Cases reported "Fever"

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1/37. 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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2/37. Histopathologic features of burkholderia cepacia pneumonia in patients without cystic fibrosis.

    We present the histopathologic features of fatal burkholderia cepacia pneumonia in three adults (one man [age 44 years] and two women [aged 40 and 43 years]). In all patients, the pulmonary infiltrates initially were localized (right middle lobe, left upper lobe, and right middle lobe) but rapidly progressed. Two open-lung biopsies and one pneumonectomy specimen showed necrotizing granulomatous inflammation merging with areas of more conventional necrotizing bronchopneumonia In one patient, a mediastinal lymph node also showed stellate necrotizing granulomas. vasculitis was absent. B. cepacia was cultured from the open-lung biopsies and bronchial wash specimens in two patients and from postmortem cultures of lung, subcarinal lymph nodes, and blood in the third. The histopathology in these patients resembles that of melioidosis, which is caused by a related organism, burkholderia pseudomallei. B. cepacia needs to be considered in the differential diagnosis of necrotizing granulomatous inflammation. In addition, given the rarity with which B. cepacia is identified as a cause of pneumonia in the immunocompetent host, isolation of B. cepacia should trigger a workup for underlying immunodeficiency or lead to an investigation to exclude the possibility of a nosocomial infection.
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3/37. The pathology of human west nile virus infection.

    west nile virus (WNV) was identified by immunohistochemistry (IHC) and polymerase chain reaction (PCR) as the etiologic agent in 4 encephalitis fatalities in new york city in the late summer of 1999. The fatalities occurred in persons with a mean age of 81.5 years, each of whom had underlying medical problems. Cardinal clinical manifestations included fever and profound muscle weakness. autopsy disclosed encephalitis in 2 instances and meningoencephalitis in the remaining 2. The inflammation was mostly mononuclear and formed microglial nodules and perivascular clusters in the white and gray matter. The brainstem, particularly the medulla, was involved most extensively. In 2 brains, cranial nerve roots had endoneural mononuclear inflammation. In addition, 1 person had acute pancreatitis. Based on our experience, we offer recommendations for the autopsy evaluation of suspected WNV fatalities.
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4/37. Deaths of children during an outbreak of hand, foot, and mouth disease in sarawak, malaysia: clinical and pathological characteristics of the disease. For the Outbreak Study Group.

    From April through June 1997, 29 previously healthy children aged <6 years (median, 1.5 years) in Sarawak, malaysia, died of rapidly progressive cardiorespiratory failure during an outbreak of hand, foot, and mouth disease caused primarily by enterovirus 71 (EV71). The case children were hospitalized after a short illness (median duration, 2 days) that usually included fever (in 100% of case children), oral ulcers (66%), and extremity rashes (62%). The illness rapidly progressed to include seizures (28%), flaccid limb weakness (17%), or cardiopulmonary symptoms (of 24 children, 17 had chest radiographs showing pulmonary edema, and 24 had echocardiograms showing left ventricular dysfunction), resulting in cardiopulmonary arrest soon after hospitalization (median time, 9 h). Cardiac tissue from 10 patients showed normal myocardium, but central nervous system tissue from 5 patients showed inflammatory changes. brain-stem specimens from 2 patients were available, and both specimens showed extensive neuronal degeneration, inflammation, and necrosis, suggesting that a central nervous system infection was responsible for the disease, with the cardiopulmonary dysfunction being neurogenic in origin. EV71 and possibly an adenovirus, other enteroviruses, or unknown cofactors are likely responsible for this rapidly fatal disease.
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5/37. Clinical onset of the Crohn's disease after eradication therapy of helicobacter pylori infection. Does helicobacter pylori infection interact with natural history of inflammatory bowel diseases?

