Cases reported "Eosinophilia"

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1/53. Markedly high eosinophilia and an elevated serum IL-5 level in an infant with cow milk allergy.

    BACKGROUND: interleukin-5 (IL-5) promotes the production and function of eosinophils, and an increase in the serum soluble CD23 (sCD23) level is suggestive of enhanced type-2 helper T-cell activity. The secretion of a large amount of the proinflammatory cytokine, tumor necrosis factor alpha (TNF-a), has been reported to alter the intestinal barrier capacity. OBJECTIVE: To determine whether or not distinct profiles of cytokine production were involved in the marked peripheral eosinophilia of as high as 20,000/mm3 and the gastrointestinal symptoms seen in an infant with cow milk allergy. methods: The levels of IL-5, sCD23, and TNF-alpha in serum and the culture supernatants of mononuclear cells were compared with those in infants with anaphylaxis to cow milk and nonallergic infants. RESULTS: interleukin-5 was detected in the serum (19 pg/mL) but became undetectable after 2 weeks on a milk-free diet together with clinical remission. A kinetic decrease in the serum sCD23 level was also observed during the administration of a milk-free diet with improvement of the eosinophilia in 2 months. The TNF-alpha produced in vitro after stimulation with cow milk protein was not different from in controls. CONCLUSION: It seems likely that the allergic inflammation due to cow milk can induce marked eosinophilia with an associated increase in IL-5 production.
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2/53. Eosinophilic enteritis observed during alpha-interferon therapy for chronic hepatitis c.

    We report a patient with chronic hepatitis c who developed eosinophilic enteritis while being treated with recombinant interferon alpha-2b. He had no history of either allergic disorders or recurring episodes of abdominal cramps, nausea, or diarrhea. He also had had a normal eosinophil count prior to the interferon treatment. After a 12-week course of interferon alpha-2b, he began to complain of severe abdominal pain, diarrhea, and abdominal fullness. His peripheral eosinophil count increased to 45% (absolute count, of 7,610/microl). Abdominal ultrasonography and computed tomography revealed diffuse thickness of the intestinal wall with gross ascites that contained numerous eosinophils. An upper gastrointestinal barium study with small bowel follow-through showed an edematous mucosal layer of the jejunum and ileum. There was a spectacular relief of the patient's subjective symptoms after the administration of prednisolone. follow-up studies revealed resolution of the ascites and the mucosal layer edema and normalization of the peripheral eosinophil count. prednisolone was tapered off, but the eosinophilic enteritis did not recur. As there had been no evident exposure to common causative factors for eosinophilic enteritis, we suggest that interferon alpha-2b could thus have played a role in the triggering of the eosinophilic enteritis.
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3/53. life threatening coronary artery spasm in childhood Kimura's disease.

    A 13 year old boy is described with hypereosinophilia associated with Kimura's disease, who showed repeated life threatening syncopal attacks during daily activities or at rest. Coronary arteriography demonstrated small aneurysms with irregular vessel walls of both coronary arteries, and the absence of organic stenotic lesions. Infusion of a minimal dose of ergonovine into the right coronary artery induced severe spasm of the vessel. ventricular fibrillation recurred even after administration of nifedipine and isosorbide was started, but was completely inhibited by prednisolone.
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4/53. Eosinophilic pustular eruption associated with transdermal fentanyl.

    A 70-year-old man developed a widespread eruption of sterile pustules on normal skin, mainly on the trunk, face and base of the limbs, 2 days after application of a fentanyl-transdermal therapeutic system (fentanyl-TTS) patch. The eruption was not accompanied by fever. The main histopathological finding was an intraepidermal pustule filled almost exclusively with eosinophils. Suspension of the fentanyl-TTS led to rapid and definitive spontaneous regression of the pustules in about 10 days. A similar pustular reaction related temporally to fentanyl-TTS administration had appeared several weeks before the current eruption.
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5/53. Immediate-Type allergy against human insulin associated with marked eosinophilia in type 2 diabetic patient.

    We describe a type 2 diabetic patient who showed immediate-type allergy against human insulin associated with marked eosinophilia at initial insulin therapy. Three months after initiation of insulin therapy, he noticed itchy skin wheals at the site of the insulin injection. Laboratory data at that time showed marked eosinophilia (2,512 /mm3) and progression of renal dysfunction. skin test with semisynthetic human insulin and protamine sulfate resulted in local immediate skin reactions such as itchy erythema and wheals. Histopathology of the biopsy specimen from skin showed perivascular infiltration of lymphocytes and numerous eosinophils in the dermis and subcutaneous fat. Although the titer of total IgE antibody was within normal range, that of insulin-specific IgE antibody was high. insulin administration was discontinued to preserve his insulin secretion, and stable control of his hyperglycemia was obtained by initiating nateglinide treatment (360 mg/day). His itchy skin lesions disappeared within two weeks after cessation of the insulin therapy and both eosinophilia and renal dysfunction gradually improved. Although the widespread use of human insulin in diabetic patients has greatly reduced the incidence of insulin allergy, the possibility of human insulin allergy should be kept in mind when initiating such therapy.
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6/53. Eosinophilic cellulitis (Wells' syndrome) successfully treated with low-dose cyclosporine.

