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Boy 15. Aspect of delayed puberty with empty scrotum and gynecomastia. Caryotype 46, XX. Presence of H.Y. Antigen. Plasmatic testosterone 1 020 pg/ml. Normal plasmatic FSH and LH. Hypotrophic uterus and tubes. No gonad found. Small right epididymis. Complete virilization by testosterone.
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A study of 252 patients with pubertal aberrancy was done at the Medical College of Georgia. Patients were classified into hypogonadal and eugonadal categories. Ovarian failure is the most common cause of delayed sexual development. Congenital absence of the uterus and vagina and physiologic delay of puberty follow as frequently diagnosed etiologies. Pubertal aberrancy is no longer considered a benign entity since it is associated with morbidity, mortality and significant compromise of reproductive potential. The physical, emotional and social well-being of these patients is dependent upon expedient evaluation and treatment and on appropriate education and counseling.
Delayed puberty in children with chronic renal failure (CRF) may be due to gonadal dysfunction, increased plasma binding of gonadal hormones, or changes of the hypothalamo-pituitary axis. Plasma androgens were studied in 17 prepubertal boys with preterminal CRF. In addition, the response of luteinizing and follicle-stimulating hormones (LH, FSH) to luteinizing-releasing hormone (LHRH) was followed in the plasma of these boys and of 12 prepubertal girls with CRF. Plasma testosterone (T) was significantly lower in the CRF boys than it was in the controls (mean, 9 vs. 22 ng/ml) and concerned also the free T fraction (2.5% in both groups). Dihydro-T was similarly reduced in CRF, resulting in a normal T/DHT ratio. Basal plasma LH levels were significantly elevated in boys (1.0 vs. 0.5 ng/ml) and in girls with CRF (1.4 vs. 0.4 ng/ml), whereas mean basal FSH values were similar to controls. After LHRH administration, peak levels of LH and FSH were not different in CRF and control children; however, the absolute differences from basal to peak values were lower in CRF. These findings may indicate that Leydig cell dysfunction in CRF already occurs before the onset of puberty. The blunted LH and FSH responses to LHRH suggest an additional disturbance at the hypothalamo-pituitary level.
The somato-psychic development in puberty should not be described isolated. It has to be brought in connexion with childhood on the one side and the age of the young adults on the other side. Puberty and adolescence generally are not used as synonyms. They accord with two different stages of development, succeeding one another between childhood and adulthood. They take a different, either harmonious or synchronous course. An asynchronism is often partial cause for a puberal crisis. Besides, one has to consider phenomenons like retardation or acceleration of development. These special kinds of development are illustrated by examples with two retarded adolescents. On the end, the author takes briefly up some therapeutical possibilities.
A brief summary of the research carried out on the problem of geophagia is reported in this paper. Geophagia was a common finding among Turkish children and women in villages, associated with severe iron deficiency anemia in addition to zinc depletion. The syndrome characterized by geophagia, iron deficiency anemia, growth retardation, hypogonadism and zinc deficiency has been observed in both sexes in Turkey for several decades. Zinc deficiency has been also shown by our group in this syndrome. The decreased concentrations of zinc in serum, plasma, RBC, hair and urine were measured by atomic absorption spectrophotometer. Oral iron (both inorganic and radioactive iron) and zinc absorption tests were carried out with and without clay and revealed decreased iron and zinc absorption in some cases with prolonged geophagia. Therefore, malabsorption of iron and zinc was considered to be an additional and/or a new finding in the syndrome. Furthermore, Turkish clay most probably inhibits zinc absorption in a way similar to its inhibition of iron absorption. It was worthy of observation that some Turkish patients with this syndrome had a thalassemia-like appearance with similar skull-bone changes. Finally, growth retardation and delayed puberty were shown to be corrected by oral zinc treatment for 6-month terms. Linear growth and sexual maturation were found to be greater in the zinc-treated group than in the controls.
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Chronic renal failure affects 1.5 children per million of the population each year. Most of these children are suitable for renal replacement therapy with the primary aim being full rehabilitation by means of a successful renal transplant. Since May 1974 12 children under the age of 16 years have entered the Christchurch dialysis-transplant programme. Six children had reflux nephropathy. Medullary cystic disease caused renal failure at the same time in identical twin girls. Dialysis was tolerated as a necessary step to transplantation. Major problems associated with home haemodialysis were the needling of the arteriovenous and the disruption of family life. After a successful transplant the children had few limitations. Chronic renal failure and its treatment in childhood were associated with growth retardation, delayed puberty and uncertainty regarding the future. With support from the family and friends these children attempted to lead a normal life.
