Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adipokines are cytokines derived from adipose tissue. Recently it has been established that adipokines are closely linked to the pathophysiology of not only metabolic diseases, such as diabetes mellitus, obesity, and atherosclerosis, but also to inflammation and immune diseases. In this study we measured serum levels of adipokines in patients with acute Kawasaki disease to investigate the role of adipokines in the pathophysiology of Kawasaki disease. Serum resistin, high-molecular-weight (HMW) adiponectin, leptin, and visfatin levels were measured by enzyme-linked immunosorbent assay in a total of 117 subjects: 56 patients with acute Kawasaki disease, 30 healthy children, and 31 patients with acute infectious diseases. Serum resistin levels in patients with Kawasaki disease were significantly higher than those of healthy children and patients with acute infectious diseases. In contrast, mean serum HMW adiponectin, leptin, and visfatin levels in patients with Kawasaki disease exhibited no statistically significant differences compared with those in healthy children and patients with infectious diseases. Serum resistin levels decreased significantly after administration of intravenous immune globulin. Serum resistin levels on admission were significantly higher in nonresponders compared with responders to intravenous immune globulin therapy. A multivariate model revealed that C-reactive protein was a factor that was significantly related to elevated serum resistin level in patients with Kawasaki disease. In patients with Kawasaki disease, serum resistin levels were elevated, but decreased to nearly normal after intravenous administration of immune globulin. In contrast, serum HMW adiponectin, leptin, and visfatin levels showed no statistically significant changes. These findings suggest that resistin plays an important role, while other adipokines do not play a major role, in the pathogenesis of Kawasaki disease.
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PMID:Serum adipokine profiles in Kawasaki disease. 2163 13

More than 40 years have passed since Kawasaki syndrome (KS) was first described. Yet KS still remains an enigmatic illness which damages the coronary arteries in a quarter of untreated patients and is the most common cause of childhood-acquired heart disease in developed countries. Many gaps exist in our knowledge of the etiology and pathogenesis of KS, making improvements in therapy difficult. In addition, many KS features and issues still demand further efforts to achieve a much better understanding of the disease. Some of these problem areas include coronary artery injuries in children not fulfilling the classic diagnostic criteria, genetic predisposition to KS, unpredictable ineffectiveness of current therapy in some cases, vascular dysfunction in patients not showing echocardiographic evidence of coronary artery abnormalities in the acute phase of KS, and risk of potential premature atherosclerosis. Also, the lack of specific laboratory tests for early identification of the atypical and incomplete cases, especially in infants, is one of the main obstacles to beginning treatment early and thereby decreasing the incidence of cardiovascular involvement. Transthoracic echocardiography remains the gold-standard for evaluation of coronary arteries in the acute phase and follow-up. In KS patients with severe vascular complications, more costly and potentially invasive investigations such as coronary CT angiography and MRI may be necessary. As children with KS with or without heart involvement become adolescents and adults, the recognition and treatment of the potential long term sequelae become crucial, requiring that rheumatologists, infectious disease specialists, and cardiologists cooperate to develop specific guidelines for a proper evaluation and management of these patients. More education is needed for physicians and other professionals about how to recognize the long-term impact of systemic problems related to KS.
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PMID:Kawasaki syndrome: an intriguing disease with numerous unsolved dilemmas. 2177 1

Kawasaki disease (KD) is acute systemic vasculitis that occurs mainly in infants and children under 5 years of age. The etiology of KD remains unknown. KD is liable to be complicated by coronary artery lesions (CALs), which develop in approximately 15-25% of untreated KD children and in approximately 5% of KD children after intravenous immunoglobulin (IVIG) therapy. A single high dose of IVIG (2 g/kg) is the gold standard therapy in the acute stage of KD. However, approximately 8--38% of children are unresponsive to initial IVIG treatment and at increased risk for CAL development. Anti-inflammatory high doses of aspirin are recommended in conjunction with IVIG, but our study demonstrated that there is no evidence of efficacy in preventing CAL development. The usefulness of steroids in initial therapy for KD or treatment of IVIG-resistant patients is not well established. Other immunosuppressive therapies, including infliximab, have been used in the treatment of refractory KD, but merit additional investigation. Subclinical atherosclerosis may develop early in KD patients, which makes early initiation of therapy to improve chronic inflammation an important issue. Future multicenter studies may help to define the optimal management of KD patients.
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PMID:Recent advances in the treatment of Kawasaki disease. 2210 15

