جستجوی مقالات مرتبط با کلیدواژه « autoimmune diseases » در نشریات گروه « پزشکی »

Infectious agents are considered one of the possible etiological factors of systemic lupus ery- thematosus (SLE). It has been suggested that human herpesvirus type 6 (HHV-6) may trigger autoimmune disorders, but few studies have been conducted on the relationship between this virus and autoimmune diseases, especially SLE. The present study aimed to compare the frequency of HHV-6 infection between SLE patients and healthy individuals.

Serum samples were collected from 60 healthy people and 60 SLE patients referred to the rheu- matology clinic of Shahid-Beheshti Hospital, Kashan, Iran, from January 2020 to January 2021. The following data were collected from the medical records of patients: sex; age; duration of disease; SLE clinical manifestations; and disease activ- ity. After the extraction of viral DNA from samples, a nested polymerase chain reaction (PCR) test was performed to detect HHV-6.

HHV-6 was detected in 12 SLE patients (20%) and in 8 healthy individuals (13.3%). A significant correlation was not obtained between SLE and the presence of HHV-6 (P = 0.09). There was no correlation between musculoskeletal involvements, skin lesions, renal manifestations, and hematological manifestations with the presence of HHV-6 (P˃0.05). HHV-6 was detected more frequently in patients with active lupus than in patients with quiescent disease, but this difference was not significant (P=0.08).

Although patients with SLE had a higher prevalence of HHV-6 compared with healthy people, there is no strong link between HHV-6 infection and SLE. Future research is necessary because this data does not support the hypothesis that human herpesvirus 6 plays a role in the pathogenesis of SLE.

Prediction of Wegener's granulomatosis diagnosis and relapse is a complex process. In this study, we applied machine learning algorithms to predict Wegener's granulomatosis relapse.

In this research, 189 patients admitted to Amiralam Hospital were studied and followed for approximately 2 years. Patient features included demographics, organ involvement, symptoms, and other clinical data. Different popular machine learning algorithms were applied for predicting Wegener's granulomatosis relapse, including Support Vector Machines, Random Forest, Gradient Boosting, and XGBoost algorithms. The prediction model performance was measured for the different candidate prediction algorithms using accuracy, precision, recall, and F1-measure. The selected prediction model performance was calculated based on different relapse rates and major relapse occurrence according to Birmingham Vasculitis Activity Score (BVAS) fields.

Applying different machine learning algorithms, the XGBoost algorithm performed the best. The results indicated that the prediction model's performance increased when calculating higher relapse rate possibilities. The XGBoost model had 82% accuracy while predicting more than one relapse rate and 92% accuracy in predicting more than twice the relapse rate. We also calculated the SHAP value for the prediction model. The results indicated that Cr, BVAS, lymphocyte percentage, vitamin D, nose involvement, alkaline phosphatase, diagnosis age, white blood cell count, erythrocyte sedimentation rate, and initial nose presentation are the 10 most important features according to SHAP value.

In this study, we have developed Wegener's granulomatosis relapse prediction model using machine learning algorithms. We achieved reasonable precision and recall for early prediction and decisionmaking regarding Wegener's granulomatosis relapse.

Infectious agents are considered as one of the possible etiological factors of systemic lupus erythematosus (SLE). It has been suggested that torque teno virus (TTV) may trigger autoimmune disorders, but few studies have been conducted on the relationship between this virus and autoimmune diseases, especially SLE. The present study aimed to evaluate the association between TTV frequency and SLE.

Serum samples were collected from a total of 116 participants, including 58 healthy people and 58 SLE patients who referred to the rheumatology clinic of Shahid-Beheshti hospital in Kashan, Iran from January 2020 to January 2021. After the extraction of viral DNA from the samples, a nested PCR test was performed using specific primers to detect TTV.

TTV was detected in 43 SLE patients (74.1%, 95% CI: 63.4-86.2) and 33 healthy individuals (56.9%, 95% CI: 44.1-69.0). A significant correlation was found between SLE and the presence of TTV (r= .32, p= .03). There was no correlation between the presence of TTV and musculoskeletal involvements, skin lesions, renal manifestations, and hematological manifestations (r< .05, p> .05). TTV was detected more frequently in patients with active lupus than in patients with quiescent disease, and this difference was significant (p= .048).

