ABSTRACT
The expression of melatonin in nasal polyps versus the histological structure of tissue was studied in 11 patients with aspirin-induced asthma (AIA), 8 patients with asthma without aspirin intolerance, 13 patients with polypous rhinosinusopathy (PR) without bronchopulmonary diseases, and 10 apparently healthy individuals without nasal polyposis. The expression of melatonin in the nasal mucosa was found to be normal in healthy individuals. It significantly increased in polyp tissue in PR. The specific feature of polyp tissue in patients with aspirin triad was its high eosinophils levels that correlated with the increased area of melatonin expression. Thus, in AIA patients, the role of eosinophils increases in the production and/or delivery of the hormone into polyp tissue along with a drastic reduction in platelet melatonin generation. The findings explain persistent recurrent PR in AIA patients and an exacerbation of the disease after polyp removal.
Subject(s)
Asthma/metabolism , Drug Hypersensitivity/metabolism , Melatonin/biosynthesis , Nasal Polyps/metabolism , Adult , Aged , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Aspirin/adverse effects , Asthma/chemically induced , Asthma/complications , Asthma/pathology , Asthma/therapy , Blood Platelets/metabolism , Blood Platelets/pathology , Drug Hypersensitivity/complications , Drug Hypersensitivity/pathology , Drug Hypersensitivity/therapy , Eosinophils/metabolism , Eosinophils/pathology , Female , Humans , Male , Middle Aged , Nasal Mucosa/metabolism , Nasal Mucosa/pathology , Nasal Polyps/complications , Nasal Polyps/pathology , Nasal Polyps/therapy , RecurrenceABSTRACT
The aim of the investigation was to study melatonin production in thrombocytes and their functional activity in correlation with 6-sulfatoximelatonin (6-SOM) urinary excretion in patients with aspirin-induced bronchial asthma (AIBA). Forty-three patients with bronchial asthma (BA) were examined. The main group consisted of 26 AIBA patients; the comparison group consisted of 17 BA patients with no intolerance to aspirin or other non-steroidal anti-inflammatory drugs; 30 practically healthy individuals constituted the control group. The study found no melatonin production in thrombocytes of AIBA patients: only 13.0 +/- 1.3% of platelets expressed melatonin, while in healthy people 97.7 +/- 0.6% of the cells did. Besides, daytime urinary excretion of 6-SOM, the main melatonin metabolite, was lower in AIBA patients. Lower daytime and higher nighttime melatonin production in AIBA patients correlated with the acceleration of the 1st phase and increased intensity of thrombocyte aggregation, which evidences high thrombocyte reactivity to the inducing agent. The presence of a pathologic reaction of thrombocytes to exogenous melatonin, manifesting by changes in the 1st stage of aggregation, suggests the presence of pathology in thrombocyte membrane-receptor complex and the calcium homeostasis of the cell, which determines constant activation and the participation of thrombocytes in the development of asthmatic syndrome.
Subject(s)
Aspirin/adverse effects , Asthma/blood , Asthma/chemically induced , Blood Platelets/drug effects , Blood Platelets/metabolism , Melatonin/biosynthesis , Melatonin/metabolism , Platelet Aggregation Inhibitors/adverse effects , Adult , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Circadian Rhythm , Female , Humans , Male , Melatonin/analogs & derivatives , Melatonin/urine , Middle AgedABSTRACT
Peculiar ultrastructural features allowed the authors to reveal M. Homminis corpuscles in placental tissues of women with genital mycoplasmosis. Mycoplasma was found in the amniotic epithelium, chorionic plate, in the lumen of villous capillaries, this showing possible hematogenic way of the infection from mother to fetus. In the placenta of women with genital mycoplasmosis immunopathological processes develop in association with formation of pathogenic immune complexes (PIC) that are fixing the C3 complement fraction. Location of PIC on the syncytiotrophoblast membranes and vascular endothelium causes immunological inflammation with the involvement of immunocompetent cells resulting in the destruction of syncytial membranes and membranes of the placental barrier. Damage to the placental barrier membranes promotes the development of placental failure, a complicated course of pregnancy and delivery, deterioration of the state of the fetus and newborn infant.
Subject(s)
Genital Diseases, Female/pathology , Maternal-Fetal Exchange/physiology , Mycoplasma Infections/pathology , Placenta Diseases/pathology , Adult , Antigen-Antibody Reactions , Complement C3/immunology , Female , Genital Diseases, Female/immunology , Genital Diseases, Female/microbiology , Humans , Microscopy, Electron , Mycoplasma Infections/immunology , Mycoplasma hominis/isolation & purification , Placenta Diseases/immunology , Placenta Diseases/microbiology , PregnancyABSTRACT
96 placentas from mothers with genital mycoplasmosis diagnosed during the pregnancy (main group), and without mycoplasmosis (group for comparison) were studied. Histological study was performed in parallel with electron microscopy of the amnion and use of fluorescent antibodies. Progression of the involutive-degenerative changes in the placenta with the development of lipophanerosis and destruction of the extra-placental amnion epithelium were observed in the main group in parallel with the increase of the immunoglobulins studied (A, M, G), fibrinogen, C3-component of the complement with fixation of pathogenic immune complexes (IC). IC are observed in the placenta of 51 +/- 6.35% and in the extra-placental coats in 100% of mothers with mycoplasmosis versus 9 +/- 4.91% and 40%, respectively, in the comparison group. The presence of IC in the placenta and extra-placental coats correlates with the neurological symptoms in newborns and the increase of infectious-allergic diseases in children of the 1st year of life.
