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

Criteria for the classification of polyarteritis nodosa were developed by comparing 118 patients who had this disease with 689 control patients who had other forms of vasculitis. For the traditional format classification, 10 criteria were selected: weight loss greater than or equal to 4 kg, livedo reticularis, testicular pain or tenderness, myalgias, mononeuropathy or polyneuropathy, diastolic blood pressure greater than 90 mm Hg, elevated blood urea nitrogen or serum creatinine levels, presence of hepatitis B reactants in serum, arteriographic abnormality, and presence of granulocyte or mixed leukocyte infiltrate in an arterial wall on biopsy. The presence of 3 or more of these 10 criteria was associated with a sensitivity of 82.2% and specificity of 86.6%. A classification tree was also constructed, with 6 criteria being selected. Three of these, angiographic abnormality, biopsy-proven granulocyte or mixed leukocyte infiltrate in arterial wall, and neuropathy, were criteria used in the traditional format. The other 3 criteria used in the tree format included the patient's sex, weight loss greater than 6.5 kg, and elevated serum aspartate aminotransferase or alanine aminotransferase levels above the range of normal. The classification tree yielded a sensitivity of 87.3% and a specificity of 89.3%.
 ...
PMID:The American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. 197 74

The actiopathogenesis of leucocytoclastic vasculitis is still unknown, but recently hepatitis C virus (HCV) has been suggested as trigger of autoimmunity. We report a case of a 26-yr-old patient with purpura due to leucocytoclastic vasculitis associated with hepatitis C virus infection. Laboratory findings showed AST, ALT, gamma GT within normal limits, positive antibodies to HCV (IIF and Riba II) and polymerase chain reaction for HCV RNA. Anti-nuclear antibodies, IgG and IgM anti-cardiolipin antibodies, anti-platelet antibodies and anti-neutrophil cytoplasmic antibodies with perinuclear pattern were also present. A skin biopsy specimen of a purpuric lesion showed leucocytoclastic vasculitis with small vessel thrombosis and perivascular deposition of IgM and fibrinogen on immunofluorescence study. This case shows a role of HCV in leucocytoclastic vasculitis; it is possible that this HCV can induce autoimmunity independently of cryoglobulins and liver involvement.
 ...
PMID:Leucocytoclastic vasculitis associated with hepatitis C virus antibodies. 911 52

Six of the 33 calves born in a Swedish dairy herd during a period of four months developed laminitis when they were eight to 12 weeks old. The clinical signs included difficulty in rising, a stiff gait, overgrown claws and haemorrhages in the sole horn. Samples of blood were taken from four of the calves when they had shown signs of laminitis for two to seven weeks; the serum concentrations of calcium, phosphorus and vitamin D3, the activities of aspartate aminotransferase and glutathione peroxidase, and the patterns of serum proteins were within their normal ranges. The feet of the same four calves were examined after slaughter; the third phalanx of each calf was rotated and its distal end osteolytic. Histologically there was separation and degeneration of the squamous cells of the white line, and thromboses and vasculitis in the fine vessels of the corium. Four of the six affected calves were persistently infected with bovine viral diarrhoea virus and one had antibodies against the virus. From six weeks of age the calves had been fed rye wheat, a hybrid seed rich in starch, and this may have contributed to the outbreak of laminitis.
 ...
PMID:Laminitis in young dairy calves fed a high starch diet and with a history of bovine viral diarrhoea virus infection. 919 98

A 66-year-old female was admitted to our hospital in January, 1998, complaining of low grade fever and muscle weakness of her legs. Physical examination revealed muscle weakness of her neck (4/5) and proximal skeletal muscles of her bilateral legs (3/5-4/5). She showed proteinuria and microhematuria. Her serum levels of ureanitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatinekinase, aldolase and myoglobin were all within the normal ranges. Antinuclear antibodies were negative, but her serum levels of pANCA (743 EU) and C reactive protein (18.0 mg/dl) were elevated. Neuroconduction velocity of her left common peroneal nerve was decreased to 40.8 m/sec and electric myograph showed neurogenic changes. Magnetic resonance images (MRI) of her bilateral thigh depicted high signal intensity in quadriceps by T 2 weighed images, but the signals were not enhanced by gadolinium injection. Muscle and renal biopsies revealed necrotizing vasculitis of the small arteries. Crescentic glomerulonephritis was also observed by renal biopsy. These findings supported the diagnosis of microscopic PN. On 16 th admission day, she developed acute cardiac and respiratory failures due to cardiac and respiratory muscle involvements with PN, and was assisted by mechanical ventilation. She was treated with methylprednisolone pulse therapy (500 mg/day, three consecutive days) on 18 th admission day, followed by 40 mg of oral prednisolone daily. However, her symptoms deteriorated, and herserum creatinine levels increased to 2.4 mg/dl. On 24 th admission day, intravenous cyclophosphamide pulse therapy (500 mg/day) was instituted. Her cardiac wall motion on echocardiography and serum creatinine levels gradually improved, but her skeletal and respiratory muscle weakness did not improve. On 38 th admission day, she was complicated with respiratory infection by methicillin resistant Staphylococcus aures. On 62 th admission day, she died of endotoxic shock. This is the first report describing respiratory muscle involvement with PN, and the second report describing MRI findings of muscle involvement by PN. Therefore, our case provides important clinical information for the diagnosis and treatment of the disease.
 ...
PMID:[A case of microscopic polyangiitis with severe cardiac and respiratory muscle involvement]. 1061 70