The nuclear protein high mobility group box 1 (HMGB1) has been suggested to be involved in the pathogenesis of several vascular diseases such as systemic vasculitis and atherosclerosis. In systemic vasculitides including ANCA-associated vasculitis and Kawasaki disease, serum HMGB1 levels are higher in patients with active disease compared to healthy controls. In atherosclerotic disease, HMGB1 displays increased expression in nuclei and cytoplasm of macrophages and smooth muscle cells in the atherosclerotic lesions, and is implicated in the progression of the atherosclerotic plaque. Experimental models of acute coronary syndromes and cerebrovascular accidents show that HMGB1 is not only involved in the amplification of the inflammatory response during acute ischemic injury, but also in the recovery and remodeling process after ischemia. Patients with acute coronary syndromes or stroke present significantly higher serum levels of HMGB1 than healthy controls and levels are associated with disease severity and mortality. Here we review clinical and experimental studies dealing with the role of HMGB1 in vascular diseases.
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PMID:HMGB1 in vascular diseases: Its role in vascular inflammation and atherosclerosis. 2249 29

Kawasaki disease (KD) is an acute systemic vasculitis syndrome occurring mostly in children younger than 5 years of age. Especially young infants (<1 year) have an increased risk of coronary artery lesions (CAL). Whereas the etiology of KD is still unknown, progress in treatment during its acute phase has decreased the incidence of CAL from 25-30% to 3-5%. In "atypical KD", the clinical picture is dominated by an unusual symptom as seizure, bloody diarrhea, compressive cervical adenopathy, nephrotic syndrome or hyponatremia. To make a diagnosis in case of "incomplete KD", the supplementary criteria (clinical and biological) suggested by the American Heart Association can be helpful. Once the diagnosis established, the treatment of choice is the intravenous administration of immunoglobulin associated to aspirin at anti-inflammatory dose. However, some patients remain feverish within 36 hours following the end of immunoglobulin administration. This treatment resistance seems increasing in some regions of the globe and can touch up 20% of patients. The unsatisfactory answer to the initial treatment is associated to a higher risk of CAL. Predictive criteria of resistance have been identified and allow to strengthen the medical treatment with a second administration of immunoglobulins. Moreover, methylprednisolone pulse therapy and tumor necrosis factor-alpha blockade (infliximab) appear to be interesting therapeutic options in the future. At last, other treatments have not been the object of controlled studies yet but are alternatives in refractory forms e.g. cytotoxic agents (cyclosporine A, cyclophosphamide, methotrexate), plasmapheresis, plasma exchange or abciximab, especially in patients with aneurysms. Sclerotic vascular changes are often observed in post-Kawasaki disease patients, including those without coronary lesions during the acute phase. Indeed, endothelial dysfunction and risk factors for the development of atherosclerosis, such as dyslipidemia, decreased vascular elasticity, increased C-reactive protein, oxidative stress, and inflammatory cytokines, are known to be present in the late phase of KD. However, it is not clearly established that the survivors of KD carry a higher risk of coronary disease. The epidemiological studies of the next decade should give clearer answers as far as these patients henceforth achieved the age of the atherosclerosis. In conclusion, the diagnosis of KD imposes a strict supervision by a pediatric cardiologist initially. The follow-up is organized according to the existence or non-existence of coronary artery lesions. Late complications as stenosis or coronary thrombosis can occur but remain rare. Thus, it is necessary to be reassuring with the parents, especially for those whose children had no or regressive CAL, while recommending a prevention of the cardiovascular risk factors in the adulthood.
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PMID:[Kawasaki disease: what you need to know]. 2292 12

Patients with different forms of systemic vasculitis experience long-term morbidity and mortality caused by cardiovascular disease due to premature atherosclerosis. Epidemiologic reports of patients with GCA suggest that long-term mortality in this disease is not increased compared with the general population of the same age. The risk of a stroke, however, in particular in the vertebrobasilar territory, is increased. In addition, the occurrence of aortic aneurysmal disease and aortic dissection is also clearly increased in GCA. Mortality due to ischaemic heart disease, however, is not increased. In Takayasu arteritis accelerated atherosclerosis has been clearly documented both clinically and in autopsy reports. Atherosclerotic plaques in the carotid artery may be present in the carotid arteries especially in patients with a documented history of arteritis involving the carotid artery. It is controversial whether Kawasaki disease is associated with accelerated atherosclerosis. Young adults with a history of Kawasaki disease may have abnormal brachial artery reactivity, increased carotid IMT values and increased arterial stiffness. At autopsy examinations of KD patients, however, no significant atherosclerotic lesions are detected and carotid IMT measurements were found to be clearly different from those in young adults with familiar hypercholesterolaemia, suggesting that the remodeling process in KD is different from atherosclerosis. In ANCA-associated vasculitis (AAV), an increased mortality as a consequence of cardiovascular disease is well-documented. In these patients the relative risk for coronary heart disease is two- to fourfold that in control subjects. In addition, a similar relative risk has been found for stroke. Diabetes, hypertension, dyslipidemia, abdominal obesity (metabolic syndrome), impaired renal function, persistent proteinuria and increased production of C-reactive protein are common risk factors for premature atherosclerosis in patients with systemic vasculitis. Furthermore, cholesterol and its modifications play a pivotal role in the pathogenesis of accelerated atherosclerosis in vasculitis. The (preventive) therapy for accelerated atherosclerosis in systemic vasculitis is based on an aggressive approach against inflammation and against risk factors of premature atherosclerosis such as smoking, inactivity, obesity and unhealthy diet. In addition, patients should be treated with angiotensin-converting enzyme inhibitors and/or angiotensin receptor-1 blockers for hypertension and statins for dyslipidemia. Finally, low dose acetylsalicylic acid should be prescribed in patients with large vessel vasculitis, i.e., both in GCA and TA, who do not have contraindications for ASA.
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PMID:Cardiovascular disease due to accelerated atherosclerosis in systemic vasculitides. 2350 55

