OR = 5.29). In addition, psoriasis patients were significantly more likely to be smokers (OR = 2.96) and to have a regular or heavy consumption of alcohol (OR = 3.33 and 3.61, respectively). In conclusion, psoriasis patients appear to be at higher risk for diabetes mellitus and cardiovascular disease. This could likely be due to the effects of chronic inflammatory changes, in particular the secretion of proinflammatory cytokines. The risk of late term cardiovascular complications might support the use of systemic treatment in psoriasis.
Arch Dermatol Res 2006 Dec
PMID:Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis. 1702 63

To date, diabetes-associated skin ulcerations represent a therapeutic problem of clinical importance. The insulin-resistant type II diabetic phenotype is functionally connected to obesity in rodent models of metabolic syndrome through the release of inflammatory mediators from adipose tissue. Here, we used the impaired wound-healing process in obese/obese (ob/ob) mice to investigate the impact of obesity-mediated systemic inflammation on cutaneous wound-healing processes. Systemic administration of neutralizing monoclonal antibodies against tumor necrosis factor (TNF)alpha (V1q) or monocyte/macrophage-expressed EGF-like module-containing mucin-like hormone receptor-like (Emr)-1 (F4/80) into wounded ob/ob mice at the end of acute wound inflammation initiated a rapid and complete neo-epidermal coverage of impaired wound tissue in the presence of a persisting diabetic phenotype. Wound closure in antibody-treated mice was paralleled by a marked attenuation of wound inflammation. Remarkably, anti-TNFalpha- and anti-F4/80-treated mice exhibited a strong reduction in circulating monocytic cells and reduced numbers of viable macrophages at the wound site. Our data provide strong evidence that anti-TNFalpha therapy, widely used in chronic inflammatory diseases in humans, might also exert effects by targeting "activated" TNFalpha-expressing macrophage subsets, and that inactivation or depletion of misbehaving macrophages from impaired wounds might be a novel therapeutic clue to improve healing of skin ulcers.
J Invest Dermatol 2007 Sep
PMID:Systemic anti-TNFalpha treatment restores diabetes-impaired skin repair in ob/ob mice by inactivation of macrophages. 1746 Jul 30

Experts on psoriasis convened with authorities from other medical specialties to discuss the recently described association between psoriasis, obesity and subsequent cardiovascular comorbidity. Similar to other diseases of increased systemic inflammation, psoriasis has been linked to a heightened risk of myocardial infarction, especially in the more severely affected, younger patients. However, unlike in other inflammatory diseases - such as rheumatoid arthritis - more severely affected patients with psoriasis are much more likely to be obese. Importantly, the pathophysiology of both psoriasis and obesity shows many shared cytokines that are known to contribute to features of the metabolic syndrome, such as hypertension, dyslipidaemia and insulin resistance. The strong association between psoriasis and obesity potentially makes psoriasis an important healthcare issue that requires an update in its standard of care. This meeting reviewed the evidence-based literature and addressed how, moving forward, dermatologists and other specialists may redefine the magnitude of health risk associated with more severe psoriasis and its comorbidities, while clarifying both the epidemiology and pathophysiology of the association with obesity.
Br J Dermatol 2007 Oct
PMID:Obesity in psoriasis: the metabolic, clinical and therapeutic implications. Report of an interdisciplinary conference and review. 1762 91

Epidemiological studies have shown that, in psoriasis patients, associated disorders may occur more frequently than expected. Such comorbidities include psoriatic arthritis, psoriatic pustular diseases, Crohn disease, and signs of metabolic syndrome, which leads to atherosclerosis with coronary heart disease. Although the disorders represent separate entities, they appear to follow overlapping pathogenic pathways. Comorbidities often become clinically manifest years after onset of psoriasis and are frequently seen in severe disease. Persistent low-grade inflammation with secretion of proinflammatory cytokines (eg, tumor necrosis factor alpha) favors the development of insulin resistance and metabolic syndrome. In addition, biochemical and immunologic observations point toward an inflammatory immune mechanism that uses tools of the innate defense armamentarium.
Clin Dermatol
PMID:Comorbidities in psoriasis. 1802 89

After an initial attempt by the WHO to define metabolic syndrome (MS) on a pathophysiologically oriented approach requiring the assessment of insulin resistance markers, the NCEP-ATPIII and more recently the IDF proposed more clinically oriented criteria to help, toward a preventive medicine goal, to identify patients who are likely to have features of the MS and be at increased risk of type 2 diabetes and cardio vascular disease. The notion of MS is built around abnormalities of the metabolism of lipids and carbon hydrates, a rise of blood pressure, and visceral obesity of abdominal localization. These parameters report only partially on mechanisms leading to the development of the MS. The physiopathology of MS is partially understood even today and likely results from the combination of environmental, genetic and epigenetic factors. Abdominal visceral obesity, a state of low-grade chronic inflammation and insulin resistance are the main processes susceptible to explain the various constituents of this syndrome.
Ann Dermatol Venereol 2008 Feb
PMID:[Pathogenesis of the metabolic syndrome]. 1846 91

