Signe Sparre Beck-Nielsen, Bendt Brock-Jacobsen, Jeppe Gram, Kim Brixen and Tina Kold Jensen
To estimate the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets.
Population-based retrospective cohort study based on a review of medical records.
Patients aged 0–14.9 years referred to or discharged from hospitals in southern Denmark from 1985 to 2005 with a diagnosis of rickets were identified by register search, and their medical records were retrieved. Patients fulfilling the diagnostic criteria of primary rickets were included.
We identified 112 patients with nutritional rickets of whom 74% were immigrants. From 1995 to 2005, the average incidence of nutritional rickets in children aged 0–14.9 and 0–2.9 years was 2.9 and 5.8 per 100 000 per year respectively. Among immigrant children born in Denmark, the average incidence was 60 (0–14.9 years) per 100 000 per year. Ethnic Danish children were only diagnosed in early childhood and the average incidence in the age group 0–2.9 years declined from 5.0 to 2.0 per 100 000 per year during 1985–1994 to 1995–2005. Sixteen cases of hereditary rickets were diagnosed during the study period giving an average incidence of 4.3 per 100 000 (0–0.9 years) per year. The prevalence of hypophosphatemic rickets and vitamin D-dependent rickets type 1 was 4.8 and 0.4 per 100 000 (0–14.9 years) respectively.
Nutritional rickets is rare in southern Denmark and largely restricted to immigrants, but the incidence among ethnic Danish children was unexpectedly high. Hereditary rickets is the most common cause of rickets in ethnic Danish children, but nutritional rickets is most frequent among all young children.
Martin Overgaard, Dorte Glintborg, Henrik Thybo Christesen, Tina Kold Jensen and Marianne Skovsager Andersen
Low circulating prolactin is a potential marker of metabolic risk during pregnancy. We aimed to investigate associations between prolactin and glucose status in pregnant women with and without gestational diabetes mellitus (GDM) or polycystic ovary syndrome (PCOS).
Prospective observational cohort study. From the Odense Child Cohort, 1497 pregnant women were included.
Blood samples were assessed during first, second (prolactin, hemoglobin A1c (HbA1c)) and third trimester (fasting prolactin, testosterone, HbA1c, insulin, glucose). Oral glucose tolerance test (OGTT) was performed around gestation week 28 in 350 women with risk factors for GDM and in 272 randomly included women. GDM was defined by 2-h plasma glucose ≥9.0 mmol/L.
The median (IQR) prolactin increased from 633 (451–829) mIU/L in first–second trimester to 5223 (4151–6127) mIU/L at third trimester. Prolactin was inversely associated with HbA1c in first (r = −0.19, P < 0.001) and third trimester (r = −0.07, P = 0.014). In third trimester, women with GDM (n = 37; 6.0%) had lower prolactin compared to women without GDM (4269 vs 5072 mIU/L, P = 0.004). Third trimester prolactin multiple of the median (MoM) was inversely associated with risk of GDM in multivariate regression analysis (OR 0.30, P = 0.034). PCOS was diagnosed in 10.0% (n = 146). Early pregnancy prolactin MoM was positively associated to PCOS diagnosis (OR 1.38, P = 0.051).
Low prolactin levels during pregnancy were associated with higher HbA1c and risk of GDM. A diagnosis of PCOS was associated with higher early pregnancy prolactin levels.