Maternal thyroid hormone homeostasis during early gestation is fundamental for fetal growth and development, yet the specific clinical implications of the ratio between free triiodothyronine and free thyroxine, a marker of peripheral deiodinase activity and metabolic status, remain insufficiently explored regarding newborn health.

Objective: To investigate the baseline thyroid function status and influencing factors in preterm infants. Methods: A cross-sectional study was conducted, enrolling 2 236 preterm infants with gestational ages of 28-<37 weeks admitted to the Department of Neonatology, Capital Center for Children's Health, Capital Medical University between September 2015 and September 2024, and 912 full-term infants hospitalized for jaundice during the same period. All neonates who enrolled to anaylized underwent first time thyroid function testing between 7-14 days of age. Clinical data, thyroid function levels, maternal pregnancy complications, birth-related and postnatal complications, and therapeutic medications were collected. Preterm infants were stratified by sex and gestational age weeks to describe thyroid function status for comparison with full-term infants. Preterm infants with thyroid function retesting between 37 and <40 weeks were further analyzed and compared thyroid hormone levels of full-term infants with gestational ages of 37-<38 weeks. Inter-group comparisons were performed using the Mann-Whitney U test, with multivariate linear regression analysis to identify influencing factors of thyroid function in preterm infants. Results: Among the 632 neonates who enrolled to anaylized, 354 cases (56.0%) were male and 278 cases (44.0%) were female; 365 cases (57.8%) were preterm infants and 267 cases (42.2%) were full-preterm infants. Female preterm infants exhibited higher serum T4 and T3 levels than males (both P<0.05).TSH was negatively associated with gestational age at birth (β=-0.18, P<0.001). In contrast, T4, FT4, T3, and FT3 were all positively associated with gestational age at birth (β=4.56, 0.39, 0.04, and 0.15, respectively; all P<0.001).In the thyroid function assay, a total of 127 preterm infants with corrected gestational ages ranging from 37 weeks to <40 weeks and 102 full-term infants were included. Comparative results between the two groups showed that the levels of T4, FT4, and T3 were all lower in the preterm infants than in the full-term group (all P<0.01), whereas no statistical difference was observed for TSH and FT3 (both P>0.05). Multivariate linear regression analysis indicated that TSH levels were positively correlated with gestational age and postnatal dopamine use (β=0.34 and 0.10, both P<0.05) and negatively correlated with the Apgar score at the first minute and the presence of patent ductus arteriosus (β=-0.16 and -0.12, both P<0.05). T3 levels were positively correlated with preterm gestational age and female sex (β=0.39 and 0.11, both P<0.05) and positively correlated with preterm gestational age and female sex (β=0.40 and 0.11, both P<0.05), but negatively correlated with the number of pregnancies and the presence of patent ductus arteriosus (β=-0.11 and -0.12, both P<0.05). FT3 levels were positively correlated with gestational age (β=0.34, P<0.05) and negatively correlated with the presence of patent ductus arteriosus (β=-0.11, P<0.05). FT4 levels were positively correlated with gestational age, postnatal neonatal respiratory distress syndrome, and pregnancy-induced hypertension (β=0.37, 0.15, 0.10; all P<0.05), but negatively correlated with the number of pregnancies (β=-0.12, P<0.05). Conclusions: The thyroid function of preterm infants differs from that of full-term infants, with lower birth gestational age being associated with a higher likelihood of transient hypothyroidism. Thyroid hormone levels in preterm infants corrected for gestational age at 37 weeks remain lower than those in full-term infants. In addition to gestational age, thyroid function in preterm infants is also influenced by gender, multiple pregnancies, Apgar score, patent ductus arteriosus, and use of dopamine medications.

A 36-year-old postpartum woman with prior intrahepatic cholestasis of pregnancy and gallstone pancreatitis presented with right upper quadrant pain, jaundice, and elevated liver enzymes. Initial workup suggested drug-induced liver injury, but laboratory results worsened after antibiotics were discontinued. Imaging and liver biopsies revealed cholestasis and progressive fibrosis. Endoscopic retrograde cholangiopancreatography finally confirmed primary sclerosing cholangitis, though overlap with pregnancy-related liver conditions delayed diagnosis. This case highlights the diagnostic challenges of postpartum cholestasis and illustrates how primary sclerosing cholangitis may emerge in temporal association with pregnancy despite initially nondiagnostic imaging and histology.

