Vitamin D is known to regulate innate and adaptive immune processes at the cellular level, but the role of vitamin D status on associated inflammatory processes across pregnancy is unclear. Our primary objective was to evaluate the relationships between serum biomarkers of inflammation (interleukin [IL]-6, IL-10, tumor necrosis factor [TNF]-α), acute-phase proteins (C-reactive protein and hepcidin) and vitamin D status, 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)D), measured across pregnancy and in the neonate at birth. A second objective was to identify associations between vitamin D status and clinically diagnosed infections. In this study, 158 racially and ethnically diverse pregnant adolescents were recruited from the Rochester Adolescent Maternity Program (RAMP) in Rochester, NY. Serum 1,25(OH)D was significantly lower in adolescents and neonates with IL-6 concentrations above the 75th percentile at delivery ( P = .04) and at birth ( P = .004), respectively. After adjusting for other potential covariates of inflammation, maternal serum 1,25(OH)D was significantly positively associated with TNF-α during pregnancy ( P = .02), but at delivery 1,25(OH)D and TNF-α were inversely associated with one another ( P = .02). Teens with 25(OH)D concentrations <30 ng/mL were more likely to test positive for candida ( P = .002) and bacterial vaginosis ( P = .02) during pregnancy. African Americans exhibited significantly lower TNF-α concentrations at both mid-gestation ( P = .009) and delivery ( P = .001) compared to the Caucasian adolescents. These results suggest that lower maternal vitamin D status may increase risk of infection across gestation.

Addressing modifiable risk factors associated with dietary intake and pre-pregnancy weight may help reduce health disparities among pregnant minority adolescents. Additionally, targeted sexual health education may greatly benefit younger female adolescents.

Here, we present a 22-year-old female patient with adult-onset Still's disease (AOSD) who was newly diagnosed in the setting of secondary macrophage activation syndrome (MAS), a rare, life-threatening inflammatory disease with 50% mortality due to multi-organ failure. She met the diagnostic criteria of AOSD and MAS, while genetic testing excluded primary causes of MAS. She had high fevers, anemia, thrombocytopenia, splenomegaly, hematophagocytosis, and elevated serum ferritin (37,950 ng/mL) and CD25 levels (11,870 pg/mL), which remained unresponsive to corticosteroids and anakinra. Her serum interferon gamma (IFN-γ) levels were elevated (7 pg/mL). She was markedly responsive to IFN-γ blockade with emapalumab that eliminated her fevers and all MAS-associated laboratory abnormalities. This report provides initial evidence for therapeutic efficacy for IFN-γ blockade in AOSD and secondary MAS.

A 42-year-old woman with juvenile idiopathic arthritis was treated with anakinra, corticosteroids, and hydroxychloroquine when she developed chronic hypoxic respiratory myopathy. She was admitted to the intensive care unit for acute hypercapnic respiratory failure and required prolonged intubation, subsequent tracheostomy, and long-term ventilatory support due to multiple failed spontaneous breathing trials after discontinuation of anakinra and steroids. Muscle biopsy revealed type II fiber atrophy with the accumulation of autophagosomes and vacuoles presenting as curvilinear bodies, elevated MHC class I antigen expression, and infiltration by CD68+ macrophages and CD8+ T cells. Type II fiber atrophy was attributed to corticosteroid use and curvilinear bodies due to blockade of autophagy by hydroxychloroquine. After hydroxychloroquine was discontinued, the patient recovered to her prehospitalization baseline.

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