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)

A case of panarteritis nodosa with positive Australia antigen is presented. Panarteritis appeared following serum hepatitis and caused arthromyalgia, abdominal pain, prolonged fever of unknown origin, peripheral polyneuropathy, blood hypertension, and renal insufficiency. A muscular biopsy showed atrophy due to denervation and necrotizing arteritis in various stages causing serious damage to the arteries. Abdominal arteriography clearly demonstrated the existence of aneurismal dilations in the liver, pancreas, and kidneys. The angiographic findings in panarteritis nodose are discussed with special reference to the aneurysms localized in several organs. Their situation is described in detail; it is usually abdominal and more specifically intrarenal. The fact that they occur in a high percentage of cases is helpful when establishing the diagnosis. Lastly, the role of Australia antigen in the development of panarteritis nodose is discussed. It stimulates an immune response and the production of circulating immunocomplexes which are depostied on the vascular walls with complement fixation and damage to the blood vessels. The possibility that other viral agents may be present in the various types of necrotizing vasculitis in humans is commented on.
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PMID:[Panarteritis nodosa with positive Australia antigen (author's transl)]. 3 58

We reported 5 patients with renal failure associated with polyarteritis nodosa (PN). In all patients the renal dysfunction became apparent from 2 to 4 weeks after the onset of fever or neuromuscular symptoms with laboratory findings supporting marked inflammatory process and took the course of either acute or rapidly progressive renal failure. The clinical diagnoses on admission were variable; fever of unknown origin, peptic ulcer disease, polyneuritis multiplex, disseminated intravascular coagulation and Buerger's disease. Microscopic examination of the kidneys in 3 by renal biopsy and in 2 by autopsy revealed crescentic glomerulonephritis without immunoglobulin deposit, segmental necrotizing glomerulonephritis, marked inflammatory infiltrate around the glomeruli, granulomatous lesion, tubular necrosis and cortical necrosis other than necrotizing vasculitis. The outcomes were favorable with prednisolone monotherapy in two patients who had biopsy-proven diagnosis and treatment early in the course. Of all PN the prevalence of renal involvement is considered to be about 70%, the prognosis of which has been considered very poor. However it seems possible to alter fatal outcome of this disease by starting treatment with confident histological proof early in the disease process.
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PMID:[Renal failure associated with polyarteritis nodosa]. 197 42

Inflammatory pseudotumor of lymph nodes (IPT), a recently described benign cause of lymphadenopathy, was studied in 14 patients using paraffin-section immunohistochemistry. All biopsies showed a proliferation of spindle cells (small blood vessels, histiocytes, and "activated" fibroblasts resembling myofibroblasts) containing a mixture of inflammatory cells without atypia and involving the connective tissue framework (hilum and sinuses) of the lymph node. Ten patients had additional histologic features of IPT originally described (extranodal extension, obliterative vasculitis, and endothelial infiltration), and nine of these had associated fever of unknown origin, which in some was relieved by biopsy alone. Additional features observed focally in some cases but not previously described included lymph node parenchymal infarction, fibrinoid vascular necrosis, karyorrhexis, and involvement of only part of the lymph node. Immunostaining showed the lymphoid infiltrate to be predominantly of T-lineage (except for plasma cells), only a minority of which marked as T-helper cells. Numerous mononuclear cells resembling histiocytes were identified, some of which had a spindled shape but reacted with an antibody (KP1) of myelomonocytic specificity. Large fibroblastic cells expressed alpha-muscle actin but not desmin, similar to myofibroblasts in granulation tissue. The morphologic and immunohistologic features were similar to those in inflammatory pseudotumors of spleens and livers also studied, but the lack of simultaneous lymph node involvement argued against a common etiology. The findings suggest that the mass lesion of IPT is produced in response to localized lymph node inflammation or injury and further exclude hematolymphoid or mesenchymal neoplasia as a cause.
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PMID:Inflammatory pseudotumor of lymph nodes. Additional observations and evidence for an inflammatory etiology. 206 12

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.
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PMID:[Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case]. 225 22

