Biomedical subjects

Liang-Shiou Ou

Publications and source records attributed to Liang-Shiou Ou.

17 recordsLinked to original sources

PubMed2006

Septic arthritis in patients with systemic lupus erythematosus: salmonella and nonsalmonella infections compared.

OBJECTIVES: To assess the clinical characteristics and outcome of systemic lupus erythematosus (SLE) with septic arthritis. METHODS: In this 20-year retrospective study, we reviewed the charts of SLE patients with septic arthritis confirmed by synovial fluid analysis and culture. To identify risk factors for septic arthritis, data of SLE patients with septic arthritis were compared with data of 100 hospitalized SLE patients without septic arthritis. RESULTS: There were 10,732 inpatient records of 3,127 SLE patients; 29 SLE patients had septic arthritis. Their ages ranged from 14 to 68 years (mean, 35.1 +/- 14.1 years). The mean SLE duration before septic arthritis onset was 30.6 months. All patients received corticosteroids; 93% had active disease (SLEDAI > or = 4). Compared with controls, avascular necrosis (AVN) of the femoral head was the most common predisposing articular disease (Odds ratio, 3.799;CI, 1.59 to 9.05). Of the 29 patients, 17 (59%) had salmonella infections and 12 (41%) had other infections. Salmonella-infected patients were younger (28.7 +/- 10.4 years) than those with nonsalmonella infections (44.1 +/- 14.0 years; P = 0.002). The hip was the most commonly affected joint, especially in the salmonella group, followed by the knees and ankles. Salmonella-infected patients were more prone to oligo-articular septic arthritis. The overall mortality rate was 10%. CONCLUSIONS: Salmonella enteritidis B is the most common pathogen causing septic arthritis in younger SLE patients. Septic arthritis tended to be oligo-articular and involve the hip joint. AVN of the femoral head was the most common predisposing articular disease. Once septic arthritis is suspected, culture specimens should be collected and appropriate antibiotics given immediately.

Adolescent↗

PubMed2006

Staphylococcal enterotoxin B inhibits regulatory T cells by inducing glucocorticoid-induced TNF receptor-related protein ligand on monocytes.

BACKGROUND: Superantigens inhibit naturally occurring CD4+CD25+ regulatory T-cell (nTreg) activity, yet the mechanism for this is unknown. OBJECTIVE: We tested the hypothesis that staphylococcal enterotoxin B (SEB), a prototypic superantigen, inhibits the ability of nTregs to suppress T-effector cell (Teff) proliferation by an antigen-presenting cell-dependent cell contact mechanism and the induction of glucocorticoid-induced TNF receptor-related protein ligand (GITR-L) on monocytes. METHODS: Cell proliferation assays were performed on immunomagnetic-bead separated CD4+CD25+, CD4+CD25- T cells and CD14+ monocytes using anti-CD3, SEB, or a neutralizing anti-GITR-L antibody for stimulation. A cytokine permeable membrane insert separating cells in culture was used to evaluate the role of cell contact. Proliferation was measured by [3H]-thymidine incorporation or a carboxyfluorescein diacetate succinimidyl ester assay. GITR-L expression was determined by RT-PCR and immunostaining. RESULTS: Antigen-presenting cell contact was required for proliferation of nTregs and loss of their ability to suppress Teff proliferation as confirmed by carboxyfluorescein diacetate succinimidyl ester. At baseline, monocytes expressed no GITR-L, but after SEB stimulation, GITR-L gene and protein expression increased significantly over a period of 24 hours (P<.05). When GITR-L activity was neutralized with blocking antibody, as opposed to isotype control, nTregs suppressed Teff proliferation despite the presence of SEB (P<.05). Likewise, loss of GITR-L at 48 hours was associated with restoration of nTreg activity (P<or=.05). CONCLUSION: Staphylococcal enterotoxin B upregulates GITR-L on monocytes and inhibits nTreg ability to suppress Teff proliferation via a cell contact interaction. CLINICAL IMPLICATIONS: Prevention of GITR-L induction on monocytes by SEB may be a novel target for control of inflammation in superantigen-driven diseases such as atopic dermatitis.

