Clinical case of demyelynating polyneuropathy of patient with autoimmune polyendocrine syndrome

Abstract

Background. The function of a nervous system (NS) has a strong correlation with a somatic state of each individual. Therefore, somatoneurology as a new branch of medicine appeared. Nowadays due to pathophysiological researches we possess the knowledge of mechanisms on NS damage at the background of diseases of endocrine, cardiovascular, digestive, respiratory and other systems. Nevertheless, practically all these processes are difficult to be separated in each case of illness because of the complexity of their simultaneous interaction and polymorphism of clinical symptoms. Autoimmune diseases are worth special attention due to their chameleon-like way of progressing when different organ systems get involved with new exacerbations. Moreover, the pathogenesis of NS damage at the background of autoimmunisation is not only connected with the response of nervous tissue on inflammation and demyelination, but it’s also a result of multiorgan disfunction – a consequence of their autoimmune disruption. According to the mentioned fact the clinical case of autoimmune polyendocrine syndrome described in this article is very representative because of the presence of combination of immune system dysfunction (what is a potential trigger of demyelination) and the impact of glucose toxicity phenomenon on NS (a symptom of diabetes mellitus caused by autoimmune pancreatitis). To sum up with, studying somatoneurological features of autoimmune diseases is a relevant topic for practitioners at the «century of autoimmune diseases». Purpose – to describe the clinical case of polyneuropathy at the background of autoimmune polyendocrine syndrome. Materials and Methods. The results of objective examination and data of instrumental and laboratory tests protocols made at «Kharkiv Regional Clinical Hospital» were used. Results. Polyneuropathic type of nervous system damage was verified due to electroneuromyographic examination and the scale «Neuropathy Impairment Score of Lower Limbs» (NIS-LL). The efficiency of combined therapy with «Nerviplex», «Dialipon» and «Gabapentin» was demonstrated in this case. Conclusions. Autoimmune diseases can lead to nervous tissue damage due to different pathophysiological mechanisms, including the direct impact on it with the processes of inflammation and demyelination but also as a secondary consequence of multiorgan dysfunction at the background of immune autoagression.