Anti-Müllerian hormone (AMH), also called Müllerian inhibiting substance or factor, is produced by Sertoli cells from fetal life until puberty. In the present study, AMH, testosterone (T), LH, and FSH were measured by immunochemical methods in the serum of 50 boys with normal or delayed pubertal development, 4 patients with suspected androgen insensitivity, and 11 patients with either central (CPP) or gonadotropin-independent (GIPP) precocious puberty to investigate the hormonal regulatory mechanisms of AMH secretion at puberty. An inverse relationship between AMH and T levels was demonstrated. In boys with normal or delayed puberty with T concentrations below 6.7 nmol/L, AMH values were elevated (mean +/- SEM, 22.4 +/- 3.1 micrograms/L) and widely dispersed. In subjects with T levels over 6.7 nmol/L, AMH levels were uniformly low (3.4 +/- 0.5 micrograms/L), except in patients with suspected androgen insensitivity. No significant relationship was found between AMH and gonadotropin levels. Similar results were obtained in patients with either CPP or GIPP. Longitudinal studies were performed on four boys with CPP and two with GIPP before and after treatment. At the time of diagnosis, the T concentration was high, and AMH levels were usually low in CPP and GIPP patients alike. When appropriate treatment was initiated, the T concentration was normalized within 2-4 weeks, but restoration of prepubertal AMH levels required several months. Mature Sertoli cells were observed in testicular biopsies performed in three patients with untreated GIPP. Our results suggest that gonadotropins are not directly implicated in repression of AMH synthesis at puberty, but, rather, that the decrease in AMH production is the consequence of an androgen-mediated, long term, reversible chain of events leading to morphological and functional maturation of the Sertoli cells. Thus, the fall in serum AMH levels appears to be an excellent marker of Sertoli cell pubertal development.
Researchers involved in the field of congenital malformations are often forced to work on an animal model. Both accurate description of its normal development and comparative staging with human development will be mandatory. To complete the lacking medical literature, we herein provide such data for the rabbit model. Sampled rabbit embryos were staged using the Carnegie criteria, in order first to determine if they were consistent with the rabbit developmental pattern, and second to compare this pattern with the human one. Our results show a suitable comparison of rabbits and humans in early developmental stages, except for the neural growth.
Background: In spite of significant therapeutic progress, the prognosis of congenital diaphragmatic hernia (CDH) remains pejorative in those forms in which the liver is herniated into the chest. The severity of this malformation relies on the pulmonary hypoplasia due to lung compression by the herniated viscera in the thoracic cavity, particularly the liver. This impaired growth concerns the whole pulmonary tissue, i.e. both the vessels and the alveoli. For the clinician, it is mandatory to know the evolution pattern of the lesions, to define the best time to treat them. Aim and Method: The aim of this work was to study the pulmonary lesions along the gestation in fetuses affected byCDH. This morphological study was carried out on 134 human fetuses aged from 22 to 40 weeks of gestation. Anatomical and histological analysis focused on lung weight, alveolar count and wall thickness of the distal vessels. Results: The results indicate that the pulmonary lesions worsen as the pregnancy continues, particularly beyond 30 weeks of gestation. Conclusion:Such an anatomical study should bring to the clinicians useful data to enhance the management of the patients.
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