[Colorectal neo- and dysplasia in acromegaly].

Colorectal disorders can be not only an independent disease, but also manifestation of acromegaly--a neuroendocrine disease which is characterized by chronic pathological hypersecretion of the growth hormone (GH) and the increased concentration of insulino-like growth factor type 1 (IGF-1). In clinical recommendations on diagnosis and treatment of acromegaly, colonic polyps are marked as one of most pathognomonic manifestations of acromegaly. Prevalence of coloni polyps in acromegalic is 2,5-3 times higher than in the general population. Moreover, frequency of diverticula and dolichocolon is increased in patients with acromegaly compared with general population (in 3,6 and 12 times, accordingly). Colorectal cancer incidence with a tendency to more aggressive current is also increased (by 4,4 times). When these colonic diseases is diagnosed, especially in patients of young age, it is necessary to define the IGF-1 blood level as the first stage of acromegaly identification. If diagnosis of acromegaly is confirmed, gastroenterologist with endocrinologist together should direct treatment on correction of intestinal pathology as well as on achievement of the biochemical control over acromegaly.

Antibodies to pituitary surface antigens during various pituitary disease states.

Autoantibodies to cell surface antigens of human somatotropinoma (ASAS), human prolactinoma (ASAP) and rat adenohypophysis (ASARA) were assayed in the serum of patients with pituitary diseases associated with GH deficiency (GHD), such as pituitary dwarfism and primary empty sella syndrome (ESS), and in the serum of patients with hyperprolactinaemia of different etiologies: idiopathic hyperprolactinaemia, prolactinoma and ESS. The investigation was carried out with a cellular variant of an ELISA. Among children with GHD, the highest percentage of antibody-positive patients was found in the group with idiopathic isolated GHD (89% of ASAS(+) patients and 30% of ASARA(+) patients vs 33.3% and 0% respectively in the group with idiopathic combined pituitary hormone deficiency, and 33.3% and 9% in patients with pituitary hypoplasia associated with isolated GHD or combined pituitary hormone deficiency). Among hyperprolactinaemic patients, the highest ASAP and ASARA frequency was observed in patients with idiopathic hyperprolactinaemia (67.7% and 41.9% respectively) where it was twice as high as in the group of patients with prolactinoma. The proportion of ASAS(+) and ASARA(+) did not differ significantly between the groups of patients with ess with or without GHD. Similarly, there was no significant difference between the number of ESS ASAP(+) and ASARA(+) patients with or without hyperprolactinaemia. The data obtained suggested that autoimmune disorders may be primary, and responsible, at least in part, for pituitary dysfunction in the cases of idiopathic isolated GHD and idiopathic hyperprolactinaemia. At the same time, the autoimmune disorders in the patients with prolactinoma or ESS are probably secondary to the organic pituitary lesion and their significance in the development of the pituitary dysfunction is obscure.

[Bone tissue in patients with hyperprolactinemic hypogonadism]. / Sostoianie kostnoi tkani u bol'nykh s giperprolaktinemicheskim gipogonadizmom.

Sixteen women with hyperprolactinemia were examined for Ca metabolism, osseous metabolism, mineral saturation of bone tissue in the thoracic portion of the spine and radius. Lowered mineral saturation of the thoracic vertebrae was detected in 69% of the examinees, that of the distal segment of the radius in 44%. Reduction of the mineral saturation of the spine was in negative correlation with the blood prolactin level and length of amenorrhea. No changes in the bone resorption biochemistry or Ca metabolism were detected. A marked reduction of blood osteocalcin level that reflects osteoblast function was detected, its blood concentration being in negative correlation with prolactin level. No relationships between mineral saturation of bone tissue, prolactin, and osteocalcin, on the one hand, and blood estradiol level, on the other, were observed. These data suggest that osteopathy in hyperprolactinemic hypogonadism is due to reduced bone formation and not to reduced estradiol production.

[Use of lysenyl-forte and methergoline in the therapy of hyperprolactinemic hypogonadism]. / Primenenie lisenila-forte i metergolina v lechenii giperprolaktinemicheskogo gipogonadizma.

The paper is concerned with a study of the effectiveness of lysenyl-forte (Hemapol, Czechoslovakia) and methergoline (Carlo Erba, Italy) for therapy of patients with different types of hyperprolactinemic hypogonadism. Altogether 49 patients were investigated, of them 33 received lysenyl-forte at a dose of 0.6 mg/day and 16-methergoline at a dose of 12 mg/day for 3 months. A degree of galactorrhea, a menstrual cycle and the blood level of prolactin were assessed before and after therapy. A prolactin inhibiting effect of both drugs comparable with that of bromocriptine was noted. However a clinical effect and good tolerance were more frequently observed in this sampling in lysenyl therapy.