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Physicians often face tight resource constraints, meaning they have to make trade‐offs between which patients they care for and the amount of care received. Studies show that patients requiring many resources disproportionately suffer a loss of care when resources are constrained. This study uncovers whether physicians' attitudes toward prioritization of healthcare predicts poor‐health patients' access to care. We combine unique survey data on Danish GPs' preferred prioritization principle with register data on their patients' contacts in general practice. We consider different types of contacts as the required effort could impact the need for prioritization. Our results show variation in GPs' prioritization principles, where a majority prefers a principle that may lead to an unequal distribution of services. We further find that GPs' attitudes toward prioritization predict some poor‐health patients' access to general practice. GPs who state they prefer the principle of prioritizing patients in the poorest health state when resources tightened provide more contacts to poor‐health patients. The additional contacts are typically high‐effort contacts such as annual status meetings and home visits, but also low‐effort contacts such as emails. Our findings indicate inequity in poor‐health patients' access to care across general practices. [ABSTRACT FROM AUTHOR]

General practitioners' (GPs') income often relies on self‐reported activities and performances. They can therefore 'game the system' to maximize their remuneration. We investigate whether Danish GPs game their travel fees for home visits. Combining administrative and geographical data, we measure the difference between GPs' traveled and billed distances. We exploit a rise in the fees for home visits. If there is a link between the rise in fees and upcoding, we interpret this finding as indicative of gaming behavior. We find that upcoding occurs slightly more often than downcoding (16% vs. 13% of visits) for visits that can be both upcoded and downcoded. Using linear probability models with GP fixed effects, we find that the fee rise is associated with a reduction in upcoding of 0.6% of home visits (2.8% for visits where upcoding is feasible) and no change in downcoding. Importantly, we find no statistically significant differences in the reduction in upcoding across distance bands despite large differences in their fee rises. We therefore conclude that there is no causal evidence of GPs gaming their fees. [ABSTRACT FROM AUTHOR]

In publicly funded health systems, waiting times act as a rationing mechanism that should be based on need rather than socioeconomic status. However, several studies suggest that individuals with higher socioeconomic status wait less. Using individual‐level data from administrative registers, we estimate and explain socioeconomic inequalities in access to publicly funded care for seven planned hospital procedures in Denmark. For each procedure, we first estimate the association between patients' waiting time for health care and their socioeconomic status as measured by income and education, controlling for patient severity. Then, we investigate how much of the association remains after controlling for (i) other individual characteristics (patients' family status, labor market status, and country of origin) that may be correlated with income and education, (ii) possible selection due to patients' use of a waiting time guarantee, and (iii) hospital factors which allow us to disentangle whether inequalities in waiting times arise across hospitals or within the hospital. Only for a few procedures, we find inequalities in waiting times related to income and education. These inequalities can be explained mostly by geographical and institutional factors across hospitals. But we also find inequalities for some procedures in relation to non‐Western immigrants within hospitals. [ABSTRACT FROM AUTHOR]

Paying on the basis of fee-for-service (FFS) is often associated with a risk of overprovision. Policymakers are therefore increasingly looking to other payment schemes to ensure a more efficient delivery of health care. This study tests whether context plays a role for overprovision under FFS. Using a laboratory experiment involving medical students, we test the extent of overprovision under FFS when the subjects face different fee sizes, patient types, and market conditions. We observe that decreasing the fee size has an effect on overprovision under both market conditions. We also observe that patients who are harmed by excess treatment are at little risk of overprovision. Finally, when subjects face resource constraints but still have an incentive to overprovide high-profit services, they hesitate to do so, implying that the presence of opportunity costs in terms of reduced benefits to other patients protects against overprovision. Thus, this study provides evidence that the risk of overprovision under FFS depends on fee sizes, patients' health profiles, and market conditions. [ABSTRACT FROM AUTHOR]

IgG-binding to the surface of Langerhans cells (LC) is a feature of primary Sjogren's syndrome and might be associated with qualitative and quantitative defects in LC. Fifteen patients with primary' Sjogren's syndrome and 15 healthy controls had a punch biopsy performed from clinically unaffected skin. LC were enumerated in epidermal sheets by an immunoperoxidase technique, as well as demonstrated by immunofluorescence in vertical sections, which were furthermore examined for in vivo deposits of immunoglobulins, fibrinogen and C3. A significant (P < 0.05) reduction in number of LC, measured on epidermal sheets, was found in patients as compared with controls. Examination of vertical sections did not reveal abnormalities in morphology or localisation of epidermal LC. Intraepidermal IgG deposits were demonstrated in 7/15 patients. In vivo deposits were not found in any of the controls, The density of epidermal LC was not correlated to the presence of intraepidermal IgG deposits. [ABSTRACT FROM AUTHOR]

