Background. The acid-alkaline state (AAS) in physiological conditions is caused by a certain ratio of acids and alkalis in blood plasma as well as in organs and tissues. Imbalances of the above ratio are observed in patients with asthma (As). Objective. To study AAS in patients with an uncontrolled course of As. Materials and methods. The study involved 27 patients having a moderately severe course of As with metabolic acidosis and without any controls. Physical examinations were made; respiratory function and AAS were assessed. The patients were divided into two groups: 13 cases – group 1 and 14 cases – group 2. Their basic treatment included budesonide / formoterol fumarate dehydrate 160/4.5 µg, with use of control questionnaires for As (ACQ-5) and life quality (SF-36). Additionally to their therapy patients from group 1 received 250 ml of 4.2 % sodium bicarbonate intravenously by drop infusions thrice daily every other day. Results and discussion. All the patients had a reduced control over As from 3.5 to 5 points (4 [3.5; 4.5] in group 1 and 4.5 [4; 5] in group 2). According to spirography data, the level of rate values before treatment in cases from group 1 was as follows: forced expiratory volume in 1 sec (FEV1) = 54.00 % [47.00; 59.00], peak expiratory flow (PEF) 25 % = 52.00 % [49.00; 57.00], PEF 50 % = 51.40 % [41.00; 57.00], PEF 75 % = 50.00 % [43.00; 57.10]. In patients from group 2 their level of rate values before treatment was as follows: FEV1 = 57.00 % [52.00; 61.00], PEF 25 % = 56.10 % [52.00; 59.70], PEF 50 % = 54.40 % [47.00; 59.00], PEF 75 % = 54.00 % [47.30; 60.10]. AAS values in cases from group 1 were: рН = 7.32±0.05, РСО2 = 33.8±1.34 mm Hg, ВЕ = -4,8±0,01 mmol/l; in patients from group 2 these were: рН = 7.31±0.04, РСО2 = 32.3±1.13 mm Hg, ВЕ = -4.25±0.01 mmol/l. After the treatment, the following changes were registered: respiratory function indices improved in both groups, but reliable changes versus pre-treatment results were revealed in 1st group – FEV1, PEF 25 % and PEF 75 % (p<0.05), while in 2nd group it was only in PEF 25 %. Both groups demonstrated positive changes of all AAS indices, but reliable changes in all examined indices were found out in patients from group 1 (р<0,05), whose treatment effectiveness was assessed as good in 8 cases and satisfactory in 4. In patients from group 2 the result of treatment was satisfactory in 9 cases, whereas in 5 patients it was unsatisfactory. Conclusions. Inclusion of sodium bicarbonate into combination therapy for patients with As is not accompanied with development of any adverse events and is recommended for using in combination therapy for exacerbations of As, particularly if metabolic acidosis develops.

The aim: Revealing of clinical-pathogenetic peculiarities in manifestations of uncontrolled As+MS. Materials and methods: Sixty-five cases, divided into 2 groups: Group I – severe As (n=20), Group 2 – severe As+MS (n=45). The general clinical examination included fasting blood glucose, insulin level, HOMA-IR index, body mass index (BMI), spirometry, levels of ММР-9, МСР-1, IL-8 and IL-12. Results: In Group I, 20 patients (100%) had obstructive respiratory dysfunction. Group II had 13 cases (28.88%) with the restrictive, 15 (33.33%) with the obstructive and 17 (37.77%) with the mixed types. BMI revealed: Group I had the normal mass (BMI averaged 24.62 [22.76; 25.71]; Group II had 21 overweighed cases (46.66%) and 24 (53.33%) with grade 1 obesity, averaging 29.70 [28.35; 31.23]. Correlation analysis in Group II showed significant correlations between: age and WHR (r=0.52, p<0.001) (increase of abdominal fat depots during life), FEV1 and BMI (r=-0.63, р<0.001) (obesity affects pulmonary function). IL-8 and IL-12 levels in Group II were increased, respectively, by 27.86 and 13.18 times versus Group I. A relationship was found between MCP-1 and MMP-9 (r=0.77, р<0.05), Group II revealed direct correlation between MCP-1 and total FEV1 (r=0.53, р<0.05). Conclusions: Overweight and obesity in As+MS deteriorate respiratory function versus the same indices in isolated As. Relationships between proinflammatory cytokines and MMP-9 and MCP-1 prove pathogenetic peculiarities of systemic inflammation and metabolic homeostasis. As and MS can cause their coexistence, facilitating development of mutual aggravation.