Lobunets' O. Role of cytokines and endothelial dysfunction in mechanisms of gastroesophageal refux disease formation with accompanying neurocirculatory dystony and their correction.

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number

0412U005797

Applicant for

Specialization

  • 14.01.02 - Внутрішні хвороби

21-09-2012

Specialized Academic Board

Д 64.600.04

Essay

The thesis is devoted to the efficiency of diagnosis and treatment of gastroesophageal reflux disease associated with NDC in young adults, based on the study of pathogenic role of the cytokine system, endothelial function in conjunction with the degree of reduction of QoL and clinical manifestations of the basic features, and comorbidity. Еxamined 105 patients with GERD, of which 62 patients with concomitant GERD NDC and 43 GERD patients without comorbidity and 20 healthy students, constituting a control group. A statistically significant decrease of ET-1, the contents of metabolites of NO, blood flow velocity in the celiac trunk and the size of its diameter while increasing the levels of cytokines - IL-1? and TNF-? in patients in both groups with significantly more profound shift in patients with concomitant GERD NDC. GERD patients with concomitant hypertension type NDC of these disorders with greater degree of certainty related to an enhanced level of ET-1, IL-1? and TNF-?, and in patients with concomitant GERD NDC to hypotonic type they are manifested in the reduction of NO, blood flow velocity in the celiac trunk and the size of its diameter, the higher the content of IL-1? and TNF-?. In parallel, we found that the depth and nature of violations are in direct correlation with the level of reduction of QoL, as manifested to a greater degree of GERD patients with concomitant NDC. It is proved that the additional inclusion of dalargin in the standard treatment regimen of patients with concomitant GERD as the NDC and without comorbidity faster onset of clinical remission, contributes to a more complete correction of violations in the spectrum of endothelial function, cytokine system.

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