A significant association between TTV and SLE was observed in the present study; however, further studies are needed to investigate the role of TTV in the pathogenesis and clinical course of SLE.

Coronavirus disease 2019 (COVID-19) is an infectious disease that has surrounded the world caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease is usually onset with symptoms like fever, cough, fatigue, respiratory problems, and loss of smell and taste. The majority of COVID-19 patients have mild or no symptoms, but a few demonstrate acute respiratory problems (ARDS) that can be life-threatening.

Authors searched English published articles in local and international journals over the period 2000 to 2022 using several databases including Scopus, PubMed, Scholar, and Science Direct. Then, the relevant articles were revised. During this period, different articles have been published, but we tried to choose and review articles that introduced effective data.

Some people show symptoms long after their negative PCR test called post-COVID-19 syndrome, which studies showed can last more than 12 weeks after infection. Other than the complications patients confront amid the period of COVID-19 infection, there is an accumulation of evidence regarding the delayed complications of COVID-19, including auto-immune outbreaks such as multisystem inflammatory syndrome (MIS), idiopathic thrombocytopenic purpura (ITP), Guillain-Barre syndrome, Miller-Fisher syndrome, Autoimmune hemolytic anemia (AIHA), Autoimmune thyroid disease and also COVID-19 associated coagulopathies, have received remarkable attention since the early months of the pandemic. Microbiome changes in the gut and nasopharynx of patients with COVID-19 affect the severity of the disease, furthermore, some genes inherited from Neanderthals increase the severity of COVID-19.

COVID-19 infection, along with the immune suppression mechanism, has the potential to evoke destructive inflammation in the host. Clarifying the pathophysiology of the COVID‐19 injuries to the host could help to develop appropriate treatment.

Major depression is a common disabling disorder that affects about 280 million people worldwide (1-3) and is predicted to become the main contributor to global Disability-Adjusted Life Years (DALY) by 2030 (4). The costs imposed by depression and its complications in the United States reach more than 200 billion annually - considering occupational problems and suicide of patients (5). There are effective treatments for depression, but about one-third of patients are resistant to treatment. In addition, Electroconvulsive Therapy (ECT) has been reported to be beneficial for only half of refractory patients (4,6). A better understanding of the neuropathophysiology of the disorder, which leads to more appropriate and useful classifications, preventions, and treatments, seems to be a solution. After the monoaminergic system, the glutamatergic system and, recently, the neuroinflammation hypothesis have been proposed in the pathophysiology of major depression. Inflammation disrupts the regulation of the Hypothalamus-Pituitary-Adrenal (HPA) axis and the production of neurons in the hippocampus (7). Inflammatory cytokines disrupt the serotonin production pathway by decreasing Brain-Derived Neurotrophic Factor (BDNF) expression and increasing tryptophan oxidation (8). Decreased levels of BDNF and decreased signaling between it and its receptor in the hippocampus and prefrontal cortex cause depression (9). The result of the oxidation of tryptophan is kynurenine, whose compositions have agonistic and antagonistic effects on the N-methyl-d-aspartate (NMDA) receptor, a major player in the glutamatergic system (8,10). In general, the evidence shows the complexity and overlap of systems in the pathoetiology of inflammatory depression. Regarding this, even a subtype called Inflammatory Cytokine-Associated Depression (ICAD) has been suggested so that different treatment approaches can be considered for these patients (10). There is clinical evidence for these proposed mechanisms. An imbalance in the levels of kynurenine metabolites in patients with depression and an increase in the levels of pro-inflammatory cytokines in patients with resistant depression have been reported. Another suggester is its higher prevalence in patients with chronic autoimmune connective tissue disorders and exacerbated activation times of the innate immune system (11). The administration of cytokine and interferon for the treatment of cancer and hepatitis C, respectively, has led to depression in patients (7,10,11). Moreover, anti-inflammatory compounds such as celecoxib, simvastatin, pioglitazone, and dexamethasone have shown antidepressant effects in various trials (8). Blood levels of Interleukin-6 (IL-6) and C-Reactive Protein (CRP) are associated with depression, so that inflammation measured through these two predicts future depression (13). The levels of peripheral inflammatory cytokines have also been helpful in predicting patients’ responses to antidepressant treatment. Specifically, lower baseline IL-8 levels have been reported to lead to a better response to antidepressants. Additionally, antidepressant responders had a significant reduction in Tumor Necrosis Factor-α (TNF-α) (10,12). It seems that any primary neuroinflammation of the brain and any chronic inflammatory condition that produces markers crossing the blood-brain barrier and even chronic stress on the vessels can cause depression (7). Also, genetics, cellular damage, obesity, stress, diet, and gut microbiome can fuel chronic inflammation (10). Considering that inflammation predicts future depression and depression is a predictor of IL-6, it is possible to suggest a bidirectional relationship between inflammation and depression. The evidence promises an important therapeutic target for major depression treatment approaches. Also, more research is necessary to investigate the possibility of using inflammatory cytokines as biomarkers of response to pharmacological treatment and even other treatments.

