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PubMed1997

Necrotizing vasculitis in Greece: clinical, immunological and immunogenetic aspects. A study of 66 patients.

The clinical spectrum and outcome of necrotizing vasculitis were evaluated in a retrospective study in order to assess: (1) the clinical expression and evolution of the disease; (2) the response to several therapeutic approaches based on major events (organ involvement causing disability or death); (3) the immunogenetic background of patients. Sixty-six Greek patients fulfilling the ACR criteria for the diagnosis of vasculitis entered the study. Thirty-seven were diagnosed with Wegener's granulomatosis (WG), 22 with polyarteritis nodosa (PAN) and seven with Churg-Strauss syndrome (CSS). The demographic characteristics of patients with WG and PAN were similar. Cutaneous manifestations, gastrointestinal and peripheral nervous system involvement occurred more often in patients with PAN, whereas pulmonary and upper respiratory tract involvement, renal, ear abnormalities and fever were more frequent in patients with WG. Muscle weakness and asthma were found exclusively in patients with PAN and CSS, respectively, while the presence of classic-antineutrophil cytoplasmic antibodies (c-ANCA) characterized WG patients. Hepatitis B surface antigen (HBsAg) was found in 22% of PAN patients. No significant differences were detected when comparing the PAN and WG groups with respect to the first major event (log-rank P = 0.50) with and without potential confounders (age, gender, therapy or c-ANCA). For WG patients, a statistically significant difference was found on different routes of administration of cyclophosphamide (oral vs pulse) (P = 0.006). Regarding the HLA antigens, an increased frequency of DR1 (26.9% vs 10.3%, P = 0.057) in WG and the absence of DR3 in patients with PAN and CSS were noted. It appears that although the immunogenetic background and the clinical expression of the diseases differ, the response to treatment as well as the evolution and the survival rate of these patients are similar in the two groups.

Adolescent↗
PubMed1991

Humoral immunity and immunogenetics in the idiopathic inflammatory myopathies.

The idiopathic inflammatory myopathies (IIMs) are a heterogeneous group of rare but increasingly recognized syndromes characterized by chronic muscle inflammation of unknown cause. The finding of other autoimmune diseases in association with IIM, the inflammatory pathology, the response to immunosuppressive therapy, and the frequent occurrence of autoantibodies all support the notion that the IIMs are autoimmune diseases. IIM patients are unique in their immune targeting of a group of autoantigens involved in protein synthesis. Recent studies of the autoantibodies that bind these autoantigens (the myositis-specific autoantibodies) suggest that they arise by mechanisms that closely resemble standard immune responses. There is increasing interest in and efforts directed toward dividing the rheumatic diseases into more uniform groups for purposes of better defining etiology and pathogenesis. This approach has been useful in the analysis of the IIMs in which new approaches, subsetting patients by autoantibodies, have produced more homogeneous groupings. Recent data on predisposing immunogenetic factors in different clinical and serologic subsets of IIM patients also suggest that these disorders result from environmental agents acting on groups of genetically restricted individuals to induce immunologic activation and subsequent tissue pathology. This review summarizes these findings about the origins of the myositis-specific autoantibodies and their epidemiologic, clinical, prognostic, and immunogenetic associations.

Antibody Formation↗
PubMed2004

Have recent immunogenetic investigations increased our understanding of disease mechanisms in the idiopathic inflammatory myopathies?

PURPOSE OF REVIEW: The idiopathic inflammatory myopathies (IIM) continue to provide a challenge given the variable effectiveness of the available treatments, and immunogenetic studies are ongoing to further elucidate IIM disease mechanisms. This review examines how recent research has improved our understanding of the mechanisms that lead to IIM. RECENT FINDINGS: HLA-DRB1 studies in a large homogenous cohort of UK Caucasian patients have confirmed that polymyositis (PM) and dermatomyositis (DM) are not genetically identical diseases while other studies have shown that tumor necrosis factor alpha is genetically implicated in disease susceptibility. Some remarkable results from an international collaboration, correlating gene-environment interactions, clearly suggest that ultraviolet light is capable of modulating both clinical and immunologic features of IIMs. Studies on microchimerism are unraveling interesting associations in juvenile DM patients, and bolstering the hypothesis that myositis may be an 'allo-immune' disease. mRNA gene expression profiling is helping to increase our understanding of myositis pathogenesis, whilst animal models have provided new information on the roles of Th1 responses and nitric oxide synthase in muscle disease. New candidate genes have been examined in inclusion body myositis (IBM), and a novel gene transfer experiment has been conducted, which led to significant changes in expression of the IBM phenotype. SUMMARY: Improving the understanding of the immunogenetics and immunopathogenesis of the IIMs may in the future provide novel therapeutic targets, and thus improve outcomes in these difficult diseases.

