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J G Hanly

Publications and source records attributed to J G Hanly.

At least 19 recordsLinked to original sources
PubMed2007

Neuropsychiatric events at the time of diagnosis of systemic lupus erythematosus: an international inception cohort study.

OBJECTIVE: To describe the prevalence, characteristics, attribution, and clinical significance of neuropsychiatric (NP) events in an international inception cohort of systemic lupus erythematosus (SLE) patients. METHODS: The study was conducted by the Systemic Lupus International Collaborating Clinics (SLICC). Patients were enrolled within 15 months of fulfilling the American College of Rheumatology (ACR) SLE classification criteria. All NP events within a predefined enrollment window were identified using the ACR case definitions of 19 NP syndromes. Decision rules were derived to determine the proportion of NP disease attributable to SLE. Clinical significance was determined using the Short Form 36 (SF-36) Health Survey and the SLICC/ACR Damage Index (SDI). RESULTS: A total of 572 patients (88% female) were recruited, with a mean +/- SD age of 35 +/- 14 years. The mean +/- SD disease duration was 5.2 +/- 4.2 months. Within the enrollment window, 158 of 572 patients (28%) had at least 1 NP event. In total, there were 242 NP events that encompassed 15 of 19 NP syndromes. The proportion of NP events attributed to SLE varied from 19% to 38% using alternate attribution models and occurred in 6.1-11.7% of patients. Those with NP events, regardless of attribution, had lower scores on the SF-36 and higher SDI scores compared with patients with no NP events. CONCLUSION: Twenty-eight percent of SLE patients experienced at least 1 NP event around the time of diagnosis of SLE, of which only a minority were attributed to SLE. Regardless of attribution, the occurrence of NP events was associated with reduced quality of life and increased organ damage.

Adult↗
PubMed2006

Mortality related to cerebrovascular disease in systemic lupus erythematosus.

The objective of this study was to examine mortality rates related to cerebrovascular disease in systemic lupus erythematosus (SLE) compared to the general population. Our sample was a multisite Canadian SLE cohort (10 centres, n = 2688 patients). Deaths due to cerebrovascular disease were ascertained by vital statistics registry linkage using ICD diagnostic codes. Standardized mortality ratio (SMR, ratio of deaths observed to expected) estimates were calculated. The total SMR for death due to cerebrovascular disease was 2.0 (95% confidence interval [CI] 1.0, 3.7). When considering specific types of events, the category with the greatest increased risk was that of ill-defined cerebrovascular events (SMR 44.9 95% CI 9.3, 131.3) and other cerebrovascular disease (SMR 8.4, 95% CI 2.3, 21.6). Deaths due to cerebral infarctions appeared to be less common than hemorrhages and other types of cerebrovascular events. Our data suggest an increase in mortality related to cerebrovascular disease in SLE patients compared to the general population. The large increase in ill-defined cerebrovascular events may represent cases of cerebral vasculitis or other rare forms of nervous system disease; alternately, it may reflect diagnostic uncertainty regarding the etiology of some clinical presentations in SLE patients. The suggestion that more deaths are attributed to cerebral hemorrhage, as opposed to infarction, indicates that inherent or iatrogenic factors (eg, thrombocytopenia or anticoagulation) may be important. In view of the paucity of large-scale studies of mortality attributed to neuropsychiatric outcomes in SLE, our findings highlight the need for additional research in large SLE cohorts.

Adolescent↗
PubMed2006

Sustained remission of lupus nephritis.

The aim of this study was to describe the clinical course of patients with lupus nephritis (LN) who attain a sustained remission (SR) and identify predictors of SR. A retrospective study of patients with biopsy-proven LN were followed for up to 10 years. SR was defined as normal renal function, urine protein <0.5g/day, and an inactive urine sediment without significant immunosuppressive maintenance therapy for no less than three years. Control patients had LN but did not fulfill the criteria for SR. Data was collected at diagnosis of LN (T0), at onset of remission (T1), and at final follow-up (T2). A total of 35 patients were identified, 16 with a SR of LN and 19 controls, with a mean +/- SD follow-up of 126.4 +/- 8.5 months. Remission of LN was achieved following 37.7 +/- 6.8 months of therapy. At diagnosis (T0) the WHO classification of nephritis, activity and chronicity scores of renal biopsies were comparable in the two groups. At final follow-up (T2), the mean estimated creatinine clearance for the SR group was significantly higher than in controls (P = 0.009) and disease activity (SLEDAI scores) was lower (P = 0.002). Cumulative damage (SDI scores) in the SR group did not increase after patients entered remission (P = 0.250), whereas the mean SDI score in the control group increased significantly (P = 0.014) even when renal variables were excluded (P = 0.016). Multivariate analysis revealed that female gender (P = 0.023), older age (P = 0.034), higher nonrenal SLEDAI scores (P = 0.016) at the time of diagnosis of LN and absence of azathioprine (P = 0.010) were predictive of SR. It was concluded that remission of LN occurs in a substantial proportion of systemic lupus erythematosus (SLE) patients and may be sustained without maintenance immunosuppressive therapy. It is associated with a significantly slower accrual of both renal and non-renal damage over the ensuing seven years.