Numerous extrahepatic manifestations have been reported in patients with both acute and chronic hepatitis B (arthralgias or arthritis, skin rashes, glomerulonephritis and neuritis), all of which are present in polyarteritis nodosa (PAN) which is the most unique and spectacular extrahepatic manifestation. In the 1970s, the frequency of PAN due to the hepatitis B (HBV) reached 30%. Immunization programs explain the decrease and it is now down to 7%. PAN usually occurs within 6 months of infection. Clinical manifestations reflect this most classic form of PAN, Hepatic manifestations including, ALT/AST elevations are mild and usually overlooked. Besides HBV, other viruses may be responsible for cases of vasculitides including PAN, HIV, Parvovirus B19, and EBV. Different pathogenic mechanisms have been identified but immune complexes are mainly thought to be responsible. In glomerulonephritis, detailed immunostaining and ultrastructural findings indicate that HBe antigen (Ag) is more likely to be the responsible antigen. In PAN, fewer reports are available and early studies with poorly defined antibodies need to be revisited. Interestingly almost all cases of HBV/PAN are associated with wild-type HBV infection, characterised by HBe antigenemia and high HBV replication, supporting the concept that lesions could result from the deposit of viral Ag/Ab complexes soluble in Ag excess, possibly involving HBe Ag. The recent observation of PAN cases associated with precore mutation which abrogates the formation of HBe Ag challenges this view. It may suggest that other, still undefined, circulating HBV-related Ag(s) distinct from HBe Ag could be involved. Remarkably, none of the HBV/PAN cases or glomerulonephritis exhibit antineutrophil cycoplasmic antibodies (ANCA) reactivity. Viral PAN can now be completely separated from other form of vasculitis mostly autoimmune in nature. Based on the efficacy of antiviral agents in chronic hepatitis B and of plasma exchanges in PAN we combined both therapies to treat HBV PAN. This was associated with swift recovery, even in the most severe forms. The perfect time correlation between inhibition of virus replication and resolution of all bioclinical signs suggest a direct pathogenic role of the virus possibly via immune complexes. Traditional immunosuppressive and steroid therapy should no longer be used for HBV PAN cases.
 ...
PMID:Polyarteritis nodosa and extrahepatic manifestations of HBV infection: the case against autoimmune intervention in pathogenesis. 1133 92

Various clinical and immunological extrahepatic manifestations were described during infection by hepatitis C virus (HCV). We reported a rare association, within the same patient, made up with a cutaneous leucytoclastic vasculitis, cryoglobulinemia and aplastic anemia. A 70 years old woman with infection by HCV diagnosed four years ago, was hospitalized due to upper members purpura and six cutaneous ulcerations. Complete blood count revealed a pancytopenia. Prothrombin time was at 65%, AST, ALT an d GT were within normal limits. Test for antibodies to HCV en serum was positive. Bone marrow aspiration showed marked hypocellularity. A skin biopsy showed leucocytoclastic vasculitis of small vessels. Interferon a therapy was not indicated because aplastic anemia. Simultaneous occurrence of cutaneous vasculitis, cryoglobulinemia and aplastic anemia during HCV infection lays the question of their mechanism. Purpura and cutaneous ulcerations can be due to cryoglobulinia.
 ...
PMID:[Leukocytoclastic vasculitis, cryoglobulinemia and medullary aplasia associated with hepatitis C]. 1177 39

We experienced a girl with polyarteritis nodosa (PN) diagnosed by myocardial biopsy. The symptoms began with high fever and skin rash. These symptoms and laboratory findings temporarily improved by oral prednisolone, however, she flared up with chest pain about 40 days after onset of the disease. Electrocardiogram indicated the elevation of ST-T levels and low voltage, and blood examination showed remarkable elevation of creatine phosphokinase (CK), white blood cell count (WBC), aspartate aminotransferase (AST) and lactic dehydrogenase (LDH) levels. We suspected systemic vasculitis and damage of coronary artery or/and heart muscle. Finally, she was diagnosed with classical polyarteritis nodosa by myocardial biopsy. Coronary angiography revealed no abnormalities. The combination therapy of cyclophosphamide pulses and plasma-exchange was very effective to suppress the disease activity.
 ...
PMID:[A case of classical polyarteritis nodosa diagnosed by myocardial biopsy]. 1204 86

