[Cerebral low T3 syndrome]. / Mozgovoi sindrom nizkogo T3.

The authors studied the time course of changes in the parameters of the cerebral thyronergic system (total and free triiodthyronine (T3) and thyroxin (T4), thyroxine-binding globulin (TBG), thyroid-stimulating hormone (TSH) by radioimmunoassay (Immunotech, Czechia; CIS, France), proinflammatory cytokine of TNF-alpha by enzyme immunoassay (Innogenetic, Belgium) in the blood and cerebrospinal fluid (CSF) in 59 patients (37 males and 22 females whose age ranged from 21 to 64 years) in acute subarachnoidal hemorrhage due to arterial aneurysmal rupture. On admission, the condition of 47 (79.7%) was rated as grades III-VI according to the Hunt-Hess scale, which was responsible for high mortality rates (33.89% in the assessment of outcomes according to the Glasgow outcome scale). The causes of death were ischemic and hemorrhagic insults, edema of the brain, cerebral stem wedging. Laboratory findings were analyzed in relation to the clinical condition of patients, outcomes, and the degree of secondary vasospasm assessed by Doppler transcranial study by the average blood flow velocity in the middle cerebral artery. They revealed a significant depression of thyroidal metabolism with developed the total low T3 syndrome just before surgical treatment in patients with deterioration in the early postoperative period. The significant correlations found by the authors between the decreased blood T3 and TSH levels and 1) the severity of neurological disorders; 2) the degree of vasospasm, and 3) the outcome of disease, as well as negative correlations of elevated TNF-alpha levels not only in the blood, but also in CSF with the content of CT3, CT4 and with the severity of neurological symptomatology are indicative of the development of isolated syndrome in the brain, which is characterized by specific thyroidal metabolic disorders, which the author propose to call the cerebral low T3 syndrome (by taking into account the presence of the autonomic systems of thyroidal homeostatic provision).

[Involvement of thyroid hormones in mental recovery following severe craniocerebral trauma]. / Rol' tireoidnykh gormonov v protsesse vosstanovleniia psikhicheskoi deiatel'nosti posle tiazheloi cherepno-mozgovoi travmy.

To study a role of thyroid hormones in the recovery of mental performance, 71 patients (60 males, 11 females) aged 7 to 66 years (mean age 32.7 +/- 3.5) with severe brain injury (TBI). According to the stage of mental recovery (1--none; 2--elementary acts; 3--verbal contact; 4--spatial orientation; 5--intellectual and mnestic processes and emotional and personality traits), the study was divided into 5 series. Immunoradiometric assay of thyroid hormones (T3 and T4) and their free fractions (FT3 and FT4), thyroid-stimulating hormone (TSH), thyroxine-binding globulin (TBG), and prolactin (P) revealed significant alterations in thyroid metabolism at stages 1 to 4, which appeared as low T3 syndrome. The thyrotropin-releasing hormone (TRH) test made in study series 3 to 5 suggests that the patients have neuroendocrine dysfunctions at the mentioned recovery stages of mental functions of the brain. There was a close relationship of clinical parameters (mental time course) to alterations in the thyroid status and metabolism and to morphological impairments of brain tissues in their traumatic damage, which is evidenced by a correlation of the levels of blood and spinal fluid markers (neurone-specific enolase--NSE and protein S-100) of brain injury with psychopathological disorders (r = -0.96 and -0.6, respectively; p < 0.05) and by the assessment of TBI outcomes (r = -0.65 and -0.62, respectively; p < 0.05). Thus, the findings clinically confirm the neurotransmitter role of thyroid hormones at the stages of mental recovery. In addition, the results show that measurement of blood T3, FT3, TSH, T4, TBH, and NSE should be included into neurochemical monitoring in SBI as prognostically significant criteria. They also may serve as a basis for timely correction of thyroid metabolism.

