Coronary Arteritis in Systemic Lupus Erythematosus

Heibel, Richard H.; O'Toole, J D; Curtiss, Edward I.; Medsger, Thomas A.; Reddy, Sudhakar P.; Shaver, James A.

doi:10.1378/chest.69.5.700

Cited by 67 publications

(19 citation statements)

References 13 publications

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“…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%

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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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Section: History Of the Present Illnessmentioning

confidence: 99%

“…Coronary vasculitis is rare but well documented as a cause of acute MI (13). Angiographically, it manifests as a coronary aneurysm or arteritis (13,14).…”

Section: Systemic Vasculitis In Slementioning

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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“…22,23 In a nested case-control study, we recently compared SLE women with a history of CVD (SLE cases) with age-matched SLE women without CVD (SLE controls) and age-matched women from the general population (controls). 24 By use of B-mode ultrasound, we measured the intima-media thickness (IMT) of the carotid artery as a surrogate measurement of atherosclerosis.…”

Section: Sle and Atherosclerosismentioning

confidence: 99%

Atherosclerosis in Patients With Autoimmune Disorders

Frostegård

2005

ATVB

205

164

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Abstract-Recent findings indicate that presence of activated immune competent cells and inflammation are typical of atherosclerosis, the main cause of cardiovascular disease (CVD). The risk of CVD is very high in a prototypic autoimmune disease, systemic lupus erythematosus (SLE), and is also raised in other autoimmune diseases such as rheumatoid arthritis. Autoimmunity-related CVD and atherosclerosis are important clinical problems. They may also shed light on interactions between immune reactions and atherosclerosis development and manifestations, not least in women, who have a much higher risk of autoimmune disease than men. In general, a combination of traditional and nontraditional risk factors, including dyslipidemia (and to a varying degree, hypertension, diabetes, and smoking), inflammation, antiphospholipid antibodies (aPLs), and lipid oxidation, contribute to CVD in autoimmune diseases. Premature atherosclerosis is likely to be a major underlying mechanism, although distinctive features, if any, of autoimmunity-related atherosclerosis compared with "normal" atherosclerosis are not clear. One interesting possibility is that factors such as inflammation, neoepitopes on endothelial cells, or aPLs make atherosclerotic lesions in autoimmune disease more prone to rupture than in "normal" atherosclerosis. Some cases of autoimmunity-related CVD may be more related to thrombosis than atherosclerosis. Whether premature atherosclerosis is a general feature of autoimmune diseases such as SLE or only affects a subgroup of patients whereas others do not have an increased risk remains to be demonstrated. Treatment of patients with autoimmune disease should also include CVD aspects and be focused on traditional risk factors as well as on disease-related factors. Hopefully novel therapeutic principles will be developed that target the causes of the inflammation present in atherosclerotic lesions.

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“…(Kozkmaz & Cansu, 2007) Not all patients with coronary arteritis do well on corticosteroids, however Heibel et al describe a patient with coronary arteritis who was treated with prednisone and cyclophosphamide, but had new myocardial damage after starting therapy. (Heibel et al, 1976) Angina did not resolve for 3 weeks. (Heibel et al, 1976) 8.…”

Section: Pathologymentioning

confidence: 97%

“…(Heibel et al, 1976) Angina did not resolve for 3 weeks. (Heibel et al, 1976) 8. Premature atherosclerosis and systemic lupus erythematosus 8.1 Background-premature atherosclerosis and systemic lupus erythematosus Despite improved life expectancy, patients with systemic lupus erythematosus (SLE) are still at considerable risk for premature death.…”

Section: Pathologymentioning

confidence: 97%