Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasma kallikrein-kinin system (KKS) participates in the pathogenesis of inflammatory reactions involved in cellular injury, coagulation, fibrinolysis, kinin formation, complement activation, cytokine secretion and release of proteases. It has been shown that KKS activation in the systemic inflammatory response syndrome results in decrease of its component plasma proteins. Similar changes have been documented in diabetes, sepsis, children with vasculitis, allograft rejection, disseminated intravascular coagulation, patients with recurrent pregnancy losses, hereditary angioedema, adult respiratory distress syndrome and coronary artery disease. Direct involvement of the KKS in the pathogenesis of experimental acute arthritis and acute and chronic enterocolitis has been documented by previous studies from our laboratory using experimental animal models. It has been found that in HK deficient Lewis rats, experimental IBD was much less severe. We showed a genetic difference in kininogen structure between resistant Buffalo and susceptible Lewis rats, which results in accelerated cleavage of HK and it is responsible for the susceptibility to the inflammatory process in the Lewis rats. It has been demostrated that therapy with a specific plasma kallikrein inhibitor (P8720) modulated the experimental enterocolitis, arthritis and systemic inflammation. Furthermore, it has been shown that a bradykinin 2 receptor (B2R) antagonist attenuates the inflammatory changes in the same animal model. We have showed that a monoclonal antibody targeting HK decreases angiogenesis and arrests tumor growth in a syngeneic animal model. In summary, these results indicate that the plasma KKS plays a central role in the pathogenesis of chronic intestinal inflammation, arthritis and angiogenesis.
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PMID:[High molecular weight kininogen in inflammation and angiogenesis: a review of its properties and therapeutic applications]. 1670 6

Ulcerative colitis (UC) can manifest with a variety of extra-intestinal disorders frequently affecting the skin, joints, and liver. An aetiologic role of alpha1-antitrypsin deficiency in chronic inflammatory bowel disease has recently been suggested. We report a patient with UC and alpha1-antitrypsin deficiency who presented with disseminated cutaneous leucocytoclastic vasculitis clinically appearing with target-like purpuric patches and haemorrhagic oedemas. In addition, he displayed acute haemorrhage of the eyes and the respiratory tract consistent with a systemic vasculitic process. Moreover, he had autoimmune haemolytic anaemia. Systemic vasculitides, such as Wegener's granulomatosis, Churg-Strauss syndrome, and microscopic polyangiitis, could widely be excluded. Systemically administered glucocorticosteroids and azathioprine led to dramatic improvement of extra-intestinal symptoms. On the basis of alpha1-antitrypsin deficiency and UC, the present patient likely developed severe systemic vasculitis with multi-organ involvement. UC should at times be viewed within the context of a more generalized immune imbalance affecting multiple organs, and not as an isolated pathological entity. Testing for alpha1-antitrypsin deficiency in UC patients may detect individuals at higher risk of severe extra-intestinal involvement.
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PMID:Complex extra-intestinal complications of ulcerative colitis in a patient with alpha1-antitrypsin deficiency. 1675 Nov 15

The most common extraintestinal manifestations of Crohn's disease and ulcerative colitis are iritis and uveitis, primary sclerosing cholangitis (PSC) and nodal erythema and pyoderma gangrenosum. Complications within the cardiovascular system seem to be uncommon, but there are no systematic investigations concerning the epidemiology of these manifestations. There are more than 100 cases reported about pericarditis and perimyocarditis in patients with inflammatory bowel disease. Other patients with Crohn's disease or ulcerative colitis suffer from vasculitis, representing a further mechanism of inflammatory diseases of the cardiovascular system. There are several case reports showing a combination of Takayasu's arteritis and Crohn's disease, and cross-reacting antibodies against gut mucosa and aortic tissue were found. Some patients developed thrombotic complications by activating the coagulation system, which can result in atrial thrombi, embolism of the pulmonary arteries, myocardial infarction and disseminated intravascular coagulopathy (DIC). Furthermore, a few case were reported about atrio ventricular blocks, amyloidosis of the heart, dilative cardiomyopathy and endomyocardial fibrosis in patients with chronic inflammatory bowel disease. Here, a 27-year-old patient with known ulcerative colitis for 2 years is reported, who presented in the authors' department with unstable angina pectoris. Coronary angiographic examination was immediately performed and diffuse intracoronary thrombi were found, which could be removed by the catheter procedure. A myocardial infarction did not develop. Because of positive anti neutrophil cytoplasmic antibodies (p-ANCA) a p-ANCA-positive arteritis of the coronary vessels with intracoronary thromboembolism due to ulcerative colitis was diagnosed. Systematic studies or investigations concerning the epidemiology of the cardiovascular complications are still lacking, so that an overview about the published data is given.
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PMID:[Chronic inflammatory bowel disease and cardiovascular complications]. 1680 21

