Терапевтический архив (Feb 2018)
Comorbid for gastroduodenal ulcers in the aspect of calcium imbalance and blockers of slow calcium channels in their treatment
Abstract
Improvement of methods of prevention and treatment led to an increase in the number of patients with comorbid occurring chronic disease that requires effective integrated therapy to reduce the polypharmacy. Aim. Find out the calcium content of the blood reflecting its balance and functional status the calcium regulatory system when it is comorbid for gastroduodenal ulcers (GDU), developed on the background of chronic erosive gastritis (CEG), chronic erosive duodenitis (CED), arterial hypertension (AH) and osteo-articular pathology with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), and the impact of his changes on the activity ulzerogennogo process, the state of regional microcirculation and the functions of the stomach. To determine the pathogenetic justification for and effectiveness of blockers of slow calcium channels (BSCaC) in complex treatment. Materials and methods. Examined 132 patients with GDU. All patients were divided into groups: the 1st (n=49) - patients with recurrent of peptic ulcer disease (PUD) and CEG/CED; the 2nd (n=23) - with recurrence of PUD and AH, the 3rd (n=14) - with GDU and osteoarticular pathology, taking NSAIDs. Patients of these three groups for the treatment of erosive ulcerous lesions of gastroduodenal zone (GDZ) has been appointed complex therapy with inclusion of nifedipine. The 4th (control) group consisted of 56 patients with recurrent BU without concomitant pathology, applying integrated therapy with nifedipine. The results and discussion. The PU relapse, comorbid her over with erosive gastroduodenitis, hypertension, GDU with of osteoarticular pathology and taking NSAIDs is accompanied by a calcium imbalance with increased levels of calcium in the blood, contributing to increase of acid-peptic factor in the formation of hypermotor dyskinesia stomach, disruption of regional microcirculation and repair processes, activation of ulcerogenesis in GDZ. Inclusion in the complex therapy of GDU of nifedipine leads to the recovery of calcium balance, functions of the stomach and regional microcirculation, accelerates the timing and increases the percentage of scarring ulcers. Conclusion. GDU accompanied by dysfunction the calcium regulatory system with increasing levels of blood calcium, contributing to the formation of the major pathogenetic mechanisms of ulcerogenesis. BSCaC application in complex therapy of GDU is pathogenetically justified and clinically effective, reduces the excessive drug treatment in the treatment.
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