[Presentations for HIV post-exposure prophylaxis in emergency departments: guideline and recommendations]. / HIV-Postexpositionsprophylaxe in der Notaufnahme: Vorgehen, Tipps & Tricks.

Patients often present to emergency departments after potential or confirmed exposure to human immunodeficiency virus (HIV) asking for recommendations concerning the initiation of post-exposure prophylaxis (PEP). These presentations may occur after occupational as well as non-occupational exposure. PEP entails taking a triple antiretroviral therapy for 28-30 days. If taken early (ideally within 2 h, but no later than 72 h) and as indicated, HIV infection can be prevented with a high level of probability. Since these presentations occur around the clock, they require basic expertise on the part of the emergency department staff regarding its indication and its side effects as well as standardized procedures in the emergency department to not delay initiation. Patients should present to an infectious disease outpatient clinic or practice specialized in HIV in order to have the indication reviewed by a specialist and, if necessary, adapted to complex cases with the aim of making individual case decisions. This review article aims to summarize core statements of the 2022 German-Austrian guideline on HIV post-exposure prophylaxis and to give emergency department staff necessary knowledge to safely and correctly begin PEP.

[Care for dying patients in the emergency department]. / Versorgung sterbender PatientInnen in der Notaufnahme.

Patients at the end of life frequently receive care in emergency departments. Emergency physicians are faced with caring for both patients who pass away suddenly following an acute illness or injury despite rescue efforts, as well as those who are dying from a chronic condition or high age. To provide proper care and respect the patients' wishes regarding invasive treatments, emergency physicians should be knowledgeable about advance directives and have effective communication skills when delivering bad news to patients and their family. In addition, a basic understanding of palliative care is necessary for physicians to effectively manage symptoms.

Disorders of selenium metabolism and selenoprotein function.

PURPOSE OF REVIEW: Inborn errors of metabolism are increasingly recognized as underlying causes in pediatric diseases. Selenium and selenoproteins have only recently been identified as causes of inherited defects. Respective case reports have broadened our understanding of selenoprotein function and their developmental importance. This review presents the characterized defects and tries to attract attention to the spectrum of potential phenotypes. RECENT FINDINGS: The characterization of patients with inherited mutations in selenoprotein N has corroborated the physiological importance of selenium for muscle function. Individuals with inherited defects in selenocysteine insertion sequence (SECIS)-binding protein 2 display a syndrome of selenoprotein-related defects including abnormal thyroid hormone metabolism, delayed bone maturation, and other more individual phenotypes. The recent identification of mutations in selenocysteine synthase causing progressive cerebello-cerebral atrophy underlines the central role of selenoproteins in brain development and protection from neurodegeneration. SUMMARY: The spectrum of diseases related to inborn defects of selenium utilization, transport, and metabolism is expanding. However, only few examples are already known, resulting from defects in one selenoprotein gene and two genes involved in selenoprotein biosynthesis, respectively. Complex syndromes with impaired muscle function, stunted growth, neurosensory and/or immune defects may point to the involvement of impaired selenium metabolism and selenoprotein function, necessitating specific diagnostic procedures.

Lack of Association between Selenium Status and Disease Severity and Activity in Patients with Graves' Ophthalmopathy.

BACKGROUND: Selenium (Se) is of importance for regular functioning of the immune system and thyroid gland, and may have a health effect in mild Graves' ophthalmopathy (GO). OBJECTIVE: As the Se status declines in inflammation, we analyzed whether GO activity or severity affects the Se status of patients. METHODS: Serum Se and selenoprotein P (SePP) concentrations were retrospectively determined in 84 consecutive GO patients before treatment and compared to their clinical activity score (CAS) and severity of eye changes (NOSPECS) status, and to the concentrations of autoantibodies targeting the TSH receptor (TRAK) or the IGF1 receptor (IGF1R-aAB). RESULTS: Serum Se and SePP were linearly associated, indicating a suboptimal Se status of our patients. In comparison to data from other European cohorts, the majority of GO patients had a relatively poor Se status ([Se] ± SD; 70.0 ± 23.8 µg/l), below the threshold needed for full expression of selenoproteins. TRAK were inversely associated with Se concentrations, while IGF1R-aAB titers were not associated with Se. Neither Se nor SePP concentrations differed between GO patients with severe versus mild or active versus inactive disease, or showed significant associations with the CAS or NOSPECS values. CONCLUSION: GO patients are at risk of a low Se status, yet disease severity or activity does not seem to affect Se or SePP concentrations directly. However, as the retrospective nature of the analysis does not allow conclusions on a potential causative role of Se on Graves' disease or GO risk, these results neither support nor discourage adjuvant Se supplementation attempts.

Autoantibodies to the IGF1 receptor in Graves' orbitopathy.

CONTEXT: Graves' disease (GD) is maintained by stimulating antibodies against the TSH receptor. Graves' orbitopathy (GO) is the main extrathyroidal manifestation of GD, potentially involving autoimmunity against the IGF1 receptor (IGF1R). OBJECTIVE: We tested for autoantibodies against the IGF1R (IGF1R-Abs) in sera of GD patients and controls and elucidated their possible implication in the disease. DESIGN: A diagnostic assay for IGF1R-Ab was established with recombinant human IGF1R as autoantigen. Serum samples or purified Ig preparations were analyzed for IGF1R binding and modulation of IGF1 signaling in vitro. A total of 108 consecutive GO patients represented on average by 5.4 separate serum samples per individual along with 92 healthy controls were analyzed. RESULTS: IGF1R-Ab were detected in 10 serum samples from control subjects (11%) and in 60 samples (10%) from the GO patient serum bank. The positive patient samples were derived from 15 individuals yielding an IGF1R-Ab prevalence of 14% in GO. More than three consecutive samples were available from 11 of the 15 positive GO patients spanning an average disease period of 2 years. IGF1R-Ab concentrations were constantly elevated in these patients demonstrating relatively stable IGF1R-Ab expression over time. IGF1R-Ab failed to stimulate IGF1R autophosphorylation but instead inhibited IGF1-induced signaling in hepatocarcinoma HepG2 cells. Similarly, growth of MCF7 breast cancer cells was inhibited by IGF1R-Ab, supporting their classification as IGF1 antagonists. CONCLUSIONS: Our data demonstrate the existence of IGF1R-Abs in humans but do not support the hypothesis that the IGF1R-Abs contribute to GO pathogenesis.