Animals↗
PubMed1989

The immunogenetic relationship between anti-Ro(SS-A)/La(SS-B) antibody positive Sjögren's/lupus erythematosus overlap syndrome and the neonatal lupus syndrome.

We have described previously the clinical features of a unique group of anti-Ro(SS-A) antibody positive Sjogren's patients who have cutaneous features of lupus erythematosus, most commonly subacute cutaneous lupus erythematosus, defined as the Sjogren's/lupus erythematosus overlap syndrome. Three of these patients are also mothers of infants with the neonatal lupus erythematosus syndrome, characterized by cutaneous lesions resembling subacute cutaneous lupus erythematosus or congenital heart block. Patients with Sjogren's/lupus erythematosus overlap syndrome, subacute cutaneous lupus erythematosus, and mothers of infants with the neonatal lupus syndrome characteristically have autoantibodies to Ro(SS-A), and in many cases, La(SS-B) antigens. The present study was designed to test the hypothesis that anti-Ro(SS-A)/La(SS-B) positive Sjogren's/lupus overlap patients and mothers of infants with neonatal lupus erythematosus syndrome are immunogenetically homogenous and closely related. We report a strong association with HLA-B8, DR3, DQw2, and DRw52 phenotypes and the HLA-B8, DR3, DQw2, DRw52 extended haplotype in both patient cohorts. Furthermore, we describe disease associations with HLA-DR3/DRw6 heterozygotes in both patient groups. These data demonstrate that anti-Ro(SS-A)/La(SS-B) positive Sjogren's/lupus overlap patients and neonatal lupus syndrome mothers are immunogenetically closely related to each other and appear to be more closely related to both primary Sjogren's syndrome and subacute lupus erythematosus, than to classical systemic lupus erythematosus.

Antibodies, Antinuclear↗
PubMed1987

Evidence against an immunogenetic basis for diabetes in chronic pancreatitis.

A possible immunogenetic basis for diabetes in chronic pancreatitis was explored by studying 19 patients with both disorders, most of whom required treatment with insulin. In contrast to patients with insulin-dependent (Type 1) diabetes, patients with diabetes and chronic pancreatitis had residual beta cell function but blunted C-peptide responses to intravenous glucagon, absence of circulating islet cell antibodies, and HLA-DR types similar to control subjects and patients with chronic pancreatitis without diabetes. Diabetes complicating chronic pancreatitis is therefore not associated with the biochemical or immunogenetic markers characteristic of Type 1 diabetes.

Adult↗
PubMed1993

Electrophysiological and immunogenetic findings in recurrent monosymptomatic-type hypersomnia: a study of two unrelated Italian cases.

MSLT and immunogenetic findings in two unrelated Italian subjects with recurrent monosymptomatic hypersomnia are reported. In both patients MSLT documented a markedly increased daytime sleep propensity during the attacks without augmented REM sleep pressure. Both patients share the same HLA haplotype (HLA-DR1, DQ1) which has been found in Kleine-Levin syndrome. This makes these subtypes of recurrent hypersomnia indistinguishable one from the other, under the immunogenetic profile, but permits differentiation from narcolepsy which is HLA-DR2, DQ1 closely linked.

Adolescent↗
PubMed2002

Immunogenetic studies on malnutrition-modulated diabetes mellitus.

Genetic studies of malnutrition-related diabetes are few. We have analyzed the HLA class II gene polymorphism in malnutrition-modulated diabetes mellitus (MMDM), which was previously referred to as protein-deficient diabetes mellitus (PDDM) in the 1985 WHO classification. Insulin-dependent diabetes mellitus (IDDM) is a polygenic disorder with an autoimmune basis for disease development. In addition to HLA, a second susceptibility locus for IDDM has been identified to lie in the major histocompatibility class III region. Both IDDM and MMDM in eastern Indians are associated with DR3-DQ2 but not DR4-DQ8. The presence of autoantibodies to IDDM autoantigens in clinical MMDM either identifies the slow-onset form of IDDM or suggests autoimmunity different from that in IDDM. Our study demonstrates that the presence of GAD65 antibody and DR3-DQ2 positivity in MMDM patients identifies the underlying autoimmune mechanism in the etiology in eastern India. In autoantibody-negative MMDM patients an association with DR7-DQ2 is identified. The date obtained also indicate the possibility that MMDM can coexist with IDDM in these patients and that malnutrition could be one of the reasons for the slower onset in IDDM-prone individuals. The association of DR7-DQ2 suggests that there is a different immunogenetic background to MMDM than to IDDM. MICA is located in the MHC class I region and is expressed by monocytes, keratinocytes, and endothelial cells. Sequence determination of MICA gene identifies trinucleotide repeat (GCT) microsatellite polymorphism in exon 5. Five alleles with 4, 5, 6, and 9 repetitions of GCT or 5 repetitions of GCT with 1 additional nucleotide insertion (GGCT) are identified. The alleles are A4, A5, A5.1, A6, and A9. We studied the association of MICA alleles with IDDM (n = 52) and MMDM (n = 41) patients and healthy controls (n = 73) from Cuttack, eastern India. MICA was typed by PCR amplification, and fragment sizes were determined in an ABI prism DNA sequencer. Allele 9 of MICA is positively and allele 4 negatively associated with MMDM patients compared to controls. Allele 5 is positively associated with IDDM (OR 2.64, P < 0.05) when compared to controls. Our findings suggest that MMDM is immunogenetically different from IDDM in eastern India and that MIC-A is important in the pathogenesis of MMDM patients from Cuttack in eastern India.

