Systemic lupus erythematosus in a multiethnic US cohort (LUMINA): XXV. Smoking, older age, disease activity, lupus anticoagulant, and glucocorticoid dose as risk factors for the occurrence of venous thrombosis in lupus patients

Calvo‐Alén, Jaime; Toloza, Sergio; Fernández, Mónica; Bastian, Holly M.; Fessler, Barri J.; Roseman, Jeffrey M.; McGwin, Gerald; Vilá, Luis M.; Reveille, John D.; Alarcón, Graciela S.

doi:10.1002/art.21149

Cited by 126 publications

(89 citation statements)

References 47 publications

(37 reference statements)

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“…In our study, 1 episode of thrombosis was observed among every 28 women who received menopause hormonal therapy. Avoiding menopause hormonal therapy in women who are positive for aPL would not be enough, since other factors, such as smoking, older age, disease activity over time, and glucocorticoid dose, are also associated with the occurrence of venous thrombosis in lupus patients (42). Therefore, we consider the real threat of menopause hormonal therapy in women with SLE to be the risk of developing thrombosis, not the effect of menopause hormonal therapy on disease activity.…”

Section: Discussionmentioning

confidence: 99%

Menopause hormonal therapy in women with systemic lupus erythematosus

Sánchez‐Guerrero

González-Pérez

Durand-Carbajal

et al. 2007

Arthritis & Rheumatism

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Objective. To evaluate the effects of menopause hormonal therapy on disease activity in women with systemic lupus erythematosus (SLE).Methods. We conducted a double-blind, randomized clinical trial involving 106 women with SLE who were in the menopausal transition or in early or late postmenopause. Patients received a continuoussequential estrogen-progestogen regimen (n ‫؍‬ 52) or placebo (n ‫؍‬ 54). Disease activity was assessed at baseline and at 1, 2, 3, 6, 9, 12, 15, 18, 21, and 24 months, according to the SLE Disease Activity Index (SLEDAI). The primary outcome measure was global disease activity, estimated by measuring the area under the SLEDAI curve. Secondary outcome measures included maximum SLEDAI score, change in SLEDAI score, incidence of lupus flares, median time to flare, medication use, and adverse events. Results were studied using intent-totreat analysis.Results. At baseline, demographic and disease characteristics were similar in both groups. Mean ؎ SD SLEDAI scores were 3.5 ؎ 3.3 and 3.1 ؎ 3.4 in the menopause hormonal therapy and placebo groups, respectively (P ‫؍‬ 0.57). Disease activity remained mild and stable in both groups throughout the trial. There were no significant differences between the groups in global or maximum disease activity, incidence or probability of flares, or medication use. Median time to flare was 3 months in both groups. Thromboses occurred in 3 patients who received menopause hormonal therapy and in 1 patient who received placebo. One patient in each group died during the trial due to sepsis.Conclusion. Menopause hormonal therapy did not alter disease activity during 2 years of treatment. However, an apparently increased risk of thrombosis seems to be a real threat in women with SLE who receive menopausal hormone therapy.

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Section: Discussionmentioning

confidence: 99%

Menopause hormonal therapy in women with systemic lupus erythematosus

Sánchez‐Guerrero

González-Pérez

Durand-Carbajal

et al. 2007

Arthritis & Rheumatism

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“…It is unclear whether GC also contributed to his thrombosis. However, data from Cushing's syndrome patients, anecdotal evidence of thrombosis after GC, and limited evidence from a lupus cohort study may support such a possibility (18,45,46). It may be prudent to try to initiate high-dose GC therapy, or at least pulse GC, only after initiation of anticoagulation therapy in patients with CAPS/probable CAPS, and thereafter make an effort to taper the dose of GC as fast as the clinical condition would allow.…”