Adrenal Cortex Hormones↗
PubMed2004

ACR classification criteria for systemic lupus erythematosus: limitations and revisions to neuropsychiatric variables.

There are a wide variety of neurologic (N) and psychiatric (P) manifestations of systemic lupus erythematosus (SLE) which extend beyond those identified in the current American College of Rheumatology (ACR) classification criteria for SLE. Several attempts have been made to devise a classification of NP-SLE manifestations. The most recent is the ACR nomenclature and case definitions for 19 NP lupus syndromes which currently provides the best means of a standardized approach to categorize NP events in SLE patients. Data from a number of studies has indicated a wide variability in the prevalence of the 19 NP syndromes. On the basis of these findings and utilizing the guidelines provided in the case definitions for diagnosis and exclusion of confounding variables, it is proposed to examine a number of NP manifestations for possible inclusion in revised classification and diagnostic criteria for SLE.

Humans↗
PubMed2001

Neuropsychiatric lupus.

Neuropsychiatric (NP) manifestations of systemic lupus erythematosus (SLE) have been recognized for more than 100 years but continue to pose a diagnostic and therapeutic challenge for rheumatologists and other physicians involved in the care of SLE patients. NP-SLE includes a plethora of clinical manifestations and the reported prevalence has varied widely between 14% and 75%. The recent introduction of a standard nomenclature, case definitions, and diagnostic criteria for 19 NP-SLE syndromes should facilitate a more consistent approach to the classification of patients and to the execution of large multicenter clinical studies. The etiology of NP-SLE is likely multifactorial and includes microangiopathy, autoantibody production, and the intrathecal production of proinflammatory cytokines. Newer imaging modalities of brain structure and function provide novel ways of understanding pathogenic mechanisms. The use of standardized neuropsychometric techniques to evaluate cognitive function has identified a high prevalence of cognitive impairment in SLE patients. The management of patients with NP-SLE includes symptomatic and immunosuppressive therapies, evidence for which is largely limited to uncontrolled clinical trials and anecdotal experience. Multicenter initiatives are required to address important issues on prognosis and management.

Cognition Disorders↗
PubMed2001

Detection of 'antiphospholipid' antibodies: a single chromogenic assay of thrombin generation sensitively detects lupus anticoagulants, anticardiolipin antibodies, plus antibodies binding beta(2)-glycoprotein I and prothrombin.

The diagnosis of the antiphospholipid syndrome (APS) requires both a typical clinical event plus a persistently positive test in an assay for either anticardiolipin (aCL) antibodies or a lupus anticoagulant (LA). Enzyme linked immunosorbent assays (ELISA) specific for autoantibodies against beta(2)-glycoprotein I (beta(2)GPI) or prothrombin are also used, but none of the tests are adequately sensitive or specific. A chromogenic assay was developed that measures the effect of test antibody or plasma samples on in vitro thrombin formation. It is able to detect both LA and beta(2)GPI-dependent aCL antibodies and may have greater specificity for APS than currently available tests. Using this method various monoclonal antibodies (MoAbs) were examined, from mice immunized with beta(2)GPI, mice with a spontaneous animal model of APS, and from three humans with APS. Plasma and affinity purified antibodies from patients with APS and control groups were also examined. Thrombin inhibition was more sensitive to perturbation by MoAbs than a combination of tests for LA (P < 0.05) and at lower antibody concentrations (12.5 microg/ml versus 100 microg/ml). There was a significant correlation between inhibition of thrombin generation and the level of MoAb reactivity to beta(2)GPI (r = 0.90; P < 0.001) but not to CL (r = 0.06; P = 0.76). Plasma and affinity purified antibodies from patients with APS also inhibited thrombin generation, and significantly more so than patients with aPL from causes other than APS. APS patient samples showed thrombin inhibition in the presence of anti-beta(2)GPI or antiprothrombin antibodies. All MoAbs binding beta(2)GPI showed inhibition of thrombin generation, while MoAbs binding domain I of beta(2)GPI had more LA effect.

