Ocular toxocariasis in schoolchildren.

Ocular toxocariasis in humans is typically a unilateral disease caused by second-stage larvae of the Toxocara species. Serological evidence of widespread infection in humans provides little information on clinical disease. There is only a single previous estimate of the prevalence of ocular toxocariasis (from Alabama). The present survey examined the extent of consultant-diagnosed toxocaral eye disease among a population of schoolchildren. More than 120,000 participants were surveyed by questionnaire and follow-up. Two sets of control subjects from the same school and from the same county were compared with persons who had ocular toxocariasis. The prevalence of consultant-diagnosed toxocaral eye disease was 6.6 cases per 100,000 persons when only cases regarded as definite by the consultant ophthalmologist were included. This increased to 9.7 cases per 100,000 persons when both definite and strongly suspected cases were included. Geophagia and a history of convulsion were associated with toxocaral eye disease in both of the case-control studies.

Inhibin B in boys from birth to adulthood: relationship with age, pubertal stage, FSH and testosterone.

OBJECTIVE: Inhibin B in males is produced principally by Sertoli cells under the influence of FSH and is thought to have a role in feedback regulation of FSH. The aims of our study were to investigate how inhibin B changes from birth to late adolescence in boys, to derive reference data and to explore its relation with pubertal stage, FSH and testosterone. DESIGN AND SUBJECTS: Blood samples were collected from (i) 366 boys aged 0--18 years to obtain age-related reference data; (ii) 195 boys who had full pubertal staging; and (iii) a cohort of 15 boys studied longitudinally as they approached and entered early puberty. MEASUREMENTS: Dimeric inhibin B was measured by double antibody enzyme-linked immunosorbent assay (ELISA), FSH by immunoradiometric assay (IRA) and testosterone by an extraction radioimmunoassay. RESULTS: Inhibin B was high in infant boys, decreased gradually to a nadir at 6--10 years of age, then increased rapidly in early adolescence to reach a new plateau at 12--17 years. It was detectable in all samples. Age-related reference ranges and data for calculation of SD scores are presented. In prepubertal boys, inhibin B correlated positively with age (P < 0.001), but not with FSH. Inhibin B increased progressively from pubertal stages G1 to G3 but then decreased slightly at stages G4 to G5 (P less-than-or-equal 0.01). At stage G2, inhibin B correlated positively with testosterone (P < 0.01) but not with FSH. From stage G3 onwards, inhibin B correlated inversely with FSH (P < 0.01) but lost its relationship with testosterone. In the cohort of boys studied longitudinally, inhibin B increased progressively prior to pubertal onset and further on entry into early clinical puberty (P < 0.05). Testosterone also increased over this period (P < 0.05) but FSH showed no significant change. CONCLUSIONS: The two peaks of inhibin B during infancy and early puberty appear to reflect the two periods of Sertoli cell proliferation in normal human males. During mid-childhood, a relatively constant amount of inhibin B is secreted constitutively. The early FSH-independent increase in inhibin B that precedes clinical puberty and continues to stage G2 may be stimulated by testosterone or other factors from Leydig cells. The inverse relationship between inhibin B and FSH that subsequently develops from mid-puberty onwards is consistent with the establishment of a negative feedback loop at this time.

Dimeric inhibins in girls from birth to adulthood: relationship with age, pubertal stage, FSH and oestradiol.

OBJECTIVE: Inhibin B is produced by granulosa cells in small antral follicles under the influence of FSH, whilst inhibin A is produced by larger follicles and the corpus luteum. The aims of our study were to investigate how these inhibins change from birth to late adolescence in girls, to derive reference data and to explore their relation with pubertal stage, FSH, oestradiol and each other. STUDY DESIGN AND SUBJECTS: Blood samples were collected from: (a) 345 girls aged 0--18 years to obtain age-related reference data, and (b) 80 pre-menarcheal girls with full pubertal staging, of whom 40 were on GH treatment at the time of sampling. MEASUREMENTS: Dimeric inhibins A and B were measured by double antibody enzyme-linked immunosorbent assay (ELISA), FSH by immunoradiometric assay (IRMA) and oestradiol by radioimmunoassay. RESULTS: Median inhibin B was low until age 6 years, slightly higher from 6 to 10 years, then increased from 10 to 12 years to reach a plateau from 12 to 18 years. Inhibin A was usually detectable in girls younger than 3 months but thereafter became undetectable in most samples until after age 10 years, when median levels rose progressively to 14 years, then stabilized from 14 to 18 years. Both inhibins displayed considerable scatter about the median throughout infancy, childhood and adolescence. Girls aged 0--10 years showed a positive correlation between inhibins A and B (P < 0.0001), whereas those aged 14--18 years showed an inverse relationship (P < 0.001), indicating the onset of ovulatory cycles. Age-related reference ranges and data for calculation of SD scores are presented. GH-treated girls at pubertal stage B2 (but not at B1 or B3--5) had higher inhibin B and FSH levels than untreated girls and were excluded from further analysis. Both inhibins A and B increased during puberty (P < 0.0001) and were positively correlated with each other (P < 0.01). Both inhibins were also positively correlated with FSH in pre-pubertal girls (P < 0.05) but not at pubertal stages B3--5. CONCLUSIONS: Although median levels of inhibins A and B remained low until after age 10 years in girls, the increased levels of both inhibins in individual samples, together with their positive relationship with FSH, provide further evidence of sporadic follicular development throughout infancy and childhood under the influence of FSH. The increase in both inhibins during puberty and their changing relationship with FSH are in keeping with the concept of follicular growth being dependent on the duration of FSH elevation above a critical threshold rather than the degree of elevation per se.