Adult↗

PubMed2006

RANTES and monocyte chemoattractant protein 1 as sensitive markers of disease activity in patients with juvenile rheumatoid arthritis: a six-year longitudinal study.

OBJECTIVE: To longitudinally investigate serum and synovial fluid (SF) levels of RANTES and monocyte chemoattractant protein 1 (MCP-1) as well as in vitro migration of mononuclear cells toward SF in patients with juvenile rheumatoid arthritis (JRA). METHODS: Serum and SF levels of RANTES and MCP-1 were determined by enzyme-linked immunosorbent assay. Chemotaxis was performed using the modified Boyden chamber method. RESULTS: Serum RANTES levels were significantly increased in all onset types of JRA, with the highest levels present in systemic-onset JRA. Serum MCP-1 levels were significantly elevated in patients with systemic-onset JRA and were associated with current systemic features. Although serum levels of RANTES and MCP-1 decreased significantly after treatment, RANTES and MCP-1 levels during disease remission were still significantly higher in JRA patients than in controls. A relationship was found between serum RANTES levels during remission and the duration of clinical remission, with low levels being associated with prolonged clinical remission and high levels with shorter clinical remission. Serum RANTES levels correlated with C-reactive protein concentrations, hemoglobin values, white blood cell (WBC) counts, and platelet counts, whereas serum MCP-1 levels correlated with WBC counts and serum ferritin levels. Levels of RANTES and MCP-1 in SF were elevated as compared with levels in serum. SF chemotactic activity for mononuclear leukocytes was significantly inhibited by either anti-RANTES or anti-MCP-1 antibody. CONCLUSION: RANTES is a key molecule in the pathogenesis of all onset groups of JRA, whereas MCP-1 is particularly important in systemic-onset JRA. Serum levels of these CC chemokines represent more highly sensitive markers of disease activity than conventional markers of inflammation.

Adolescent↗

PubMed2005

Sequential evaluation of clinical and laboratory changes amongst children suffering from lupus nephritis during intermittent intravenous cyclophosphamide therapy.

We prospectively evaluated the efficacy and safety of a 24-month course of intermittent intravenous cyclophosphamide (IC) therapy for children suffering from lupus nephritis soon after the diagnosis of systemic lupus erythematosus (SLE) was made. Eight children with severe lupus nephritis were treated with IC monthly for 6 months and then every 3 months, totaling 24 months. The repeated measurements of sequential serological parameters of lupus nephritis, monitored over the course of the study, were analyzed statistically. The urine creatinine clearance rate (Ccr), the 24-h urine protein excretion, and the serum creatinine level significantly improved (p<0.05) after 6, 9 and 12 months of treatment, respectively. The serum C3, C4, albumin, and triglyceride level, the hemoglobin level, and the erythrocyte sedimentation rate significantly improved (p<0.05) 1 month after treatment. The IC appeared to elicit a significant effect (p<0.05) upon the mean leukocyte and neutrophil counts but had no effect (p>0.05) on the platelet count. The lymphocyte count decreased (p<0.05) during the first six monthly IC, whereas the lymphocyte count returned to the baseline level during the quarterly IC events. From a total of 96 IC doses given to those SLE patients, severe myelotoxicity occurred in one patient when lymphocyte count declined to 98 mm(-3); however, no sign of clinical infection was observed. The daily steroid dosage can be tapered rapidly, and the SLE-associated hyperlipidemia resolved parallel to the resolution of the acute lupus nephritis. We concluded that the efficacy of a 24-month IC course for a child suffering from lupus nephritis is significant.

Adolescent↗

PubMed2005

Factors that regulate naturally occurring T regulatory cell-mediated suppression.