Animals↗
PubMed2001

Positive effect of etidronate therapy is maintained after drug is terminated in patients using corticosteroids.

Following a 52-wk randomized controlled trial of intermittent cyclic etidronate therapy in patients using corticosteroids, we performed a 52-wk open-label trial of calcium alone in 114 corticosteroid-treated patients to determine whether the beneficial effect of etidronate is maintained after the drug is discontinued. All patients were given 500 mg/d of elemental calcium. Sixty-one and 53 patients made up the former placebo and etidronate groups, respectively. A total of 89 (98%) of patients in the former placebo and etidronate groups remained on corticosteroids throughout the second year. The mean (SE) percentage change in bone mineral density of the lumbar spine, femoral neck, and trochanter were compared between groups. The difference between groups in mean percentage change from baseline (wk 0, initiation of etidronate or placebo therapy) in the bone density of the lumbar spine, femoral neck, and trochanter, following 104 wk, was 3.8 (0.9), 3.0 (1.1), and 4.3 (1.1), respectively (p < 0.05, all sites), in favor of the former etidronate group. While not significant, the former placebo group demonstrated a slightly larger rate of decline in bone density over the second year than the former etidronate group at all three sites. Following the discontinuation of etidronate therapy, there was no accelerated bone loss and there was evidence of a residual protective effect in both the lumbar spine and femoral neck for up to 1 yr posttreatment.

Adult↗
PubMed2001

Manpower in Canadian academic rheumatology units: current status and future trends. Canadian Council of Academic Rheumatologists.

OBJECTIVE: To examine manpower and activity profiles of attending staff, and enrollment in training programs over 3 years in academic rheumatology units in Canada. METHODS: In 1998, the Canadian Council of Academic Rheumatologists (CCAR) established a database to annually monitor trends in manpower, activity profiles, and recruitment in 15 academic rheumatology units in Canada. Information was also collected on residents pursuing subspecialty training in rheumatology. RESULTS: Between 1998 and 2000, the total number of rheumatologists increased from 157 (137 adult; 20 pediatric) to 162 (139 adult; 23 pediatric). Male to female ratio was about 2:1 and mean age increased from 48 to 49 years. About 60% of rheumatologists held fulltime positions within their academic units. In the year 2000, 57% of individuals had a substantial commitment (> or = 50% time) to clinical care activities compared to 17% for research and 3% for teaching. There were 21 unfilled positions, mainly full-time in adult rheumatology, across 12 centers. A substantial commitment (> or = 50% time) for research was identified in 11 of the unfilled positions, for clinical care activities in 6, and for teaching in one. Significant barriers to recruitment as identified by 11 centers were lack of suitable applicants (9), financial resources (5), and physical resources (3). From 1998 to 2000 the number of trainees in pediatric and adult rheumatology fell from 38 to 29 and the number of active training programs from 12 to 11. The mean age of trainees was 30-32 years, with equal representation for males and females. Over the 3 years studied, funding of trainees was provided by government (range 41-51% of trainees), The Arthritis Society (21-26%), and alternative sources (23-38%). Based on current recruitment, anticipated changes in population growth, and increased prevalence of rheumatic diseases, there will be a 64% shortfall in rheumatologists required in Canada by 2026. CONCLUSION: Rheumatology manpower in Canadian academic units needed to fulfill responsibilities in delivery of clinical services and academic programs is inadequate. Enrollment in rheumatology training programs is falling and is insufficient to meet the present and future manpower needs for patients with rheumatic diseases in Canada.

Academic Medical Centers↗
PubMed2000

Anti-beta2-glycoprotein I (GPI) autoantibodies, annexin V binding and the anti-phospholipid syndrome.