Young adults suffered from acute cardiac event, such as acute coronary syndrome, ischemic-associated arrhythmia and sudden death, are frequently encountered without known etiology and significant risk factors. Coronary vasculitis due to Kawasaki disease contributes to be a risk factor in young adult population to develop acute coronary event. Afflicted predominantly during childhood, Kawasaki disease gives rise to vasculitis of coronary artery which becomes major concern since it leads to coronary aneurysm and stenosis. Self-limited nature of Kawasaki disease make those suffered in childhood survive into adult life. Accelerated coronary atherosclerosis in the Kawasaki disease-related lesion occurring in young adult and subsequent acute coronary syndrome and sudden death in this population are devastating impacts of the sequel of Kawasaki disease. It is expected that internists and adult cardiologists become familiar with this sequel and provide better care for the patients.
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PMID:Coronary artery sequel of Kawasaki disease in adulthood, a concern for internists and cardiologists. 2358 13

Coronary ectasia is rare in patients with Noonan syndrome. When suspected during echocardiography more common causes including Kawasaki disease in children and atherosclerosis coronary artery disease in adults should be ruled out. Coronary CT angiogram, a non-invasive imaging tool may be preferred over conventional coronary angiogram in the initial diagnosis and monitoring the progression of coronary ectasia in such patients. Aspirin may be considered to prevent coronary thrombosis.
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PMID:Coronary artery ectasia in an adult Noonan syndrome detected on coronary CT angiography. 2360 65

Coronary aneurysms represent anomalies identified in 0.15%-4.9% of patients undergoing coronary angiography. At present, there is no uniform definition of this pathology. Aneurysms of the left main coronary artery (LMCA) are extremely uncommon, with an incidence of 0.1%. It has been demonstrated that atherosclerosis is the main cause of these anomalies in adults, and Kawasaki disease in children and adolescents. Other causes include connective tissue disorders, trauma, vasculitis, congenital, mycotic, and idiopathic. These dilated sections of the coronary artery are not benign pathology because they are subject to spasm, thrombosis, and subsequent distal embolism, spontaneous dissection and rupture. Treatment options include anticoagulation, custom-made covered stents, reconstruction, resection, and exclusion with bypass. Our report on an old case illustrates the giant saccular LMCA aneurysm leading to myocardial ischemia due to coronary steal phenomenon.
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PMID:Giant saccular aneurysm of the left main coronary artery. 2361 May 81

Kawasaki disease (KD) is an acute medium vessel vasculitis seen in children. The most significant long-term complication is related to coronary artery abnormalities. Use of intravenous immunoglobulins, however, has led to significant reduction in incidence of coronary aneurysms. What is more alarming is the fact that higher risk of cardiovascular disease is seen in even those children who do not have coronary artery aneurysms during subacute phase. Various factors like abnormal lipid profiles, abnormal vessel wall reactivity and endothelial dysfunction have been implicated for this. Carotid intima-media thickness (cIMT) has been used as a surrogate marker for atherosclerosis. This study was planned to evaluate cIMT in children with KD. Twenty-seven children with diagnosis of KD at least 1 year prior to enrolment were evaluated for cIMT at enrolment and then after 3 months. Fasting lipid profile was done for all patients. Mean cIMT was significantly higher in children with KD compared to controls. In lipid profiles, undesirable HDL-C and triglyceride levels were seen in 2 and 3 children, respectively. Undesirable and borderline LDL-C levels were seen in 1 and 2 patients, respectively. Undesirable and borderline total cholesterol levels were seen in 1 and 3 patients, respectively. Higher cIMTs were seen in our cohort of KD patients. Proatherogenic abnormalities in lipid profile were seen in a few patients. Both abnormalities may predict a higher risk of atherosclerosis in future. The results of this study need to be replicated on a larger study sample and over longer follow-up periods.
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PMID:Carotid intima-media thickness in children with Kawasaki disease. 2392 93


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