Section: Discussionmentioning

confidence: 99%

“…An extensive evaluation revealed elevated inflammatory markers, including erythrocyte sedimentation rate (ESR; 102 mm/hour), C-reactive protein level (56 mg/liter), positive antinuclear antibodies (ANAs; Ͼ1:640), strongly positive anti-doublestranded DNA (anti-dsDNA) titers, low levels of C4 (9 mg/dl, normal range 16 -38), prolonged prothrombin time (16.2 seconds, normal range 10 -13), prolonged activated partial thromboplastin time (60 seconds, normal range [27][28][29][30][31][32][33][34][35][36][37][38], and positive lupus anticoagulant (LAC) by dilute Russell's viper venom time. His urine analysis showed proteinuria (0.440 gm protein/gm creatinine), hematuria (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) …”

Section: History Of the Present Illnessmentioning

confidence: 99%

A 26‐year‐old white man with a systemic lupus erythematosus flare and acute multiorgan ischemia: Vasculitis or thrombosis?

Cherian¹,

Duculan²,

Amigues³

et al. 2011

Arthritis Care & Research

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A 26-year-old white man with a systemic lupus erythematosus (SLE) flare and acute multiorgan ischemia. History of the present illnessThe patient was in his usual state of health until 2 months before admission, when he developed pain and stiffness in his right shoulder, neck, and back after playing softball. His symptoms progressively worsened despite manipulation by a chiropractor, and he developed new pain in his soles. This was diagnosed as plantar fasciitis and he was given a topical steroid injection and a short course of methylprednisolone. This treatment improved his pain, but at its completion, he developed disabling diffuse arthralgias in his shoulders, elbows, knees, and feet, along with fevers, anorexia, and weight loss. Worsening symptoms prompted hospitalization in another institution 3 weeks before admission, where he was febrile up to 103°F and hypertensive (144/100 mm Hg). An extensive evaluation revealed elevated inflammatory markers, including erythrocyte sedimentation rate (ESR; 102 mm/hour), C-reactive protein level (56 mg/liter), positive antinuclear antibodies (ANAs; Ͼ1:640), strongly positive anti-doublestranded DNA (anti-dsDNA) titers, low levels of C4 (9 mg/dl, normal range 16 -38), prolonged prothrombin time (16.2 seconds, normal range 10 -13), prolonged activated partial thromboplastin time (60 seconds, normal range 27-38), and positive lupus anticoagulant (LAC) by dilute Russell's viper venom time. His urine analysis showed proteinuria (0.440 gm protein/gm creatinine), hematuria (11-25 red blood cells [RBCs]/high-power field [hpf]), and pyuria (3-10 white blood cells [WBCs]/hpf). Antibodies to Sm/RNP, Ro/SSA, and La/SSB; anticardiolipin antibodies; antineutrophil cytoplasmic antibodies (ANCAs); and anticyclic citrullinated peptide antibodies were negative, and creatine phosphokinase was normal. An infectious disease evaluation was performed and was negative for all pathogens, including Lyme disease, human immunodeficiency virus, and viral hepatitis. Renal ultrasound and Doppler were performed and were negative for renal pathology and venous thrombosis. He was placed on prednisone 10 mg orally twice daily, losartan 50 mg daily, and aspirin 81 mg daily, and his fevers resolved with some improvement in joint pains. Two weeks before admission, he was evaluated by a rheumatologist who discontinued aspirin in anticipation of a kidney biopsy to rule out lupus nephritis. Laboratory evaluation again revealed persistent proteinuria (2ϩ), hematuria (10 -20 RBCs/hpf), C4 hypocomplementemia (C3 111 mg/dl, C4 9 mg/dl), and strongly positive anti-dsDNA. The patient could not tolerate tapering of prednisone to 15 mg and he stayed at 17.5 mg daily.He presented to our clinic 3 days before admission and his scheduled kidney biopsy. Over the course of the previous week he had developed a few small tender erythematous skin lesions and some skin excoriation on his fingers and palms. He also experienced numbness of his fingertips and bilateral soles for 2 or 3 days. Weight loss of 30 -33 pounds over the cou...