Pyoderma gangrenosum (PG) is an uncommon cutaneous disease of unknown etiology. In 50 percent of affected patients, PG is associated with systemic disease including inflammatory bowel disease, arthritis, and hematologic malignancies.(1) Diagnosis of PG is based on clinical presentation, histopathology and on the exclusion of other diseases that can produce clinically similar lesions, e.g. infection, vasculitis, malignancy, collagen vascular diseases, diabetes, and trauma. Four variants of PG have been described: ulcerative, pustular, bullous, and vegetative.(2) We report a woman with renal failure who developed PG in the absence of any obvious triggering trauma in a distinctive unilateral crop just distal to an arteriovenous dialysis shunt.
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PMID:Pyoderma gangrenosum occurring near an arteriovenous dialysis shunt. 1686 25

A clinically and pathologically distinct form of chronic pancreatitis is now widely recognized and has been designated variably as lymphoplasmacytic sclerosing pancreatitis, duct-destructive (duct-centric) pancreatitis or autoimmune pancreatitis. This entity is currently defined by a constellation of clinical and pathologic findings, including the lack of both conventional risk factors for pancreatitis, such as alcohol use and gallstones, and their hallmark pattern of injury, including calcifications and pseudocysts. Histologically, it is characterized by lymphoplasmacytic inflammation with abundant IgG4-positive plasma cells that exhibit an affinity for ducts as well as venules ("peri-venulitis," with or without frank vasculitis). Inflammation is often associated with sclerosis and expansion of periductal tissue. In some cases, fibroblastic activity is prominent and resembles "inflammatory pseudotumor" or is even misdiagnosed as "inflammatory myofibroblastic tumor." In what appears to be a distinct subset of this entity, intraepithelial granulocytic infiltrates may be seen. Well-developed examples are readily recognized; however, lesser ones may be difficult to distinguish from other forms of pancreatitis based on morphology alone. This type of pancreatitis is considered an autoimmune process. In about 15% to 20% of patients, the clinical stigmata of autoimmune conditions are present at the time of diagnosis, and in many others, discovered subsequently. The usual "lymphoplasmacytic sclerotic" type tends to be associated with Sjogren, whereas the "granulocytic" subset, with inflammatory bowel disease. Most patients present with a pancreatic head mass, often with an accompanying stricture of the distal common bile duct, which thus radiologically resembles "pancreas cancer." In fact, this entity accounts for more than a third of the cases of pseudotumoral pancreatitis (mass-forming inflammatory lesions that resemble carcinoma). Elevated serum IgG4 levels are characteristic and may be very helpful in the differential diagnosis from tumors and tumor-like lesions of the pancreas which seldom result in levels above 135 mg/dL. The mean age of the patients with this condition is in the mid-50s; the subset with granulocytic intraepithelial lesions seem to be younger (mid 40s). Despite the autoimmune association, males are afflicted as commonly as (if not more than) females. Following resection, emergence of new fibro-inflammatory lesions in the remaining pancreaticobiliary tree has been noted in some cases; however, the process typically responds to steroids. It is important to recognize the distinctive clinicopathologic features of this entity, so that it can be diagnosed accurately and managed appropriately.
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PMID:Diagnostic features and differential diagnosis of autoimmune pancreatitis. 1693 59