    Eosinophilic cellulitis (Wells'syndrome) is an uncommon skin disorder. We report two adult male patients who had recurrent erythematous plaques and a nodular lesion on the abdomen. The histopathologic feature of their skin biopsies similarly indicated a marked infiltrate of eosinophils in the dermis with the fashion of "flame figures". One of the patients demonstrated blood eosinophilia. Given the clinicohistological findings, the patients fulfilled the criteria for the diagnosis of eosinophilic cellulitis. The skin lesions remained refractory to medications such as corticosteroids, sulfones, antihistamines, and minocycline. Considering the beneficial effect of cyclosporine in the treatment of eosinophilia-associated dermatoses, we speculated that eosinophilic cellulitis might respond to cyclosporine therapy. Thus, each of the two patients was given cyclosporine (microemulsion formulation) at a daily dose of 1.25 or 2.5 mg/kg, i.e., 100 or 200 mg, respectively. Complete remission of the skin eruptions was obtained in both patients during a 3- or 4-week period of treatment. No side effects were observed. Neither of the patients experienced relapse of the disease at least over 10 months after the discontinuation of the cyclosporine therapy. We suggest that administration of low-dose cyclosporine be a safe and useful therapeutic option in patients with eosinophilic cellulitis.
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7/53. hiv seronegative eosinophilic pustular folliculitis successfully treated with metronidazole.

    We describe a patient with eosinophilic pustular folliculitis (EPF) who initially responded to oral indomethacin, the most often-used therapy for EPF, but eventually became refractory to continuous administrations. Treatment with metronidazole resulted in complete clearance of the lesion.
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8/53. Progressive systemic sclerosis-polymyositis overlap syndrome with eosinophilic pleural effusion.

    Pleural fluid rarely occurs in patients with progressive systemic sclerosis (PSS) or polymyositis (PM) with no lesions in the pulmonary area. Pleural fluids in patients with autoimmune diseases are mostly dominated by monocytes and lymphocytes but very rarely contain increased eosinophils. We report a 55-year-old male with PSS-PM overlap syndrome and eosinophilic pleural effusion. air invasion into the pleural cavity and the antituberculous therapy could be ruled out as causes for the patient's eosinophilic pleural effusion, because the differential eosinophil count was already as high as 19% from the first thoracentesis before the start of antituberculous therapy. Infections and malignant tumor also were unlikely causes based upon the negative pleural fluid results and the negative pleural biopsy findings, except for nonspecific inflammation. After the administration of corticosteroid, the pleural effusion decreased promptly, with normalization of serum creatine phosphokinase and c-reactive protein concentrations.
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9/53. Drug-induced rash with eosinophilia and systemic symptoms syndrome with bupropion administration.

    BACKGROUND: Sustained-release bupropion is commonly used for the symptomatic relief of depressive illness and as an adjuvant in smoking cessation therapy. OBJECTIVE: To report a case of bupropion-induced drug rash with eosinophilia and systemic symptoms syndrome, including acute hepatitis, obstructive lung disease, and myositis. methods: After the patient discontinued use of bupropion, serologic tests, muscle biopsies, pulmonary function tests, a chest x-ray examination, venous Doppler ultrasounds, and an electrocardiogram were performed. RESULTS: On discontinuation of bupropion and prolonged systemic corticosteroid therapy, there was complete resolution of symptoms. CONCLUSIONS: To our knowledge, this is the first reported case of drug rash with eosinophilia and systemic symptoms syndrome induced by bupropion therapy. We report this case to notify clinicians of the potential serious multisystem complications that can occur with sustained-release bupropion therapy.
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10/53. Successful treatment of refractory vasospastic angina with corticosteroids: coronary arterial hyperactivity caused by local inflammation?

    BACKGROUND: Although vasospastic angina usually responds well to treatment with calcium antagonists and/or nitrates, there have been anecdotal case reports of refractory vasospastic angina resistant to intensive treatment with high doses of calcium antagonists and nitrates. methods AND RESULTS: Four patients with vasospastic angina, which was refractory to intensive treatment with high doses of calcium antagonists and nitrates, were completely controlled after administration of corticosteroids. Although none of the 4 patients showed eosinophilia, all had bronchial asthma or chronic thyroiditis, and in 2 cases, the activity of vasospastic angina corresponded with that of bronchial asthma. CONCLUSIONS: These findings suggest that in these patients, coronary spasm may have been induced by arterial hyperreactivity because of local inflammation in the coronary arterial wall and that the corticosteroids suppressed the arterial hyperreactivity by alleviating the inflammation. Corticosteroids may be considered as a treatment choice for patients with refractory vasospastic angina, particularly when the patient has an allergic tendency, such as bronchial asthma.
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