Vitiligo is the most common cause of skin depigmentation, which relates to a wide range of psychological disorders. Stigma is defined as a negative attitude towards oneself that results from one's perception of being different from the general population. In this study, we have evaluated the quality of life and stigmatization degree among vitiligo patients. In this cross-sectional study, 323 patients with vitiligo referred to Razi Hospital, Tehran, Iran, were evaluated. All patients were asked to fill out a questionnaire containing age, gender, marital status, educational level, employment status, duration of vitiligo, location of lesions, history of underlying diseases, history of previous treatments, as well as history of depression or suicide. Quality of life and stigmatization among patients were assessed by DLQI (dermatology life quality index) and FSQ (feeling stigmatization questionnaire) questionnaires. The prevalence of moderate and severe stigmatization were 49.8 % and 13.3%, respectively. Women were significantly more stigmatized than men. The presence of vitiligo lesions on the face, hands, or forearms, previous topical and oral treatments, and prior depressive disorders were significantly associated with an increased sense of stigma. Patients with thigh or trunk lesions faced less stigmatization. Additionally, stigmatization was meaningfully related to the level of quality of life impairment. In the present study, 63% of patients with vitiligo experienced moderate to severe stigmatization levels related to gender, lesion site, history of prior treatments, and depression. Moreover, there was a significant correlation between the level of stigma sensation and the life quality disturbance.

Hashimoto's thyroiditis is a chronic inflammation and an autoimmune disease of the thyroid gland that causes hypothyroidism. Genetic, internal, and environmental factors are the causes of this disease. Because human herpes viruses such as herpesvirus type 6 (HHV-6) are involved in some autoimmune disorders, they may also play a role in causing this disease. This study aimed to evaluate the association between human herpes virus 6 (HHV-6) with Hashimoto's thyroiditis.

In the present study, 64 samples of thyroid paraffin tissue including 32 samples of thyroid paraffin tissue of healthy individuals as control, and 32 samples of thyroid paraffin tissue of Hashimoto's thyroiditis patients were taken from the pathology department of Loghman Hakim Hospital in Tehran. A questionnaire collected demographic information of patients. After DNA extraction from the samples, the nested-PCR technique was performed using specific primers for HHV-6.

Totally, the HHV6-DNA was found in 34.4% of thyroid tissues of healthy individuals (81.8% female and 18.2% male) and 46.9% of patients with Hashimoto's thyroiditis (73.3% female and 26.7% male). It was found that this difference in virus frequency between the two groups was not statistically significant (P value=0.309). There was also no statistically significant relationship between the prevalence of human herpesvirus type 6 and age or sex.

Based on the present study, the number of HHV-6-infected individuals in Hashimoto's patients and controls did not differ significantly; therefore, HHV-6 appears not to be associated with Hashimoto's thyroiditis.

Inflammatory cytokines play roles in the pathogenesis of celiac disease. To introduce new diagnostic markers in patients with celiac disease for easy, fast, low cost, and non-invasive diagnosis, we evaluated the peripheral blood expression levels of interleukin-15 (IL-15), interleukin-17A (IL-17A), interleukin23A (IL-23A), granzyme B (GzmB), T-box transcription factor 21 (TBX21), and tumor necrosis factor alpha-induced protein 3 (TNFAIP3) of patients compared with the healthy controls, which were extracted from public databases organized in a protein-protein interaction network, in this group.

