PATHOMORPHOLOGICAL CHANGES OF THE SKELETAL MUSCLES UNDER FORMATION OF THE REPERFUSION SYNDROME.

Analysis of pathomorphological changes which taking place in muscle tissue after reperfusion of previously ischemic rats limbs allowed to identify three phases of the experimental reperfusion syndrome (RS): the first or ischemic, the second or initial reperfusional, the third or late reperfusional. Morphological changes of the skeletal muscles in the first stage are characterized by presence of dystrophic-necrotic processes and reflect the compensatory-adaptive reaction of the organism to hypoxia. In the third stage one can see the progress of morphological damages, which develop during the ischemic period against a background of exhaustion of proteinase inhibitors. This indicates the intensity of endogenous intoxication of the organism with the products of disturbed metabolism and determines the irreversibility of destructive processes and probability of multiple organ failure. Proceeding from the character of the pathomorphological changes and the state of proteinase-inhibitor system one can suppose, that the optimal time for medical measures is the first stage and the first hours of the second stage (to increase the ischemic tolerance of the skeletal muscles). Taking into account the direct relation between the intensity of pathomorphological injuries and the imbalance of proteinase-inhibitor system, the usage of proteinase-inhibiting medicines for correction of RS-development and reduction of the destructive changes during first and second stages is substantiated. When reperfusion syndrome lasts for a long time, medical measures become ineffective due to the high degree of pathological changes.

Endometrial hyperplasia-related inflammation: its role in the development and progression of endometrial hyperplasia.

BACKGROUND: Endometrial hyperplasia (EH) is one of the most common gynecologic diseases in the world. Different statistical categories implicate an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a key role in the progression of endometrial hyperplasia. OBJECTIVE: The aim of this study is to evaluate the role of inflammation in the transformation and progression of endometrial hyperplasia, using local inflammatory cytokines and nonspecific protease levels, CD 45(+) expression, and histological examination. DESIGN: The study included 107 patients (ages 29-49 years) with different forms of endometrial hyperplasia. The enrolled patients were randomized into one of the four groups: normal endometrium (n = 18) as the control group, simple hyperplasia (n = 41), complex hyperplasia without atypia (n = 36), complex atypical hyperplasia or endometrioid adenocarcinoma (n = 12). METHODS: The following were evaluated for patients with different forms of EH: steroid hormone levels in blood serum and uterine flushings, immunohistochemical estrogen and progesterone receptor expression patterns in the endometrial tissue, CD 45(+) (common leukocyte antigen) expression, the levels of the cytokines IL-1ß, IL-6, and TNF-α, and nonspecific proteases and their inhibitors. RESULTS: The level of estradiol in blood serum and especially in uterine flushings was elevated dramatically in simple EH as compared to that of controls, but there was no significant difference between estradiol levels among the different forms of EH. The estimation of CD 45(+), the levels of the cytokines IL-1ß, IL-6, and TNF-α, and the activity of proteases (elastase-like and trypsin-like activities) and their inhibitors showed that levels of nonspecific inflammatory markers increase with EH progression. CONCLUSIONS: We suggest that the initial responsibility for the development of simple endometrial hyperplasia belongs to systemic hyperestrogenemia and, in particular, local hyperestrogenia, but that the role of inflammatory processes increases in complex and atypical EH. Development of inflammatory changes in endometrial hyperplasia may be considered as a factor in the promotion and progression of pathology, as well as an attributed risk factor for malignancy in endometrial hyperplasia. In this study, we have established a role for CD 45(+) expression cells, non-specific proteases, and the inflammatory cytokines IL-1ß, IL-6, and TNF-α in endometrial hyperplasia-related inflammation.