Pathophysiology : the official journal of the International Society for Pathophysiology最新文献

{"title":"Vitamin D Serum Levels and the Development of Intensive Care Unit-Acquired Weakness: Insights from a COVID-19 Intensive Care Cohort.","authors":"Jelena Gulišija, Vesna Čapkun, Stefan Golic, Sanda Stojanović Stipić","doi":"10.3390/pathophysiology32020021","DOIUrl":"10.3390/pathophysiology32020021","url":null,"abstract":"<p><p><b>Background/Objectives</b>: The pathogenesis of intensive care unit-acquired weakness (ICU-AW) is multi-factorial, with some of the main risk factors being sepsis, multiorgan failure, and the inflammatory response related to critical illness. Vitamin D is crucial for muscle function, the immune response, and inflammation, and has been identified as a predictor of negative outcomes in intensive care unit (ICU) patients with COVID-19. The objective of this preliminary study was to examine the relationship between vitamin D serum levels and the incidence of ICU-AW in a cohort from the University Hospital of Split. <b>Methods</b>: A prospective observational cohort study was conducted in the University Hospital of Split in ICU from December 2021 to March 2022. The inclusion criteria were as follows: patients over 18 years old who had a confirmed severe acute respiratory coronavirus disease 2 (SARS-CoV-2) infection, patients who were mechanically ventilated for more than 48 h, and patients who were weaned from a ventilator over at least 24 h. The exclusion criteria were a history of neurological or musculoskeletal disorders and a pre-existing poor functional status. Vitamin D was detected in the first routine blood sample. <b>Results</b>: A total of 77 patients were observed, with 36 patients who were successfully weaned from a ventilator over at least 24 h and 1 patient who could not be examined because of impaired consciousness (this patient was excluded from further analysis), and thus a total of 35 patients were analyzed. Of these 35 patients, 12 (34%) developed ICU-AW. The median vitamin D serum level in the ICU-AW group was 17 (7.5-73.3), while that in the non-ICU-AW group was 25.2 (12.3-121). The difference in vitamin D serum levels between the groups was not significantly different from zero (<i>p</i> = 0.567). All patients, except for one, were vitamin D insufficient. <b>Conclusions</b>: Vitamin D serum levels in the ICU-AW group were not statistically different from the non-ICU-AW group, possibly due to the small sample size. Given the known roles of vitamin D in muscle function, immune modulation, and inflammation, a potential etiopathogenetic role in ICU-AW cannot be excluded without additional studies. Therefore, further studies with larger sample sizes than ours are necessary to determine whether vitamin D deficiency contributes to the development of ICU-AW and whether supplementation could have preventive or therapeutic value.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":"32 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resting State of Dementia of the Alzheimer's Type and Healthy Older Adults Using fNIRS.","authors":"In-Sop Kim, Jaejin Hwang, Chorong Oh, Richard J Morris","doi":"10.3390/pathophysiology32020020","DOIUrl":"10.3390/pathophysiology32020020","url":null,"abstract":"<p><strong>Background/objectives: </strong>This study explores variations in brain activity between individuals with dementia of the Alzheimer's type (DAT) and healthy older adults during a resting state using functional near-infrared spectroscopy (fNIRS).</p><p><strong>Methods: </strong>FNIRS measured brain activity in ten AD patients and six healthy individuals. A device with 16 channels was placed on each participant's forehead to measure oxygenation levels while they kept their eyes closed. The data were analyzed using a support vector machine (SVM) model.</p><p><strong>Results: </strong>The results indicated differences in oxygenated hemoglobin (HbO) levels between the two groups. Specifically, HbO levels were generally higher in the dementia group in the left hemisphere, with a sharp increase after 26 s. Conversely, HbO levels were consistently lower in the right hemisphere of the dementia group. The SVM analysis demonstrated high accuracy in differentiating between the AD and healthy groups based on HbO levels.</p><p><strong>Conclusions: </strong>The study indicates that differences in brain activity during resting state can potentially distinguish people with DAT from healthy individuals. We found relatively reduced hemoglobin activity in the prefrontal areas of those with DAT. Furthermore, the concentration changes in the HbO in the left lateral prefrontal and right medial brain regions emerged as the most informative in distinguishing individuals with DAT from healthy individuals. The results of the current study show that this method could improve current DAT diagnostic practices due to its efficiency.