Improving senior house officer training in accident and emergency medicine: the benefits of a diploma.

Accident and emergency is a fascinating specialty providing exposure to a wide range of acute and chronic conditions from all branches of medicine. To ensure a minimal standard of training nationally we propose the introduction of a diploma for junior doctors.     

Subtenon's depot corticosteroid injections in patients with a history of corticosteroid-induced intraocular pressure elevation.

PURPOSE: To determine whether a history of intraocular pressure elevation from local corticosteroid administration could predict subsequent intraocular pressure elevation after posterior subtenon's corticosteroid injection. METHODS: A retrospective review was performed of 64 consecutive patients (64 eyes) receiving posterior subtenon's corticosteroid injection. Patients were categorized as either historical corticosteroid responders or nonresponders based on intraocular pressure response to topical corticosteroid drops in the same eye or to previous posterior subtenon's corticosteroid injection of the fellow eye. Historical responders were defined as having a relative intraocular pressure increase of 5 mm Hg and absolute intraocular pressure greater than 24 mm Hg with an anatomically open angle. Relative risk of intraocular pressure elevation was evaluated based on historical response and presenting diagnosis. RESULTS: Nine eyes were historical responders, and 55 eyes were historical nonresponders. A higher rate of recurrent intraocular pressure elevation developed in historical responder eyes (4 of 9, 44%) compared with nonresponders (7 of 55, 13%) after posterior subtenon's injection (P = .04, Fisher's test; P = .07, Kaplan-Meier analysis). Historical responders with uveitis were at significantly higher risk of intraocular pressure elevation than nonresponders without uveitis (hazard ratio = 10.8, P = .04, Cox proportional hazards). All but one eye that developed intraocular pressure elevation from posterior subtenon's injection was adequately controlled with topical antiglaucoma therapy. CONCLUSION: In nonglaucomatous eyes, a previous history of corticosteroid-induced intraocular pressure elevation is a relative, not absolute, contraindication to posterior subtenon's corticosteroid injection, because the risk of intraocular pressure elevation is not absolute, and because it can usually be well controlled with topical antiglaucoma therapy.     

Relationship of factor XIIIa-positive dermal dendrocytes to Kaposi's sarcoma.

The histogenesis of Kaposi's sarcoma (KS) has been the subject of controversy, much of which has centered around whether the spindle cells of KS are derived from vascular endothelium or from lymphatics. Recently, some investigators have speculated that the spindle cells of KS are derived from dermal dendrocytes, a population of mononuclear dendritic cells normally present in the papillary and upper reticular dermis. These cells have been shown to proliferate in response to a variety of stimuli and have been reported to express the plasma proenzyme factor XIIIa. We examined immunohistochemically sections fixed in formaldehyde solution and embedded in paraffin from 20 tumor-stage, 15 patch-stage, and 15 plaque-stage lesions of KS with antibodies directed against factor XIIIa, factor VIII-related antigen, Ulex europaeus lectin, and LN3 (anti-HLA-DR) to investigate the relationship of dermal dendrocytes to KS in general and to try to clarify the histogenesis of this tumor. Our results revealed that the dermis of patch- and plaque-stage KS lesions contains an increased number of factor XIIIa-positive dermal dendrocytes compared with normal dermis and that some of these cells are spindle shaped. Many of the spindle cells in patch- and plaque-stage lesions of KS, however, are negative for factor XIIIa. The cells lining the slitlike spaces and some spindle-shaped cells in close proximity to the vascular spaces stain for factor VIII-related antigen and for Ulex europaeus lectin. LN3 labeled many cells resembling macrophages within the lesions and in papillary dermis. Less than 25% of the dendritic cells within the lesions and in the adjacent dermis expressed both factor XIIIa and LN3. Tumor-stage lesions showed focal but unequivocal staining of the spindle cells for factor VIII-related antigen and Ulex europaeus lectin. Tumor spindle cells were negative for factor XIIIa. Factor XIIIa-positive dendrocytes were plentiful in the uninvolved dermis and were aggregated around the periphery of the tumor nodules. The expression of factor VIII-related antigen and Ulex europaeus lectin by the spindle cells of nodular KS, and their lack of expression of factor XIIIa, suggests that the spindle-shaped tumor cells in all stages of KS are derived from endothelial cells and not from dermal dendrocytes. Dermal dendrocytes appear to undergo hyperplasia in response to KS of all stages. In patch- and early plaque-stage KS lesions, dermal dendrocytes are near factor VIII-related antigen-positive spindle cells and tumor vessels. The mechanism reactive dermal dendrocyte hyperplasia in KS remains obscure.     

HLA antigens in Omanis with blinding trachoma: markers for disease susceptibility and resistance

AIM—To determine the presence of HLA antigens in people with blinding trachoma.METHODS—Fifty Omanis with blinding trachoma were serologically typed for HLA A, B, C, DR, and DQ antigens and DNA typed for class II DRβ and DQβ alleles and compared with a population of 100 healthy controls.RESULTS—χ² analysis of serological reactions did not reveal any significant differences in HLA antigen frequencies after correction of probability, although DR4, DR7, and DR53 were completely absent in the patients and all of the patients were HLA DQ1 positive. In the case of DQ1 the relative risk was 22.6 (95% confidence interval of 20.7-24.7). Class II DNA low resolution DRβ typing showed a significant increase in HLA DR16 (p_c = 0.036, relative risk = 3.8) and a significant decrease in HLA DR53 (p_c = 0.018, relative risk = 0.05 ).CONCLUSION—The finding that HLA DR16 (a DR2 subtype) is associated with susceptibility to blinding trachoma, a disease that is caused by an intracellular micro-organism, is consistent with reports of an HLA DR2 association with leprosy and tuberculosis, diseases also caused by an intracellular micro-organism. Similarly, resistance to leprosy is associated with HLA DR53 as is the case with blinding trachoma described here. It is postulated that HLA DR2 or subtypes in association with HLA DQ 1 may enable an intracellular micro-organism to enter the cell or are involved in presentation of peptides derived from intracellular micro-organisms to T lymphocytes initiating a delayed hypersensitivity or autoimmune reaction. These findings are the first report that genetic factors are of major importance in the development and protection against blinding trachoma.