After completion of this article, the reader should be able to recall that paroxysmal nocturnal hemoglobinuria (PNH) during pregnancy increases adverse events for both the mother and the fetus, state that maternal and fetal mortality are both high, and explain that the major complications occur in the postpartum period.

SummaryBackgroundHyponatremia and vitamin D deficiency are frequent disorders, and both have been associated with gait disturbances, falls and fractures. The aim of this study was to evaluate the existence of an association between serum sodium and vitamin D serum levels.MethodsWe performed a retrospective investigation to establish whether hyponatremia and vitamin D deficiency may be associated in a general population of unselected outpatients. An electronic search was performed in the laboratory information systems of the Hospital of Verona and the Hospital of Parma (Italy), to retrieve combined results for total vitamin D and sodium obtained in all outpatients referred for health check-up in the year 2013.ResultsCombined results of vitamin D and sodium could be retrieved for 5097 outpatients (3859 females and 1238 males; mean age 64±17 years). Vitamin D deficient subjects displayed significantly lower levels of serum sodium (140 versus 141 mmol/L; p<0.001), along with a significantly higher rate of hyponatremia (6.3% versus 5.1%; p=0.037). Accordingly, hyponatremic subjects had significantly lower levels of serum vitamin D (55 versus 60 nmol/L; p=0.015), along with a significantly higher rate of vitamin D deficiency (41.8% versus 36.1%; p=0.030). A highly significant correlation was found between sodium and total vitamin D after adjustment for age and gender (p<0.001).ConclusionsThe results of this study demonstrate for the first time the existence of a significant correlation between the serum levels of sodium and total vitamin D in a general population of unselected outpatients.

LDH-X, an isoenzyme of lactate dehydrogenase specific for germinal epithelium activity, has been measured in the seminal plasma of infertile subjects whose infertility had different origins. In the same samples, seminal transferrin, an index of Sertoli cell function, was also measured. In this investigation, seminal LDH-X was not detectable in the vasectomized subjects, in patients with azoospermia due to seminiferous tubular damage, nor in patients who showed a marked decrease in sperm concentration (less than 1 X 10(6)/ml). In oligozoospermic patients (sperm concentration less than 20 X 10(6)/ml) seminal LDH-X levels were reduced to about one-third of those found in normal controls. Seminal LDH-X levels correlated (r = 0.7237) with total sperm count better than seminal transferrin levels (r = 0.5511), while no correlation was found between these two biochemical parameters and sperm motility, viability and morphology. To study their spontaneous variations with time, LDH-X and transferrin were also measured in semen specimens collected monthly from five healthy men, over 1 year. In these samples (N = 60), sperm count variability (43.1%, calculated in terms of the coefficient of variation), was similar to that of LDH-X (40.4%) and higher than for transferrin (23.0%).

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Somatomedin C is a Sertoli cell peptide and since measurements of other Sertoli cell products in semen have provided a useful indices of testicular function, it was considered pertinent to measure the semen levels of Somatomedin C. Somatomedin C was measured by RIA in seminal plasma of vasectomized subjects (n = 18), subjects with agenesis of the seminal vesicles and vasa deferentia (n = 6) and subjects with azoospermia resulting from seminiferous tubule damage without obstruction (n = 23). Normal fertile subjects (24 men with a sperm concentration > 20 × 106/ml) were used as controls. In all subjects, seminal levels of transferrin were also measured as an index of Sertoli cell function. The majority of seminal Somatomedin C appears to derive from the testis and/or epididymis. However, in several normal controls seminal levels of Somatomedin C (median = 3.52; range = 1.10–15.67 U/ejaculate) were found to be within the range for vasectomized subjects (median = 0.78; range = 0.46–4.20 U/ejaculate). In subjects with azoospermia the seminal levels of Somatomedin C (median = 2.06; range = 0.60–10.12 U/ejaculate) were significantly lower (P < 0.02) than in fertile controls. However, values for these two groups overlapped. It is concluded that Somatomedin C in semen is not a reliable index of seminiferous tubule function and does not appear to be of diagnostic value in male infertility.