    BACKGROUND: There are conflicting reports concerning the prevalence of helicobacter pylori infection in patients with inflammatory bowel diseases: some studies connected Sulphasalazine therapy and lower incidence of helicobacter pylori infection, but others showed lower prevalence of helicobacter pylori infection in inflammatory bowel diseases despite the choice of therapy. CASE REPORT: A 28-year-old male patient presented in January 1996 with the symptoms of ulcer like dyspepsia. There was no significant abnormality on physical examination, laboratory testing and abdominal ultrasound. histology examination of the biopsy specimen taken during the upper endoscopy revealed helicobacter pylori associated active gastritis only in the corporal part of the stomach. After two weeks eradication therapy (omeprazole, amoxicillin) he was well. Three months later, at the control endoscopy, granulomatous gastritis of the corporal localization was detected, without helicobacter pylori present. Antral mucosa appeared normal, both, on endoscopy and histology examination. In July 1996 he started with cramping abdominal pain, mild periodical fever and episodes of watery diarrhea. In laboratory results we found nonspecific signs of inflammation. We repeated upper endoscopy, colonoscopy and enteroclysis--with evidence of segmental stenotic lesions of the upper part of ileum and jejunum. Again, we confirmed granulomatous gastritis and small granuloma in the proximal jejunum. After starting the 5-ASA therapy in combination with Metronidazol, patient was better clinical condition, and laboratory results were normal. We suggested mesalamine maintenance therapy 1 gr. every day, and three years later he is well, in clinical remission of Crohn's disease. CONCLUSION: The clinical course of the Crohn's disease maybe "sui generis" connected with helicobacter pylori infection- but the exact mechanisms remain to be discovered.
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6/37. Progressive bouts of acute abdomen: pet the peritoneum.

    The recent discovery of the mutated gene responsible for familial mediterranean fever (FMF) is supposed to facilitate its diagnosis which up till now is a clinical one because there are no specific laboratory tests. The sensitivity of genetic testing is limited because these tests search only for known mutations. In this case report we describe a patient with periodic abdominal pain in whom the diagnosis of FMF was wrongly discarded because of lack of a durable effect of colchicine and negative genetic testing. Diffuse peritoneal inflammation was nicely demonstrated by a FDG-PET (fluoro-deoxy-glucose positron-emission tomography) performed during a typical crisis. We discuss the possible diagnostic pitfalls and conclude that a crisis-PET might upgrade the level of diagnostic certainty in equivocal cases.
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7/37. Persistent flank pain, low-grade fever, and malaise in a woman treated with indinavir.

    This case report describes a 32-year-old woman treated with indinavir who developed mild to moderate flank pain, malaise, and low-grade fever. Sterile pyuria preceded increased serum creatinine levels. Workup revealed persistent pyuria, normal-sized kidneys, a normal intravenous pyelography, and negative urinary cultures. Renal biopsy showed interstitial nephritis and chronic inflammation. Collecting ducts contained crystals. Two months after treatment with indinavir was discontinued, serum creatinine levels returned to normal and pyuria disappeared. Sterile pyuria in patients taking indinavir may help to identify patients at risk for renal dysfunction and interstitial nephritis. Markedly increasing the fluid intake above the recommended dosage may ameliorate or even reverse the process of tubulointerstitial disease.
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8/37. Intracardiac thrombosis and fever possibly triggered by ovulation induction in a patient with antiphospholipid antibodies.

    We report on a 28-year old patient with polycystic ovary syndrome (PCOS) who presented with fever and laboratory markers of inflammation. Her medical history was relevant for multiple ovulation inductions (OI) and ovarian hyperstimulation syndrome (OHSS). She had two miscarriages and one preterm delivery. Intracardiac thrombosis was diagnosed in the presence of antiphospholipid antibodies. We suggest that primary antiphospholipid syndrome (APS) was possibly triggered by OI.
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9/37. Atypical presentation of churg-strauss syndrome: another "forme fruste" of the disease?

    vasculitis is a clinicopathologic process characterized by inflammation and damage to blood vessels. A broad and heterogenous group of syndromes may result from this process, because any type, size, and location of blood vessel may be involved. The cause of these conditions remains unclear, but an autoimmune inflammatory process, characterized by involvement of both neutrophils and endothelial cells, seems to play an important role. In 1951, Churg and Strauss described a clinical syndrome of severe asthma, hypereosinophilia with eosinophilic infiltrates, eosinophilic vasculitis, and granulomata in various organs. asthma may precede this vasculitis by many years. We report a case of anti-neutrophil cytoplasmic antibody-positive, pauci-immune, crescentic, necrotizing glomerulonephritis with peripheral and interstitial eosinophilia but without asthma. This is very unusual in churg-strauss syndrome.
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10/37. A case of cutaneous sensory neuropathy associated with churg-strauss syndrome.

    Cutaneous sensory neuropathy manifests as multiple, sharply demarcated areas of hypoesthesia with a variable degree of pain. This rare neuropathy is caused by a multifocal infection or inflammation of the small sensory nerves of the skin. We report a case in a patient with febrile arthritis and eosinophilia. Her chronic cough and the presence of extravascular infiltrates of eosinophils in a neuromuscular biopsy specimen suggested churg-strauss syndrome. The course was favorable under corticosteroid therapy.
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