Search

Pasqualini and Bur published the first case of eunuchoidism with preserved spermatogenesis in 1950 in Revista de la Asociación Médica Argentina. The hypoandrogenism with spermatogenesis syndrome included: (a) eunuchoidism, (b) testis with normal spermatogenesis and full volume, with mature spermatozoa in a high proportion of seminiferous tubes and undifferentiated and immature Leydig cells (c) full functional compensation through the administration of chorionic gonadotropin hormone, while hCG is administered (d) total urinary gonadotrophins within normal limits (e) this definition supposes the normal activity of the pituitary and the absence of congenital malformations in general. A first step in the understanding of the physiopathogeny of Pasqualini syndrome or the so called "fertile eunuch" syndrome was the absence of LH in plasma and urine of patients. The second breakthrough was the functional and genetic studies that validated the hypothesis of a functional deficit of LH in these men: it will then also be described in some women. Different groups including ours demonstrated in these cases a LH with varying degrees of immunological activity but biologically inactive in most of the patients, due to one or more inactivating mutations in the LHB gene. Finally, the full comprehension of Pasqualini syndrome allowed to reverse the hypoandrogenic phenotype and to restore fertility in these patients through the use of chorionic gonadotropin and the modern in-vitro fertility techniques. This article is an historical review and a tribute to the memory of Rodolfo Q. Pasqualini.

Spermatogenesis is a well defined, complex,long and very orderlyprocess of cellular division and differentiation that is under regulation by endocrine signals (GnRH, LH, Inhibin and FSH ): paracrine signals, derived from the interrelation of the various types of cells in the tubules and interstitium (even in a juxtacrine way), and autocrine signals of self communication of the cell with itself. Testosterone plays an essential role in this process. In the testicular tubules, testosterone reaches concentrations 100 times higher than circulating testosterone in the blood stream. From a reproduction point of view, we can find two completely different scenarios in relation to testosterone deficit syndrome with a similar final clinical result: The difficulties of the male to have children. On one side the presence of hypogonadism, which requires a different management depending of the clinical priority and wishes of parenthood of the patient an his partner. On the other side, the opposite situation, the patient who requires or is already under testosterone therapy. In patients with hypogonadotropic hypogonadism, when patient's clinical priority is fertility, the treatment to restore normal spermatogenesis requires external administration of gonadotropins. Treatment must be prolonged, at least 12-18 months. 95% of the cases will have a favorable response, meaning the finding of spermatozoids in ejaculation sperm as a consequence of spermatogenesis restoration.

Spermatogenesis arrest is a complex process of interruption in the differentiation of germinal cells of specific cellular type, which elicits an altered spermatozoa formation. In contrast, hypospermatogenesis is defined as a decrease in number of germ cells and its proportion. Factors identified intervening upon spermatogenesis arrest are: genetic, hormonal, growth factors, interaction between Sertoli and germ cells and ectoplasmic specialization integrity of spermatozoa. In addition, environmental toxic effects have shown to exert subletal and letal cellular damage with gene disruption. Hence in this work we review sperm physiology along with etiologic elements associated to spermatogenesis arrest delineating the most appropriate conduct for diagnosis and treatment.

The normal development and function of the male and female gonads is characterized by a massive cell decrease in which apoptosis plays a key role. This event is a controlled program of cell death, fundamental for development and homeostasis. In the male gonad up to 75% of the germinal cells undergo this process, probably as a mechanism to eliminate the germinal cells incompatible with the preservation of the species. It has been demonstrated the participation of the transforming growth factors beta 1 and beta 2, as well as the role of the Fas system, polypeptide and steroidal hormones in the regulation of this process. The study of apoptosis in physiological and pathological events among insects, nematodes and mammals has allowed to understand the role of genes, endonucleases and the deoxyribonucleic acid fragmentation as part of the molecular mechanisms involved in this event. In this paper were analyzed the molecular mechanisms mentioned above, during different stages of the development and function of the male gonad.

In this work, the seric and hypophysial concentrations of the hormones alpha-melantopin and prolactin of male specimens of Leptodactylus ocellatus from the province of Cordoba are studied during a complete annual period. This amphibian presents a continuous reproductive cycle with a wave of greater spermatogenic activity in early summer months (December-January). The results corresponding to hormones show a very similar pattern: both present their maximal seric value in the December-January period, coincidently with the greatest spermatogenic wave. Maximal hypophysial values precede seric concentration maximum by two months. Although the influence of these hormones on amphibian spermatogenesis is not well understood, the observations here described would indicate that alpha-melanotropin as well as prolactin could play a role in the spermatogenic process in Leptodactylus ocellatus.