A prospective clinical study (1974-1988) was carried out in 33 patients with several types of systemic vasculitis (SV) presenting as fever of unknown origin (FUO) according to the 1961 Petersdorf and Beeson's criteria. Histological confirmation, either from biopsy or necropsy, was available in all cases. The types of SV with FUO were: panarteritis nodosa (PAN) (14 cases), giant cell arteritis (GCA) (13 cases), and overlapping polyangiitic syndrome (OPS) (6 cases). In PAN, the clinical features associated with fever at the onset of the disease were remarkably nonspecific: constitutional symptoms (85%), arthromyalgia (50%), nonspecific abdominal pain (28%), and irritative cough (28%). In the whole course of the cases of GCA a significantly smaller frequency of presentation of local arterial symptoms and polymyalgia rheumatica (p less than 0.01) was found in the subgroup of patients with FUO than in those without it. As regard laboratory data, a higher increase of serum alkaline phosphatase (p less than 0.05) was found in the cases of PAN and OPS with FUO. Striated muscle biopsy and arteriography were the most useful investigations in the diagnosis of PAN. The study that gave the diagnosis in the cases of GCA was temporal artery biopsy.
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PMID:[Systemic vasculitis as a cause of fever of unknown origin]. 260 77

We report an unselected series of eight patients younger than 6 months of age with Kawasaki disease evaluated between January 1982 and May 1984. The incidence of coronary artery aneurysms (six patients) and the mortality (two patients) were unusually high in this small series. Because of the confusing clinical presentation in three patients, diagnosis was delayed until pathologic or echocardiographic evidence of coronary vasculitis or aneurysm was discovered. The currently accepted clinical criteria for Kawasaki disease may not always identify patients with the pathologic findings of the syndrome who are younger than 6 months of age. The diagnosis of Kawasaki disease and echocardiographic evaluation of the coronary arteries should be considered in young infants with prolonged fever of unknown origin.
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PMID:Clinical spectrum of Kawasaki disease in infants younger than 6 months of age. 377 56

The authors describe 3 cases of left atrial myxoma confirmed by two-dimensional echocardiography and at operation. One patient had the symptoms of embolisms to the cerebral and renal vessels in the absence of heart disease, 2 patients presented with the symptoms of congestive heart failure. In one patient, loud first sound as well as systolic and diastolic murmur at the heart apex were documented. The nonspecific manifestations (weight loss, fever, high ESR, dysproteinemia, and rheumatoid factor) were observed in all the cases. The difficulties encountered in the clinical diagnosis of heart myxoma are discussed. The differential diagnosis is made between valvular heart disease and infective endocarditis, systemic vasculitis, cardiomyopathy, etc. Echocardiography to exclude myxoma should be performed in patients with thromboembolism, rheumatic valvular disease, subacute endocarditis (particularly in the absence of the classical symptoms) and in those with fever of unknown origin.
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PMID:[Clinical characteristics of myxoma of the heart]. 401 32

A 57-year-old Dutch woman, who had lived and worked in Tanzania for 26 years, developed serious, progressive bilateral retinitis after suffering from a fever of unknown origin. Fundus abnormalities in both eyes suggested that the woman had been infected with Rift Valley fever virus. Serologic studies confirmed this suspicion. White macular lesions accompanied to extensive vasculitis appear to be specific for Rift Valley fever retinitis.
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PMID:Rift Valley fever retinitis. 719 57

Infarcted peribiliary lymph nodes were found at laparotomy in a 56-year-old man who had a fever of unknown origin and transient abdominal pain. Despite thorough clinical and laboratory investigation, a cause was not demonstrated. A review of the reported cases of idiopathic or spontaneous lymph node infarction revealed a clinical presentation characterized by the sudden appearance of a painful mass, often associated with otherwise unexplained fever. Most clinical laboratory test results were negative. Although the pathogenesis is not known, histologic changes in involved lymph nodes are indistinguishable from those produced experimentally by occlusion of the vascular supply of lymph nodes. The histologic differential diagnosis includes lymphoma, metastatic carcinoma, vasculitis, and infection.
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PMID:Idiopathic infarction of intraabdominal lymph nodes. A cause of fever of unknown origin. 744 75

A 24-year-old woman with SLE since the age of 12 developed sensory-motor peripheral neuropathy in 1990. Her sensory neuropathy was symmetrical in all limbs and distally dominant. Electrophysiological study showed marked reduction of motor and sensory conduction velocities. Sural nerve biopsy revealed vasculitis and axonopathy. Symptoms of neuropathy and nerve conduction velocities were improved by high dose steroid treatment. After one year she had a fever of unknown origin, and then presented limb myokymia with involuntary finger movement which was fine, irregular, and continuous. Needle EMG revealed myokymic discharge at dorsal interosseous and flexor pollicis brevis muscles. Because myokymia was increased by hyperventilation and suppressed by local anesthesia at the wrist, her myokymia was thought to originate in the peripheral nerve. This is the first case report of limb myokymia with finger involuntary movement caused by peripheral neuropathy due to SLE.
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PMID:[Limb myokymia with involuntary finger movement caused by peripheral neuropathy due to systemic lupus erythematosus (SLE)--a case report]. 795 31


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