We examined the role of autoantibodies to beta2-GPI and prothrombin (PT) in the inhibition of annexin V binding to cardiolipin (CL) and the association with clinical manifestations of the anti-phospholipid syndrome (APS). Plasma samples from 59 patients with anti-phospholipid (aPL) antibodies were studied. Affinity purification of total IgG and IgG anti-ss2-GPI antibodies was performed using staphylococcal protein A and phospholipid liposomes. Annexin V binding to CL was significantly inhibited by 31/59 (53%) aPL+ plasma samples. There was a significant association between annexin V inhibition and elevated levels of IgG anti-cardiolipin (aCL) (r = -0.62; P < 0.001), IgG anti-ss2-GPI (r = -0.67; P < 0. 001) and a weaker association with lupus anti-coagulant (r = -0.27; P = 0.05). There was no association with other isotypes of aCL and anti-ss2-GPI or with anti-PT of any isotype. In patients with clinical manifestations of the APS there were higher levels of IgG aCL (median (range) Z score): 10.0 (0-17.6) versus 5.0 (0-16.1); P = 0.03), IgG anti-ss2-GPI (4.5 (0-11.3) versus 0.9 (0-9.7); P = 0.02) and greater inhibition of annexin V binding to CL (-3.4 (-11.4-0.6) versus -1.1 (-10.8-1.2); P = 0.22). Odds ratios for the laboratory assays and the presence of clinical manifestations of the APS varied between 0.38 and 4.16, with the highest values for IgG aCL (4.16), IgG anti-ss2-GPI (3.28) and annexin V inhibition (2.85). Additional experiments with affinity-purified IgG antibodies indicated that inhibition of annexin V binding was dependent upon the concentration of ss2-GPI and anti-ss2-GPI antibodies. These results indicate that inhibition of annexin V binding to procoagulant phospholipid surfaces is dependent upon anti-ss2-GPI antibodies and suggest a role for annexin V in the pathogenesis of the APS.

Annexin A5↗
PubMed2000

Autoimmune antiphospholipid antibodies and cryoglobulinemia.

In addition to their role in the thrombotic manifestations of the antiphospholipid syndrome (APS), autoimmune antiphospholipid (aPL) antibodies may also be responsible for direct injury to the blood vessel wall, although the mechanism is unclear. Cryoglobulinemia has been reported infrequently in patients with APS and is one potential means of blood vessel injury. The aim of the present study was to determine if autoimmune aPL antibodies and their target antigens contribute to the formation of cryoprecipitates. Cryoglobulins were identified and isolated from 5 of 8 patients with autoimmune aPL antibodies. Using identical concentrations of immunoglobulins isolated from matched sera and washed cryoprecipitates there was a significant enrichment (at least 100%) of aCL antibodies in the cryoprecipitates from 4 of 5 patients. This involved IgG, IgM and IgA isotypes with specificity for both beta2-glycoprotein I (GPI) and prothrombin (PT). The target antigens were detected in cryoprecipitates from all 5 aPL positive patients and in cryoprecipitates from 3 controls. These results suggest that anti-beta2-GPI and anti-PT antibodies in association with their target antigens are integrally involved in the formation of cryoprecipitates in patients with autoimmune aPL antibodies and provide insight into a potential mechanism for blood vessel injury.

Antibodies, Antiphospholipid↗
PubMed2000

The Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index for Systemic Lupus Erythematosus International Comparison.

OBJECTIVE: To compare patients with systemic lupus erythematosus (SLE) from different centers with respect to demographics and Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SLICC/ACR DI) scores, and to assess whether the SLICC/ACR DI changed over time, and whether initial DI scores were related to outcome. METHODS: Members of SLICC completed DI scores and patient demographics on patients followed in their centers. Information was provided at 2, 5-10, and > 10 years of followup. Data were entered on computer and analyzed on SPSS/PC+ and SAS using descriptive statistics and analysis of variance. RESULTS: Information for 1297 patients within 2 years of first clinic visit was submitted from 8 centers. There were 1187 women and 110 men with a mean age at diagnosis of SLE of 32 years. Seven hundred sixty-two were Caucasian, 423 were black, and the remainder were of other races. There were more blacks in the American centers than in Canadian or European centers. Five centers provided information for the 3 time periods. The DI increased over time. Ninety-nine patients had died. Higher SLICC/ACR DI scores were documented in patients who went on to die. CONCLUSION: The SLICC/ACR DI is a valid measure for damage in SLE.

American Medical Association↗
PubMed2000

Efficacy of sacroiliac corticosteroid injections in patients with inflammatory spondyloarthropathy: results of a 6 month controlled study.