The effect of altered nutrition on sexual maturation may depend in part on the nature and timing of the dietary change. The data are conflicting as to whether rats undernourished before weaning but normally fed after weaning have delayed puberty, but such undernourished rats clearly weigh less at vaginal opening than do normally fed animals. Altered nutrition after weaning can change the timing of puberty, and in such cases the body weight at puberty of the animals given the modified diet is frequently abnormal. The factors regulating the age and weight at puberty of rats fed altered diets seem to include the degree of underfeeding, as reflected in the growth rate, and the composition of the diet. Undernourished immature male rats have low serum testosterone secondary to gonadotropin deficiency. Basal luteinizing hormone (LH) in these animals is either low or "inappropriately normal" relative to their hypoandrogenic state (low serum testosterone and sexual accessory gland weights), and serum LH increases after luteinizing hormone-releasing hormone (LHRH) or castration are normal or minimally reduced. Serum follicle-stimulating hormone (FSH) in undernourished rats is subnormal basally and after administration of LHRH, but not after castration, which suggests that the low basal serum FSH is due to inhibition of FSH output by a testicular factor. Spermatogenesis may be unaltered by dietary changes severe enough to cause hypoandrogenism, although very severe under-nutrition will impair sperm production.
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The syndromes described are often related to primary endocrine or development defects, but may also result from purely educational or psychological problems. Adolescents may find it difficult to seek help, particularly in the younger age range where early medical intervention is important. While psychotherapy alone is often advisable, the use of anxiolytic agents may be an effective adjunctive treatment. Benzodiazepines are particularly useful because they do not stimulate enzyme activity as do some sedative agents. Teenagers are dependent on the expectations of their parents, and as ANTHONY and RIZZO [1971] have emphasized, the administration of drugs to a member of a family demands an understanding of such expectations, as well as a subtle awareness of the dynamic homeostasis and interactional patterns prevalent in the family at the time. The expectations of parents and the physician concerning the changes due to the drugs prescribed should be synchronized by mutual discussions and questioning. The adolescent has less anxiety tolerance, fewer brakes, less facilities for elaborating his symptoms on symbolic levels, and diminished capacities for postponement of impulsive gratifications; all these factors are important in achieving results by psychological methods alone. The time factor urges us to combine psychotherapy and pharmacotherapy; a well-selected drug in moderate dosage will not necessarily impair the transference. We may take the advise of Plato, who said that the drug effect should be supplemented with parleys ("epodai") which will guieten down or cheer up the soul. The modern sex therapist dealing with adolescents might follow this direction.
A 27-year-old man was admitted to the Urological Department of Tokyo University, with complaints of delayed puberty and growth retardation. At the age of 14 years, he found his skeletal growth retarded. Since then he had not shown any development of secondary sex characters, such as change of voice, appearance of public and axillary hair and development of external genital organs. He had not experienced the ejaculation and libido, while the excretion has been maintained. This feminized patient showed poorly developed external genitalia, while there was no evidence of galactorrhea or gynecomastia. Ophthalmologic examinations were normal. Endocrinological studies revealed moderate hyperprolactinemia (185-200 ng/ml) and marked disorder for GH secretion. Gonadotropins were low normal and their responses to LH-RH were moderately disturbed. Serum testosterone level was extremely low and its responses to HCG were insufficient. Under the diagnosis of prolactinoma, he was referred to the Neurological Department. Plain skull film and tomography of the sella showed a deformed and slightly expanded sella, the measurement of which were within normal limits. No supra-sellar extention was demonstrated by pneumoencephalography and CT scan. A diagnosis of PRL producing microadenoma was made, and a radical removal of the tumor was performed through the transsphenoidal route. In most tumor cells the presence of PRL was revealed by immunohistochemical stains. Postoperatively, PRL levels returned to normal, while other hormonal deficiencies remained unchanged. With the administration of testosterone, he gradually became masculine and reportedly gained normal libido and potency.
A primitive gonadal failure was observed in 2, 20 and 18 years old galactosemic female patients. The conditions was clinically suspected because of primary amenorrhea in one case and delayed puberty, followed by spaniomenorrhea in the other case, and confirmed by very low plasma estradiol and very high plasma gonadotropin levels. Galactose-free diet was started at 9 months of age in the first case and soon after birth in the second. Several similar cases have been recently reported. Primitive gonadal failure associated with galactosemia suggests a possible toxic' destruction of the ovaries during the intrauterine life by a galactose metabolite.
Understanding the physical, physiological and psychological components of puberty is essential for diagnosis and optimal management of problematic growth and development. The relationships between these components should be considered also.
Adolescent anorexia nervosa is characterised by its relationship to pubertal conflicts. The authors report two cases showing that this syndrome is not confined to girls. In boys, it usually results in delayed puberty. The diagnostic criteria are detailed. The concept of pathological process, causing stereotyped syndrome, is distinguished from the notion of psychological organisation which gives rise to wide individual variation. The pathological outcome is considered in the context of pubertal dynamics, marked by the reemergence of the oedipus conflict and the rearrangement of the patients identificatory systems, and also in the continuity of the particular libidinal behaviour, characterised by important points of fixation of the oral pulsion. The role of the family group in the initiation and maintenance of the anorectic behaviour is also discussed.