The dissertation is devoted to the study of the clinical-pathogenetic
relationship between the gut microbiota and non-alcoholic fatty liver disease
(NAFLD) in patients with type 2 diabetes mellitus (T2DM); as well as assessing the
impact of correction of changes in the gut microbiota on the course of these diseases.
The relevance of the chosen area is due to the fact that the number of patients
with type 2 diabetes has increased significantly in recent decades and this trend
continues to grow rapidly. About 80% of patients with type 2 diabetes are
overweight or obese. Non-alcoholic fatty liver disease is the most common noninfectious liver disease in the world. Recent studies indicate that various disorders
of the intestinal microbiota, including intestinal dysbiosis and bacterial overgrowth
syndrome (SIBO) can play a significant role in the development and progression of
NAFLD. It has been shown that changes in the intestinal microbiota can also lead to
the development of obesity, and subsequently to the formation of type 2 diabetes.
The influence of changes in the large and small intestinal microbiota on the
development of nonalcoholic fatty liver disease in patients with type 2 diabetes
remains unclear.
The aim of the work was to improve the efficiency of diagnosis and treatment
of patients with non-alcoholic fatty liver disease in type 2 diabetes mellitus in
combination with disturbances of the gut microbiota by using various methods of
correction of the gut microbiota in these diseases.
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A prospective, cohort, comparative, randomized study was conducted, which
included 122 patients (70 men and 52 women) aged 19 to 75 years. The main group
included 61 patients aged (47,1 ± 3,3) years with a combination of NAFLD and
T2DM; to the first comparison group – 31 patients aged (44,4 ± 3,9) years with
NAFLD without diabetes; to the second comparison group – 30 patients aged
(52,2 ± 4,1) years with T2DM without fatty liver disease. The control group
consisted of 30 practically healthy individuals aged (46,3 ± 3,5) years, in whom
NAFLD and T2DM were excluded.
Research results.
In the clinical study of patients with NAFLD and T2DM, there were no
patients with normal body weight in the main and both comparison groups. In all
three groups of patients, body mass index (BMI) was significantly higher than in the
control group (p < 0.001). The frequency of obesity detection ranged from ranged
from 93,5% of the NAFLD group to 83,3% of the T2DM group, in all groups, grade
1 obesity prevailed, which was abdominal in nature (the Waist-Hip Ratio (WHR)
varied from 1,2 to 1,45) and in all groups of patients was significantly higher than
in the control group (p < 0.001). In patients with type 2 diabetes mellitus who had
NAFLD, a longer course of T2DM was determined; with a duration of T2DM over
10 years, NAFLD was almost 2,5 times more frequent than in patients with less than
3 years of illness. The majority of patients in the NAFLD group with T2DM had
subcompensated diabetes mellitus – 25 (41,0%), while among patients with isolated
diabetes mellitus, the majority were at the stage of diabetes compensation –
16 (53,3%) (p = 0,05).
In 33 (54,1%) patients with NAFLD and T2DM, macrovascular lesions
(coronary artery disease (CAD), cerebral atherosclerosis(СА) and peripheral arterial
disease of the lower extremities) were diagnosed, which in 27 (44,2%) were
combined with hypertension. In patients with isolated NAFLD, the incidence
of hypertension was 51,6%.
In the study of the clinical symptoms of NAFLD, both with and without
diabetes, the most commonly observed nonspecific symptoms were heaviness in the
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right hypochondrium, epigastric discomfort, and unstable stools. When comparing
the group of patients with NAFLD and diabetes with the group of patients with
NAFLD, we found no significant differences in clinical symptoms (p > 0,05). At the
same time, comparing with the second group of patients with isolated T2DM, we
found significantly more frequent detection of heaviness in the right hypochondrium
(p = 0,002) and liver enlargement on palpation (p < 0,001).