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“…12 aPLs were strongly associated with thrombosis in this cohort. In the LUMINA Study, 9% of SLE patients had at least one VT. 13 VT was independently associated with LAC and several other risk factors (smoking, older age, disease activity, and glucocorticoid dose).…”

Section: Apls and Risk Of Thrombosismentioning

confidence: 93%

Venous Thrombosis in the Antiphospholipid Syndrome

Farmer-Boatwright

Roubey

2009

ATVB

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Abstract-The antiphospholipid syndrome is a relatively common acquired cause of venous thrombosis. Up to 20% of cases of deep vein thrombosis, with and without pulmonary embolism, may be associated with antiphospholipid antibodies. These antibodies are typically detected in lupus anticoagulant assays and tests for anticardiolipin antibodies. Most antiphospholipid antibodies are directed against several phospholipid-binding plasma proteins. The most common antigens are ␤ 2 -glycoprotein I and prothrombin. Immunoassays using these purified antigens are now available. In addition to being markers for thrombotic risk, antiphospholipid antibodies have been shown to directly contribute to hypercoagulability in animal models and in various in vitro studies. Prevention of recurrent venous thrombosis in patients with the antiphospholipid syndrome requires long-term anticoagulation. The optimal intensity of warfarin therapy is an ongoing issue, but most clinicians currently favor a target INR in the 2.0 to 3.0 range. In certain patients, antiphospholipid antibodies may interfere with determination of the INR, requiring other approaches to monitor and adjust the warfarin dose. Low-dose aspirin is typically recommended for primary prevention of thrombosis in asymptomatic patients with moderate to high levels of antiphospholipid antibodies, although strong supporting data are lacking. Key Words: antiphospholipid Ⅲ anticardiolipin Ⅲ lupus anticoagulant Ⅲ ␤2-glycoprotein I Ⅲ thrombosis T he antiphospholipid syndrome (APS) is the association of thrombosis or recurrent pregnancy loss with persistent antiphospholipid antibodies (aPLs). The spectrum of thrombosis in APS includes both venous and arterial events and thrombosis at nearly every site in the vasculature has been reported. This review will focus on venous thrombosis (VT) in the setting of APS. The most common type of venous thrombosis associated with APS is lower extremity deep vein thrombosis (DVT) with or without pulmonary embolism (PE). APS is one of the more common acquired causes of venous thrombophilia. In one prospective cohort study, approximately 20% of patients with DVT or PE had moderate to high levels of aPLs before the thrombotic event. 1 About one-third of patients present with VT at the time of diagnosis of APS. 2 APS occurring in the absence of other autoimmune diseases is termed primary APS. Secondary APS refers to APS in the setting of other autoimmune diseases, most commonly systemic lupus erythematosus (SLE). International consensus criteria for the classification of definite APS were initially published in 1999 3 and updated in 2006. 4 The classification criteria, summarized in the Table, are useful in research studies but are not intended as diagnostic criteria for clinical purposes. The criteria do not include a number of clinical manifestations associated with aPLs including thrombocytopenia, livedo reticularis, valvular heart disease (LibmanSacks endocarditis), a form of nephropathy, and certain neurological abnormalities. 4 Antiphospholipid Anti...

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Systemic lupus erythematosus in a multiethnic US cohort (LUMINA): XXV. Smoking, older age, disease activity, lupus anticoagulant, and glucocorticoid dose as risk factors for the occurrence of venous thrombosis in lupus patients

Cited by 126 publications

References 47 publications

Menopause hormonal therapy in women with systemic lupus erythematosus

Menopause hormonal therapy in women with systemic lupus erythematosus

A 26‐year‐old white man with a systemic lupus erythematosus flare and acute multiorgan ischemia: Vasculitis or thrombosis?

Venous Thrombosis in the Antiphospholipid Syndrome

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