Inflammation is traditionally viewed as a physiological reaction to tissue injury. Leukocytes contribute to the inflammatory response by the secretion of cytotoxic and pro-inflammatory compounds, by phagocytotic activity and by targeted attack of foreign antigens. Leukocyte accumulation in tissues is important for the initial response to injury. However, the overzealous accumulation of leukocytes in tissues also contributes to a wide variety of diseases, such as atherosclerosis, chronic inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, vasculitis, systemic inflammatory response syndrome, juvenile diabetes and psoriasis. Many therapeutic interventions target immune cells after they have already migrated to the site of inflammation. This review addresses different therapeutic strategies, used to reduce or prevent leukocyte-endothelial cell interactions and communication, in order to limit the progression of inflammatory diseases.
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PMID:Therapeutic targeting of molecules involved in leukocyte-endothelial cell interactions. 1695 69

Worldwide, over 400,000 patients have been treated with tumour necrosis factor (TNF)-alpha antagonists for indications that include rheumatoid arthritis, juvenile rheumatoid arthritis, inflammatory bowel disease, psoriatic arthritis and ankylosing spondylitis. Since their approval, concerns regarding safety have been raised. There is a risk of re-activation of granulomatous diseases, especially tuberculosis, and measures should be taken for detection and treatment of latent tuberculosis infections. Preliminary data suggest that anti-TNF therapy may be safe in chronic hepatitis C. However, TNF-alpha antagonists have resulted in re-activation of chronic hepatitis B if not given concurrently with antiviral therapy. Solid tumours do not appear to be increased with anti-TNF therapy. Variable rates of increased lymphoma risk have been described with anti-TNF therapy compared with the general population, although no increased risk was found compared with a rheumatoid arthritis population. Large phase II and III trials with TNF-alpha antagonists in advanced heart failure have shown trends towards a worse prognosis, and should therefore be avoided in this population. Both etanercept and infliximab are associated with the formation of autoantibodies, and these autoantibodies are rarely associated with any specific clinical syndrome. Rare cases of aplastic anaemia, pancytopenia, vasculitis and demyelination have been described with anti-TNF therapy. This chapter will discuss the safety profile and adverse events of the three commercially available TNF-alpha antagonists: etanercept, infliximab and adalimumab. The data presented in this review have been collected from published data, individual case reports or series, package inserts, the Food and Drug Administration postmarketing adverse events surveillance system, and abstracts from the American College of Rheumatology and European Congress of Rheumatology meetings for 2005.
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PMID:Problems encountered during anti-tumour necrosis factor therapy. 1697 37

Ulcerative colitis and Crohn's disease are associated with a variety of systemic manifestations. Pulmonary disease has been described much less frequently than other organ systems, yet more than 400 cases have been reported. Lung and gastrointestinal system are originated from primitive gut and they have same pathogenetic changes in these patients. Major patterns of pulmonary disease associated with inflammatory bowel disease (IBD) are pleuritis, airway disease, interstitial lung disease, necrobiotic nodules, pulmonary eosinophilia, thromboembolic disease, vasculitis, granulomatous lung disease, etc. Colectomy may aggravate respiratory symptoms. Drug induced disease must be kept in mind in patients taking sulfasalazine, mesalamine, methotrexate, and anti-TNF-alpha. Latent pulmonary abnormalities are evident either at pulmonary function tests or induced sputum or bronchoalveolar lavage, have been also reported in patients with inflammatory bowel disease in the absence of clinical evidence of airway disease. The treatment of IBD related respiratory involvement depends on the specific pattern of involvement, if left untreated, especially in airway disease, puts the patient at risk of developing irreversible destruction of the air passage. A high degree of suspicion is necessary to detect early the respiratory disease in association with any form of bowel disease.
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PMID:[Inflammatory bowel disease and lung]. 1700 50

