Hormonal dysfunction is a known consequence of moderate and severe traumatic brain injury (TBI). In this study we determined the incidence, time course, and clinical correlates of acute post-TBI gonadotroph and somatotroph dysfunction. Patients had daily measurement of serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, estradiol, growth hormone, and insulin-like growth factor-1 (IGF-1) for up to 10 days postinjury. Values below the fifth percentile of a healthy cohort were considered abnormal, as were non-measurable growth hormone (GH) values. Outcome measures were frequency and time course of hormonal suppression, injury characteristics, and Glasgow Outcome Scale (GOS) score. The cohort consisted of 101 patients (82% males; mean age 35 years; Glasgow Coma Scale [GCS] score 8 in 87%). In men, 100% had at least one low testosterone value, and 93% of all values were low; in premenopausal women, 43% had at least one low estradiol value, and 39% of all values were low. Non-measurable GH levels occurred in 38% of patients, while low IGF-1 levels were observed in 77% of patients, but tended to normalize within 10 days. Multivariate analysis revealed associations of younger age with low FSH and low IGF-1, acute anemia with low IGF-1, and older age and higher body mass index (BMI) with low GH. Hormonal suppression was not predictive of GOS score. These results indicate that within 10 days of complicated mild, moderate, and severe TBI, testosterone suppression occurs in all men and estrogen suppression occurs in over 40% of women. Transient somatotroph suppression occurs in over 75% of patients. Although this acute neuroendocrine dysfunction may not be TBI-specific, low gonadal steroids, IGF-1, and GH may be important given their putative neuroprotective functions.

No abstract

Background and Aim There is limited research on the use of histamine‐H2 receptor antagonists and proton pump inhibitors for treating COVID‐19. We compare clinical outcomes between patients hospitalized with COVID‐19 receiving famotidine or pantoprazole. Methods This retrospective study included 2184 patients (famotidine: n = 638, pantoprazole: n = 727, nonuse: n = 819) aged 18 years or older treated for COVID‐19 from March 2020 to March 2021. Patients who received both famotidine and pantoprazole treatments were excluded. Multivariate logistic regression was used for the primary outcome, namely all‐cause mortality, and the secondary outcomes, namely mechanical ventilation, vasopressor use, acute kidney injury, and gastrointestinal bleeding. The main predictor variable was the use of famotidine or pantoprazole. Covariates were demographics, chronic diseases, and symptoms. Results As compared to nonuse, famotidine (OR: 0.30, 95% CI: 0.20–0.44, P < 0.001) and pantoprazole (OR: 0.47, 95% CI: 0.33–0.66, P < 0.001) were significantly associated with lower odds for all‐cause mortality. Comparison of famotidine and pantoprazole showed that the former had lower odds for all‐cause mortality (OR: 0.65, 95% CI:0.45–0.95, P < 0.05), mechanical ventilation (OR: 0.38, 95% CI: 0.25–0.58, P < 0.001), vasopressor use (OR: 0.33, 95% CI: 0.22–0.48, P < 0.001), acute kidney injury (OR: 0.40, 95% CI: 0.30–0.54, P < 0.001), and gastrointestinal bleeding (OR: 0.15, 95% CI: 0.08, 0.29, P < 0.001). Conclusions Famotidine is associated with lower odds for all‐cause mortality, mechanical ventilation, vasopressor use, acute kidney injury, and gastrointestinal bleeding as compared to pantoprazole in patients hospitalized with COVID‐19. We recommend that clinicians consider the use of famotidine over pantoprazole for hospitalized COVID‐19 patients. Future research with a clinical trial would be beneficial to further support such use of famotidine.

Introduction: Hepatitis E virus (HEV) can cause acute or chronic viral hepatitis and is a common cause of acute viral hepatitis worldwide and is an important public health concern. A high level of HEV, hepatitis A virus (HAV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) cross reactivity can occur, which indicates that serology can sometimes be unreliable in the diagnosis of acute viral hepatitis. Case Description/Methods: A 28-year-old Pakistani male presented with right upper quadrant abdominal pain, general malaise, and deranged liver function tests. Work-up for his abnormal liver tests was unremarkable except for detection of Hepatitis E antibody, Hepatitis E IgM antibody, and Epstein-Barr Virus IgM antibody with polymerase chain reaction (PCR) analysis revealing no detection of Epstein-Barr Virus DNA. The patient was diagnosed with acute hepatitis E with a false-positive EBV infection due to serological cross-reactivity. Supportive care was continued, liver function tests trended down, and the patient clinically improved and was discharged with outpatient follow-up. Discussion: The incubation time for HEV infection can last up to six weeks and HEV RNA, anti-HEV IgM, and anti-HEV IgG antibodies can be detected at the time of diagnosis. Anti-HEV IgM antibodies have a short window of positivity at three to four months, whereas HEV RNA can be detected in the blood within three weeks with viral shedding lasting up to six weeks in the stool. The enzyme immunoassay is the most widely used serological method for the identification of anti-HEV IgG and IgM antibodies, but the identification of anti-HEV IgM and rising titers of anti-HEV IgG antibodies are inadequate for diagnosis due to the lack of specificity for these antibodies. Confounding the diagnosis of HEV is the incidence of HEV, HAV, CMV, and EBV cross reactivity, which is posited to be due to polyclonal B-cell stimulation. The diagnosis of HEV infection in the clinical setting relies on the performance of assays of anti-HEV IgM, and subsequently the awareness of factors influencing diagnostic accuracy is crucial regarding potential treatment options. This case suggests that both anti-HEV IgM and EBV IgM should be interpreted with caution in acute HEV infection and that confirmatory testing with PCR analysis should be conducted to evaluate for false-positive serological cross-reactivity. We conclude that the diagnosis of viral hepatitis should be based on characteristic symptoms, elevated liver enzymes, serology, and confirmatory PCR testing.

transplants have yet been reported. Given the serious implications of this disease and the number of vaccines against COVID-19 given world-wide, further research is needed to better understand this entity and its pathophysiology.