OBJECTIVE: To evaluate changes in articular symptoms, spinal mobility, and global function over 6 months after intraarticular injections of long acting corticosteroid into the sacroiliac (SI) joints of patients with inflammatory low back pain (ILBP). METHODS: Nineteen patients with symptoms of ILBP were studied. Thirteen (68%) had radiographic evidence of sacroiliitis. The remaining 6 patients (32%) had normal imaging studies and thus were considered to have mechanical low back pain. All patients received bilateral SI joint injections of triamcinolone hexacetonide (40 mg/joint) under computer tomographic guidance. Outcome variables included the duration of low back morning stiffness, back pain (by visual analog scale, McGill Pain Questionnaire), spinal mobility (chest expansion, Schober test, 10 cm segments test, finger-fibula distance), and self-report health status (SF-36). RESULTS: Both groups of patients showed a transient improvement in stiffness and pain, spinal mobility, and general health status that was most pronounced at 1-3 months after intraarticular therapy. This did not reach statistical significance (p > 0.05) and by 6 months, followup all outcome variables had reverted to pretherapy levels in both groups. CONCLUSION: These preliminary observations suggest that SI corticosteroid injections are ineffective in the management of patients with inflammatory spondyloarthropathy.

Administration, Topical↗
PubMed2000

Anti-beta2-glycoprotein I autoantibodies, in vitro thrombin generation, and the antiphospholipid syndrome.

OBJECTIVE: Thrombin plays a pivotal role in the regulation of hemostasis. We examined the effect of antiphospholipid (aPL) antibodies, in particular those with specificity for beta2-glycoprotein I (beta2-GPI), on in vitro thrombin generation, and examined the association with clinical manifestations of the antiphospholipid syndrome (APS). METHODS: We studied plasma samples from 59 patients with aPL antibodies determined by the presence of either elevated anticardiolipin (aCL) antibodies or lupus anticoagulant (LAC). Direct antibody binding of IgG, IgM, and IgA to beta2-GPI and prothrombin (PT) was determined by ELISA. Affinity purification of total IgG and IgG anti-B2-GPI antibodies was performed using staphylococcal protein A and phospholipid liposomes. A chromogenic assay was used to determine the effect of plasma samples and purified autoantibodies on in vitro thrombin generation. RESULTS: Thirty-three of 59 (56%) plasma samples inhibited in vitro generation of thrombin and 7/59 (12%) accelerated thrombin formation. There was a strong negative correlation between thrombin generation and IgG aCL (r = -0.72, p < 0.001) and IgG anti-beta2-GPI (r = -0.71, p < 0.001) antibody levels, and a weaker correlation with LAC (r = -0.46, p = 0.001). This association was not found with anti-PT antibodies and could not be attributed to concurrent therapy with warfarin. Additional experiments with affinity purified IgG antibodies indicated a dose dependent inhibition of thrombin generation, which was restricted to anti-beta2-GPI antibodies. Patients with a history of core clinical manifestations of the APS [venous and arterial thrombosis, recurrent (> or = 2) fetal loss] had significantly greater inhibition of in vitro thrombin generation (mean +/- SEM Z score: -3.38 +/- 0.51 vs -1.42 +/- 0.56; p = 0.01) and higher levels of IgG aCL (mean +/- SEM Z score: 8.39 +/- 1.12 vs 5.39 +/- 0.88; p = 0.04) and IgG anti-beta2-GPI antibodies (mean +/- SEM Z score: 4.49 +/- 0.69 vs 2.26 +/- 0.54; p = 0.01). Odds ratios for these variables and clinical manifestations of the APS were 5.43, 4.17, and 3.28, respectively. CONCLUSION: aPL antibodies may accelerate or inhibit the rate of in vitro thrombin formation. The predominant effect is inhibition that is restricted to IgG anti-beta2-GPI antibodies and it is strongly associated with clinical manifestations of the APS.

Antiphospholipid Syndrome↗
PubMed1999

A prospective analysis of cognitive function and anticardiolipin antibodies in systemic lupus erythematosus.