T regulatory (Treg) cells play a key role in the modulation of allergic and autoimmune responses. This review will discuss the factors that regulate naturally occurring Treg (nTreg) cell-mediated suppression. The involvement of cytokines, costimulatory molecules, and ligands on antigen-presenting cells in the inhibition of nTreg cell-mediated suppression in vitro is summarized. Understanding the events that control suppressive function of nTreg cells will allow manipulation of these cells to inhibit or enhance their functions in the development of novel therapies for autoimmune and allergic diseases.

Adrenal Cortex Hormones↗

PubMed2005

Prevalence and severity of symptoms of asthma, rhinitis, and eczema in 13- to 14-year-old children in Taipei, Taiwan.

BACKGROUND: The prevalence of asthma and allergic diseases in children has increased worldwide. OBJECTIVE: To perform the phase 3 survey of the International Study of Asthma and Allergies in Children (ISAAC) to report the time trend of the prevalence and severity of asthma and allergic diseases in children in Taipei. METHODS: Two junior high schools in each of the 12 school districts in Taipei were randomly chosen to enter the study. All students aged 13 to 14 years in the chosen schools were invited to participate in written and video questionnaires in Chinese (identical to those of the ISAAC phase 1 survey). The study was performed between December 1, 2001, and January 31, 2002. All data analysis followed the protocol of the ISAAC and then was submitted to the ISAAC International Data Center. RESULTS: Of 6653 eligible children from 23 high schools (1 school refused participation), 6381 (95.9%) participated. The prevalence of symptoms of asthma, allergic rhinitis, and atopic eczema in the past 12 months in 13- to 14-year-old children increased by 37%, 51%, and 193%, respectively, on written questionnaires during a 7-year period. The severity of asthma symptoms, including more than 4 wheezing attacks in the past 12 months, wheezing that disturbs sleep more than once per week, and wheezing that limited speech in the past 12 months, did not show any significant changes on written questionnaires during the 7 years. CONCLUSION: The increasing prevalence of symptoms of asthma, allergic rhinitis, and atopic eczema in 13- to 14-year-old children in Taipei in a 7-year period is a significant burden on public health systems in Taiwan.

Adolescent↗

PubMed2005

The prevalence, severity and seasonal variations of asthma, rhinitis and eczema in Taiwanese schoolchildren.

The prevalence of asthma is increasing in Taiwan but data remain limited. The aim of this study was to determine the prevalence, severity, demographic and seasonal variations of asthma, rhinitis, and eczema in Taiwan. Using a one-stage stratified cluster random sampling, first grade (aged 6-8) and eighth grade (aged 13-15) students from Taoyuan, northern Taiwan, were invited to participate in this survey. The results showed a total of 6190 students, 3079 aged 6-8 and 3111 aged 13-15, completed this survey. In general, children aged 6-8 had significantly higher prevalence rates of diagnosed asthma, rhinitis, and eczema than children aged 13-15 (12.2%, 29.8%, and 10.2% vs. 9.6%, 18.3%, and 4.7%, respectively). Similarly, children aged 6-8 had significantly higher proportions of allergic symptoms, except for exercise-induced wheezing (5.8% vs. 17.8%, p < 0.0001). Among those with allergic disorders, children aged 6-8 presented a greater severity of wheezing attacks in the last 12 months. As regards gender, boys aged 6-8 had a significantly higher proportion of asthma or rhinitis symptoms than girls aged 6-8 but not in children aged 13-15. In children aged 6-8, asthma and rhinitis peaked in winter, especially in December. However, children aged 13-15 had two peaks (winter and summer) for asthma or rhinitis.

Adolescent↗

PubMed2005

Central nervous system infections in patients with systemic lupus erythematosus.