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":"32 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Efficacy of Mesenchymal Stem Cells in Modulating Oxidative Stress in Puromycin-Induced Nephropathy.","authors":"Yusuke Iizuka, Masanori Sasaki, Kojiro Terada, Takuro Sakai, Yoshinobu Nagaoka, Shinobu Fukumura, Jeffery D Kocsis, Takeshi Tsugawa, Osamu Honmou","doi":"10.3390/pathophysiology32020019","DOIUrl":"10.3390/pathophysiology32020019","url":null,"abstract":"<p><p><b><i>Background:</i></b> Podocytes are essential for kidney function, and their dysfunction can result in nephrotic syndrome, such as minimal change disease (MCD). Oxidative stress contributes to podocyte damage. We investigated the therapeutic potential of intravenously infused mesenchymal stem cells (MSCs) in a puromycin aminonucleoside (PAN)-induced rodent MCD model, focusing on oxidative stress modulation. <b><i>Methods:</i></b> Sprague-Dawley rats were divided into three groups: intact, PAN-Vehicle, and PAN-MSC. MCD was induced through subcutaneous PAN injection. MSCs were infused intravenously in the PAN-MSC group on day 7. Urinary albumin, serum albumin, and creatinine levels were assessed. Histological analysis of the renal cortex was performed. Podocyte protein (NPHS1, NPHS2, and PODXL) and antioxidant enzyme (SOD1, SOD2, and GPX1) levels were measured using quantitative real-time reverse-transcription PCR (qRT-PCR). <b><i>Results:</i></b> MSC infusion significantly reduced proteinuria and restored podocyte structure in the PAN-MSC group. Electron microscopy revealed that infused MSCs could inhibit the fusion of the foot process induced by PAN injection. qRT-PCR showed that intravenous infusion of MSCs rescued the inhibition of GPX1 expression. GFP-labeled MSCs accumulated at the podocyte injury sites. <b><i>Conclusion:</i></b> Systemic MSC infusion mitigates PAN-induced MCD by reducing proteinuria, preserving podocyte structure, and modulating oxidative stress via the GPX1 pathway, offering a potential therapeutic approach for nephrotic syndrome.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":"32 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomolecular Mechanisms of Autoimmune Diseases and Their Relationship with the Resident Microbiota: Friend or Foe?","authors":"Skender Topi,&nbsp;Lucrezia Bottalico,&nbsp;Ioannis Alexandros Charitos,&nbsp;Marica Colella,&nbsp;Marina Di Domenico,&nbsp;Raffaele Palmirotta,&nbsp;Luigi Santacroce","doi":"10.3390/pathophysiology29030041","DOIUrl":"https://doi.org/10.3390/pathophysiology29030041","url":null,"abstract":"<p><p>The use of innovative approaches to elucidate the pathophysiological mechanisms of autoimmune diseases, as well as to further study of the factors which can have either a positive or negative effect on the course of the disease, is essential. In this line, the development of new molecular techniques and the creation of the Human Genome Program have allowed access to many more solutions to the difficulties that exist in the identification and characterization of the microbiome, as well as changes due to various factors. Such innovative technologies can rekindle older hypotheses, such as molecular mimicry, allowing us to move from hypothesis to theory and from correlation to causality, particularly regarding autoimmune diseases and dysbiosis of the microbiota. For example, <i>Prevotella copri</i> appears to have a strong association with rheumatoid arthritis; it is expected that this will be confirmed by several scientists, which, in turn, will make it possible to identify other mechanisms that may contribute to the pathophysiology of the disease. This article seeks to identify new clues regarding similar correlations between autoimmune activity and the human microbiota, particularly in relation to qualitative and quantitative microbial variations therein.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"507-536"},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9505211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33469972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mimicry between SARS-CoV-2 and Human Endocrinocytes: A Prerequisite of Post-COVID-19 Endocrine Autoimmunity?","authors":"Leonid P Churilov,&nbsp;Muslimbek G Normatov,&nbsp;Vladimir J Utekhin","doi":"10.3390/pathophysiology29030039","DOIUrl":"https://doi.org/10.3390/pathophysiology29030039","url":null,"abstract":"<p><p>Molecular mimicry between human and microbial/viral/parasite peptides is common and has long been associated with the etiology of autoimmune disorders provoked by exogenous pathogens. A growing body of evidence accumulated in recent years suggests a strong correlation between SARS-CoV-2 infection and autoimmunity. The article analyzes the immunogenic potential of the peptides shared between the SARS-CoV-2 spike glycoprotein (S-protein) and antigens of human endocrinocytes involved in most common autoimmune endocrinopathies. A total of 14 pentapeptides shared by the SARS-CoV-2 S-protein, thyroid, pituitary, adrenal cortex autoantigens and beta-cells of the islets of Langerhans were identified, all of them belong to the immunoreactive epitopes of SARS-CoV-2. The discussion of the findings relates the results to the clinical correlates of COVID-19-associated autoimmune endocrinopathies. The most common of these illnesses is an autoimmune thyroid disease, so the majority of shared pentapeptides belong to the marker autoantigens of this disease. The most important in pathogenesis of severe COVID-19, according to the authors, may be autoimmunity against adrenals because their adequate response prevents excessive systemic action of the inflammatory mediators causing cytokine storm and hemodynamic shock. A critique of the antigenic mimicry concept is given with an assertion that peptide sharing is not a guarantee but only a prerequisite for provoking autoimmunity based on the molecular mimicry. The latter event occurs in carriers of certain HLA haplotypes and when a shared peptide is only used in antigen processing.