The marked pituitary tumor shrinkage achieved by continuous sc infusion (CSI) of the long-acting somatostatin analog octreotide in one acromegalic patient led us to treat 16 other acromegalic patients for up to 24 months by CSI. This therapy, given in doses ranging from 100-600 micrograms/day, resulted in normalization of the mean daily serum GH (mGH) and insulin-like growth factor I levels in 9 of the 17 patients (53%). In 7 patients, mean daily serum GH decreased but not to normal; 3 of these patients had hyperprolactinemia which was not influenced by octreotide. One patient was completely unresponsive. In contrast to the biochemical results, 80% of the patients had marked clinical improvement. Side-effects consisted of slightly impaired carbohydrate tolerance in 2 patients and cholelithiasis in 2 patients. Pituitary tumor size decreased in only 3 patients; in 1 of them visual field defects disappeared rapidly. These results suggest that octreotide treatment may prove beneficial before surgery in patients with macroadenomas, although its efficacy varies widely. Potential responsivity can usually be determined by a short course (24 h) of CSI of octreotide.
SMS 201-995, a long-acting somatostatin analog, was given as the initial treatment to an acromegalic patient. SMS 201-995 (200 micrograms, sc, three times daily) reduced, but did not normalize, serum GH levels. Complete and prolonged control of GH secretion was obtained with a 600-micrograms daily continuous sc infusion (CSI), and the patient was treated in this way for 6 months. Rapid improvement of clinical signs and symptoms of acromegaly occurred, as did major tumor shrinkage. The other pituitary functions did not change. After 6 months, the daily SMS 201-995 dose was progressively reduced; GH secretion remained suppressed. After 12 months of treatment, GH secretion was controlled with a CSI of 100 micrograms SMS 201-995 daily, but not with two daily sc 100-micrograms injections. Further significant reduction in tumor size occurred. We conclude that CSI of SMS 201-995 resulted in constant GH normalization and marked clinical and morphological improvement. This form of treatment should be considered as an alternative to ablative treatment of acromegaly.
Male factors account for approximately 50% of reproductive pathology. Different disorders, including urogenital and endocrine system development abnormalities, lead to testicular and gametogenesis defects. Parallely, studies have reported that somatic and germ cell genome decay are a major cause of male infertility. It has been shown that in somatic karyotype, there is a higher incidence of chromosomal aberrations in infertile men than neonatal population and significant chromosome Y microdeletion or specific gene alterations in affected spermatogenesis. Karyotyping and FISH application at somatic and germ cell levels are no longer sufficient to investigate the potential contribution of genome disorders on male infertility. A wide range of molecular methods are required for better understanding of male infertility causes. Molecular omes and omics techniques have become a great tool to investigate male infertility from chromosome to protein. This review reports different molecular tests and methods that can be offered for male infertility investigation.
The recovery of exocrine and endocrine testicular function was studied in six patients orchidectomized for an estrogen-producing Leydig cell tumor. Gynecomastia disappeared in four patients. The contralateral testis, whose volume was reduced, returned to normal size after 30 days. Sperm density returned to normal in only one of the four patients in whom the preoperative sperm count was reduced. One day after unilateral orchidectomy, plasma estradiol decreased to normal and testosterone (T) fell about 50%. On the 10th postoperative day, plasma T [5.60 +/- 1.20 ng/ml (SD)] was normal. On day 120, T was higher than on day 10 (6.83 +/- 1.20 ng/ml). There was no significant increase of T after a single injection of hCG (5000 IU) on day 10, and the T response was similar to that of normal men on day 120. Plasma FSH and LH were increased on the 10th postoperative day; they then decreased between 60 and 120 days after the operation but were still above the normal values on day 120. The FSH/LH ratio, which was 0.43 +/- 0.17 preoperatively returned to normal (1.60 +/- 0.25) 10 days postoperatively. In conclusion, after hemicastration for an estrogen-secreting tumor, testicular hormonal secretion returns to normal within 120 days but spermatogenesis may still be impaired at this time.
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