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Query: UMLS:C0042384 (vasculitis)
20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Branch thrombosis is an occlusion of an arterial branch while the main artery driving blood into the limb is normal. This situation may be observed in iliaca interna or femoralis profunda arteries; ankle systolic pressure is normal despite typical intermittent claudication. Diagnosis of branch thrombosis must be confirmed by arteriography. There are 3 different kinds of arterio-arterial emboli, i.e. emboli coming from proximal arterial wall: (1) emboli deriving from an arterial aneurysm, (2) emboli of atheromatous plaques, often caused by an invasive medical procedure, and (3) cholesterol emboli, often spontaneous, occluding 50-500 micron diameter arteries. Clinically, the disease resembles vasculitis and may simulate periarteritis nodosa.
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PMID:[Clinical aspects of arterial insufficiency of the lower extremities. Side-branch thrombosis and arterio-arterial embolism]. 667 33

A 45-year-old woman developed cold paraesthesias, severe pain in the finger-tips of both hands and acral necroses, at first pinhead-sized but gradually enlarging. She had been a heavy smoker for many years, was hypertensive and had sustained a myocardial infarction 10 years previously. Angiography demonstrated bilateral occlusion of digital arteries and Doppler-ultrasound showed occlusion of both internal carotid arteries. Erythrocyte sedimentation rate was greatly increased to 101/130 mm. The symptoms improved during rheological treatment and administration of methylprednisolone, but then nonspecific abdominal pain occurred, together with intermittent claudication of the left leg, and she had numerous haemoptyses. The chest radiograph showed finely reticular shadows in both lungs. Histological examination of peribronchial tissue revealed typical signs of vasculitis. The patient became oliguric (creatinine up to 5.5 mg/dl). The titre of antineutrophil cytoplasm antibodies (cANCA) was very high. Despite treatment with cyclophosphamide and glucocorticoids the renal failure got worse, she had a stroke and severe anginal attacks developed. She died 25 weeks after the first admission from cardiocirculatory failure. As the patient's signs were those of several kinds of vasculitis, the polyangitis overlap syndrome seems the most likely diagnosis in retrospect.
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PMID:[Polyangiitis overlap syndrome]. 816 23

Arterial ulcers occur because of inadequate perfusion of skin and subcutaneous tissue at rest. Arterial occlusive disease, common among smokers, diabetics and the elderly, can lead to claudication, rest pain and gangrene, in addition to localized ulceration. Other processes, such as venous stasis, pressure, trauma, and vasculitis, can also cause ischemia. However, a thorough patient history and physical assessment can help discriminate between ischemic ulcers caused by arterial disease and other types of ulcers. The key to the diagnosis of arterial occlusive disease is the patient history. Pain while walking is the most common presenting complaint and can indicate intermittent claudication. Physical assessment should include both a general exam, looking for problems relating to lungs, heart and nervous system, and a focused exam of the affected extremities and arterial pulses. Vascular laboratory findings can also help confirm a diagnosis of arterial ischemic ulceration. The key to treatment is improvement in the vascular perfusion to the affected area. Surgical revascularization is the mainstay of treatment, with some interventional procedures becoming accepted. Medical options, in addition to correction of underlying medical problems, include good wound and supportive care, but pharmaceutical interventions have generally not proven effective, and should be considered only if interventional procedures are not possible. With an adequate blood supply reestablished, most arterial ulcers will progress to healing unless there are complicating factors.
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PMID:Arterial ulcers: assessment and diagnosis. 871 33