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"486-494"},"PeriodicalIF":0.0,"publicationDate":"2022-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9504401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33469971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Critical Functions of Histone Deacetylases (HDACs) in Modulating Inflammation Associated with Cardiovascular Diseases.","authors":"Supaporn Kulthinee,&nbsp;Naohiro Yano,&nbsp;Shougang Zhuang,&nbsp;Lijiang Wang,&nbsp;Ting C Zhao","doi":"10.3390/pathophysiology29030038","DOIUrl":"https://doi.org/10.3390/pathophysiology29030038","url":null,"abstract":"<p><p>Histone deacetylases (HDACs) are a superfamily of enzymes that catalyze the removal of acetyl functional groups from lysine residues of histone and non-histone proteins. There are 18 mammalian HDACs, which are classified into four classes based on the primary homology with yeast HDACs. Among these groups, Class I and II HDACs play a major role in lysine deacetylation of the N-terminal histone tails. In mammals, HDACs play a pivotal role in the regulation of gene transcription, cell growth, survival, and proliferation. HDACs regulate the expression of inflammatory genes, as evidenced by the potent anti-inflammatory activity of pan-HDAC inhibitors, which were implicated in several pathophysiologic states in the inflammation process. However, it is unclear how each of the 18 HDAC proteins specifically contributes to the inflammatory gene expression. It is firmly established that inflammation and its inability to converge are central mechanisms in the pathogenesis of several cardiovascular diseases (CVDs). Emerging evidence supports the hypothesis that several different pro-inflammatory cytokines regulated by HDACs are associated with various CVDs. Based on this hypothesis, the potential for the treatment of CVDs with HDAC inhibitors has recently begun to attract attention. In this review, we will briefly discuss (1) pathophysiology of inflammation in cardiovascular disease, (2) the function of HDACs in the regulation of atherosclerosis and cardiovascular diseases, and (3) the possible therapeutic implications of HDAC inhibitors in cardiovascular diseases. Recent studies reveal that histone deacetylase contributes critically to mediating the pathophysiology of inflammation in cardiovascular disease. HDACs are also recognized as one of the major mechanisms in the regulation of inflammation and cardiovascular function. HDACs show promise in developing potential therapeutic implications of HDAC inhibitors in cardiovascular and inflammatory diseases.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"471-485"},"PeriodicalIF":0.0,"publicationDate":"2022-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40412848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Belyaeva et al. Tuberculosis and Autoimmunity. <i>Pathophysiology</i> 2022, <i>29</i>, 298-318.","authors":"Irina V Belyaeva,&nbsp;Anna N Kosova,&nbsp;Andrei G Vasiliev","doi":"10.3390/pathophysiology29030037","DOIUrl":"https://doi.org/10.3390/pathophysiology29030037","url":null,"abstract":"<p><p>The authors would like to make the following correction to the published paper [...].</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"469-470"},"PeriodicalIF":0.0,"publicationDate":"2022-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40412847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiology of Nociception and Rare Genetic Disorders with Increased Pain Threshold or Pain Insensitivity.","authors":"Marco Cascella,&nbsp;Maria Rosaria Muzio,&nbsp;Federica Monaco,&nbsp;Davide Nocerino,&nbsp;Alessandro Ottaiano,&nbsp;Francesco Perri,&nbsp;Massimo Antonio Innamorato","doi":"10.3390/pathophysiology29030035","DOIUrl":"https://doi.org/10.3390/pathophysiology29030035","url":null,"abstract":"<p><p>Pain and nociception are different phenomena. Nociception is the result of complex activity in sensory pathways. On the other hand, pain is the effect of interactions between nociceptive processes, and cognition, emotions, as well as the social context of the individual. Alterations in the nociceptive route can have different genesis and affect the entire sensorial process. Genetic problems in nociception, clinically characterized by reduced or absent pain sensitivity, compose an important chapter within pain medicine. This chapter encompasses a wide range of very rare diseases. Several genes have been identified. These genes encode the Nav channels 1.7 and 1.9 (<i>SCN9A</i>, and <i>SCN11A</i> genes, respectively), <i>NGFβ</i> and its receptor tyrosine receptor kinase A, as well as the transcription factor PRDM12, and autophagy controllers (<i>TECPR2</i>). Monogenic disorders provoke hereditary sensory and autonomic neuropathies. Their clinical pictures are extremely variable, and a precise classification has yet to be established. Additionally, pain insensitivity is described in diverse numerical and structural chromosomal abnormalities, such as Angelman syndrome, Prader Willy syndrome, Chromosome 15q duplication syndrome, and Chromosome 4 interstitial deletion. Studying these conditions could be a practical strategy to better understand the mechanisms of nociception and investigate potential therapeutic targets against pain.