Background. Postmenopausal endometriosis is rare. The purpose of this presentation is to give a review of the topic based on existing literature. Methods. A Medline search concerning postmenopausal endometriosis was carried out. Hormone therapy and risk of malignancy in these patients are discussed. Results. Some 32 case reports on postmenopausal endometriosis were found. The most common location is in the ovaries. Estrogens stimulate endometriosis. There is a risk of recurrence or de novo occurrence of endometriosis after the menopause in patients who take hormone therapy (HT); especially estrogen only therapy (ET). So far, treatment has primarily been surgery (hysterectomy (TAH) and bilateral oophorectomy (BSO)). There is little experience with medical treatment (aromatase inhibitors). The risk of malignant transformation of premenopausal endometriosis is around 1%. Furthermore, patients with endometriosis have an increased risk of ovarian cancer, and, apparently, other malignancies. The risk of malignant transformation appears to be further elevated in patients who take ET, although this subject is not fully elucidated. Conclusions. Although the condition is rare, it is important to be aware of endometriosis after the menopause. Postmenopausal endometriosis infers a risk of recurrence and malignant transformation. Although solid evidence is lacking, the risk of malignant transformation appears to be lower during combined HT compared to ET. Thus, hormone replacement therapy should generally be reserved for patients with severe climacteric complaints, and if indicated, combined therapy should be used. [ABSTRACT FROM AUTHOR]

In Philadelphia, one of the nation's judicial battlegrounds, a clinical practice group of 360 physicians responded to the medical malpractice insurance crisis by creating a reciprocal risk retention group that has supported the group's best practices while almost eliminating the number of claims going to trial. This article describes how the insurance crisis helped change the culture of its physician practice group, restore the close physician-patient relationship that lies at the heart of medicine, and shows how elements of this revolutionary program can be adopted by all professional liability insurers. [ABSTRACT FROM AUTHOR]

The in vivo and in vitro effects of indomethacin on the natural killer (NK) cell activity against K 562 target cells were studied. In vivo administration of indomethacin, 3 × 50 mg for 7 days to normal donors did not influence baseline NK cell activity, which means that treatment with prostaglandin (PG) inhibitors can be allowed in studies on NK cell activity of persons with normal PG production. The NK cell activity of fresh mononuclear cells was boosted with pharmacological concentrations of indomethacin in vitro, while frozen cells were not. Our results indicate that indomethacin enhances the NK cell activity in vitro by blocking the prostaglandin production of monocytes, since monocyte depleted effector cells were not boosted by indomethacin. [ABSTRACT FROM AUTHOR]

This article focuses on thrombocyte involvement in immune inflammatory reactions. The immune inflammatory reaction is a complex interaction between antigens, leucocytes, thrombocytes, blood vessels, connective tissue and an extensive number of soluble tissues. Thrombocytes are cell fragments without nuclei and therefore without ability to synthesize proteins. Based on the description of normal thrombocyte structure and physiological characteristics, this article presents contemporary knowledge on thrombocyte involvement in immune inflammatory reactions.

The ability of human lymphocytes to produce soluble mediator(s) with thrombocyte aggregating activity (TAA) was investigated in an in vitro technique. Isolated human mononuclear cells were stimulated with phytobaemagglutinin or purified protein derivative of tuberculin. The supernatants were investigated for lymphokine activity in a leucocyte migration inhibitory factor assay. Supernatants were then tested for their ability to aggregate human thrombocytes, and in contrast to the results of previous studies, we were not able to demonstrate any TAA. Most likely, lymphokines with TAA are not involved in the thrombotic processes seen in human cell-mediated immune inflammatory reactions. [ABSTRACT FROM AUTHOR]

SSjögren's syjögren's syndrome (SS) is an autoimmune exocrinopathy. The salivary glands arc the site of activated T- and B-lymphocytes, along with gradual parenchymal destruction, diminished flow and altered composition of the secretory product. At present, sialochemistry has achieved no significance for the evaluation of SS patient. However, the number of sialochemical publications is steadily growing. This study review current sialochemical findings in patients with SS and relate the observations to the present concept of diagnosis, pathogenesis and prognosis of SS. An ideal combination of the collection of low-stimulated pure secretion, measurements of absolute flow-rates, and biopsy from the same glands seem to be unobtainable in SS patients. But two procedures may be appropriate: stimulated parotid secretion combined with parotid biopsies, or absorbance of low-stimulated labila saliva combined with labial gland biopsy. Sufficient data on disease-specific alterations in salivary composition in SS are still lacking. However, detection of specific changes in protein synthesis or in glycosylation as well as the detection of inflammatory cell products should be possible with the use of sensitive biochemical assays. [ABSTRACT FROM AUTHOR]

The article focuses on toxic epidermal necrolysis due to erythromycin. A 20-year-old woman had psoriasis since the age of 13. To treat a sore throat she was given erythromycin. 0.5 g twice daily for a week before admission to hospital. However, she did not take it consistently and had no erythromycin during the 2 days before admission, following the sudden development of a skin eruption. This case is remarkable because it is the first reported grave skin eruption due to erythromycin substantiated by oral provocation and a positive epicutaneous test. Toxic epidermal necrolysis is a well-known drug reaction usually due to phenylbutazones, sulphonamides, barbiturates, phenolphthalein and hydantoin.