OBJECTIVE: To evaluate the clinical profiles of patients with systemic lupus erythematosus (SLE) with central nervous system (CNS) infections. METHOD: We retrospectively reviewed patients with SLE with CNS infections from January 1983 to June 2003. The clinical features, laboratory data, and prognoses of these patients were recorded. RESULTS: During the 20-year review period, 17 SLE patients with CNS infections were identified. The mean age at CNS infection was 29.6 +/- 15.3 years. Cryptococcal infection was identified in 10 patients and bacterial meningitis in 7. Most patients (94%) had active SLE at the time of CNS infection. Fifteen patients received corticosteroid therapy and of these, 7 received it in conjunction with immunosuppressive agents. The most common presentation was headache, fever, and vomiting. The mortality rate among the 17 patients was high (41.2%). CONCLUSION: Cryptococcal meningitis played the major role in CNS infection of patients with SLE, and it cannot be ruled out even when the cerebrospinal fluid (CSF) white blood cell count is within normal range. CSF India ink and latex agglutination testing for cryptococcal antigen should be performed and are effective screening tools to establish an early diagnosis.

Adolescent↗

PubMed2005

Advances in atopic dermatitis.

Atopic dermatitis (AD) is a highly pruritic, chronic, and relapsing inflammatory skin disorder affecting 10-20% of children worldwide. During the past year there have been significant advances in our understanding of the cellular and immunologic mechanisms underlying AD as well as the immunologic triggers involved in its pathogenesis. The introduction of a new class of topical anti-inflammatory medications, topical calcineurin inhibitors, has significantly increased our treatment options and led to the rethinking of potential management approaches in AD.

Antigen-Presenting Cells↗

PubMed2004

CD56+ cells induce steroid resistance in B cells exposed to IL-15.

Interleukin-2 can induce steroid resistance in T cells. IL-15 shares biological activities with IL-2, as both cytokines use IL-2Rgamma for signal transduction. We therefore sought to determine whether IL-15 contributes to induction of PBMC corticosteroid resistance. Surprisingly, we found that incubation of unfractionated PBMC with IL-15 for 48 h resulted in the inhibition of glucocorticoid receptor (GCR) nuclear translocation in response to dexamethasone (DEX) treatment in CD19-positive B cells significantly greater than CD19-negative non-B cells (p < 0.01). However, pure B cells incubated with IL-15 responded normally with nuclear translocation of GCR in response to steroids, but failed to translocate GCR when they were grown in the presence of CD19(-) cells. Coculture of B cells with CD3(+) (T cells), CD14(+) (monocytes), or CD56(+) (NK and NKT cells) in the presence of IL-15 revealed that only CD56(+) cells contributed to the steroid insensitivity of B cells. IL-15 stimulation significantly increased production of IL-4 by CD56(+) cells (p < 0.02). Treatment of purified B cells with combination IL-15/IL-4 resulted in abrogation of glucocorticoid receptor nuclear translocation and the inability of DEX to suppress cytokine production by B cells. In the presence of IL-4-neutralizing Ab, when B cells were cocultured with CD56(+) cells and IL-15, the B cells were found to be steroid sensitive, i.e., DEX induced GCR nuclear translocation. This study demonstrates that B cells develop steroid resistance in the presence of CD56(+) cells after IL-15 stimulation. Furthermore, IL-15 and IL-4 have the capacity to induce B cell insensitivity to steroids.

B-Lymphocytes↗

PubMed2004

T regulatory cells in atopic dermatitis and subversion of their activity by superantigens.