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"435-452"},"PeriodicalIF":0.0,"publicationDate":"2022-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397076/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40719466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated IgG and IgM Autoantibodies to Advanced Glycation End Products of Vascular Elastin in Hypertensive Patients with Type 2 Diabetes: Relevance to Disease Initiation and Progression.","authors":"Krasimir Kostov,&nbsp;Alexander Blazhev","doi":"10.3390/pathophysiology29030034","DOIUrl":"https://doi.org/10.3390/pathophysiology29030034","url":null,"abstract":"<p><p>The increased glycation of elastin is an important factor in vascular changes in diabetes. Using the ELISA method, we determined serum levels of IgM and IgG autoantibodies to advanced glycation end products of vascular elastin (anti-AGE EL IgM and anti-AGE EL IgG) in 59 hypertensive patients with type 2 diabetes (T2D) and 20 healthy controls. Serum levels of matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) and the C-reactive protein (CRP) were also determined. The levels of anti-AGE EL IgM antibodies in the T2D group were similar to those in the control group, while those of anti-AGE EL IgG antibodies were significantly higher (<i>p</i> = 0.017). Significant positive correlations were found between the levels of anti-AGE EL IgM antibodies and MMP-2 (<i>r</i> = 0.322; <i>p</i> = 0.013) and between the levels of anti-AGE EL IgG antibodies and CRP (<i>r</i> = 0.265; <i>p</i> = 0.042). Our study showed that elevated anti-AGE EL IgG antibody levels may be an indicator of the enhanced AGE-modification and inflammatory-mediated destruction of vascular elastin in hypertensive patients with T2D. Anti-AGE EL IgM antibodies may reflect changes in vascular MMP-2 activity, and their elevated levels may be a sign of early vascular damage.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"426-434"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9396981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40719465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmune Autonomic Dysfunction Syndromes: Potential Involvement and Pathophysiology Related to Complex Regional Pain Syndrome, Fibromyalgia, Chronic Fatigue Syndrome, Silicone Breast Implant-Related Symptoms and Post-COVID Syndrome.","authors":"Naim Mahroum,&nbsp;Yehuda Shoenfeld","doi":"10.3390/pathophysiology29030033","DOIUrl":"https://doi.org/10.3390/pathophysiology29030033","url":null,"abstract":"<p><p>The pathophysiological mechanisms involved in chronic disorders such as complex regional pain syndrome, fibromyalgia, chronic fatigue syndrome, silicone breast implant-related symptoms, and post-COVID syndrome have not been clearly defined. The course of the pain in some of the syndromes, the absence of evident tissue damage, and the predominance of alterations in the autonomic nervous system are shared similarities between them. The production of autoantibodies following a trigger in the syndromes was previously described, for instance, trauma in complex regional pain syndrome, infectious agents in fibromyalgia, chronic fatigue syndrome, and post-COVID syndrome, and the immune stimulation by silicone in women with breast implants. In fact, the autoantibodies produced were shown to be directed against the autonomic nervous system receptors, leading to the amplification of the perception of pain alongside various clinical symptoms seen during the clinical course of the syndromes. Therefore, we viewed autoantibodies targeting the autonomic nervous system resulting in autonomic dysfunction as likely the most comprehensive explanation of the pathophysiology of the disorders mentioned. Based on this, we aimed to introduce a new concept uniting complex regional pain syndrome, fibromyalgia, chronic fatigue syndrome, silicone breast implant-related symptoms, and post-COVID syndrome, namely \"autoimmune autonomic dysfunction syndromes\". Due to its etiological, pathophysiological, and clinical implications, the suggested term would be more precise in classifying the syndromes under one title. The new title would doubtlessly facilitate both laboratory and clinical studies aimed to improve diagnosis and make treatment options more directed and precise.</p>","PeriodicalId":520741,"journal":{"name":"Pathophysiology : the official journal of the International Society for Pathophysiology","volume":" ","pages":"414-425"},"PeriodicalIF":0.0,"publicationDate":"2022-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9396987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40719464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}