Low back pain: justification of treatment standards (literature review)
Authors: Byelyavsky S.K. , Borysov B.M. , Svyrydova N.K. , Trinus K.F. , Shipilo L.M. 
Published: May 2024

The American Association of Neurological Surgeons reported that approximately 75–85 % of Americans experience low back pain (LBP) during their lifetime. There is considerable heterogeneity among epidemiologic studies of LBP, which limits the ability to compare and generalize the data. One-year incidence of the first episode of LBP ranges from 6.3 to 15.4 %, while 1-year incidence of any episode of low back pain is from 1.5 to 36 %. In hospital-based studies, episode remission after one year ranges from 54 to 90 %. Experts from Europe, Australia and Latin America identified 15 clinical practice guidelines for the treatment of low back pain in primary care settings. The authors pay attention to the fact that the data on the use of nonsteroidal anti-inflammatory drugs (NSAIDs) in the mentioned guidelines are contradictory. Enzymatic oxidation of arachidonic acid has been shown to lead to the formation of potent pathological agents by two main pathways. Those in the prostaglandin (PG) pathway, particularly PGE2, have been considered inflammatory mediators for many years. The discovery of the biological activity of thromboxane A2 and prostacyclin, as well as the destructive oxygen-centered radical as additional products of this biosynthetic pathway now require their consideration as potential inflammatory mediators. Like PGE2, their biosynthesis is inhibited by nonsteroidal anti-inflammatory drugs. There is also an alternative lipoxygenase pathway that yields arachidonic acid oxygenation products called leukotrienes and eicosanoids, which have also been shown to be important inflammatory mediators resistant to NSAIDs. It was shown that dexamethasone suppresses the release of arachidonate from human epithelial cells by inducing the synthesis of the p11 protein and inhibiting the activity of phospholipase A2, that is, it affects the pathological mechanisms of inflammation that are lacking in NSAIDs, namely, it blocks the release of arachidonic acid salts. Dexamethasone has been shown to affect both exudative and proliferative phases of inflammation. Inflammatory mediators block active sulfhydryl groups of proteins, enzymes, receptors, and ion channels. The positive role of donors of such groups in the treatment of LBP is shown in the literature. In the treatment of allodynia, bisphosphonates, which normalize calcium metabolism and reduce calcification of cartilage and ligaments, have proven themselves to be the best: they cause a decrease in the intensity of pain and swelling and improve nerve function. Racetams have been shown to be useful for the treatment of not only neuropathic pain, but also cognitive impairment. Racetams are especially active in combination with choline donors. Peripheral neuropathy (PN) is a common disease with an incidence of approximately 8 % in the elderly. Neuropathic pain has a high prevalence in the general population and affects more than half of all patients with PN. The pathophysiology of PN is characterized by damage to myelin-producing Schwann cells in peripheral nerves. Regeneration/protection of the myelin sheath after nerve injury is a fundamental element of recovery in PN. Nucleotides such as uridine monophosphate have been shown to be effective in treating the cause of myelin damage in several experimental and clinical models. B vitamins such as В12, В6, В3, В1 are essential for nerve health. These vitamins can aid in the healing of damaged nerves and relieve symptoms of nerve damage like numbness and tingling, that is why they are called neurotropic vitamins. In confirmation of the clinical value of these arguments, a clinical case is presented, when the patient was managed with a combination of the discussed drugs and felt significantly better.