Approximately one third of people with diabetes are diagnosed with diabetic polyneuropathy. [1] The frequency of detected cases during clinical examination is 20%, and during ENMG it reaches 80%. Asymptomatic course occurs in 50% of patients. [7] Pain, paresthesia, numbness and ulceration of the feet significantly reduce the quality of life of patients. The vulnerability of the nervous tissue and its inability to limit the supply of glucose under the influence of hyperglycemia in the absence of therapy leads to the progression of the disease and the deterioration of the function of various parts of the nervous system, metabolic and vascular disorders.
The risk of developing DPN increases with the age of patients, in the presence of hypertension, with a history of hypoglycemic coma. There is a dependence with indicators of glycosylated hemoglobin, cholesterol, LDL and HDL, triglycerides. There are studies on the influence of genetic risk factors, and the role of inflammatory cytokines in the development of the disease is being actively studied. [2]
First, the distal parts of the lower extremities are involved in the pathological process, and then shorter nerve fibers are also affected. Sensitivity decreases or is lost, tendon reflexes weaken, the speed of propagation of excitation slows down. The muscles of the foot, interosseous muscles atrophy, deformation of the fingers occurs. The process is accompanied by neuropathic pain.
Lack of early diagnosis and treatment of complications of diabetes leads to the development of diabetic foot and limb amputations, more than 50% of which could be prevented. [8]
In recent years, three priorities have been identified in the treatment of diabetic polyneuropathy:
- lifestyle correction, lipid profile control, glycemia reduction and normalization of glycated hemoglobin levels; [3]
- pathogenetic-oriented therapy;
- symptomatic pain relief: analgesics, antidepressants, opioids, and anticonvulsants that relieve symptoms but are limited by CNS side effects . [1]
Today, enough evidence has been accumulated of the positive effect of B vitamins on the progression of complications of diabetes. A review of 43 studies at once shows that B vitamins should be considered as a therapy for diabetic polyneuropathy and an agent that affects the development of the disease. [4]
It has been shown that vitamin B12 deficiency worsens the prognosis, and its administration can change neuropathic symptoms, improving the quality of life of patients. [5]
B vitamins have a number of neurotropic functions, improve the regeneration of nervous tissue and have an analgesic effect.
Thiamine (B1) is involved in the regeneration of damaged nerve tissues, and its deficiency accompanies the pathogenesis of the disease. Transketolase activity decreases during hyperglycemia, which causes the accumulation of intermediate products of glucose metabolism. Taking thiamine interferes with this process. [7]
Pyridoxine (B6) is involved in the synthesis of transport proteins of the nervous tissue, affects its structure and functions. And cyanocobalamin (B12) forms the components of cell membranes, promotes the restoration of the myelin sheath, accelerates the regeneration of nervous tissue, reduces pain, exerting an antinociceptive effect on the endings of pain receptors.
The effectiveness of B vitamins has been proven in the treatment of DPN in animal studies and in a number of human studies and continues to be discussed. One of them showed a significant reduction in pain when taking a fat-soluble form of thiamine. However, there was no improvement in vibration sensitivity, which the authors attribute to a short course of treatment that lasted three weeks. [7]
It is noted that the functions of vitamin B1, B6 and B12 mutually potentiate each other's effects. What makes it expedient to prescribe Neuromultivit to patients with diabetic polyneuropathy as part of complex therapy. The convenience of its use is due to the oral intake of several B vitamins at once, and not separate tablet forms. [8]
There is evidence that oral administration of this drug in patients with DPN is more effective than the standard parenteral regimen. [6]
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