Churg-Strauss Syndrome in Patients Receiving Montelukast as Treatment for Asthma

Wechsler, Michael E.; Finn, David P.; Gunawardena, Dineli; Westlake, Robert M.; Barker, Alan F.; Haranath, Sai Praveen; Pauwels, Romain; Kips, Johan; Drazen, Jeffrey M.

doi:10.1378/chest.117.3.708

Cited by 231 publications

(100 citation statements)

References 14 publications

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“…Within a few months of LRA coming on the market, cases now recognized as CSS began to appear. Initially, Wechsler reported eight such patients who had been taking zafirlukast (37) and raised the question of whether this was a toxic drug effect (38,39). Similar findings followed shortly when montelukast was introduced (38,39).…”

Section: Disease Unmasked By Manipulating Steroid Therapy: Formes Frumentioning

confidence: 94%

“…Initially, Wechsler reported eight such patients who had been taking zafirlukast (37) and raised the question of whether this was a toxic drug effect (38,39). Similar findings followed shortly when montelukast was introduced (38,39). However, careful review of the data, including careful comparisons of incidence rates in asthmatics, has led to the conclusion that these are all cases of CSS unmasked by decreasing steroid use (38 -42); that is, represent formes frustes disease.…”

Section: Disease Unmasked By Manipulating Steroid Therapy: Formes Frumentioning

confidence: 99%

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Recent Advances in the Diagnosis of Churg-Strauss Syndrome

Churg

2001

Modern Pathology

162

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Most pathologists assume that a diagnosis of ChurgStrauss syndrome (CSS) requires the finding of necrotizing vasculitis accompanied by granulomas with eosinophilic necrosis in the setting of asthma and eosinophilia. However, recent data indicate that this definition is too narrow and that adherence to it leads to cases of CSS being missed. CSS has an early, prevasculitic phase that is characterized by tissue infiltration by eosinophils without overt vasculitis. Tissue infiltration may take the form of a simple eosinophilia in any organ, and a fine-needle aspirate showing only eosinophils may suffice for the diagnosis in this situation. The prevasculitic phase appears to respond particularly well to steroids. Even in the vasculitic phase of CSS, many cases do not show a necrotizing vasculitis but often only an apparently nondestructive infiltration of vessel walls by eosinophils. In modern biopsy materials, granulomas frequently cannot be found. In the postvasculitic phase of CSS, healed vascular lesions resemble organized thrombi but typically show very extensive destruction of elastica and, often, an absence of eosinophils. The widespread use of steroids as therapy for asthma has led to the peculiar and confusing situation in which the steroid therapy accidentally suppresses CSS and changes in steroid treatment uncover the disease; this type of "formes frustes" CSS is now well recognized with leukotriene receptor antagonist treatment and will be seen with increasing frequency as other steroid-sparing therapies for asthma are introduced.

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Section: Disease Unmasked By Manipulating Steroid Therapy: Formes Frumentioning

confidence: 94%

Section: Disease Unmasked By Manipulating Steroid Therapy: Formes Frumentioning

confidence: 99%

Recent Advances in the Diagnosis of Churg-Strauss Syndrome

Churg

2001

Modern Pathology

162

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“…These authors postulate that Churg-Strauss syndrome developed in these patients as a result of disinhibition of hypereosinophilia, arising from cessation of systemic and pulmonary corticosteroids and initiation of leukotriene inhibitors. 10 In conclusion, this case demonstrates that Churg-Strauss syndrome may be the initial manifestation of HIV disease. Recognizing the possible associations between varying rheumatologic syndromes and HIV is important because corticosteroid and cytotoxic therapy may potentially worsen HIV infection.…”

Section: Resultsmentioning

confidence: 63%

Churg-Strauss Syndrome Associated with HIV Infection

Nguyen¹,

Ferentz²,

Patel³

et al. 2005

The Journal of the American Board of Family Medicine

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CASE REPORTA 28-year-old woman with history of moderate persistent asthma, recurrent sinusitis, and a recently diagnosed deep venous thrombosis presented to her physician for follow-up of anticoagulation on enoxaparin and warfarin. A month before presentation, the patient had been diagnosed with deep venous thrombosis of her right leg; a Doppler sonogram was used to make the diagnosis. She had a hypercoagulable workup, including normal levels of protein C, protein S, and antithrombin 3 levels. She had no clinical risk factors, including trauma, immobility, pregnancy, obesity, or medications associated with thrombosis.At this follow-up, she complained of a 5-day history of fever, pleuritic chest pain, dyspnea, and malaise accompanied by nausea, emesis, anorexia, and loose stools. She denied any recent travels or contacts with ill persons. Complete blood count revealed a leukocytosis of 50,000 cells/mm 3 with 65% eosinophils.Enoxaparin was discontinued because of the possibility of drug allergy. Two days later, a complete blood cell count revealed worsening leukocytosis and hypereosinophilia. The patient was admitted. She had been hospitalized 1 month previously for an asthma exacerbation and had been discharged from the hospital on triamcinolone inhaler, albuterol inhaler, and a 60-mg prednisone taper over 2 weeks. She was subsequently readmitted to the hospital 2 weeks later for acute deep venous thrombosis, and discharged from the hospital in stable condition on enoxaparin and warfarin.Vital signs at admission were: temperature, 102.6°F; respiratory rate, 20 breaths/min; blood pressure, 110/60 mm Hg; pulse, 110 beats/min; and pulse oximetry of 98% on room air. Pertinent physical findings on physical examination include generalized cervical lymphadenopathy and faint expiratory wheezing on lung auscultation. Abdominal examination revealed mild diffuse tenderness, and rectal examination revealed heme-negative brown stool. Extremity examination was consistent with a resolving deep venous thrombosis.Leukocyte count at admission was 52,800 with 67% eosinophils. Platelet count was 122,000, and hematocrit was 0.248 with mean corpuscular volume of 69.2. Results of a metabolic panel were normal. Urinalysis revealed 3ϩ blood, 1ϩ protein, negative nitrite, and leukocyte esterase, no casts, and 18% eosinophils. Chest radiograph revealed increased interstitial markings, and abdominal radiographs revealed non-specific bowel gas pattern without evidence of obstruction or free air. Electrocardiogram revealed sinus tachycardia.A hematology-oncology consultation was obtained. Laboratory tests were requested for HIV, IgE, stool ova and parasites, blood cultures, antinuclear antibody, rheumatoid factor, and antineutrophil cytoplasmic antibodies. HIV testing was positive, with a CD4 count of 682 and 1004 RNA copies/mL. IgE was 1005 mg/dL, and anti

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“…Similar cases have been described in patients with zafirlukast (3)(4)(5). Further reports described patients with CSSin whomorally administered corticosteroids were being tapered during or after treatment with the other CysLTl -receptor antagonists such as montelukast (6) or pranlukast (7). Wechsler et al (6) discussed the mechanism of CSSonset in such cases.…”

mentioning

confidence: 72%

Allergy and Angitis: Two aspects of Churg-Strauss Syndrome

Morishita

2001

Intern. Med.

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Churg-Strauss Syndrome in Patients Receiving Montelukast as Treatment for Asthma

Cited by 231 publications

References 14 publications

Recent Advances in the Diagnosis of Churg-Strauss Syndrome

Recent Advances in the Diagnosis of Churg-Strauss Syndrome

Churg-Strauss Syndrome Associated with HIV Infection

Allergy and Angitis: Two aspects of Churg-Strauss Syndrome

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