A 49-year-old woman with a history of chronic hepatitis C virus infection and Hashimoto disease was admitted to our hospital because of proteinuria, hematuria, purpura, and edema in the lower extremities. Laboratory data on admission revealed proteinuria (0.2 g/day), microscopic hematuria (3+) with RBC casts, renal dysfunction(serum creatinine 1.4 mg/dl), positive anti nuclear antigen (x640, speckled type), hypocoplementemia, mixed cryoglobulinemia (type III), and hepatitis C virus infection (AST 45 IU/l, ALT 33 IU/l). MPO-ANCA level was found to be high (356 EU). In renal biopsy, most glomeruli showed crescentic formation with the weak deposition of IgG, IgM, and C3 in the mesangial area and along the capillary wall. She was diagnosed as having systemic vasculitis associated with MPO ANCA. Methylprednisolone pulse therapy followed by oral prednisolone (40 mg/day) effectively normalized MPO ANCA level. It has been reported that ANCA is found in patients with HCV-associated mixed cryoglobulinemia. Therefore, in chronic hepatitis C patients with systemic vasculitis, we should consider the possibility of ANCA-related microscopic polyangiitis and make a correct diagnosis by renal biopsy.
 ...
PMID:[A case of MPO-ANCA-related microscopic polyangiitis with mixed cryoglobulinemia]. 1678 Jan 8

A 3-month-old male Golden Retriever puppy was evaluated for lethargy and fever of 2-days duration. Results of a CBC and biochemical profile revealed marked eosinophilia (6.3 X 10(3)/microL; reference interval 0.1-1.2 X 10(3)/microL), moderate thrombocytopenia, and increased activities of alanine aminotransferase, aspartate aminotransferase, and creatine kinase. Hepatomegaly and peritoneal effusion were found using abdominal ultrasound. Peritoneal fluid analysis revealed eosinophilic inflammation (23,000 nucleated cells/microL with 88% eosinophils). Despite supportive treatment the puppy's condition deteriorated rapidly; euthanasia was requested, and a necropsy performed. Microscopically, there was marked necrosuppurative and eosinophilic hepatitis with vasculitis. Numerous hepatocytes contained protozoal organisms suspected to be Toxoplasma gondii or Neospora caninum. However, serum was negative for both T gondii and N caninum antibodies; polymerase chain reaction assay on hepatic tissue was negative for both organisms; and immunohistochemical evaluation of hepatic tissue using serum raised against T gondii, N caninum, and Sarcocystis neurona also was negative. Schizont morphology suggested that merozoites replicated by endopolygeny, forming rosettes around a central residual body. Transmission electron microscopy revealed that merozoites lacked rhoptries. These findings were consistent with a diagnosis of Sarcocystis canis, an apicomplexan parasite with an unknown life cycle.
 ...
PMID:Fatal hepatic sarcocystosis in a puppy with eosinophilia and eosinophilic peritoneal effusion. 1696 26

Case 1. A 23-year-old white housewife presented with an erythematous violaceous rash on her face, neck, chest, and limbs, particularly over the dorsum of the hands and fingers; diffuse alopecia; and an inability to climb stairs and get up from a low seat. The clinical examination showed red to violaceous well-demarcated plaques on sun-exposed areas on the dorsum of the fingers and hands, with periungual erythema and telangiectasia; facial erythema; and heliotrope rash. There was also symmetric involvement of proximal muscles of the limbs. Laboratory examination showed hypergammaglobulinemia, elevated serum aspartate aminotransferase, and serum alanine aminotransferase; normal activities of creatinokinase, lactate dehydrogenase, and aldolase; an antinuclear antibody titer of 1:40 with a speckled pattern; negative anti-DNA and anti-Scl70; and normal serum complement levels (C3, C4, and CH50). Urinalysis results were within normal limits. Skin biopsy histopathology showed hyperkeratosis, edema of the upper epidermis, scattered inflammatory infiltrate, and focal accumulation of mucin in the form of acid mucopolysaccharides. Deep asymptomatic nodules on the inner upper limbs appeared later. Histopathology of these lesions showed focal areas of lobular panniculitis in the subcutaneous tissue, with lymphoplasmocytic inflammatory infiltrate without vasculitis (Figure 1 and Figure 2). Case 2. A 29-year-old white housewife presented with an erythematous violaceous rash on her face, neck, chest, and lower extremities. Clinical examination showed red to violaceous well-demarcated aching plaques on the internal surface of the thighs and tips of the fingers; periungual erythema and digital petechiae; Raynaud's phenomenon; and bilateral ulnar and cervical enlarged lymph nodes. Laboratory examination showed elevated serum aspartate aminotransferase, alanine aminotransferase, creatinokinase, lactate dehydrogenase, and aldolase; negative venereal disease research test results; an antinuclear antibody titer of 1:1024 with speckled pattern; negative anti-DNA and anti-Scl70; and normal serum complement levels (C3, C4, and CH50). Urinalysis results were within normal limits. Histopathology of the deep asymptomatic nodule on the inner left thigh showed lobular panniculitis with a scattered inflammatory infiltrate and diffuse fat necrosis, in addition to calcium deposition between the lipocytes and microcysts without vasculitis (Figure 3).
 ...
PMID:Dermatomyositis with panniculitis. 1721 24


1 2 Next >>