Peripheral blood mononuclear cells were collected from 30 patients with celiac disease and 30 healthy subjects. Total RNA was extracted, and mRNA expression levels of targeted genes were investigated by the quantitative realtime polymerase chain reaction (PCR) method. SPSS software was used for statistical analysis. Receiver operating characteristic (ROC) curve analysis was performed to characterize the diagnostic ability of the studied genes.

The expression of IL-15, IL-17A, IL-23A, GzmB, TBX21, and TNFAIP3 genes in peripheral blood mononuclear cells of patients with celiac disease showed a significant increase compared with the control group. Among them, TNFAIP3, IL23A, and GzmB have better resolution and diagnostic value in differentiating patients with celiac disease from healthy controls.

Our results suggest that TNFAIP3, IL23A, and GzmB could be useful and sensible markers in differentiating patients with celiac disease from healthy controls. However, the diagnostic relevance of other genes recognized by pathway analysis needs to be further investigated.

Guillain-Barré Syndrome (GBS) is an autoimmune disease that may occur after infections. As Coronavirus Disease 2019 (COVID-19) may bring about GBS, it is important to assess the effect of the COVID-19 pandemic on this disease

This study aimed to compare the distribution and characteristics of GBS during and before the COVID-19 pandemic in an academic referral hospital in the north of Iran.

This retrospective study assessed GBS distribution and characteristics during the COVID-19 pandemic period (from March 2020 to the end of February 2021) and before the pandemic (from March 2019 to the end of February 2020) on 5340 patients referred to the Neurology Ward of Poursina Hospital of Guilan Province, in Iran.

There was no significant difference between GBS distribution during (0.03%) and before (0.04%) the COVID-19 pandemic (P=0.413). There were also no differences between the two periods regarding the gender (P=0.659) and age (P=0.417) of the patients. The most common subtype of GBS during the COVID-19 pandemic was Acute Motor and Sensory Axonal Neuropathy (AMSAN) (71.4%). In both periods, the most common type of treatment was intravenous administration of immune globulin. There was no significant difference between the two periods (P=0.838) regarding the patients’ treatment response.

The distribution of GBS, its subtypes, type of treatment, and response to treatment were not different between the two study periods.

Autoimmune myelofibrosis (AIMF) is considered as an infrequent cause of bone marrow fibrosis (BMF) and a rare complication of systemic lupus erythematosus (SLE). Due to its rarity, it is mistakenly diagnosed as primary myelofibrosis (MF).We describe the clinicopathologic features of a secondary form of AIMF in a 33- year- old female patient with an undiagnosed SLE which presented with acute bicytopenia. Absence of splenomegaly, leukopenia, anemia, BMF (grade MF-1), and presence of autoantibodies were some of noticeable features. Treatment with corticosteroid led to complete regeneration of the bone marrow and subsequently to an improved hematological status. Six- month follow-up showed that the patient was in good clinical condition.Identification of AIMF is a diagnostic challenge and pitfall and it is actually a diagnosis of exclusion. It could be the first and only presenting feature of SLE and results in hematologic disturbances. So, we should consider SLE-associated AIMF in the differential diagnosis of pancytopenia.

The purpose of this study was to test and present a causal model of psychological self-esteem based on self-knowledge and feelings of shame and guilt, with self-critical mediation and compassion in three groups of healthy individuals, autoimmune patients and non-autoimmune patients in Bandar Abbas.

The design of this study is correlational. The statistical population of the present post-event study included 360 patients including 120 patients with autoimmune diseases, 120 patients with non-autoimmune diseases referring to the Great Prophet's Therapeutic Complex in Bandar Abbas in 2019, and 120 healthy individuals. In the present study, autoimmune patients will be selected by simple or accessible sampling (easy sampling). All subjects will complete a self-report questionnaire, personal feelings (shame and guilt), compassion, and self-criticism. Descriptive statistics (mean, standard deviation and correlation) were used for data analysis. Confirmatory factor analysis, Cronbach's alpha, Spearman-Brown split, and Gutman split will be used to determine validity and reliability.

