Global Journal of Digestive Diseases

Description

Children frequently suffer from nocturnal enuresis, but its pathophysiology is still poorly understood. Nocturnal polyuria, nocturnal bladder dysfunction, and sleep disorders are all recognized as major pathways, but their interrelationships remain elusive. It’s possible that NE is greatly influenced by the autonomic nervous system, which is also involved in sleep and diuresis. Articles reporting on the role of the autonomic nervous system in neurotic children regarding regulation, cardiovascular function, and diuresis-related hormones and neurotransmitters were identified through a comprehensive electronic search of the Medline database. Based on inclusion criteria published between, of an initial total of were ultimately selected for data extraction. Ten of these studies reported on cardiovascular functions, 12 on hormones and neurotransmitters associated with ANS, and one on sleep regulation. Parasympathetic or sympathetic overstimulation in neurotic patients suggests that ANS dysregulation may be the cause of NE. Patients with overactive bladder experience non-rapid eye movement-related neurotic episodes, which could be linked to parasympathetic stimulation, whereas polyuria-neurotic children sleep for longer periods of time with rapid eye movement, pointing to sympathetic over activity. While heart rate analysis revealed parasympathetic hyper function, 24-hour blood pressure monitoring revealed phenomenon that suggested sympathetic involvement. Polyuria children with NE have lower nocturnal levels of arginine-vasopressin than non-polyuria children and controls, and dopamine and serotonin may play a role in sleep and urination, suggesting that ANS-associated hormones and neurotransmitters play a role in the pathogenesis of NE. We propose that a unified model for understanding the pathogenesis of NE in various neurotic subpopulations may be provided by ANS dysregulation linked to either sympathetic or parasympathetic over activity.

Chronic Fatigue Syndrome, and Fibromyalgia

 New treatment options and new insights into future research are provided by this observation. Silicone breast, chronic fatigue syndrome, and fibromyalgia. The hypothesis that various conditions lead to the onset of autonomic nervous system imbalance in autoimmune diseases. Variable triggers or the presence of an autoimmune disease overstimulate the immune system in people with HLA-predisposition, resulting in the production of various anti-GPCR. The following symptoms are brought on by anti-GPCR damage to the organs or altered cell function damage to the central nervous system, such as chronic fatigue syndrome damage to the peripheral nervous system: cardiovascular, gastrointestinal, and glandular dysfunction are all examples of peripheral neuronal system damage damage to the immune system, including vasculitis, arthritis, and myositis. The idea that various conditions cause an autoimmune imbalance in the autonomic nervous systematic-GPCR damage the organs or alter the function of cells, which contributes to the following symptoms: central neuronal system damage - chronic fatigue syndrome; Variable triggers or the presence of an autoimmune disease overstimulate the immune system in people with HLA-predisposition. Damage to the peripheral nervous system, such as problems with the cardiovascular, digestive, and glandular systems, which combine changes in the central and peripheral nervous systems In this review, all published data on an imbalance of autoantibodies against GPCR, clinical symptoms, and pathogenic mechanisms in CFS, fibromyalgia, SBIs, and some autoimmune diseases were analysed. Immune system damage includes vasculitis, arthritis, and myositis. The autoimmune autonomic nervous system imbalance was identified and possible diagnostic criteria were developed. The idea that various conditions lead to an autonomic nervous system imbalance that causes autoimmune disease. Variable triggers or the presence of an autoimmune disease overstimulate the immune system in people with HLA-predisposition, resulting in the production of various anti-GPCR. The following symptoms are brought on by anti-GPCR damage to the organs or altered cell function: damage to the central nervous system, such as chronic fatigue syndrome; damage to the peripheral nervous system, such as problems with the cardiovascular, digestive, and glandular systems, which combine changes in the central and peripheral nervous systems; Damage to the immune system, such as arthritis, myositis, vasculitis, the implants syndrome, the sick building syndrome, and the post-orthostatic tachycardia syndrome, as well as autoimmune diseases and autoimmune inflammatory syndromes caused by adjuvants, frequently come with the clinical symptoms of dysautonomia severe exhaustion, drowsiness, dizziness, memory loss, dry mouth and eyes, hearing loss, tachycardia, and other symptoms Researchers were able to speculate on the novel mechanism underlying these conditions, autoimmune autonomic nervous system imbalance, following the recent discovery of an imbalance of autoantibodies against G protein-coupled receptors in post-COVID syndrome, SBIs, and other autoimmune diseases. Memory loss, severe fatigue, pains, sweating, hair loss, paresthesia, deafness, sight, tachycardia, vertigo, allergy, depression, and autoimmune, inflammatory syndromes induced by adjuvants are common complaints among patients with chronic fatigue syndrome, fibromyalgia, silicone breast implant syndrome, sick building syndrome, and autoimmune diseases.

Autoantibodies to G Protein-Coupled Receptors

In the meantime, neither instrumental nor laboratory analyses reveal any deviations from the normal value. As a result, the patients receive ineffective psychiatric treatment because they are deemed to have psychosomatic conditions. It is evident that some of the clinical symptoms that have been described are similar to those of dysautonomic conditions. These conditions could be caused by an imbalance of autoantibodies to G protein-coupled receptors, which are expressed in almost all types of cells, including immune and nonimmune cells. Different intracellular signaling pathways that regulate cell trafficking and migration, the secretion of inflammatory cytokines, vasoconstriction or vasodilatation, neurotransmission, and the function of exocrine and endocrine glands are activated depending on the cell type and exogenous or endogenous factors. It is evident that some of the described clinical symptoms are similar to dysautonomic conditions, which may be associated with an imbalance of autoantibodies to G protein-Different intracellular signaling pathways that control cell trafficking and migration, inflammatory cytokine secretion, vasoconstriction or vasodilatation, neurotransmission, and the function of exocrine and endocrine glands are activated by these factors, which can be exogenous or endogenous. Psychiatric disorders like schizophrenia and bipolar disorder are known to have higher insulin resistance, but depression is not as well understood. We wanted to find out if depression changes insulin resistance, test the metabolic subgroup hypothesis of depression, and see if antidepressants changed things. Studies that assessed fasting insulin or glucose levels or the Homeostatic Model Assessment for Insulin Resistance index and included adult subjects with depression, as well as either a control group or follow-up after treatment with antidepressants, met the inclusion criteria. Included were 70 studies with participants. Acute depression was accompanied by an increase in the HOMA-IR index and insulin levels. During remission, neither insulin nor the HOMA-IR index changed. Atypical depression, but not typical depression, had elevated insulin levels. Insulin variation was greater in depression sufferers than in controls. Treatment for depression did not alter insulin resistance. During acute episodes, depression increases insulin resistance. The majority of analyses showed a lot of heterogeneity. In accordance with the standards of precision psychiatry, a laboratory assessment of insulin resistance may have clinical utility for the diagnosis of the metabolic subtype and treatment selection in depression patients.