BACKGROUND: Atopic dermatitis (AD) is a chronic inflammatory skin disease involving colonization by superantigen (SAg)-secreting Staphylococcus aureus. CD4+CD25+ T regulatory (Treg) cells are thought to play an important role in controlling inflammatory responses. OBJECTIVE: In this study we examined whether Treg cells might be deficient in patients with AD. METHODS: CD4+CD25+ and CD4+CD25- T cells were isolated from PBMCs by using immunomagnetic beads. Cells were cultured with anti-CD3 or SAg, staphylococcal enterotoxin B (SEB), for 72 hours. Proliferation was measured by means of tritiated thymidine incorporation. CD4, CD8, CD25, and cutaneous lymphocyte-associated antigen expression on PBMCs was assessed by means of flow cytometry. RNA was extracted from isolated subsets of T cells, and the results of real-time PCR for FoxP3 mRNA were determined. RESULTS: Surprisingly, CD4+CD25+ T cells were significantly (P <.01) increased in patients with AD (6.68%+/-0.99%, n=15) compared with in asthmatic patients (3.42%+/-0.58%, n=12) or nonatopic healthy control subjects (3.34%+/-0.43%, n=14). Patients with AD also had a higher expression of CD25+ in skin-homing, CD4+, cutaneous lymphocyte-associated antigen-positive T cells than asthmatic and nonatopic subjects, with values of 35.95% versus 22.44% versus 23.03%, respectively (P <.006). Only CD4+CD25+ cells expressed FoxP3, whereas CD4+CD25- T cells and CD4- cells did not. Consistent with known properties of Treg cells, CD4+CD25+ cells were anergic to anti-CD3 stimulation. When CD4+CD25+ cells from each study group were mixed with CD4+CD25- cells, proliferative responses were equally suppressed after anti-CD3 stimulation. In contrast, after SEB stimulation, CD4+CD25+ cells were no longer anergic. Furthermore, when CD4+CD25+ cells were mixed with CD4+CD25- cells and stimulated with SEB, the suppressive function of Treg cells was reversed. CONCLUSION: Patients with AD have significantly increased numbers of peripheral blood Treg cells with normal immunosuppressive activity. However, after SAg stimulation, Treg cells lose their immunosuppressive activity. These data suggest a novel mechanism by which SAgs could augment T-cell activation in patients with AD.

Adult↗

PubMed2004

Superantigen-induced corticosteroid resistance of human T cells occurs through activation of the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK-ERK) pathway.

BACKGROUND: Microbial superantigens induce human T-cell resistance to corticosteroids. OBJECTIVE: Understanding the molecular pathways resulting in corticosteroid-resistant T cells is important because this condition can complicate the treatment of inflammation. METHODS: The response of human PBMCs to steroids was assessed by using proliferation assays after stimulation with superantigens or anti-CD3 in the presence of various kinase inhibitors. Glucocorticoid receptor alpha (GCRalpha) localization was defined on the basis of intracellular staining. Protein phosphorylation was measured by means of Western blotting. RESULTS: In the current study we found that PBMCs stimulated with superantigen, but not anti-CD3, induced corticosteroid-resistant T cells. However, the purified T cells stimulated either with staphylococcal enterotoxin B (SEB) or anti-CD3 are susceptible to corticosteroid inhibition. These results imply that signals on antigen-presenting cells might act in concert with the T-cell receptor to cause steroid resistance. Blockade of CD40-CD40 ligand interaction had no effect on superantigen-induced corticosteroid resistance. However, CD28 costimulation with T-cell receptor activation induced corticosteroid resistance of human T cells in a dose-dependent manner. Superantigen stimulation, compared with anti-CD3 stimulation, was found to induce a more rapid and sustained phosphorylation of mitogen-activated extracellular signal-regulated kinase (ERK). Treatment with PD98059 and UO126 (specific mitogen-activated protein kinase kinase [MEK]/ERK inhibitors), but not a p38 inhibitor or a c-Jun N-terminal kinase inhibitor, restored the response to steroids, as indicated by proliferation assays. Furthermore, purified ERK1 and ERK2 were able to phosphorylate recombinant human GCRalpha directly in an in vitro kinase assay. Of note, superantigen-induced corticosteroid resistance was associated with abrogation of GCRalpha nuclear translocation. This effect could be reversed by treatment with MEK/ERK pathway inhibitors. CONCLUSIONS: These data are compatible with the hypothesis that superantigen-induced corticosteroid resistance involves the Raf-MEK-ERK1/ERK2 pathway of T-cell receptor signaling, which leads to GCRalpha phosphorylation and inhibition of dexamethasone-induced GCRalpha nuclear translocation.

