Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune encephalitis that may present with acute psychiatric symptoms, seizures, movement disorders, impaired consciousness and autonomic dysfunction. A 30-year-old previously healthy woman at 10-11 weeks of gestation was admitted to the intensive care unit after an approximately 2-3-week history, reported by relatives, of insomnia, behavioral change, auditory and visual hallucinations, psychomotor agitation, aggressive behavior, and a generalized tonic-clonic seizure before admission. On admission, the patient had severe encephalopathy and subsequently required mechanical ventilation because of hypoventilation. Cerebrospinal fluid testing detected IgG antibodies against NMDAR at a titer of 1:160. Brain magnetic resonance imaging showed a right hippocampal lesion consistent with limbic encephalitis, and pelvic ultrasonography identified adnexal masses suspicious for teratoma. Prolonged EEG demonstrated diffuse delta-theta slowing with a delta-brush pattern, without findings consistent with focal or myoclonic seizures. The patient received high-dose methylprednisolone, intravenous immunoglobulin, plasma exchange, rituximab, pregnancy-conscious antiseizure therapy, individualized pregnancy management, and laparoscopic removal of bilateral mature ovarian teratomas. Following combined immunotherapy, ventilatory and supportive ICU care, antiseizure therapy, individualized maternal-fetal management, and tumor removal, the recurrent motor events ceased by the end of the first postoperative week. The patient's consciousness, speech, and motor function gradually improved. This case highlights that anti-NMDAR encephalitis in pregnancy requires early cerebrospinal fluid antibody testing, exclusion of infectious mimics, supportive neurocritical care, prompt immunotherapy, timely teratoma removal and individualized reasoning regarding pregnancy management.

Pregnancy is characterized by progressive hemostatic adaptation: increased fibrinogen synthesis, enhanced thrombin generation, and reduced fibrinolytic potential together prepare the maternal circulation for delivery-related blood loss. A fall in fibrinogen during pregnancy or the immediate postpartum period therefore does not carry the same meaning as an equivalent value outside of pregnancy. It may instead represent loss of a pregnancy-specific hemostatic reserve. Fibrinogen concentration is consistently associated with the severity of postpartum hemorrhage, but randomized trials have not shown that empirical replacement in all women with early postpartum hemorrhage improves clinical outcomes. This narrative review summarizes current evidence on pregnancy-associated fibrinogen deficiency and dysfunction, with emphasis on pathophysiology, trial findings, fibrinogen thresholds, replacement strategies, congenital fibrinogen disorders, and research gaps. Current data support using fibrinogen as both a severity marker and a selective treatment target, interpreted according to gestational age, bleeding phenotype, placental involvement, and resource setting. Direct evidence generated in low-resource settings is limited; no randomized trial of fibrinogen measurement or replacement has been conducted in such a setting.

Gestational diabetes mellitus (GDM) is conventionally diagnosed at 24–28 weeks of gestation, although hyperglycaemia may be detected earlier. Early gestational diabetes mellitus (eGDM), defined here as hyperglycaemia diagnosed before 24 weeks in the absence of overt diabetes, is characterised by limited but emerging molecular and metabolic evidence. In women with eGDM diagnosed before 20 weeks, DALI phenotyping identified insulin-resistant, secretion-dominant and mixed phenotypes using HOMA-IR and the OGTT-derived Stumvoll first-phase index, with greater obstetric risk in the resistance-dominant group. In the TOBOGM cohort, eGDM was associated with higher diacylglycerol and fatty-acid species, which remained associated with eGDM and glycaemic indices after adjustment for clinical risk factors. Early-pregnancy SHBG provides additional evidence, with a further reduction reported in women diagnosed before 20 weeks. The principal limitation is that eGDM-specific evidence remains sparse. Most early-pregnancy biomarker studies measured women before 24 weeks but diagnosed GDM later and therefore describe antecedents of subsequent disease rather than eGDM diagnosed before 24 weeks. Most mechanistic evidence also derives from conventional-window GDM or placental tissue obtained at delivery, preventing determination of whether reported abnormalities precede, accompany or result from early hyperglycaemia. Longitudinal studies with early diagnosis, concurrent assessment of insulin sensitivity and secretion, adjustment for adiposity and independent validation are therefore needed to define the molecular phenotype of eGDM.