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POLYNEUROPATHY: MODERN ASPECTS OF METABOLIC THERAPY
Kodirova Nargizakhon Umarovna
Assistant of the Department of Propadeutics of internal diseases of Bukhara
State Medical Institute named after Abu Ali ibn Sina
https://doi.org/10.5281/zenodo.15104446
Annotation
The article presents a review of the literature on the problem of therapy of
metabolic polyneuropathy in patients with diabetes mellitus type 2 (DM2) and
chronic alcohol intoxication. The most common variant of diabetic neuropathy
(30-50% of patients with DM) is diabetic polyneuropathy (DPN), manifested by
severe pain syndrome. The development of symmetrical distal sensory
polyneuropathy (SDSP) in patients with DM2, which is characterized by intense
pain neuropathic syndrome, occurs in 20-30%, and the frequency of its
representation increases as the disease progresses. Vitamins B1, B6, B12 have a
neurotropic effect, the deficiency of each of which leads to the formation of
polyneuropathy. The appointment of a combination of thiamine, pyridoxine,
cyanocobalamin well relieves pain and eliminates sensitivity disorders..
Key words:
polyneuropathy, diabetes mellitus type 2, B vitamins,
Neuromultivit.
Peripheral nerve lesions that occur against the background of primary and
secondary metabolic disorders (diabetes mellitus, chronic alcohol intoxication,
deficiency of B vitamins, etc.) are referred to as metabolic polyneuropathies. The
most common cause of their development is type 2 diabetes, which has acquired
the character of an “epidemic of the 21st century” [1]. The most common (30–
50% of patients with diabetes) variant of diabetic neuropathy is diabetic
polyneuropathy (DPN) [2], a severe complication of type 2 diabetes, which is not
always diagnosed in a timely manner, characterized by severe pain symptoms, a
number of severe clinical disorders, early disability and a significant
deterioration in the quality of life of patients [3]. Population studies have shown
that varying degrees of peripheral nerve lesions are detected in almost half (15
90%) of patients with diabetes [4, 5]. The frequency and severity of
complications detected increases with the duration of the disease and the
severity of metabolic disorders. In 5–10% of cases, patients with newly
diagnosed type 2 diabetes already have signs of peripheral nerve damage.
According to modern concepts, blockade plays a leading role in the formation of
the pathological process in nerve fibers, endothelium and vascular wall in DPN
hexosamine pathway of glucose utilization with accumulation of intermediate
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products of glucose metabolism, in particular glucose-6 phosphate and
glyceraldehyde-3-phosphate. Increased concentration of intermediate products
of metabolism triggers activation of protein kinase-C and formation of large
amount of AGEs (Advanced Glycation end products), which leads to disruption
of endothelium-dependent reactions and functions of nerve cell structures.
Blockade of glucose metabolism is caused by activation of special polymerases,
which occurs in response to destruction of mitochondrial DNA by superoxide.
Oxidative stress, which is caused by formation of large amount of free radicals
against the background of weakness of own antioxidant system (reduced
content of antioxidant enzymes), is responsible for disruption of glucose
metabolism in cytoplasm of cells. It is assumed that the correlation between the
number of nerve fibers in the peripheral nerve and the wall thickness of the
endoneural vessels is fundamental for the development of DPN in diabetes
mellitus [2]. The toxic effect caused by the metabolic disorder has a direct effect
on the nervous tissue. An additional aggravating factor in the suffering of
peripheral nerves in diabetes mellitus is the damage to small vessels that
provide blood supply to the nerve trunks. A common clinical syndrome of
peripheral nervous system damage in diabetes and other somatic diseases is
symmetrical distal sensory polyneuropathy (SDSP), which is characterized by
predominant damage to the nerves of the lower extremities. With SDSP, an
intense neuropathic pain syndrome is observed, which is associated with a high
risk of developing diabetic foot. Neuropathic pain syndrome is manifested by
hyperpathy - intense pain that persists after stimulation is stopped,
hyperalgesia, and allodynia [6]. Neuropathic pain syndrome of varying severity
occurs in 20-30% of patients 38 medical advice with SDSP, the frequency of its
presence correlates with the severity of the disease [7].
Population studies have shown that varying degrees of peripheral nerve
damage are found in 15–90% of patients. with diabetes. The frequency and
PERIPHERAL DISEASES NS severity of complications increases with the duration
of the disease and the severity of metabolic disorders, in 5-10% of cases in
patients with newly diagnosed type 2 diabetes there are already signs of
peripheral nerve damage
.
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