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POLYARTERITIS NODOSA
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ESSENTIALS OF DIAGNOSIS
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Classic polyarteritis nodosa characterized by the following: only medium-sized arteries are affected; smaller arterioles are sometimes involved; lung is spared but kidney often affected, causing reninmediated hypertension Clinical findings depend on the arteries involved Common features include fever, abdominal pain, livedo reticularis, mononeuritis multiplex, anemia, and elevated acute phase reactants (ESR or C-reactive protein or both) Associated with hepatitis B (10% of cases)
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B Laboratory Findings
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Most patients with polyarteritis nodosa have a slight anemia, and leukocytosis is common Acute phase reactants are often (but not always) strikingly elevated A major challenge in making the diagnosis of polyarteritis nodosa, however, is the absence of a disease-specific serologic test (eg, an autoantibody) Patients with classic polyarteritis nodosa are ANCA-negative and may have low titers of rheumatoid factor or antinuclear antibodies, both of which are nonspecific findings In patients with polyarteritis nodosa, appropriate serologic tests for active hepatitis B infection must be performed
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Polyarteritis nodosa, described in 1866, is acknowledged widely as the first form of vasculitis reported in the medical literature For many years, all forms of inflammatory vascular disease were termed polyarteritis nodosa In recent decades, numerous subtypes of vasculitis have been recognized, greatly narrowing the spectrum of vasculitis called polyarteritis nodosa Although the term is reserved currently for necrotizing arteritis of medium-sized vessels that has a predilection for involving the skin, peripheral nerves, mesenteric vessels (including renal arteries), heart, and brain, the disease can involve most organs Polyarteritis nodosa is relatively rare, with a prevalence of about 30 per 1 million people Approximately 10% of cases of polyarteritis nodosa are caused by hepatitis B Most cases of hepatitis B associated disease occur within 6 months of hepatitis B infection
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The diagnosis of polyarteritis nodosa requires confirmation with either a tissue biopsy or an angiogram Biopsies of symptomatic sites such as skin (from the edge of an ulcer or the center of a nodule), nerve, or muscle have sensitivities of approximately 70% The least invasive tests should usually be obtained first, but biopsy of an involved
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organ is essential If performed by experienced physicians, tissue biopsies normally have high benefit-risk ratios because of the importance of establishing the diagnosis Patients in whom polyarteritis nodosa is suspected eg, on the basis of mesenteric ischemia or new-onset hypertension occurring in the setting of a systemic illness may be diagnosed by the angiographic finding of aneurysmal dilations in the renal, mesenteric, or hepatic arteries Angiography must be performed cautiously in patients with baseline renal dysfunction
CMDT 2008
POLYMYALGIA RHEUMATICA & GIANT CELL ARTERITIS
ESSENTIALS OF DIAGNOSIS
Giant cell (temporal) arteritis is characterized by headache, jaw claudication, polymyalgia rheumatica, visual abnormalities, and a markedly elevated ESR The hallmark of polymyalgia rheumatica is pain and stiffness in shoulders and hips lasting for several weeks without other explanation
Treatment
For polyarteritis nodosa, corticosteroids in high doses (up to 60 mg of oral prednisone daily) may control fever and constitutional symptoms and heal vascular lesions Pulse methylprednisolone (eg, 1 g intravenously daily for 3 days) may be necessary for patients who are critically ill at presentation Immunosuppressive agents, especially cyclophosphamide, lower the risk of disease-related death and morbidity among patients who have severe disease For patients with polyarteritis nodosa associated with hepatitis B, the preferred treatment regimen is a short course of prednisone accompanied by lamivudine (100 mg/d orally) and plasmapheresis (three times a week for up to 6 weeks)
General Considerations
Polymyalgia rheumatica and giant cell arteritis probably represent a spectrum of one disease: Both affect the same population (patients over the age of 50), show preference for the same HLA haplotypes, and show similar patterns of cytokines in blood and arteries Polymyalgia rheumatica and giant cell arteritis also frequently coexist The important differences between the two conditions are that polymyalgia rheumatica alone does not cause blindness and responds to low-dose (10 20 mg/d) prednisone therapy, whereas giant cell arteritis can cause blindness and large artery complications and requires high-dose therapy (40 60 mg/d)
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