Alpha-thalassemia (α-thalassemia) has two clinically significant forms: hemoglobin Bart hydrops fetalis (Hb Bart) syndrome (caused by deletion/inactivation of all four α-globin genes; --/--), and hemoglobin H (HbH) disease (most frequently caused by deletion/inactivation of three α-globin genes; --/-α). Hb Bart syndrome, the more severe form, is characterized by prenatal onset of generalized edema and pleural and pericardial effusions as a result of congestive heart failure induced by severe anemia. Extramedullary erythropoiesis, marked hepatosplenomegaly, and a massive placenta are common. Death usually occurs in the neonatal period. HbH disease has a broad phenotypic spectrum: although clinical features usually develop in the first years of life, HbH disease may not present until adulthood or may be diagnosed only during routine hematologic analysis in an asymptomatic individual. The majority of individuals have enlargement of the spleen (and less commonly of the liver), mild jaundice, and sometimes thalassemia-like bone changes. Individuals with HbH disease may develop gallstones and experience acute episodes of hemolysis in response to infections or exposure to oxidant drugs.

Fever after a caesarean section is often believed to be caused by infections, which usually require an escalation of antimicrobial treatment. Although caesarean delivery can be lifesaving for both mother and baby, the procedure carries risks, with emergency caesarean sections being associated with a higher chance of complications, including infection and haemorrhage, compared to elective caesarean sections.  Drug-induced fever is an important yet often overlooked alternative diagnosis in obstetrics and can be difficult to recognise in patients receiving antibiotics for suspected postoperative infection. Persistent fever in a postoperative patient is a significant concern, as it may indicate ongoing or worsening infection and require systematic evaluation and a multidisciplinary approach. We report a case of a 31-year-old woman in her first pregnancy who developed a fever of 39.8°C, abdominal pain, and cough on day two following an emergency caesarean section. Her blood culture, urine culture, high vaginal swab, and viral panel were negative. Her white cell count (WBC), lactic acid, and procalcitonin levels were within normal limits, but C-reactive protein (CRP), a non-specific inflammatory marker, was the only elevated inflammatory marker. Pelvic ultrasound showed a small hematoma at the surgical site, and a chest X-ray indicated bilateral bronchopneumonia. A diagnosis of bronchopneumonia and pelvic haematoma was made. She was started on intravenous β-lactam antibiotics. Her cough resolved within two days, and she remained relatively well, but her high-grade fever persisted.  Despite escalating her antibiotics, she continued to experience a high-grade fever, which led to her transfer to a tertiary hospital. There, she was managed by a multidisciplinary team (MDT) of infectious disease specialists (ID team), pharmacists, physicians, and obstetricians, but her high-grade fever persisted. Repeat blood cultures, urine cultures, and high vaginal swabs were all negative. Similarly, her WBC, lactic acid, and procalcitonin levels, markers of infection, were within normal limits, but her CRP remained elevated. A further CT scan to exclude infected pelvic vein thrombosis or retained products of conception was negative, but raised concerns about worsening abdominal infection and possible peritonitis, even though the patient felt well with no abdominal pain or tenderness on examination. The CT report created diagnostic and management dilemmas. The MDT discussed the report extensively and recommended an exploratory laparotomy, which was explained to the patient and her family, but she declined. The next day, she developed jaundice and drug-induced hepatitis, leading to suspicion of drug-induced fever. All her antibiotics were stopped, and she became fever-free within days. The worsening ultrasound and CT scan findings are most likely due to an unusual response to a systemic hypersensitivity immune complex reaction to drug-induced fever rather than infection.  This case underscores the challenges of managing patients with persistent fever and highlights the importance of vigilance and awareness of drug-induced fever as a potential cause. Regular comprehensive assessments, including clinical examinations and investigations, are essential to identify infectious causes. A delayed diagnosis can lead to longer hospital stays, unnecessary tests, increased healthcare costs, and possible harm to the patient.

This article addresses the diagnostic challenges encountered and resolution of a neonate with blocked D phenomenon, where maternal anti-D had masked the D sites on the neonate's red blood cells (RBCs), initially resulting in false-negative D typing. This article emphasizes the importance of integrating serologic and molecular methods for accurate blood type determination, which is crucial for managing hemolytic disease of the fetus and newborn. A mother, whose RBCs typed as D- and with a history of D isoimmunization, gave birth to a neonate who presented with anemia and jaundice. Initial D typing revealed the neonate had D- RBCs. The mother's blood sample tested as group B, D- with a high anti-D titer (512). The neonate's direct antiglobulin test (DAT) was strongly positive for IgG, and eluate testing confirmed anti-D specificity, indicating that maternal anti-D was coating the neonate's RBCs. Treatment of the neonate's RBCs with a commercial ZZAP reagent removed bound IgG antibodies, converting the DAT to negative and revealing the neonate's RBCs to be group B, D+, thereby resolving the initial serologic dilemma. Further polymerase chain reaction-based molecular testing of the neonate's RBCs confirmed the D+ phenotype (R1R1), demonstrating the utility of molecular methods in complex cases.