Diabetes Complications↗
PubMed2004

Genetics of liver disease: immunogenetics and disease pathogenesis.

Understanding the genetic basis of "complex disease" has been heralded as one of the major challenges of the post genome era. However what are "complex diseases" and how will understanding the genetics of such diseases advance medical science? There has been a great deal of "hype" about the potential of the human genome mapping project. The three major claims are that this information will: (a) be used in diagnosis; (b) provide useful prognostic indices for disease management (including the development of individualised treatment regimens, based on the findings of both immunogenetic and pharmacogenetic studies); and (c) provide insight into the pathogenesis of these diseases. Of these three objectives the last has the greatest potential and is the least exaggerated claim. In this review I shall highlight major associations, discuss some of the practical issues that arise, and outline how current knowledge of the immunogenetic basis of chronic liver disease is beginning to inform the debate about disease pathogenesis.

Autoimmune Diseases↗
PubMed1983

Immunogenetic and clinical findings in idiopathic pulmonary fibrosis. Association with the B-cell alloantigen HLA-DR2.

In order to assess the role of immunogenetic factors in the pathogenesis of idiopathic pulmonary fibrosis (IPF), HLA-A, B, C, and DR typing was performed on 20 Caucasian patients with IPF seen from 1978 to 1980 and in 200 healthy blood donors. An increase in the frequency of the B-cell alloantigen, HLA-DR2, was observed; HLA-DR2 was found in 65% of patients with IPF compared with 26% of the control subjects (corrected p value = 0.005, chi-square = 11.476, relative risk = 5.286). Although not significant, increases were observed in HLA-B7 and HLA-A3, antigens known to be in linkage disequilibrium with HLA-DR2. The HLA-DR2 was observed in 12 of 14 patients with "ground glass linear" and "cystic honeycombing" radiographic patterns, whereas it was observed in only 1 of 6 patients with "ascinar nodular" radiographic patterns (p = 0.01). No other correlation was observed between HLA type and clinical, laboratory, or pathologic parameters. We conclude that immunogenetic factors, perhaps genes within the major histocompatibility complex, are relevant to the pathogenesis of IPF.

Adult↗
PubMed2003

Clinical, immunogenetic and outcome features of Hispanic systemic lupus erythematosus patients of different ethnic ancestry.

The aim of this study was to compare and contrast the clinical, immunogenetic and outcome features of two subgroups of Hispanic patients with systemic lupus erythematosus (SLE), one from Northern Spain (Spaniards) and one of from the USA (Hispano-Americans: Hispanics primarily of Mexican ancestry (Amerindian and Spaniard backgrounds). Patients with SLE as per the American College of Rheumatology classification criteria, from two University-affiliated Hospitals (Universidad de Cantabria) and disease of five or less years in duration (n = 28) and with four years of follow up constituted the Spaniard subgroup. Fifty-two patients of Hispano-American ancestry from the LUMINA (Lupus in Minority populations: Nature versus Nurture) cohort constituted the Hispano-American subgroup. Patients were studied using a similar protocol. In short, sociodemographic, clinical, immunological, immunogenetic and psychosocial and behavioral features were obtained at enrollment into the study (baseline visit) and yearly thereafter. The relationship between these variables and disease activity at baseline and over time, as measured by the systemic lupus activity measure (SLAM) and disease damage, as measured by the SLICC (Systemic Lupus International Collaborating Clinics) Damage Index (SDI) were determined. Variables found to be significant at P = 0.10 were then entered into multivariable linear regression models with disease activity at baseline and over time, and damage as the outcome measures. Patients of Hispano-American and Spaniard ethnicity had comparable sociodemographic features except for home density, which was higher among the Hispano-Americans. HLA-DRB1*08 was associated with SLE among the Hispano-Americans but not among the Spaniards. Hispano-American patients had more severe disease as manifested by more frequent clinical manifestations (renal and neurological), higher SLAM scores at baseline and over time and higher SDI scores at the year 4 visit (that despite the fact that Hispano-American patients had overall shorter disease duration than the Spaniard patients). Hispano-American ethnicity, younger age at disease onset and the number of ACR criteria at baseline and over time were consistently associated with disease activity, whereas increased home density and the absence of HLA-DRB1*0301 were significant predictors only over time. Disease damage was associated with disease activity over time, the number of ACR criteria at baseline, increased home density and the presence of HLA-DRB1*08. This is the first longitudinal study of SLE in two different Hispanic subgroups. Hispanics with a strong Amerindian background have a more serious disease than that observed in Spaniards. Genetic and socio-economic differences between these two Hispanic subgroups probably account for these findings.

