Резюме. У статті висвітлено поняття ектопічних АКТГ-пухлин нейроендокринної системи. Описано рідкісний випадок ектопічного АКТГ-синдрому Кушинга, зумовленого бронхіальним карциноїдом, у клініці якого, поряд з типовою симптоматикою, домінував тромбоемболічний синдром. Хірургічне видалення бронхіального карциноїда призвело до регресу кушингоїдної та іншої симптоматики. Ключові слова: синдром Кушинга, тромбоемболія, карциноїд, гіпофізектомія, торакотомія.

Diabetes insipidus is a rare endocrinological disease and occurs in 2–4 per 100,000 pregnancies. Diagnosis of gestational diabetes insipidus is very difficult because it develops against the background of physio­logical mechanisms that accompany pregnancy: thirst threshold decreases leading to polydipsia and plasma osmolarity decreases causing hypotonic polyuria. Understanding of pathophysiology of the disorder is very important for further management of these vulnerable patients. A 32-year-old patient at 36 weeks of gestation, primigravida, was referred to an endocrinologist with complaints of polyuria (6.5 l/day), nocturia — up to 5 times, severe polydipsia. At 12 weeks of gestation, there was a risk of abortion for prevention of which the patient received progesterone 100 mg intravaginally twice a day until 34 weeks. She has a history of subacute thyroiditis, with no family history of endocrine pathology. Physical examination revealed a decrease in skin turgor, blood pressure 110/85 mm Hg. Heart rate 115 bpm, weight 71 kg (body mass index 26.9 kg/m2). The patient was at high risk of developing preeclampsia. Laboratory data: analysis of urine according to Zimnitsky: volume per day — 6.8 l, specific gravity in portions: 1.012; 1.008; 1.010; 1.005; 1.012; 1.014; 1.010. Total blood count, total urine test, serum sodium and potassium, liver function tests, level of thyroid-stimulating hormone, free thyroxine, thyroid peroxidase antibodies and morning free cortisol level were normal. The patient was administered desmopressin 10 μg intranasally twice daily. Six weeks after delivery, desmopressin was stopped and she had no further evidence of polyuria, polydipsia or nocturia.

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Hypoglycemic syndrome is often noted in clinical practice in the treatment of patients with diabetes mellitus (DM), especially with insulin. This syndrome is manifested by symptoms caused by neuroglycopenia (insufficient supply of glucose to the brain, which utilizes 20 % of all glucose). Hypoglycemia occurs quite often, in about 40 % of people with type 1 DM. The clini­cal syndrome of postprandial (reactive) hypoglycemia of various etio­logies is considered, which is manifested by a hypoglycemic condition in the next hours after eating, especially easily diges­tible carbohydrates. In most cases, there is a violation of the hypothalamic regulation of carbohydrate metabolism, and the clinical picture is dominated by symptoms of activation of the sympathoadrenal system. Such hypoglycemia is usually transient, as glucose levels return to normal rapidly due to the release of counterinsular hormones. The importance of the latter in the regulation of insulin secretion is evidenced by the fact that after oral glucose loa­ding, a higher level of insulin secretion is determined than in the case of intravenous administration of an equivalent dose. Elderly patients with hypoglycemia are more likely to deve­lop neurolo­gical disorders than adrenergic disorders (palpitations, tremors, hunger). These symptoms may be mistaken for signs of cerebrovascular ischemia, as a result, hypoglycemia is not adequately detected and treated. In addition to the acute adverse effects of hypoglycaemia, a hypoglycaemic episode may have long-term consequences. Frequent hypoglycemic conditions have a significant psychological impact and are also a risk factor for dementia. The paper presents the data, based on scientific sources and own observations, on etiopathogenesis of hypoglycemia, as well as their most frequent clinical varieties, in particular, in the syndrome of unrecognization of hypoglycemia, postprandial hypoglycemia, in chronic insulin overdose in patients with diabetes mellitus in old age and insulinism.

Recently, in the foreign scientific literature there have been reports that boys and young men with the classic virile form of congenital adrenal hyperplasia or congenital dysfunction of the adrenal cortex as a result of inadequate glucocorticoid therapy in 21–28 % of cases have testicular adrenal rest tumors, which increases under the influence of excessive production of adrenocorticotropic hormone (ACTH). This benign formation up to 2 cm in diameter and larger is detected by palpation and ultrasound. The formations can press on the testicular tissue and lead to hypogonadism. Such individuals may have low testosterone levels due to decreased Leydig cell function. Testicular adrenal rest tumors usually decrease after treatment optimization. Unreasonable surgery is sometimes performed in suspected cancer. A clinical case is presented of the classic form of congenital adrenal hyperplasia, manifested itself in isosexual precocious puberty, cryptorchidism and testicular adrenal rest tumors rare, increased under the influence of excessive ACTH production as a result of inadequate glucocorticoid replacement therapy. Formations detected during ultrasound decrease when treatment is optimized. Observation of the patient in the dynamics showed that ones of the main diagnostic hormonal tests are blood levels of ACTH and 17-hydroxyprogesterone, which at the time of disease detection were excessively high. Continuous glucocorticoid replacement therapy maintains the level of these indicators within the reference values. Timely diagnosis of the nature of the pathology, constant corrective hormone therapy ensured the patient’s abi­lity to adapt to life and society in accordance with his status. Clinical mani­festations of hypocorticism and/or hyperandrogenism in the parents of our patient were not detected, which indicates autosomal recessive inheritance of congenital adrenal hyperplasia. In the future, it is important to provide genetic counseling to expectant parents, especially with manifestations of hyperandrogenism, to assess the possible development of such pathology in their offspring.