Fever of unknown origin (FUO) was originally defined as recurrent fever of 38.3 degrees C or higher, lasting 2-3 wk or longer, and undiagnosed after 1 wk of hospital evaluation. The last criterion has undergone modification and is now generally interpreted as no diagnosis after appropriate inpatient or outpatient evaluation. The 3 major categories that account for most FUOs are infections, malignancies, and noninfectious inflammatory diseases. The diagnostic approach in FUO includes repeated physical investigations and thorough history-taking combined with standardized laboratory tests and simple imaging procedures. Nevertheless, there is a need for more complex or invasive techniques if this strategy fails. This review describes the impact of (18)F-FDG PET in the diagnostic work-up of FUO. (18)F-FDG accumulates in malignant tissues but also at the sites of infection and inflammation and in autoimmune and granulomatous diseases by the overexpression of distinct facultative glucose transporter (GLUT) isotypes (mainly GLUT-1 and GLUT-3) and by an overproduction of glycolytic enzymes in cancer cells and inflammatory cells. The limited data of prospective studies indicate that (18)F-FDG PET has the potential to play a central role as a second-line procedure in the management of patients with FUO. In these studies, the PET scan contributed to the final diagnosis in 25%-69% of the patients. In the category of infectious diseases, a diagnosis of focal abdominal, thoracic, or soft-tissue infection, as well as chronic osteomyelitis, can be made with a high degree of certainty. Negative findings on (18)F-FDG PET essentially rule out orthopedic prosthetic infections. In patients with noninfectious inflammatory diseases, (18)F-FDG PET is of importance in the diagnosis of large-vessel vasculitis and seems to be useful in the visualization of other diseases, such as inflammatory bowel disease, sarcoidosis, and painless subacute thyroiditis. In patients with tumor fever, diseases commonly detected by (18)F-FDG PET include Hodgkin's disease and aggressive non-Hodgkin's lymphoma but also colorectal cancer and sarcoma. (18)F-FDG PET has the potential to replace other imaging techniques in the evaluation of patients with FUO. Compared with labeled white blood cells, (18)F-FDG PET allows diagnosis of a wider spectrum of diseases. Compared with (67)Ga-citrate scanning, (18)F-FDG PET seems to be more sensitive. It is expected that PET/CT technology will further improve the diagnostic impact of (18)F-FDG PET in the context of FUO, as already shown in the oncologic context, mainly by improving the specificity of the method.
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PMID:18F-FDG PET and PET/CT in fever of unknown origin. 1720 97

Erythema nodosum, a painful disorder of the subcutaneous fat, is the most common type of panniculitis. Generally, it is idiopathic, although the most common identifiable cause is streptococcal pharyngitis. Erythema nodosum may be the first sign of a systemic disease such as tuberculosis, bacterial or deep fungal infection, sarcoidosis, inflammatory bowel disease, or cancer. Certain drugs, including oral contraceptives and some antibiotics, also may be etiologic. The hallmark of erythema nodosum is tender, erythematous, subcutaneous nodules that typically are located symmetrically on the anterior surface of the lower extremities. Erythema nodosum does not ulcerate and usually resolves without atrophy or scarring. Most direct and indirect evidence supports the involvement of a type IV delayed hypersensitivity response to numerous antigens. A deep incisional or excisional biopsy specimen should be obtained for adequate visualization. Erythema nodosum represents an inflammatory process involving the septa between subcutaneous fat lobules, with an absence of vasculitis and the presence of radial granulomas. Diagnostic evaluation after comprehensive history and physical examination includes complete blood count with differential; erythrocyte sedimentation rate, C-reactive protein level, or both; testing for streptococcal infection (i.e., throat culture, rapid antigen test, antistreptoly-sin-O titer, and polymerase chain reaction assay); and biopsy. Patients should be stratified by risk for tuberculosis. Further evaluation (e.g., purified protein derivative test, chest radiography, stool cultures) varies based on the individual. Erythema nodosum tends to be self-limited. Any underlying disorders should be treated and supportive care provided. Pain can be managed with nonsteroidal anti-inflammatory drugs.
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PMID:Erythema nodosum: a sign of systemic disease. 1737 16


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