The olfactory sense and neuropsychiatric manifestations in systemic lupus erythematosus

Abstract

Summary: Antibodies found in higher concentrations in patients with autoimmune diseases may lead to the onset of depression and decreased olfactory sense, these antibodies penetrate cells in the hippocampus and amygdala leading to apoptosis celular.Pretendemos assessing olfactory function held in pens odorized (Sniffin'Sticks kit (Medizintechnik Burghart, Wedel, Germany), analyze the possible brain lesions by magnetic resonance imaging and dose anti-P antibodies by ELISA Introduction of the project: Systemic lupus erythematosus (SLE) is a connective tissue disorder of unknown etiology and characterized by periods of remission and exacerbation, with intense participation of the immune system. The clinical manifestations in SLE are diverse and range from constitutional symptoms to severe multiorgan involvement. Neuropsychiatric manifestations occur in 12-95% of patients, depending on the diagnostic criteria applied and are associated with high morbidity and mortality. The clinical presentations are varied and include, among others, seizures, cerebrovascular accidents (stroke), depression and psychosis. Symptoms such as headache and cognitive disorders are also common findings in clinical practice. The symptoms may present alone or together, in episodes occurring only during the exacerbation of the disease, with or without other signs of SLE activity. The main diagnostic problems involve the distinction between neurological disorders caused by SLE, with immune abnormalities, and secondary events leading role, as a complication of hypertension (HBP), diabetes, coagulation disorders, severe infection, steroids and atherosclerosis. The assessment of neuropsychiatric manifestations in SLE involves a series of neuropsychological tests, laboratory and neuroimaging techniques, and magnetic resonance imaging (MRI) is considered the gold standard for evaluation. As shown in recent years, patients with SLE have structural changes, as well as functional, detectable by MRI techniques. Thus, techniques were developed to determine the prevalence and diagnosis of brain atrophy in addition to assessing the white matter, especially of the corpus callosum, and some gray matter structures, such as the hippocampus. In recent years evidence has grown of the interrelationship between the immune and central nervous system (CNS), particularly the olfactory system. In animal models has been shown that intracerebral injection of anti-P triggers a depressive behavior and reduced olfaction. Histologic examination of the brains of these mice revealed that anti-P entered in the limbic system neuronal cells, including cells of the amygdala and hippocampus, inducing apoptosis. In bees whose immune system was partially inhibited, we observed a decrease in the association of odor with the reward of sugar, it was concluded that effects on the immune response can affect the smell and subsequent memory formation. The bilateral olfactory bulbectomia in mice resulted in numerous immunologic abnormalities, including reduced phagocytosis by neutrophils, lymphocyte mitogenesis, increased adhesion of leukocytes, phagocytosis of monocytes, a positive acute phase proteins, among others. Although rarely reported by patients with autoimmune diseases, smell is often damaged and can be correlated with the severity of neurological impairment. In SLE, we observed that olfactory dysfunction was associated with depression, cognitive decline and disease activity. In clinical studies involving other diseases such as Alzheimer's, Parkinson's, multiple sclerosis and schizophrenia has been shown that the ability to identify odors involves the medial temporal lobe structures.