A 52-year-old man was admitted to our hospital in July 1995, because of intermittent claudication, paresthesia on foot and gross hematuria. Chest radiograph in 1988 revealed bilateral interstitial shadows and proteinuria had been pointed out since 1992. On admission, chest X-ray and computed tomography showed diffuse interstitial shadow, however it had not been changed for several years. Laboratory tests revealed elevated level of erythrocyte sedimentation rate, C-reactive protein, immunoglobulin, rheumatoid factor, IgG-rheumatoid factor, and immune complex. Serum MPO-ANCA were positive. Although serum creatinine level and renal function test were normal, renal biopsy demonstrated crescentic formation and necrotizing vasculitis. Immunofluorescence and electron microscopy demonstrated no remarkable deposit in glomerulus. A diagnosis of microscopic polyarteritis necrotizing and crescentic glomerulonephritis (NCGN) was made. Treatment was initiated with 30 mg of prednisolone, followed by marked improvement of intermittent claudication, and decreased titer of serum MPO-ANCA. Previous reports have demonstrated the association of MPO-ANCA with rapidly progressive NCGN, microscopic polyarteritis, and occasionally pulmonary hemorrhage recognized as pulmonary-renal syndrome. However, the present case suggests the possibility that another disease subset may also be associated with MPO-ANCA, which is characterized by interstitial pneumonitis and slowly progressive glomerulonephritis.
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PMID:[Case of MPO-ANCA positive interstitial pneumonitis and necrotizing, crescentic glomerulonephritis]. 912 27

A 33-year-old man was admitted to our hospital because of intermittent claudication and finger tip ulceration with a skin rash on the upper and lower extremities. He later developed a massive melena. Angiography revealed arterial occlusion in the hand and foot, skin biopsy showed vasculitis with eosinophilic infiltration, and biopsy of the colon showed mucosal vasculitis with thrombosis. A diagnosis of polyangiitis overlap syndrome was made, and all these symptoms improved after corticosteroid therapy.
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PMID:Polyangiitis overlap syndrome. 924 May 6

Thromboangiitis obliterans or Winiwarter-Buerger's disease is a primary systemic vasculitis of an unknown etiology, which affects medium-sized arteries and veins mainly in the lower and upper extremities, causing multiple segmental arterial occlusions especially in young male smokers. The aim of our study is to compare the knowledge on the etiology, epidemiology, clinical presentation, diagnostic and therapeutic possibilities in the time of Leo Buerger (90 years ago) and now. Between 1994 and 1998, 26 patients (19 men and 7 women) were investigated with clinical suspicion for Winiwarter-Buerger's disease. Laboratory and arteriographic investigation revealed typical signs for this disease in 22 of them. To the most common clinical signs or symptoms belong smoking and the onset of the disease before the age of 50 years (in 95.5%), intermittent claudication (in 72.7%), rest pain and ischaemic ulcers or gangrenes in the fingers (in 68.2%). In slightly more than half of the patients migrating superficial thrombophlebitis was present and similarly in one half of the patients Raynaud's phenomenon was found. In conclusion--What has changed from the times of Leo Buerger? 1. Prevalence of TAO increased in women. 2. Older patients (more than 40 years old) are being diagnosed. 3. Upperextremity involvement is more frequently present. 4. Diagnosis of TAO is being more proper, especially due to up-to-date diagnostic methods, like digital subtraction angiography. 5. The treatment is more effective, amputation number is decreased. And what has not changed? Similarly like Leo Buerger we do not known the precise etiology of the disease. Ceasation of smoking has still the most important therapeutic procedure. The clinical course of the disease is individual and in spite of the treatment is the clinical course unpredictable. (Tab. 5, Ref. 47.)
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PMID:90 years of Buerger's disease--what has changed? 1045 53

A 26 year old Albanian woman presented with intermittent claudication of upper limbs in association with alleviation of radial pulses, reduction of arterial pressures, bilateral axillary bruits and subocclusive lesions of proximal part of both humeral arteries on arteriography and MRI. Takayasu's arteritis was diagnosed according to ACR criteria. A treatment of prednisone was started together with methotrexate. The response was favourable and symptoms like claudication and malaise vanished. Takayasu's arteritis is a vasculitis which affects large vessels such as aorta and its main branches. This disease involves mainly premenopausal women; it is very rare in Europe. Diagnosis is lying on clinical features and arteriography results. Treatment of choice is corticosteroids, and immunosuppressors; sometimes a surgical procedure is necessary if stenosis is fixed.
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PMID:[Takayasu's arteritis--case report and review of the literature]. 1110 6

