The use of PPIs is a risk factor for development of osteoporosis and osteoporotic fractures. However, as the direct pathogenesis remains unclear, specific points of intervention are lacking, other than being vigilant in regard to the indication for prescribing PPIs and to use the lowest effective dose where PPIs cannot be avoided.
The majority of hip fractures-and in particular hip fractures in men-occur without a previously treated MOF that could have resulted in early detection and treatment of osteoporosis. With current treatment modalities, a maximum of one in six hip fractures in Denmark can be prevented through FLS initiatives. Identification of patients with vertebral fractures for assessment and treatment is therefore critical for successful prevention of hip fractures using this strategy.
The immediate, 1 day and 14 days skin reaction was determined in 23 female SLE patients and 23 age-matched controls after standardized exposure to ultraviolet light of the UV-A wavelengths (320-440 nm). Eighteen of the patients and 12 of the controls were photosensitive by history. Eight separate sites on the buttocks were exposed to UV-A light, four sites at doses between 42 and 252 kJ/m2 and four sites with longpass filters (320, 345, 360 and 375 nm). The reactions on test sites were graded by two independent observers unaware of given doses or filter location. All patients and controls reacted with immediate erythema irrespectively of the presence or absence of photosensitivity. After 1 day, 39% of controls and 78% of patients had erythema and the reactions were more pronounced to longwave UV-A light (>320 nm) in the patients (P < 0.001). After 14 days, six patients, but no control, had persistent erythema (P = 0.04). Interestingly, three of the four patients without anamnestic photosensitivity did not react on days 1 or 14, while the pattern seen in the controls on day 1 was totally unpredictable with regard to reported photosensitivity. These findings strongly suggest that a considerable proportion of SLE patients show pathological skin reactions to physiological doses of longwave UV-A and not only the far more studied shortwave UV-B (290-320 nm). The responsible chromatophore for the UV-A reaction is not known.
The immediate, 1 day and 14 days skin reaction was determined in 23 female SLE patients and 23 age-matched controls after standardized exposure to ultraviolet light of the UV-A wavelengths (320-440 nm). Eighteen of the patients and 12 of the controls were photosensitive by history. Eight separate sites on the buttocks were exposed to UV-A light, four sites at doses between 42 and 252 kJ/m2 and four sites with longpass filters (320, 345, 360 and 375 nm). The reactions on test sites were graded by two independent observers unaware of given doses of filter location. All patients and controls reacted with immediate erythema irrespectively of the presence or absence of photosensitivity. After 1 day, 39% of controls and 78% of patients had erythema and the reactions were more pronounced to longwave UV-A light (> 320 nm) in the patients (P < 0.001). After 14 days, six patients, but no control, had persistent erythema (P = 0.04). Interestingly, three of the four patients without anamnestic photosensitivity did not react on days 1 or 14, while the pattern seen in the controls on day 1 was totally unpredictable with regard to reported photosensitivity. These findings strongly suggest that a considerable proportion of SLE patients show pathological skin reactions to physiological doses of longwave UV-A and not only the far more studied shortwave UV-B (290-320 nm). The responsible chromatophore for the UV-A reaction is not known.
Purpose: Treatment of rheumatic diseases with tumor necrosis factor inhibitors leads to improved clinical outcomes. Therapeutic drug monitoring (TDM) may assist in guiding clinical decisions. This study investigates the impact of TDM on clinical outcome, decisionmaking and biologics cost expenditure. Patients and Methods: In a retrospective observational study of 306 patients with rheumatic diseases treated with four different tumor necrosis factor inhibitors, drug levels and antidrug antibodies were measured over a period of one year. Primary outcomes were the clinicians' response to each TDM result and the clinical outcome two years after TDM initiation. Outcomes were compared between the 111 TDM-guided patients and the 195 empirically guided patients. Results: Treatment change occurred in 55% of the patients in the TDM group, but in only 38% in the empirically guided group. In the TDM group, 89 (79.5%) patients were in remission or had low disease activity after two years follow-up compared to 128 (65.6%) patients in the empirical group. The average cost of biologics per patient per year was lower in the TDM group than in the empirical group for patients receiving infliximab, adalimumab or etanercept at baseline but not for golimumab. Conclusion: TDM-guided decision-making is useful in rheumatic patients receiving TNFi and may optimize therapeutic decisions, leading to a better control of disease activity. Proactive TDM may support decisions on dose tapering, resulting in lower drug consumption and biologics cost expenditure.
Homozygous C4A deficiency was found at a prevalence of 16% (13/80 patients) in systemic lupus erythematosus (SLE). The patients represented all diagnosed cases retrieved from a defined population in Southern Sweden, which minimizes the influence of patient selection. Photosensitivity was more common among C4A‐deficient patients than among other SLE patients (p<0.05). Otherwise, clinical features were similar in the two groups. In addition, no differences were found with regard to presence of various autoantibodies (anti‐dsDNA, anti‐Sm, anti‐RNP, anti‐SSA, anti‐SSB, rheumatoid factors and anti‐cardiolipin). In patients expressing both C4A and C4B isotypes, C4B/C4A quotients were fairly stable in plasma irrespective of disease activity. This argues against preferential break‐down of either isotype during complement activation in the disease. The increased photosensitivity of C4A‐deficient patients partly resembles the findings in patients with complete deficiencies of classical pathway components.
Fourteen individuals with complete C2 deficiency from 11 families and 3 heterozygous C2-deficient individuals from two families were investigated. In all the 24 independent C2-deficient haplotypes, the complotype S042 was present and the majority (21/24) was [HLA-B18,S042,DR2]. All carried the type I C2 deficiency C2 pseudogene with its characteristic 28 bp deletion. All but two haplotypes had 10 AC/GT repeats in the TNF alpha microsatellite polymorphism and all but one of the haplotypes were identical at or near HLA-B as assessed by RFLP using BstEII digestion and two genomic probes, R5A and M20A, located 100 and 38 kb centromeric to HLA-B, respectively. The exceptional haplotype was HLA-B40 with four AC/GT repeats at TNF-alpha. Three of the haplotypes were not DR2 based on generic and sequence-specific oligonucleotide typing. Another four haplotypes showed different DO-variants detected by RFLP analysis using BglIIand Mspl digestion. Thus, the [HLA-B18,S042,DR2] haplotype appears to be more fixed in the region between the complement genes and the HLA-B locus (96%) than in the region between the complement genes and DR (88%) and DO loci (71%). Of the 14 individuals studied, six had SLE or SLE-like syndromes and six had a history of severe infections although two were apparently healthy. Three of the six SLE patients and two individuals with repeated infections were homozygous for [HLA-B18,S042,DR2] and also homozygous for DQB1*0602 and the common DO variant. Thus, MHC class II genes linked to the C2 pseudogene do not appear to determine different clinical consequences of C2 deficiency.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.