Active Transport, Cell Nucleus↗

PubMed2003

The RANTES promoter polymorphism: a genetic risk factor for near-fatal asthma in Chinese children.

BACKGROUND: RANTES promoter polymorphisms were found associated with asthma/atopy in some studies but not others, possibly reflecting the genetic heterogeneity among different ethnicities and different asthma severity. OBJECTIVE: The purpose of this investigation was to test the genetic association between the RANTES -28C/G and -403G/A polymorphisms and asthma/atopy in a cohort of Chinese children, with particular emphasis on those patients who had experienced life-threatening asthma attacks. METHODS: Forty-eight children with near-fatal asthma, 134 children with mild-to-moderate asthma, 69 children with allergic disorders but no asthma, and 107 nonasthmatic nonatopic control children were genotyped through use of a PCR-based assay. RESULTS: No significant difference was demonstrated for frequency of the RANTES -28C/G polymorphism when the mild-to-moderate asthma, atopic/nonasthmatic, and normal control groups were compared. The RANTES -28G allele was present in a significantly higher proportion of the children with near-fatal asthma compared with the nonasthmatic nonatopic controls (odds ratio, 2.93 [1.41-6.06]; P =.006) and the children with mild-to-moderate asthma (odds ratio, 3.52 [1.73-7.16]; P =.001). The frequency of -28G allele carriage correlated with asthma severity. The RANTES -28G allele was also associated with an increased blood eosinophil count and a higher degree of bronchial hyperresponsiveness. The RANTES -403G/A polymorphism did not influence asthma/atopy susceptibility, blood eosinophil count, or bronchial hyperresponsiveness. Interestingly, a higher frequency of -403A allele carriage was observed in the moderate asthma subgroup compared with the mild asthma analog. CONCLUSIONS: We conclude that the RANTES -28C/G polymorphism exacerbates asthma severity, representing a genetic risk factor for life-threatening asthma attacks in Chinese children. In addition, the linkage disequilibrium between these 2 polymorphisms is a potential confounder that must be considered in the design and interpretation of RANTES gene association studies.

Asthma↗

PubMed2003

Primary school nurses' knowledge/competence pertaining to childhood asthma and its management prior to and following a National Asthma Education Program in Taiwan.

The main purpose of the National Asthma Education Program was to provide asthma education to school nurses in Taiwan. It was also designed to enhance the knowledge and competence of school nurses in managing the asthmatic problems that children experience while in school. In addition to providing instruction about current asthma management skills, tools, and other relevant information, the program demonstrated the use of the peak flow meter for asthmatic children. A single, 4-hr session conducted in each county and city in Taiwan, the National Asthma Education Program began on August 1, 1999, and ended December 31, 2000. A total of 829 school nurses joined the program, with an overall attendance rate of 74%. Significant effects of this program on nurses' asthma care knowledge and competence and case management efficacy were noted. The participating school nurses' demographics, however, were found to be irrelevant to these effects. Expecting the training activities to help relieve the anxieties of managing asthmatic cases in the school environment, participants reported that the training was of much benefit to them. Development of a teaching program to elevate school nurses' capabilities in asthmatic student care in the school environment and the implications of such a program within Taiwanese schools were also discussed.

Adult↗

PubMed2002

Reduced expression of CD69 and adhesion molecules of T lymphocytes in asthmatic children receiving immunotherapy.

