Interleukin-5 production by T lymphocytes in atheroembolic disease with hypereosinophilia

Cogan, Elie; Schandené, Liliane; Papadopoulos, Theodoros Athanassios; Crusiaux, Alain; Goldman, Michel

doi:10.1016/s0091-6749(95)70065-x

Cited by 19 publications

(10 citation statements)

References 5 publications

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“…A reactive infl ammation around the crystals is suggested by eosinophilia, a cytokine-mediated occurrence, 98 and has a role in causing or worsening ischaemia. However, anti-infl ammatory benefi ts might be counterbalanced by harmful eff ects of steroids on the cardiovascular system.…”

Section: Future Researchmentioning

confidence: 99%

Atheroembolic renal disease

2010

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Atheroembolic renal disease develops when atheromatous aortic plaques rupture, releasing cholesterol crystals into the small renal arteries. Embolisation often aff ects other organs, such as the skin, gastrointestinal system, and brain. Although the disease can develop spontaneously, it usually develops after vascular surgery, catheterisation, or anticoagulation. The systemic nature of atheroembolism makes diagnosis diffi cult. The classic triad of a precipitating event, acute or subacute renal failure, and skin lesions, are strongly suggestive of the disorder. Eosinophilia further supports the diagnosis, usually confi rmed by biopsy of an aff ected organ or by the fundoscopic fi nding of cholesterol crystals in the retinal circulation. Renal and patient prognosis are poor. Treatment is mostly preventive, based on avoidance of further precipitating factors, and symptomatic, aimed to the optimum treatment of hypertension and cardiac and renal failure. Statins, which stabilise atherosclerotic plaques, should be off ered to all patients. Steroids might have a role in acute or subacute progressive forms with systemic infl ammation.

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Section: Future Researchmentioning

confidence: 99%

Atheroembolic renal disease

2010

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“…Histological examination of renal biopsy samples revealed a significant infiltration of T cells and macrophages around cholesterol cleft vessels [7]. A significant increase in interleukin-5 production from activated T cells was also reported in a patient with CCE [8]. In addition, a favorable effect of low-dose (0.3 mg/kg/day) corticosteroid treatment is reported in some patients with acute aggravation of chronic renal failure, mesenteric ischemia or lower limb pain [4, 9, 10].…”

Section: Discussionmentioning

confidence: 96%

Recovery from Hemodialysis Therapy in a Patient with Renal Cholesterol Crystal Embolism

Kato

Ohtsuji

Terada

et al. 2002

Nephron

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The prognosis of renal cholesterol crystal embolism (CCE) is poor, and many patients progressively develop to the end-stage of chronic renal failure. We herein experienced a 66-year-old male patient who recovered from hemodialysis (HD) shortly after an amputation of inflammatory toes. The patient complained of painful digital cyanosis at bilateral toes and livedo reticularis at right lower leg 4 weeks following aortic angiography. Laboratory examinations revealed eosinophilia and overt proteinuria (3.0 g/day). His serum creatinine level increased from 2.18 to 8.57 mg/dl over 6 weeks, and HD treatment was started. Treatment with simvastatin (5 mg/day) did not reverse renal failure and hypereosinophilia, but the amputation of right gangrene toes promptly increased urine output and eosinophilia completely disappeared concomitantly with a decline of C-reactive protein from 9.7 to 0.7 mg/dl. Serum creatinine level was also reduced to 3.46 mg/dl, and he eventually stopped HD totally after 32 sessions. This case suggested that the surgical amputation promptly recovered renal function. Reversal of inflammation may be more effective than lipid-lowering therapy for renal failure in our patient.

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“…Complement activation, leukocyte aggregation, release of leukocyte enzymes and oxidants, endothelial injury, and intravascular coagulation probably aggravate the initial insult [19]. In this inflammatory context, atheroembolic-related eosinophilia has been shown to be related to interleukin-5 (IL-5) release by activated T cells [20] and has been reported to be seen in up to 88% of cases [3,17,21]. Cholesterol crystals may also act as a foreign body, producing vasculitis with fibrinoid necrosis [22].…”

Section: Discussionmentioning

confidence: 99%

Atheroembolic renal disease with rapid progression and fatal outcome

et al. 2010

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Atheroembolic renal disease is caused by foreign-body reaction to cholesterol crystals flushed from the atherosclerotic plaques into the small-vessel system of the kidneys. It is an underdiagnosed entity, mostly related to vascular procedures and/or anticoagulation, and prognosis is considered to be poor. Besides the benefit of aggressive medical prevention of further embolic events, use of steroid therapy has been associated with greater survival. Here we report a case of a patient with a multisystemic presentation of the disease days after performance of percutaneous coronary intervention and anticoagulation initiation due to an episode of myocardial infarction. Renal, cutaneous, ophthalmic, neurological, and possibly muscular and mesenteric involvement was diagnosed. Although medical treatment with corticosteroids and avoidance of further anticoagulation was applied, the patient rapidly progressed to end-stage renal disease requiring hemodialysis and died 6 months after diagnosis. This is a case of catastrophic progression of the disease resistant to therapeutic measures. Focus on diagnosis and more efficient preventive and therapeutic protocols are therefore needed.

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Interleukin-5 production by T lymphocytes in atheroembolic disease with hypereosinophilia

Cited by 19 publications

References 5 publications

Atheroembolic renal disease

Atheroembolic renal disease

Recovery from Hemodialysis Therapy in a Patient with Renal Cholesterol Crystal Embolism

Atheroembolic renal disease with rapid progression and fatal outcome

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