The prevalence of the metabolic syndrome is rising, particularly in developed countries, and this is largely driven by increasing obesity and sedentarity rates. Regardless of the definition, the prevalence found in France was lower than in North America and in other European countries; it varied from 11.7 p. cent in men and 7.5 p. cent in women according to the National Cholesterol Education Program (NCEP) definition to 26 p. cent in men and 18.4 p. cent in women according to the International Diabetes Federation (IDF) definition. The presence of the metabolic syndrome promotes the occurrence of type 2 diabetes and clinical atherosclerosis. Relative risk of cardiovascular morbidity and mortality is close to 2 in subjects with metabolic syndrome. The informative value of identifying metabolic syndrome has been demonstrated in the general population as well as in hypertensive subjects. However, it could provide only limited clinical value for cardiovascular disease risk stratification in type 2 diabetes mellitus.
Ann Dermatol Venereol 2008 Feb
PMID:[Metabolic syndrome: epidemiology and its risks]. 1846 92

Psoriasis is a chronic immune-inflammatory-mediated disease that can predispose patients to other inflammatory conditions. For example, individuals with psoriasis are at increased risk for insulin resistance, obesity, dyslipidemia, and hypertension--components that characterize the metabolic syndrome. The metabolic syndrome is an important driver of adverse cardiovascular outcomes. Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), and other factors that are overproduced in patients with psoriasis likely contribute to the increased risk for development of metabolic syndrome. This article reviews the association of psoriasis with metabolic syndrome, as well as the impact of biologic agents that are currently used to treat psoriasis (ie, TNF antagonists) on risk factors for metabolic syndrome.
J Drugs Dermatol 2008 Jun
PMID:Psoriasis and the metabolic syndrome. 1856 88

For this What's new in clinical dermatology?, I have selected some important publications mainly in the field of the infectious dermatosis and drugs allergy. The Chikungunya virus which is responsible of several epidemics since 2005 seems to be a virus with a cutaneous tropism. Sexually transmitted diseases are still a public health problem and we shall review the situation for syphilis, lymphogranuloma venereum and the new dynamic profile of HIV in France. Lyme disease has been the subject of consensus conference in France and in the United States. Original clinical presentations in relation with infectious agent will be also presented. We shall give a large place to what I call the toxidermatology. During the year 2007, the role of gadolinium in the nephrogenic systemic fibrosis has been confirmed, many publications have reported the side effects of biotherapies on the skin and we shall emphasize the paradoxical of some of them. Hypersensitivity syndrome and notably the controversial role of viral reactivations has been reported. The relationship between psoriasis and metabolic syndrome or cardiovascular risks has been discussed since 2006. New clinical features have been described and will be presented during this session.
Ann Dermatol Venereol 2007 Dec
PMID:[What's new in clinical dermatology?]. 1867 39

Psoriasis is a chronic, inflammatory, immune-mediated skin disease associated with substantial comorbidity. Traditional comorbid conditions include psychological/psychiatric disorders, psoriatic arthritis and inflammatory bowel disease. Increasingly, an association with metabolic dysfunction, including obesity and the metabolic syndrome, and cardiovascular disease, with consequent effects on morbidity and mortality, has been recognized in psoriasis. The underlying inflammatory mechanisms of both psoriasis and psoriasis-associated comorbidities involve mediation by proinflammatory T-helper type 1 cytokines. For effective management of psoriasis and related comorbidities, an integrated approach targeting both cutaneous and systemic inflammation may be beneficial, and strategies to improve overall management of the patient should be encouraged to reduce the disease burden. This paper discusses the emerging role of biological agents in this approach, and offers an appreciation of the role of existing anti-psoriasis and adjunctive therapies.
Br J Dermatol 2008 Aug
PMID:Long-term prognosis in patients with psoriasis. 1870 Sep 9

Psoriasis is a systemic inflammatory disease whose cutaneous involvement is the most visible component. Treating the skin and the psychological effects is the main objective of today's treatments. However, the discovery of comorbidities and their effects on the frequently associated cardiac and cerebral vascular risk and on metabolic syndrome has led to substantial modification of patient management and to new therapeutic strategies. This review of the comorbidities associated with cutaneous psoriasis and the impacts of systemic treatments for psoriasis on these comorbidities aims to outline what the future may hold in terms of patient management.
Ann Dermatol Venereol 2008 Jul
PMID:[Severe psoriasis: beyond the skin, what are the risks of not treating the disease?]. 1872 66


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