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Data are submitted on the time course of immunologic indices in 50 patients with myocardial infarction (MI) presenting with complication-free course, and 58 patients with MI complicated by thromboendocarditis. Important changes were revealed in the immune status--both cellular and humoral--during the development of thrombosis of the left ventricle secondary to MI. The cellular immunity was characterized by a decline in the levels of T-lymphocytes, particularly those of T-suppressors, augmentation of B-lymphocytes. Thrombosis evolving in MI was associated with changes in humoral immunity, such as persistent and lasting rise in immunoglobulins of all classes, especially Ig G, as well as combinations thereof, together with the increase in the content of circulating immune complexes.

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Using RIA, 188 patients with acute pneumonia were examined over time for the blood ACTH, cortisol, TTH, T3 and T4 content as well as for T4/T3, TTH/T3 and TTH/T4 correlations. Under discussion are causes, approaches to the prevention and correction of the hormonal disorders revealed in the pituitary-adrenal system in patients with an unfavourable course of pneumonia. The majority of the patients manifested thyroid hypofunction and TTH hypersecretion, which remained unchanged even during the clinical recovery, since the first days of the disease. It is advisable that microdoses of thyroidine may be included into the multimodality treatment of patients afflicted with acute pneumonia and iodine-containing expectorants excluded from it.

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Endocrine cells of the duodenal bulb producing adrenalin, noradrenalin, serotonin, histamine and beta-endorphine were assayed in 12 patients with preulcer and 39 patients with duodenal ulcer. It is shown that preulcer was mainly characterized by hyperplasia of endocrine cells in the duodenal bulb mucosa, secreting adrenalin and noradrenalin in the presence of the deficiency of beta-endorphine-producing cells. The recurrent duodenal ulcer was associated with a dramatic fall in the number of catecholamine-containing endocrine cells in the duodenal bulb.

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A study has been carried out to substantiate the assumption that excessive proliferation of major gastroduodenal endocrine cells may be predetermined genetically. Hereditary predisposition to the hyperplasia of cells belonging to the APUD system may be inherited both through the male and female lines. Duodenal ulcers (DU) undoubtedly involves multifactorial inheritance. Acquired capacity for endocrine cell hyperplasia cannot be excluded in some of DU patients. The development of DU is, apparently, related to the formation of a pathological system, based on pathologic structure-linked neurohormonal relationships between the duodenum and peripheral and central nervous systems that enhance nerve impulses in the duodenal bulbar portion. A sudden "total" catecholamine release occurs at a certain stage and is followed by a change of production/utilization ratios of various hormones that weakens pathologic neurohormonal relationships, destroys the pathologic system and activates the healing process around the ulcer. The pathologic system, active in peptic ulcers, is doubtless counteracted by a system, whose activity must be determined by the number of endocrine cells with beta-endorphine-like and, perhaps, serotonin-like immunoreactivity. The antagonistic regulation principle is of great universal significance for general biology. It is essential for healing and chronization processes.

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The activity of the kallikrein-kinin, prostaglandin and cyclase systems was assessed in 117 patients with chronic pyelonephritis with and without arterial hypertension. Pyelonephritis is shown to be associated with a dysfunction of the pressor-depressor mechanisms examined, featuring a depression of vasodepressor reactions. Patients with normal, increased and depressed humoral parameters could be found in each study group, the changes being particularly marked in patients with chronic pyelonephritis, combined with arterial hypertension.

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Comparison of the clinical and laboratory tests with the findings of post-mortem examination of 82 hearts of patients who had died in different periods after the onset of the disease allowed the authors to distinguish three periods in the clinical course of myocardial infarction: necrotic, inflammatory and adaptational. Fever, leukocytosis, the time course of MB CPK activity, and the results of polyelectrode ECG are reliable indicators of the duration of the necrotic period. The content of the protein-carbohydrate complexes in the blood adequately reflect the exudative-proliferative phase, while the content of collagen metabolites in blood and urine reflect the collagenization phase of the inflammatory period. These tests allow the physical activity of each patient to be individualized under objective control over the rate of healing of the myocardial infarct. Most patients become fully adapted to life with a reduced mass of contractile myocardium three months after the onset of the disease.

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Comparative study of the renal and blood kinin system in patients with hypertensive disease and in those with chronic pyelonephritis revealed its different reaction to a similar character of arterial pressure in these patients, which suggests that the kinin system differs in its significance in the pathogenesis of hypertension in these diseases. It is recommended to use the values of the renal and blood kinin system in practice for the differential-diagnostic purpose in the planned stage-by-stage examination of patients with arterial hypertension.

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