Widespread cutaneous necrosis in a patient with rheumatoid arthritis associated with anticardiolipin antibodies

Wolf, P.

doi:10.1001/archderm.127.11.1739

Cited by 10 publications

(3 citation statements)

References 1 publication

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“…To note, widespread cutaneous necrosis is associated with massive thrombosis of the small and medium-sized dermal vessels in primary APS,39 SLE,40 rheumatoid arthritis,41 and mycosis fungoides 42. Erythematous macules and painful nodules have been reported in aPL-positive patients as being due to thrombotic skin disease,43,44 and they can possibly improve with salicylates 45.…”

Section: Aps and Vaso-ischemic (Occlusive) Diseases With Neuropsychiamentioning

confidence: 99%

Antiphospholipid Syndrome and Vascular Ischemic (Occlusive) Diseases: An Overview

Atanassova

2007

Yonsei Med J

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Antiphospholipid syndrome (APS) is primarily considered to be an autoimmune pathological condition that is also referred to as "Hughes syndrome". It is characterized by arterial and/or venous thrombosis and pregnancy pathologies in the presence of anticardiolipin antibodies and/or lupus anticoagulant. APS can occur either as a primary disease or secondary to a connective tissue disorder, most frequently systemic lupus erythematosus (SLE). Damage to the nervous system is one of the most prominent clinical constellations of sequelae in APS and includes (i) arterial/venous thrombotic events, (ii) psychiatric features and (iii) other non-thrombotic neurological syndromes. In this overview we compare the most important vascular ischemic (occlusive) disturbances (VIOD) with neuro-psychiatric symptomatics, together with complete, updated classifications and hypotheses for the etio-pathogenesis of APS with underlying clinical and laboratory criteria for optimal diagnosis and disease management.

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Section: Aps and Vaso-ischemic (Occlusive) Diseases With Neuropsychiamentioning

confidence: 99%

Antiphospholipid Syndrome and Vascular Ischemic (Occlusive) Diseases: An Overview

Atanassova

2007

Yonsei Med J

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“…Skin lesions of Dego's disease (a rare multisystem vasculopathy), characterized pathologically by cutaneous collagen necrosis and atrophy of the epidermis with ' an absence of inflammatory cells have been linked to the other consequences of the disease, such as cerebral and bowel infarction and anticardiolipin antibodies or a lupus anticoagulant (105). Vascular thromboses may be manifest as ischemia or necrosis of entire extremities as demonstrated in association with disseminated intravascular coagulation (106), with resultant cutaneous necrosis or more patchy, widespread, demarcated areas of cutaneous necrosis, manifest by areas of painful purpura and necrosis with underlying dermal necrosis (107).…”

Section: Anticardiolipins and Cardiac Diseasementioning

confidence: 99%

State-of-the-Art Review: Antiphospholipid Thrombosis Syndromes

Bick

2001

Clin Appl Thromb Hemost

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Antiphospholipid antibodies are strongly associated with thrombosis and are the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagutable state remain unclear, numerous theories, as previously discussed, have been advanced. The most common thrombotic events associated with anticardiolipin antibodies are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type II syndrome); occasionally, patients present with mixtures of these types (type IV syndrome). Type V patients are those with antiphospholipid antibodies and RMS. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of anticardiolipin antibodies in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through VI) should be defined if possible, as this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually experience venous thrombosis. Because the aPTT is unreliable inpatients with lupus anticoagulant (prolonged in only about 40 to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests, including ELISA for anticardiolipin antibodies, the dRVVT for lupus anticoagulant, hexagonal phospholipid neutralization procedure, and beta-2-GP-I (IgG, IgA, and IgM) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If results of these tests are negative, in the appropriate clinical setting, subgroups should also be assessed. Finally, most patients with antiphospholipid thrombosis syndrome will fail warfarin therapy and, except for retinal vascular thrombosis, may fail some types of antiplatelet therapy; thus it is of major importance to make this diagnosis so that patients can be treated with the most effective therapy for secondary prevention--LMWH or UH in most instances, and clopidogrel in some instances.

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“…Vascular thromboses may be evident as ischemia or necrosis of entire extremities. Other cutaneous manifestations include peripheral gangrene, necrotizing purpura, hemorrhage (ecchymosis and hematoma formation), and crusted ulcers about the nail beds (238,245,(257)(258)(259)(260).…”

Section: Antiphospholipid-thrombosis Syndromementioning

confidence: 99%

Syndromes of Thrombosis and Hypercoagulability: Congenital and Acquired Thrombophilias

Bick

Kaplan

1998

Clin Appl Thromb Hemost

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This article stresses the common hereditary and acquired blood protein defects associated with thrombosis. The most common of the hereditary defects apear to be APC-R, SPS, antithrombin, protein C, and protein S deficiency, and the most common acquired defects are anticardiolipin antibodies and the lupus anticoagulant (antiphospholipid antibodies). Therefore, these are the defects that should first be looked for in an individual with unexplained thrombosis. If these more common defects are not found, then the rarer defects including HC II, plasminogen or TPA deficiency, dysfibrinogenemia, el evated PAI-1 and hyperhomocysteinemia should be sought. The importance of finding these defects has significant impli cations for therapy of the individual patient and for institutions of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipopro tein (a) or defects of extrinsic (tissue factor) pathway inhibitor (EPI, TFPI), may be associated with enhanced risks of throm bosis. Finally, it must be recalled that a diagnosis of thrombo sis, like that of anemia, is only a generic and partial diagnosis; just as in the anemic patient, the etiology must be clearly de fined. Only in this manner can cost-effective and appropriate therapy for both primary treatment and secondary prevention be designed. In addition, the demonstration of a hereditary defect will allow primary prevention in afflicted family mem bers by allowing the choice of appropriate therapy.

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Widespread cutaneous necrosis in a patient with rheumatoid arthritis associated with anticardiolipin antibodies

Cited by 10 publications

References 1 publication

Antiphospholipid Syndrome and Vascular Ischemic (Occlusive) Diseases: An Overview

Antiphospholipid Syndrome and Vascular Ischemic (Occlusive) Diseases: An Overview

State-of-the-Art Review: Antiphospholipid Thrombosis Syndromes

Syndromes of Thrombosis and Hypercoagulability: Congenital and Acquired Thrombophilias

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