Some arguments are in favor of the role of Chlamydia in the pathogenesis of atherosclerosis and some vasculitis. Illustrating this possible relation, we report the case of a patient developing consecutively a Chlamydia psittacci infection and a temporal arteritis. A 73-year-old woman, with no significant medical history, was hospitalized for constitutional symptoms. Three weeks before, she had described fever and sore throat of two days' duration. Since that time, she had remained exhausted and developed a mild intermittent claudication of the jaws. Clinical examination was poor. A biological inflammatory syndrome was noticed. Chest X-ray revealed bilateral interstitial opacities. The titer of anti-C. psittaci antibodies was significant (positive 1g G at 1/2048). Soon after initiation of doxycycline, a temporal arteritis biopsy was performed, due to the persistence of clinical symptoms and high inflammatory syndrome, conclusive for the diagnosis of temporal arteritis. Corticotherapy was added to antibiotic therapy, resulting in the decrease of inflammatory syndrome and an improvement in the general status of the patient. X-ray opacities decreased in three weeks. Serological control after three months showed a decrease of the titer of anti-C. psittacci antibodies to 1/256, confirming the initial diagnosis of Chlamydia pneumopathy. Our observation could provide one more argument for the role of bacteria-like Chlamydia in the pathogenesis of vascular diseases. Prospective seroepidemiological and molecular biology studies could allow us to clarify the association between Chlamydia infections and inflammatory vasculitis-like temporal arteritis.
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PMID:A possible association between Chlamydiae psittacci infection and temporal arteritis. 1119 20

A 32 years old female was admitted to hospital due to acute abdominal pain, nausea, vomiting and liquid stools. Physical examination was normal except for pain on her left inferior abdominal quadrant without peritoneal irritation signs. An abdominal CAT-scan suggested thrombosis at celiac trunk, although the echo Doppler showed no alterations except for signs of ischemia in the distal branch of the superior mesenteric artery. An exploratory laparotomy was performed disclosing a necrosis of the distal ileum and cecum, diffuse peritonitis and thrombosis of the ileocecoapendiculocolic artery. No vasculitis lesions were found in the arteries of medium size examined. A history of intermittent claudication for the past 3 years as well as acrocyanosis, asymmetry of pulses and blood pressure in the superior extremities was ascertained after the surgery. A MRI angiogram showed multiple stenoses and irregularities at the celiac trunk, hepatic, superior mesenteric and fibular arteries. No abnormalities at the aortic arch and its main branches were documented. A sepsis due to Candida sp complicated her postoperative period. After recovery, prednisone 1 mg/kg/day was started and the anticoagulation continued. The abdominal pain, intermittent claudication and superior limb acrocyanosis disappeared. This is an unusual case of type IV Takayasu's arteritis with acute abdominal signs as the first manifestation.
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PMID:[Intestinal necrosis as clinical presentation of Takayasu arteritis]. 1249 34

Arterial ischaemic ulcers develop because of inadequate perfusion leading to local ischaemia in the skin and underlying tissue. The most common cause is peripheral arterial disease, giving rise to symptoms like intermittent claudication, rest pain and gangrene, in addition to local ulceration. Diabetes mellitus increases the risk of ulcer formation; admittedly mainly neuropathic ulcers with a low component of peripheral arterial disease. Yet a combination of neuropathy and ischaemia is common ("neuro-ischaemic ulcer"). A thorough patient history and clinical examination can help discriminate arterial ulcers from venous, pressure, traumatic and vasculitis ulcers. Reduction of ankle systolic pressure and calculated ankle/brachial index, sometimes additional other non-invasive laboratory tests, confirm peripheral arterial disease. The primary treatment of arterial ischaemic ulcer is to increase blood supply to the affected area, primarily by endovascular treatment or open arterial reconstruction. Endovascular treatment (balloon angioplasty) is the method of choice because of graft infection risk in patients with open ulcers. Most arterial ischaemic ulcers will progress to healing if the blood supply is reestablished.
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PMID:[Arterial ischemic ulcers]. 1581 38


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