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Sjögren syndrome and mixed connective tissue disease
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Cutaneous vasculitis is a marker of more severe disease. Apart from the risk of lymphoma, patients with Sjögren syndrome who develop vasculitis are also more likely to have systemic involvement such as arthritis, peripheral neuropathy, Raynaud phenomenon, and glomerulonephritis. Waldenstrom macroglobulinemia is a relatively common vasculitic manifestation of primary Sjögren syndrome. It presents as palpable purpura, polyclonal hypergammaglobulinemia, and elevated titers of rheumatoid factor and anti-SS-A/SS-B autoantibodies. Though itself benign, it is associated with sensory peripheral neuropathy [5].
Non-Neoplastic Disorders of Vasculature in HIV Infection
Published in Clay J. Cockerell, Antoanella Calame, Cutaneous Manifestations of HIV Disease, 2012
Benjamin K. Stoff, Antoanella Calame, Clay J. Cockerell
Biopsy is the standard for diagnosing cutaneous vasculitis. Ideally, specimens from the lesion should be obtained within 48 hours of onset, as samples taken after that point may reveal healing rather than the original injury.17 Supporting laboratory data may be useful as well, particularly if the vasculitis is suspected to be an element of a larger disease process. When considering HSP, for instance, blood urea nitrogen and creatinine levels as well as urinalysis should be pursued to assess renal involvement. Serologic markers classically used in the work-up of vasculitis, such as C-reactive protein and complement levels, may also be of use. In the rare HIV-infected patient in whom Wegener’s disease is suspected, a positive antineutrophilic antibody (ANA) finding should be interpreted with caution, as false-positives are reportedly common.18 It is important to note that the development of vasculitis in the HIV-positive patient has not been tightly correlated with CD4+ T cell count.2
Polyarteritis nodosa: an evolving primary systemic vasculitis
Published in Postgraduate Medicine, 2023
Because of a substantial overlap in manifestations and vessel involvement, it is important to rule out forms of primary small vessel vasculitis. These include ANCA-associated vasculitis (i.e. granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis, and renal limited vasculitis) and immune complex-mediated small vessel vasculitis (i.e. cryoglobulinemic vasculitis, IgA vasculitis, urticarial vasculitis, and anti-GBM disease). Secondary causes of vasculitis should also be considered. Drug-induced vasculitis can cause a small-to-medium vessel vasculitis mimicking PAN, most commonly presenting as cutaneous vasculitis. Connective tissue diseases can also cause a vasculitis of medium vessels (e.g. systemic lupus erythematosus and rheumatoid vasculitis). Lab tests that can be used to evaluate these diseases include anti-neutrophilic cytoplasmic antibodies (ANCA), cryoglobulins, anti-nuclear antibodies (ANA) with specific nuclear antibodies as needed, anti-GBM antibodies, rheumatoid factor, and complements.
Immunoglobulin A vasculitis associated with inflammatory bowel disease: a retrospective cohort study
Published in Scandinavian Journal of Rheumatology, 2021
M Villatoro-Villar, CS Crowson, KJ Warrington, A Makol, MJ Koster
Determination of causality of TNFi in patients developing cutaneous vasculitis can be clinically difficult. Rechallenge with drug provocation testing is often considered the gold standard for confirming hypersensitivity response, but is variably performed, particularly if the clinical manifestations attributed to the medication were considered severe or life threatening. Studies composed predominantly of patients with inflammatory arthritis have demonstrated recurrence of cutaneous vasculitis on re-exposure to the same TNFi in 33–75% of the few patients rechallenged (22–24). A class effect has also been proposed, but not confirmed, owing to the return of cutaneous vasculitis in patients with rheumatoid arthritis despite switching to a different TNFi (20, 23). Much less guidance is available regarding the potential causality in patients, with the question of potential TNFi-associated IgAV during treatment for rheumatic diseases in general and IBD in particular. Indeed, only three cases of biopsy-confirmed IgAV with subsequent relapse on TNFi rechallenge have been reported: one patient with inflammatory arthritis (etanercept) (22) and two patients with Crohn’s disease (both adalimumab) (26, 27).
Symmetric polyneuropathy after viral symptomatology – not always Guillain-Barré Syndrome
Published in Acta Clinica Belgica, 2021
Michiel Keyzer, Anne Hoorens, Jo Van Dorpe, Anne-Marie Bogaert
Shortly after initiating induction therapy, decreased inflammation was seen with progressive and complete recovery of the patient’s kidney function after 2 months (Figure 3). Eosinophilia reached maximum 18% of white blood cell (WBC) formula 5 days prior to treatment and was completely resolved (0.1%) just 3 days after starting induction therapy. Clinically, the patient improved significantly with a resolution of his polyneuropathy and increased mobility by means of intensive kinesitherapy. Signs of cutaneous vasculitis disappeared completely after 3 weeks of treatment. The patient was discharged from the hospital four weeks later in good condition.