ABSTRACT
Transgender law is complex and developing. Increasing general practitioner referrals for gender dysphoria without sufficient resources for specialist units have left gaps in transgender healthcare. Surveys repeatedly find transgender patients have lower satisfaction with healthcare experiences, stating doctors have a poor understanding of their needs. Meanwhile, waiting times for referrals remain high.This review article outlines UK laws and guidelines relevant to trans healthcare, including practical advice for clinicians. Current issues are explored, including the referral process for gender dysphoria.Transgender law is continually evolving; currently, individuals require a diagnosis of gender dysphoria to legally change gender. However, the gender on NHS records can be changed without legally changing gender.Clinicians may find support from the General Medical Council for this area. Specifically, guidance exists for including trans patients in screening programmes relevant to their assigned sex at birth. Similarly, advice exists for ensuring the privacy of patients' gender history.
Subject(s)
Intestinal Diseases/diet therapy , Nurse Clinicians/trends , Nutritional Sciences/methods , Consultants , Female , Gastrostomy/methods , History, 21st Century , Humans , Intestinal Diseases/physiopathology , Nurse Clinicians/ethics , Nutrition Therapy/methods , Parenteral Nutrition/methodsABSTRACT
Gastritis due to Helicobacter pylori is induced by a Th1-mediated response that is CD4 cell and gamma interferon (IFN-gamma) dependent. T-bet is a transcription factor that directs differentiation of and IFN-gamma secretion by CD4+ Th1 T cells. The goal of this study was to use two mouse models to elucidate the role of T-bet in gastritis due to H. pylori. C57BL/6J mice, congenic T-bet knockout (KO) mutants, or congenic SCID (severe, combined immunodeficient) mutants were given live H. pylori by oral inoculation. SCID mice were given CD4+ splenocytes from C57BL/6J or T-bet KO mice by intraperitoneal injection. Twelve or 24 weeks after bacterial inoculation, C57BL/6J mice developed moderate gastritis but T-bet KO mice and SCID mice did not. In contrast, SCID recipients of either C57BL/6J T cells or T-bet KO T cells developed gastritis 4 or 8 weeks after adoptive transfer. In recipients of C57BL/6J CD4+ cells but not recipients of T-bet KO cells, gastritis was associated with a delayed-type hypersensitivity response to H. pylori antigen and elevated gastric and serum IFN-gamma, interleukin 6, and tumor necrosis factor alpha. In spite of the absence of IFN-gamma expression, indicating failure of Th1 differentiation, CD4+ T cells from T-bet KO mice induce gastritis in H. pylori-infected recipient SCID mice. This indicates that Th1-independent mechanisms can cause gastric inflammation and disease due to H. pylori.
