Effect of lifestyle intervention for people with diabetes or prediabetes in real-world primary care: propensity score analysis

Background

It is important to keep the level of antibiotic prescribing low to contain the development of resistant bacteria. This study was conducted to reveal new knowledge about how GPs think in relation to the prescribing of antibiotics - knowledge that could be used in efforts toward rational treatment of infectious diseases in primary care. The aim was to explore and describe the variations in GPs' perceptions of infectious disease management, with special reference to antibiotic prescribing.

Methods

Twenty GPs working at primary care centres in a county in south-west Sweden were purposively selected based on the strategy of including GPs with different kinds of experience. The GPs were interviewed and perceptions among GPs were analysed by a phenomenographic approach.

Results

Five qualitatively different perceptions of infectious disease management were identified. They were: (A) the GP must help the patient to achieve health and well-being; (B) the management must meet the GP's perceived personal, professional and organisational demands; (C) restrictive antibiotic prescribing is time-consuming; (D) restrictive antibiotic prescribing can protect the effectiveness of antibiotics; and (E) patients benefit personally from restrictive antibiotic prescribing.

Conclusions

Restrictive antibiotic prescribing was considered important in two perceptions, was not an issue as such in two others, and was considered in one perception although the actual prescribing was greatly influenced by the interaction between patient and GP. Accordingly, to encourage restrictive antibiotic prescribing several aspects must be addressed. Furthermore, different GPs need various kinds of support. Infectious disease management in primary care is complex and time-consuming, which must be acknowledged in healthcare organisation and planning.     

Management of osteoporosis in rheumatoid arthritis patients

Introduction: In rheumatoid arthritis (RA) patients, the risk of both vertebral and non-vertebral fractures is roughly doubled, which is for an important part caused by inflammation-mediated amplification of bone loss and by immobilization. New treatments have become available in the last two decades to treat both RA and osteoporosis.

Areas covered: Epidemiology and assessment of osteoporosis and fracture risk (including the influence of RA disease activity and bone-influencing medications such as glucocorticoids), the importance of vertebral fracture assessment in addition to bone density measurement in patients with RA, the use of disease-modifying antirheumatic drugs and their effects on generalized bone loss, and current and possible future anti-osteoporotic pharmacotherapeutic options are discussed with special focus on RA.

Expert opinion: Assessment of osteoporosis in RA patients should include evaluation of the effects of disease activity and bone-influencing medications such as (the dose of) glucocorticoids, above standard risk factors for fractures or osteoporosis as defined by the FRAX instrument. Disease-modifying antirheumatic drugs are now well able to control disease activity using treat to target strategies. This lowering of disease activity by antirheumatic medications such as anti-TNF-α results in hampering of generalized bone loss; however, no fracture data are currently available. When treating osteoporosis in RA patients, additional focus should be on calcium supplementation, particularly in glucocorticoid users, and also on sufficient vitamin D use. Several anti-osteoporotic medications are now on the market; oral bisphosphonates are most commonly used, but in recent years, more agents have entered the market such as the parenteral antiresorptives denosumab (twice yearly) and zoledronic acid (once yearly), and the anabolic agent parathyroid hormone analogues. New agents, such as odanacatib and monoclonal antibodies against sclerostin, are now being tested and will most likely enlarge the possibilities of osteoporosis treatment in RA patients.     

羟考酮对左旋氧氟沙星在人体内药物动力学的影响

目的研究羟考酮对左旋氧氟沙星(LVFX)在人体内药物动力学的影响。方法8名健康志愿者,单用LVFX或合用羟考酮,用HPLC法测定血药浓度。结果单用LVFX500mg后的药物动力学参数分别为tmax(1.562±1.050)h,cmax(6.6419±0.15860)μg/ml,AUC(47.65±11.29)h*μg/ml,T1/2(β)(7.034±0.941)h;合用羟考酮时,LVFX的药物动力学参数分别为tmax(1.125±0.641)h,cmax(7.652±2.594)μg/ml,AUC(48.74±10.58)h*μg/ml,T1/2(β)(6.275±0.588)h。两者除T1/2ka和cmax外,无显著性差异。结论羟考酮对LVFX在人体内药物动力学参数无影响。     

Tissue and blood superoxide dismutase activity and malondialdehyde level in leprosy

Background Oxidative stress (OS) results from an imbalance between free radical generating and scavenging systems. The end product of lipid peroxidation, malondialdehyde (MDA) serves as a marker of cellular damage. Superoxide dismutase (SOD) traps free radicals and acts as a free radical scavenging system. Objective To study OS indices in paucibacillary (PB) and multibacillary (MB) leprosy in tissues and blood. Materials and methods The study group comprised untreated PB patients (n = 14), untreated MB patients (n = 18) and normal human volunteers (n = 20). SOD activity, MDA level and MDA/SOD ratio were estimated in both blood and tissue. Results Compared with controls, SOD activity in tissues decreased significantly in both PB and MB patients, while SOD activity in erythrocytes decreased significantly only in MB. In addition, MDA levels increased significantly in tissues of both PB and MB patients. Moreover, the mean level of MDA in plasma of MB patients was significantly higher, whereas there was no significant difference in that of PB patients. This study showed significant increase in OS index (MDA/SOD ratio) in tissue of PB and MB patients and in blood of MB patients only, whereas there was no significant difference in OS index in blood of PB patients compared with that in the controls. Conclusion Oxidative stress was observed in both tissues and blood of MB patients and in tissues of PB patients, denoting its crucial involvement in the pathogenesis of leprosy. This can constitute an important tool in prognosis, treatment and control of leprosy.     

Inhibitors of complement derived from the erythrocyte membrane in paroxysmal nocturnal hemoglobinuria

Extracts of the membranes of normal red cells and red cells from all subpopulations of paroxysmal nocturnal (PNH) red cells inhibited antibody-mediated complement activation. These extracts were shown to accelerate decay of the complement complex. C42, and the relative amount of inhibitory activity was similar in normal and PNH membranes. Inhibitors derived from normal red cells markedly decreased lysis of both PNH and normal cells when antibody was present in excess and complement was limiting. These same inhibitors decreased PNH cell lysis to a much lesser degree when complement was activated with cobra venom or acidified serum. The susceptibility of the PNH cell to complement lysis because of an increased fixation of C3 to its membrane is not due to a difference in membrane-associated accelerator of the decay of the C42 complex.