Biomedical subjects

Dana Jerome

Publications and source records attributed to Dana Jerome.

3 recordsLinked to original sources

PubMed2006

Office capillaroscopy in systemic sclerosis.

The aims of this study are to assess the reliability of two office techniques, the ophthalmoscope and the Dermlite dermatoscope, and to detect nailfold capillaroscopy abnormalities in systemic sclerosis (SSc). Two separate studies were performed. In the first, the nailfolds of two fingers on one hand of 13 SSc patients and two normals were examined by four rheumatologists using an ophthalmoscope. In the second, the nailfolds of the two fingers of each hand of six SSc patients and two normals were examined by six rheumatologists with a Dermlite dermatoscope. Widefield capillary microscopy was performed by one observer in the ophthalmoscope study to assess validity. The examiners determined the presence or absence of dilated loops, giant capillary loops, and/or avascular areas on each digit. The kappa coefficient was calculated to demonstrate agreement. With the ophtalmoscope, the inter-observer kappa coefficients were 0.43, 0.54, and 0.19; the average intra-observer agreements were 0.61, 0.56, and 0.31; and the ophthalmoscope-microscope agreement were 0.63, 0.52, and <0.1 for dilated capillaries, giant capillaries, and avascular areas, respectively. With the dermatoscope, the kappa values for inter-observer reliability were 0.63, 0.40, and 0.20; and intra-observer reliability was 0.71, 0.55, and 0.40 for dilated capillaries, giant capillaries, and avascular areas, respectively. The ophthalmoscope and the dermatoscope provide moderate to substantial reliability to detect the presence of giant and dilated capillaries but poor inter-observer agreement for avascular areas. The ophthalmoscope is valid when compared to the microscope for detecting giant or dilated capillaries. We conclude that these techniques are useful office tools to detect capillary abnormalities in SSc.

Dermoscopy↗

PubMed2006

The effect of menopause on disease activity in systemic lupus erythematosus.

OBJECTIVE: To determine the effect of menopause on disease activity and course of systemic lupus erythematosus (SLE). METHODS: Patients were identified from the University of Toronto lupus clinic database. Menopause was diagnosed on the basis of 12 months of amenorrhea. A 3 part study was carried out. Part 1 included an inception cohort of 190 women with SLE diagnosed in the premenopausal years (Group A) and an inception cohort of 55 women with SLE diagnosed in the postmenopausal years (Group B), both followed for a minimum of 3 years. Part 2 included 49 patients followed in the clinic for at least 3 years before and 3 years after their menopause (Group C). Part 3 included 193 patients followed for 6 years entirely in the premenopausal period (Group D) and 76 patients followed for 6 years entirely in the postmenopausal period (Group E). Disease activity was measured by the SLE Disease Activity Index 2000 (SLEDAI-2K) and the adjusted mean SLEDAI-2K (AMS). Damage was assessed by the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) damage index. Comparisons were made using t-tests and chi-square and McNemar tests. A multivariate linear regression model was used to establish the impact of menopausal status on change in disease related features. RESULTS: In the first 3 years of disease, AMS was higher in Group A than Group B (6.6 +/- 3.8 vs 5.0 +/- 3.3, p = 0.003). Damage accrual was higher in Group B than in Group A both in the first year and at 3 years. For Group C, AMS and the number of flares per 3 year interval were lower in the postmenopausal period. SLICC/ACR damage index was greater during the 3 years in the postmenopausal period then in the premenopause (p = 0.006). SLEDAI-2K was higher among Group D than Group E at the start of the study (6.71 vs 4.86, p = 0.04). AMS for the 6 years was higher in the premenopausal than postmenopausal women (5.14 vs 3.54, p </= 0.0001), however, the magnitude of change in the first and second 3 year periods was not different between Group D and E. The 3 year AMS of patients in Groups C, D, and E was plotted by age and menopausal status. The slopes of AMS in the pre- and postmenopausal periods were identical, indicating that time and not menopausal status is associated with the decrease in disease activity. On the other hand, SLICC damage index showed a greater damage in postmenopausal women at any of the time points of the study. To further delineate the effect of menopausal status on changes in disease activity and damage, multiple linear regressions were performed including age at diagnosis, disease duration, and SLEDAI-2K at presentation as independent variables. No changes in AMS, number of flares, or SLICC/ACR damage index score were associated with the menopausal status. CONCLUSION: Although premenopausal women with SLE have more disease activity than postmenopausal women with SLE, we have shown that there is a constant rate of improvement over time, be it in the premenopause, across the menopause, or postmenopause. This improvement is not due to change in menopausal status. Thus clinicians should not be anticipating the postmenopausal era in a patient's course as a period of natural disease improvement.

Adult↗

PubMed2003

Frequency of adverse drug reactions in patients with systemic lupus erythematosus.

OBJECTIVE: The literature suggests that patients with systemic lupus erythematosus (SLE) have a higher frequency of adverse drug reactions (ADR). We performed this case control study to compare the prevalence of ADR in patients with SLE and controls with inflammatory arthritis. METHODS: We surveyed 249 patients, 145 with SLE and 104 age and sex matched controls with other types of inflammatory arthritis, such as rheumatoid arthritis (RA), probable RA, and psoriatic arthritis. We asked about exposure and ADR to the following classes of drugs: (1) beta-lactam antibiotics, (2) sulfonamides, (3) other antibiotics, (4) disease modifying antirheumatic drugs (DMARD), and (5) nonsteroidal antiinflammatory drugs (NSAID). Personal and family atopic histories were obtained. The 2 groups were obtained from a single rheumatologic practice and had similar characteristics and drug exposures. RESULTS: The response rate was 63% in the SLE patients and 64% in the control group. The mean age was 47.8 +/- 1.5 years in patients with SLE and 46.1 +/- 1.7 years in controls (p < 0.51). Ninety-two percent of SLE patients and 88% of controls were female (p < 0.42). Both groups had been exposed similarly to all antibiotics, as there were no significant differences between groups (exposure to sulfa antibiotics 53% in SLE patients vs 46% in controls), and to NSAID (84% SLE group vs 93% controls). Few patients from the SLE group had DMARD exposure, with the exception of plaquenil (65% SLE group vs 30% controls; p < 0.0001) and azathioprine (18% SLE group vs 4% controls; p < 0.006). There were between-groups differences with respect to total number of ADR with sulfa antibiotics (exposed had 25/48 reactions in SLE group vs 6/31 in controls; p < 0.003), but not with other drugs. Most ADR to sulfa antibiotics were cutaneous (rash). Subjects with an allergic or atopic history had more ADR (p < 0.0005). There were no differences between SLE patients and controls in having an allergic history (p < 0.88). Subjects with a positive family history of allergies were more likely to have ADR (p < 0.0043). SLE patients and controls with a personal versus family history of environmental allergies did not differ in having ADR (p < 0.16 and p < 0.83, respectively). CONCLUSION: Both intolerances and true allergic reactions were not dissimilar in patients with SLE compared to controls with inflammatory arthritis, with the exception of cutaneous reactions to sulfa antibiotics in SLE patients. This has not been the experience of other investigators (with increased ADR with several antibiotics in SLE groups) who used healthy, best friend, and relative controls with dissimilar frequencies of drug exposures. Perhaps differences observed in the past (where SLE patients have more ADR than healthy controls) are true of other inflammatory arthritis subjects (who have different drug exposures than healthy individuals) rather than just SLE. Differences could also exist in the pharmacogenetics, as our sample population was mostly Caucasian.

Angioedema↗