The analyzes of the underlying assumptions of structural equation modeling as well as broader and more sophisticated analyzes will be performed to evaluate the fitness of the proposed model, all of which will be applied through statistical equation modeling, using maximum likelihood estimation. Indirect path relations will also be used by the proposed method of Baron and Kenny and Cohen and Cohen. In the proposed model of the present study, psychological self-destruction based on self-knowledge (dependent variable) as a latent variable, variables of feelings of shame and guilt (independent variable), as exogenous variables and variables of self-compassion and self-criticism, as endogenous or mediating variables defined.

The results showed that feelings of shame and guilt and self-criticism bears a positive and significant relation with self-destruction based on self-knowledge, and self-compassion bears a negative and significant relation with self-destruction based on self-knowledge. The average of feelings of shame and guilt and self-destruction based on self-knowledge in men is higher than women, and the average of self-criticism in women is higher than men. The findings were discussed in accordance with the teleological coherence’s hypothesis in the coordinated function of the immunological, neurological and psychological systems and the basis for designing appropriate cognitive therapies for autoimmune patients.

The results showed a relatively good fit of the data model. The mediating effect of self-criticism and self-compassion on the relationship between self-destruction and feelings of shame and guilt was also confirmed.

Hashimoto thyroiditis (HT) and Graves’ disease (GD) are autoimmune inflammatory thyroid disorders. The evolution from GD into HT is the most common scenario while the conversion from HT into GD seems to be less common.

A 20-year-old female patient referred to the endocrinology clinic with a threemonth history of fatigue, lethargy, lack of appetite, constipation, menorrhagia, cold intolerance, and 5 kg weight gain in the last two months. Clinical examination showed dry skin, scalp hair loss, and painless hard goiter whereas thyroid ultrasound revealed generalized homogeneous hypoechoic thyroid hypertrophy. Laboratory tests demonstrated increased serum thyroid-stimulating hormone (TSH) 210 µIU/L (normal: 0.25-4.50), decreased free thyroxine (FT4) 0.37 ng/L (normal: 0.8-1.8) and free triiodothyronine (FT3) 1.94 pg/mL (normal: 1.8-4.6), and finally, increased thyroid peroxidase antibodies (anti-TPO) 462 IU/mL (normal: up to 34). Based on observations, HT was diagnosed and thus daily treatment with levothyroxine 75 mcg was started for the patient. Two months later, she referred with symptoms suggestive of hyperthyroidism with reduced TSH levels, which did not improve after levothyroxine cessation, thus more laboratory tests were conducted and revealed decreased TSH levels, increased T3 and T4, and TSH receptor stimulating antibody (TSAb)levels, and increased radioactive iodine uptake at 24 hours. Therefore, the diagnosis of GD was made. Five weeks after treatment, she was in full remission.

Although the switch from HT into GD is rare, it can occur at any time during the disease. Nonetheless, early diagnosis and treatment would improve the quality of care.

Primary immune thrombocytopenia (ITP) decreases platelet count as well as increases the risk of bleeding due to platelet destruction in an autoimmune disorder. For many years, prednisone (PDN) has been the standard first-line treatment in ITP practical guidelines. The current randomized clinical trial compared the efficacy of treatments between three-pulse high-dose dexamethasone (HD-DXM) and the traditional PDN regimen among untreated patients with ITP in accordance with platelet count responses and adverse events.

We randomly assigned eligible patients with ITP to receive PDN or a three-pulse regimen of HD-DXM. In the HD-DXM group, 40 mg of DXM was administered intravenously for 4 consecutive days and was repeated in 14-day intervals for three pulses of treatment. Patients in the PDN group received 1.0 mg/kg of PDN orally per day for 4 consecutive weeks. The Mann–Whitney test was used for comparing the median of platelet count between the two groups, and logistic regression was used to evaluate odds ratio (OR) in the response rate of platelet count between the two groups. Blindness was not applied for both patients and physicians.

The initial response rate of platelet count in the HD-DXM group was significantly higher than the PDN group (P < 0.05). According to the results of logistic regression, the initial and sustained response (SR) rate of platelet count in the HD-DXM group was significantly higher than the PDN group (OR: 5.68 and 4.17, respectively, P < 0.05). In fact, in the HD-DXM group, more patients reached SR after the 8-month follow-up (88.9% vs. 66.6%, P < 0.05).

In patients with ITP disease who have not received any kind of treatment, HD-DXM was more effective than conventional PDN therapy.