Observations on Recent Studies Showing Increased Co-occurrence of Autoimmune Diseases

Sloka, Scott

doi:10.1006/jaut.2002.0588

Cited by 46 publications

(39 citation statements)

References 48 publications

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“…Some IMIDs lack established clinical criteria, while others overlap significantly in symptom manifestations. To address this issue, IMIDs were classified into subgroups that had disparate organ system involvement, were physiologically distinct, and presented with contrasting symptoms (37). Patients were classified as IMID subjects in the presence of a previously diagnosed IMID or newly discovered systemic disorder comprising the following: vasculitides, connective tissue diseases, rheumatologic diseases, and others (Table 1).…”

Section: Study Population (I) Dcm Subjectsmentioning

confidence: 99%

Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

Dennert¹,

Paassen²,

Wolffs³

et al. 2012

Clin. Vaccine Immunol.

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dInfections with cardiotrophic viruses and immune-mediated responses against the heart have been suggested to play a dominant role in the pathogenesis of idiopathic dilated cardiomyopathy (DCM). Furthermore, immune-mediated inflammatory diseases (IMIDs) may result in DCM. It has not previously been assessed whether DCM patients with and without an IMID have different prevalences and quantities of cardiotrophic viruses in the heart. Therefore, we compared the profiles of cardiotrophic viruses in heart tissue of DCM patients with and without an IMID. Serum and myocardial tissue samples were obtained from 159 consecutive patients with DCM and 20 controls. Patients were subdivided into three groups, the first two based on the presence (n ‫؍‬ 34) or absence (n ‫؍‬ 125) of an IMID and the third being a control group. The parvovirus B19 virus genome was detected in equal quantities in the non-IMID DCM patients (100/125) and the control group (15/20) but in lower quantities in the IMID patients (21/34, P ‫؍‬ 0.02). Both the non-IMID and IMID DCM patients demonstrated increased myocardial inflammation compared to controls: 12.5 ؎ 1.8 and 14.0 ؎ 3.2 CD45-positive inflammatory cells, respectively, versus 5.1 ؎ 0.7 for the controls (P < 0.05 for both). Importantly, significantly higher parvovirus B19 copy numbers could be amplified in non-IMID than in IMID patients (561 ؎ 97 versus 191 ؎ 92 copies/g DNA, P < 0.001) and control subjects (103 ؎ 47 copies/g DNA, P < 0.001). The present study shows decreased parvovirus B19 prevalence and copy numbers in hearts of DCM patients with an IMID compared to those without an IMID. These findings may suggest that DCM patients with an IMID have a different pathophysiologic mechanism from that which is present in the virus-induced form of DCM.

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Section: Study Population (I) Dcm Subjectsmentioning

confidence: 99%

Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

Dennert¹,

Paassen²,

Wolffs³

et al. 2012

Clin. Vaccine Immunol.

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“…A review of studies of comorbidity, which included case reports on single individuals, located about two dozen studies in total (8). A systematic review of 52 studies of comorbidity of Thyroiditis, Type 1 Diabetes, Rheumatoid Arthritis, and Multiple Sclerosis appeared recently (9).…”

mentioning

confidence: 99%

Epidemiology of autoimmune diseases in Denmark

Eaton¹,

Rose²,

Kalaydjian³

et al. 2007

Journal of Autoimmunity

371

299

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An epidemiologic study of the autoimmune diseases taken together has not been done heretofore. The National Patient Register of Denmark is used to estimate population prevalence of 31 possible or probable autoimmune diseases. Record linkage is used to estimate 465 pairwise comorbidities in individuals among the 31 diseases, and familial aggregation among sibs, parents and offspring. The prevalence of any of the 31 diseases in the population is more than 5%. Within individuals, there is extensive comorbidity across the 31 diseases. Within families, aggregation is strongest for individual diseases, and weak across diseases. These data confirm the importance of the autoimmune diseases as a group, and suggest that common etiopathologies exist among them.

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“…The first comes from clinical observations indicating the possible shift from one disease to another or to the fact that more than one AD may coexist in a single patient (i.e., polyA, MAS) [24,[36][37][38][39] in the same family (i.e., familial autoimmunity) [40]. The second level of evidence refers to known shared pathophysiological mechanisms between ADs [41]; and the third level of evidence corresponds to the evidence implying common genetic factors [38]. The importance of this concept focuses on the probability of having multiple ADs simultaneously in one patient, which goes beyond epidemiologic inferences.…”

Section: Discussionmentioning

confidence: 99%

Homozygosity Analysis in Autoimmunity Affected Individuals and Multiplex Autoimmune Disease Families

Castiblanco¹,

Anaya²

2017

Immunome Res

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Autoimmune diseases (AD) are responsible for a substantial amount of disability and morbidity worldwide. Research generally focuses on a single disease, although autoimmune phenotypes could represent pleiotropic outcomes of non-specific disease genes underlying similar immunogenetic mechanisms. This report examined the effect and importance of the homozygosity status, using genome-wide interspersed markers, in individuals and multiplex families affected with AD. This study presented two approaches: (I) a case-control comparison and evaluation on the effect of homozygosity at the genome-wide level and per marker, including 453 unrelated individuals (121 late-, 79 early-onset AD, 40 polyautoimmunity (PolyA), 30 multiple autoimmune syndrome (MAS) and 183 healthy control individuals); and (II) a model-free affected pair linkage approach which included 35 MAS, 49 polyA, 104 late-, and 83 early-onset multiplex families. A total of 372 genome-wide markers were used in the analysis. The standardized observed homozygosity (S OH ) was calculated and the association of the homozygosity status and the autoimmune trait was evaluated. The multipoint model-free linkage analysis was applied by using RELPAL from S.A.G.E v6.3. Results for the S OH showed significant differences between controls and early-onset individuals, where early-onset affected individuals showed lower homozygosity relative to controls. No differences were observed relative to controls for MAS, polyA and late-onset disease at the genome-wide level. The local marker homozygosity effect showed share and specific risk and/or protective effects for 24 markers. The model-free affected pair linkage approach lacked any suggestive linkage signals, but marginal signals displayed excess allele sharing for extreme phenotypes in autoimmunity. This study presumed autoimmunity as a trait rather than a clinical phenotype and tried to approach AD as a continuous trait presenting extreme phenotypes. Future approaches would be expected to dwell on the data presented here to corroborate and expand on sample size, marker coverage and their effects.

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Observations on Recent Studies Showing Increased Co-occurrence of Autoimmune Diseases

Cited by 46 publications

References 48 publications

Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

Epidemiology of autoimmune diseases in Denmark

Homozygosity Analysis in Autoimmunity Affected Individuals and Multiplex Autoimmune Disease Families

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