T lymphocytes play a fundamental role in the initiation and regulation of chronic inflammatory responses in patients with asthma. CD69 is an early marker of T-cell activation. The levels of intercellular adhesion molecule-1 (ICAM-1, CD54) and L-selectin have been reported to increase in patients with allergic diseases and asthma. The present study was therefore undertaken to investigate the expression of CD69, CD54, and L-selectin by T lymphocytes of children with asthma, before and after immunotherapy. Eighteen children newly diagnosed with asthma, 11 good and nine poor responders to immunotherapy, and 16 normal subjects, were enrolled in this study. The percentages of CD69+, CD54+, and CD62L+ cells in T lymphocytes were measured by using flow cytometry. The levels of CD69, CD54, and CD62L in serum and culture supernatants were determined by using enzyme-linked immunosorbent assay (ELISA). The expression of CD69 and CD54 on CD3+ T lymphocytes was significantly higher in children with asthma than in control patients. All the patient groups expressed (spontaneously and following stimulation with phorbol myristate acetate and ionomycin together with mite-extract proteins) greater amounts of CD69 and CD54 than did control subjects. With long-term immunotherapy, the percentages of CD69+ and CD54+ T lymphocytes were significantly lower in patients with a good response to immunotherapy. Our results also showed significantly lower serum L-selectin levels following immunotherapy. In conclusion, successful immunotherapy resulted in decreased expression and production of CD69 and CD54. These results may explain, in part, the clinical efficacy of immunotherapy.

Adolescent↗

PubMed2002

Risk factors of mortality for salmonella infection in systemic lupus erythematosus.

OBJECT: To investigate the risk factors of mortality for Salmonella infection in patients with systemic lupus erythematosus (SLE). METHODS: Between 1995 and 1999 we reviewed 37 cases of Salmonella infection in 31 patients with SLE from a total of 1191 hospitalized patients with SLE at a medical center in Taiwan. Contrasting cases of patients who died with those who survived, we compared clinical and laboratory characteristics of SLE at the time of Salmonella infection, with special attention to potential risk factors (sex, age, complete blood count and differential count, erythrocyte sedimentation rate, C-reactive protein, complements, Salmonella species, infection site, reinfection, SLE presenting with Salmonella infection, associated non-Salmonella infection, etc.). RESULTS: The mean age at the onset of SLE in the 8 mortality cases was significantly higher than the 23 cases of survivors (p < 0.05). Other factors significantly related to death included associated infections other than Salmonella species, reinfection of Salmonella species, and cases of SLE presenting with Salmonella infection. Reinfection and SLE presenting with Salmonella infection were the most important risk factors of mortality for SLE with Salmonella infections: relative risk (CI) 84 (4.3-1638.8) and 63 (3.1-1296.5), respectively. CONCLUSION: Patients with SLE who are older or have associated infections other than Salmonella have an increased mortality rate when they have concurrent Salmonella infection. Patients with Salmonella infection occurring concurrently with the first presentation of SLE and patients with SLE reinfected with Salmonella species are at higher risk of mortality.

Adolescent↗

PubMed2002

Childhood idiopathic hypereosinophilic syndrome: report of a case.

We described a 15-year-old girl who presented with persistent fever, bilateral flank pain, and worsening dyspnea. The peripheral blood cell count showed remarkable eosinophilia at the time of admission. Severe pleural effusion with eosinophilic Infiltrations as well as pericardial effusion were noted thereafter. Bone marrow examination disclosed markedly increased eosinophils. Bilateral ectasia of the renal pelvis was found in an ultrasonographic study of the kidneys. Spiking fever and progressive shortness of breath persisted despite treatment with empiric antibiotics for infection. Based on the clinical course and histological findings, a tentative diagnosis of idiopathic HES was made. After treatment with oral prednisolone daily (1 mg/kg/day) for one week, there was a rapid improvement in her clinical condition. She was discharged a few days later and the steroids were withdrawn gradually when she was asymptomatic. The absolute eosinophil count (AEC) was monitored during follow-up. At 3 weeks, the AEC had fallen from 8,060/mm3 to 4,792/mm3 and it further fell to 1,591/mm3 at 5 months, and to 855/mm3 at 8 months during follow-up. There is no evidence of any other organ involvement until now. The clinical manifestations, diagnosis and management of idiopathic HES in children are also reviewed.

Adolescent↗