Medical Child Abuse: An Unusual “Source” of Vaginal Bleeding

BackgroundMedical child abuse (MCA) is challenging to diagnose. Although young children are often affected, adolescents can be victims through caregiver coercion. Presentation is highly variable. Diagnosis is essential because of high associated morbidity and mortality.CaseWe describe the case of a 12-year-old girl who presented to multiple subspecialty clinics with reported menorrhagia. Despite reassuring clinical examinations, the family described menorrhagia that failed to respond to standard treatment. After an urgent evaluation for reported heavy bleeding revealed only scant blood, the diagnosis of MCA was made.Summary and ConclusionVaginal bleeding is a rare presentation of MCA, but must be considered whenever reported symptomatology does not follow physiologic patterns, respond to standard medical treatment, or correspond to clinical evaluation. Prompt identification is important to prevent further harm.     

Host MyD88 signaling protects against acute graft-versus-host disease after allogeneic bone marrow transplantation

Recent experimental strategies to reduce graft-versus-host disease (GVHD) have focused largely on modifying innate immunity. Toll-like receptor (TLR)-driven myeloid differentiation primary response 88 (MyD88)-dependent signalling pathways that initiate adaptive immune function are also critical for the pathogenesis of GVHD. This study aimed to delineate the role of host MyD88 in the development of acute GVHD following fully major histocompatibility complex-mismatched allogeneic bone marrow transplantation (BMT). When myeloablated BALB/c MyD88 knock-out recipients were transplanted with C57BL/6 (B6) donor cells, they developed significantly more severe GVHD than wild-type (WT) BALB/c hosts. The increased morbidity and mortality in MyD88^–/– mice correlated with increased serum levels of lipopolysaccharide and elevated inflammatory cytokines in GVHD target organs. Additionally, MyD88 deficiency in BMT recipients led to increased donor T cell expansion and more donor CD11c⁺ cell intestinal infiltration with apoptotic cells but reduced proliferation of intestinal epithelial cells compared with that in WT BMT recipients. Decreased expression of tight junction mRNA in epithelial cells of MyD88^–/– mice suggested that MyD88 contributes to intestinal integrity. Cox-2 expression in the GVHD-targeted organs of WT mice is increased upon GVHD induction, but this enhanced expression was obviously inhibited by MyD88 deficiency. The present findings demonstrate an unexpected role for host MyD88 in preventing GVHD after allogeneic BMT.     

Additive Maßnahmen in der Reproduktionsmedizin – Hoffnung oder Irrung

Gynäkologische Endokrinologie -