Prevention of vertical transmission of hepatitis B: A retrospective review of a 5-year maternal-infant cohort in London.

AIMS: The World Health Organization (WHO) estimates that 3.5% of the population live with hepatitis B virus (HBV); migrants to Europe are disproportionately affected. UK birth dose HBV vaccination is limited to infants born to those living with HBV (LWHBV). High-risk infants (high maternal infectivity, low birthweight) also receive HBV immunoglobulin (HBIG). The Family Hepatitis Clinic follows infants and those LWHBV working towards WHO goals of combating viral hepatitis by 2030. METHODS: A trust-wide electronic note review of outcomes for infants born to those LWHBV (2016-2020). RESULTS: Two hundred and eighty-three infants, 134 (47%) females, born to those LWHBV were referred. Two hundred and thirty-one (82%) attended follow-up with a vertical transmission rate of 0%. Twenty (7%) individuals LWHBV received tenofovir disoproxil fumerate in pregnancy; median viral load (VL) at initiation 125 416 376 DNA IU/mL, one having birth VL. Twenty-eight (10%) infants were stratified as high risk and all received HBIG and birth dose vaccination with 9 (32%) subsequently lost to follow-up, compared to 48 (19%) low-risk infants. 267/283 (94%) had birth dose vaccination documented and 206/283 (73%) received at least four vaccine doses. 215/283 (76%) infants had serology by 24 months; 17 (6%) with suboptimal vaccine responses: hepatitis B surface antibody <100 IU/mL. Serology before 18 months resulted in higher rates of maternal hepatitis B core antibody detection (15% vs. 3%). CONCLUSION: Prevention of vertical transmission of HBV was universal in those attending, although high-risk infants were more likely lost to follow up. HBV post-vaccine serological protection was comparable with national data from 2021 (77% >4 doses, 77% HBsAb >100).

Persisting embryonal infundibular recess in a case of TITF-1 gene mutation.

The thyroid transcription factor 1 (TITF-1) gene plays an important role in the development of the ventral forebrain, thyroid and lungs. Mutations of this gene are known to cause benign hereditary chorea (BHC) and can cause the full spectrum of abnormalities seen in the brain-thyroid-lung syndrome. Abnormalities of the ventral forebrain on imaging have been variably documented in the literature. Multiple previous reports describe a cystic pituitary mass, as well as duplication of the pituitary stalk and communication between an intrasellar cyst and the third ventricle. The initial MRI performed in our case was interpreted as an intrasellar cyst, but the high-resolution MRI performed later was able to resolve this as a persisting embryonal infundibular recess (PEIR), rather than the cystic pituitary mass which has previously been described. This case illustrates the role of the TITF-1 gene in the development of the pituitary and hypothalamus.

Evaluation of Acute and Convalescent Antibody Concentration Against Pneumococcal Capsular Polysaccharides for the Diagnosis of Pneumococcal Infection in Children with Community-Acquired Pneumonia.

We evaluated whether the quantification of IgG to pneumococcal capsular polysaccharides is an accurate diagnostic test for pneumococcal infection in children with pneumonia in Nepal. Children with pneumococcal pneumonia did not have higher convalescent, or higher fold change, IgG to pneumococcal polysaccharides than children with other causes of pneumonia. Caution is needed in interpreting antibody responses in pneumococcal infections.

Effects of dexmedetomidine sedation on the EEG in children.

OBJECTIVES: To examine the effects of dexmedetomidine sedation on EEG background and epileptiform activity in children, comparing it to natural sleep. AIM: To provide quantitative and qualitative descriptions of the effect of dexmedetomidine sedation on the EEG of children. BACKGROUND: Children with intractable epilepsy admitted for surgery undergo 5 days of continuous EEG monitoring as well as nuclear medicine imaging studies with dexmedetomidine for sedation. Continuous EEG monitoring of each child during both natural sleep and dexmedetomidine-induced sedation provides a unique opportunity to evaluate the effects of dexmedetomidine on the EEG of children. MATERIALS/METHODS: Sixteen children undergoing dexmedetomidine sedation for nuclear medicine studies and simultaneous continuous EEG monitoring were studied. EEG segments during sedation were compared to samples of naturally occurring stage II sleep from the same child. Standard visual EEG analysis, quantification of delta, theta, alpha, beta, and total RMS power, number and location of spike foci, and frequency of spike activity were compared. RESULTS: The EEG during dexmedetomidine sedation resembled stage II sleep. During sedation, statistically significant increases in power of 16% for theta (P = 0.01), 21% for alpha (P = 0.03), and 40% for beta (P < 0.01) were observed, but not for delta (P = 0.63) or total EEG power (P = 0.61). Spike frequency increased by 47% during sedation but no new spike foci or seizures were observed. CONCLUSION: Dexmedetomidine sedation elicited an EEG pattern similar to that of Stage II sleep with modest increases in theta, alpha, and beta activity. Dexmedetomidine does not hinder interpretation of the EEG, suggesting that it may be a uniquely useful agent for EEG sedation in children.

Propofol infusion syndrome: an unusual cause of renal failure.

Propofol infusion syndrome has been increasingly recognized as a syndrome of unexplained myocardial failure, metabolic acidosis, and rhabdomyolysis with renal failure. It has been described only with acute neurologic injury or acute inflammatory diseases complicated by severe infections or sepsis. It appears to develop in the context of high-dose, prolonged propofol (100 microg/kg/min) treatment in combination with catecholamines and/or steroids. This was first noted in children but is increasingly recognized in adults. This is a case report of 2 patients (a 42-year-old man and a 17-year-old girl) who had acute renal failure associated with use of propofol in the appropriate clinical setting. It examines the pathophysiology and the possible mechanisms of this condition and illustrates the need to consider it as the cause of rhabdomyolysis and acute renal failure in critically ill patients.