OBJECTIVE: To prospectively analyze the association between changes in cognitive function and circulating anticardiolipin antibodies (aCL) over a period of 5 years in patients with systemic lupus erythematosus (SLE). METHODS: Cognitive function was assessed in 51 unselected female SLE patients at baseline and after a mean followup of 64.5 months (range 52-71 months), using standardized tests of cognitive function, i.e., the Wechsler Adult Intelligence Scale-Revised, the Wechsler Memory Scale-Revised, and the California Verbal Learning Test. Circulating IgG, IgA, and IgM aCL and anti-double-stranded DNA (anti-dsDNA) antibody levels were determined by enzyme-linked immunosorbent assay on 4-7 occasions over the same time period. Persistent antibody reactivity was defined as levels more than 2 standard deviations (moderately positive) and more than 5 standard deviations (highly positive) above the mean for normal controls over the duration of the study. Changes in overall cognitive performance and in raw scores on individual cognitive tests were compared in patients who were persistently positive or negative for aCL. RESULTS: At baseline 11 patients (22%) were cognitively impaired, compared with 7 (14%) at followup. Between 16% and 37% of patients had persistently elevated aCL levels of different isotypes. There was no significant difference in the prevalence of overall cognitive impairment in patients who were persistently positive for aCL compared with those who were not. In contrast, over the period of study, patients who had persistent IgG aCL positivity had a reduction in psychomotor speed, and patients who had persistent IgA aCL positivity had a reduction in conceptual reasoning and executive ability. Similar associations with anti-dsDNA antibodies were not found. CONCLUSION: These results suggest that IgG and IgA aCL may be responsible for long-term subtle deterioration in cognitive function in patients with SLE.

Adult↗
PubMed1999

Complications of nonsteroidal antiiflammatory drug gastropathy and use of gastric cytoprotection: experience at a tertiary care health center.

OBJECTIVE: To determine what proportion of patients admitted to an academic medical center with complications of nonsteroidal antiinflammatory drug (NSAID) gastropathy had true indications for NSAID use, and whether patients with risk factors for NSAID gastropathy were receiving appropriate cytoprotection. METHODS: A retrospective chart review was carried out of all patients admitted with upper gastrointestinal (GI) bleeding, ulcer perforation, or gastric outlet obstruction during 1990-91 and 1995-96. NSAID or acetylsalicylic acid (ASA) use and medical indications were determined. Risk factors for NSAID gastropathy were documented and included concomitant steroid use, history of peptic ulcer disease or GI bleeding, history of cardiovascular disease, age > 60 years, and use of more than one NSAID. GI medication coprescription for patients with risk factors for gastropathy was evaluated. RESULTS: A total of 296 cases were identified. Use of NSAID was a contributing factor in 24% of patients admitted with upper GI bleeding, ulcer perforation, or gastric outlet obstruction. Use of ASA was a contributing factor in 25%. A true indication for NSAID/ASA use was identified in only 55% of cases. Fifty-nine patients had a single risk factor for NSAID gastropathy. Of these, 24% were receiving a coprescription for any GI medication at the time of admission to hospital and 8% were receiving misoprostol. In the 64 patients with 2 or more risk factors for NSAID gastropathy, 23% were concurrently receiving and GI medication and 2% were receiving misoprostol. In the 46 patients identified with a history of peptic ulcer disease or GI bleeding 28% were coprescribed a GI medication and 2% were taking misoprostol. There were no significant differences in the proportion of patients in any of the high risk groups who were receiving GI medications between 1990-91 and 1995-96. CONCLUSION: Inappropriate use of NSAID/ASA and failure to adequately cytoprotect patients at risk of NSAID gastropathy may account for a significant proportion of patients who develop life threatening complications.

Aged↗
PubMed1999

Otitis media in infants aged 0-8 weeks: frequency of associated serious bacterial disease.

OBJECTIVE: To determine the frequency of serious bacterial infection in well appearing infants aged 0-8 weeks with isolated otitis media (OM). METHODS: Infants with confirmed OM underwent tympanocentesis with middle ear fluid (MEF) culture and complete sepsis evaluation. Enrolled infants were admitted to the hospital for parenteral antibiotics until blood, urine, and CSF cultures were negative for 48 hours. RESULTS: Forty non-toxic appearing infants were enrolled between January 1994 and April 1995, of whom 15 (38%) had a documented rectal temperature > or =38 degrees C. Bacterial pathogens were isolated from MEF cultures in 25 (62.5%) infants. All afebrile infants had negative blood, urine, and cerebrospinal fluid cultures (upper limit (UL) 95% CI 0.11). Only two febrile infants had positive cultures from sites other than the MEF (UL 95% CI 0.36). CONCLUSION: In our study population, previously healthy, non-toxic appearing afebrile infants aged 2-8 weeks and having isolated OM infrequently have an associated serious bacterial infection, suggesting that outpatient treatment with oral antibiotics and close follow-up may be an option. Further studies with large numbers of infants are necessary to confirm this conclusion.

Administration, Oral↗