[Mechanism of glucose tolerance disorders in tumors located in the sellar-diencephalic area]. / Mekhanizmy narusheniia tolerantnosti k gliukoze pri opukholiakh selliarno-dientsefal'noi lokalizatsii.

Clinical and biochemical examination carried out in 20 patients with tumors of the sellar-diencephalic area and 10 healthy persons revealed a dependence between functional disorders of the thalamus and hypophysis and the pancreatic beta-cells, which was attended by the development of obesity in patients with large endosuprasellar tumors of the hypophysis and diminution of glucose tolerance in all patients. Hyperinsulinemia revealed during intravenous glucose tolerance test and reduced glucose tolerance are evidence of relative insular insufficiency and substantiate pathogenetically the inclusion of insulin in the complex of intensive therapy applied in the early postoperative treatment of patients with tumors located in the sellar-diencephalic area.

[Regulation of carbohydrate metabolism in patients with tumors of the sellar-diencephalic area before and after surgery]. / Reguliatsiia uglevodnogo obmena u bol'nykh s opukholiami selliarno-diéntsefal'noi lokalizatsii do i posle operatsii.

Clinical and biochemical examination conducted in 40 patients with tumors of the sellar-diencephalic region before and after operation and in 8 healthy individuals revealed in the patients disorders of the function of the hypothalamus and alpha- and beta-cells of the pancreas in the presence of neurological and endocrine disorders. Radioimmunologic determination of insulin and glucagon in the blood disclosed activation of alpha- and beta-cells of the islets of Langerhans in patients with normal blood glucose content before surgery and inadequacy of the reaction of the pancreatic alpha- and beta-cells to the operation stress in patients with diminished or increased concentration of glucose in blood before surgery. Dysfunction of the hypothalamus and endocrine cells of the pancreas in tumors of the sellar-diencephalic region gives grounds for applying postoperative corrective therapy including preparations of insulin and glucagon in patients with progressive signs of a brain lesion.

[Endocrine function of the pancreas in tumors of the chiasmal-sellar region]. / Sostoianie endokrinnoi funktsii podzheludochnoi zhelezy pri opukholiakh khiazmal'no-selliarnoi oblasti.

A clinicobiochemical study of 10 patients with tumors of the chiasmal sellar region and 8 healthy persons using the i. v. glucose tolerance test (IGTT) made it possible to reveal disorder of pancreatic alpha- and beta-cell function in the patients with tumors. A distinct picture of the chiasmal sellar process with the involved hypothalamus was clinically determined in all the patients. Radioimmunoassay of immunoreactive insulin, glucagon, C-peptide and glucose revealed fasting hyperinsulinemia in the presence of both hypo- and hyperglycemia. The latter was accompanied by a raised level of glucagon in the blood. The IGTT revealed in the patients with tumors of the chiasmal sellar region hyperreactivity of beta-cells and a decrease in the sensitivity of alpha-cells to glucose as well as glucose tolerance that may be both regarded as pathogenetic factors of the development of a prediabetic condition in such patients.

[Elastase activity in experimental pancreatitis]. / Aktivnost' élastazy pri éksperimental'nom pankreatite.

The activity of elastase, elastase inhibitor and isozymes of lactate dehydrogenase (LDH) was studied in 11 dogs with experimental pancreatitis and 5 control dogs. All dogs with experimental pancreatitis died 6--14 hours after the induction of pancreatitis. Morbid anatomy studies proved severe pancreonecrosis. The results obtained show that after the induction of pancreatitis the elastase blood activity increased 3-fold as compared with the initial level, and remained unchanged up to the animals' death. At the same time the activity of elastase inhibitor fell, correlating with the rise in elastase activity. Also there was a disproportion between LDH 1 and LDH 2 which became more conspicuous to the 3d hour, and an increase in LDH 5 by the end of the experiment. A conclusion is made that dysfunction of the liver may be one of the causes of the decreased inhibitory activity of elastase in pancreonecrosis.