Adult↗
PubMed1985

Immunogenetics of Hashimoto's and Graves' diseases.

Haplotypes of the human major histocompatibility complex (HLA) and the immunoglobulin allotype (Gm) were analyzed in all 243 members of 37 families in which 2 or more first degree relatives had Graves' disease. In 10 families with 70 members where 1 or more first degree relatives had Hashimoto's disease, 26 (37%) had Graves' disease, and 14 (20%) had Hashimoto's disease. In the other 27 families, consisting of 173 members, 70 (40%) had Graves' disease, and none had Hashimoto's disease. The disease-associated haplotypes of HLA and Gm for each family were identified by determining the haplotypes concordant in 2 members with Graves' disease. In 10 families with Graves' and Hashimoto's diseases, all 14 members with Hashimoto's disease had the same disease-associated haplotypes of both HLA and Gm as had members with Graves' disease in each family. Among 96 members with Graves' disease in 37 families, 74 were used for the determination of the disease-associated haplotypes. In the remaining 22 members with Graves' disease, 21 had both disease-associated haplotypes in their families. Our findings in these families suggest that 1) in Hashimoto's disease as in Graves' disease, two genes linked to HLA and Gm, respectively, control the susceptibility of the disease; 2) common immunogenetic factors are involved in the pathogenesis of both Hashimoto's and Graves' disease, and 3) those who do not have immunogenetic factors are very unlikely to develop Hashimoto's or Graves' disease.

Female↗
PubMed2006

Multiple sclerosis with and without CSF bands: clinically indistinguishable but immunogenetically distinct.

We sought to determine whether Swedish patients with multiple sclerosis (MS) with and without oligoclonal bands (OCBs) in the CSF constitute distinct subpopulations, clinically and immunogenetically. Our findings indicate that OCB-negative MS shares the same clinical features as OCB-positive MS regarding female predominance, age at onset, proportion of primary progressive cases, rate of MRI positivity, and disease severity. Our HLA-DRB1 genotyping results suggest, however, that OCB-positive and OCB-negative MS are immunogenetically distinct.

Female↗
PubMed1985

Development of a semi-inbred line of Landrace pigs. I. Breeding performance and immunogenetic characteristics.

During 15 years of inbreeding of pigs (Canadian Landrace) a semi-inbred line has been developed. The inbreeding coefficient (FX) is 0.84, which theoretically corresponds to between 8-9 generations of brother/sister matings. At the highest inbreeding level (0.84) the mean number of newborn piglets in the litter was 7.2 (5 litters, n = 36) including 5 stillborn (13.8%). The mean birth weight of the litter was 8.56 kg (5 litters, n = 31) the mean piglet birth weight was 1.23 kg and at the age of 21 days the mean weight of a litter was 33.24 kg with a mean piglet weight of 5.44 kg. During inbreeding, immunogenetic alloantigenic systems were investigated. Of 15 known erythrocyte systems, alleles of loci J, K, and of the most polymorphic system E, segregated. As to other immunogenetic systems (histocompatibility, leucocyte and allotypes) 2 SLA haplotypes (major histocompatibility complex) and 2 alleles of the SLC leucocyte system segregated. Allotransplants of the skin in SLA compatible siblings survived for a mean of 50.7 days (n = 77) compared with 10.8 days (n = 29) in non-inbred siblings. Tests of blastic transformation activated by T and B lymphocyte mitogens revealed a normal cell-mediated immune response. After immunization with some cell membrane alloantigens a normal humoral response was also recorded. All tested animals were halothane-resistant and tolerated a 10-min exposure to 5% without developing malignant hyperthermia. Depression due to inbreeding was manifested by a reduced reproductive ability (smaller number of piglets, frequent incidence of gonadal hypoplasia, diminution or loss of libido).

Animals↗
PubMed2005

[Greater survival among patients with immunogenetic markers of rapid progression to AIDS: subsidies for nursing care].

This study sought subsidies for improving nursing care programs for AIDS patients and aimed to verify the influence of changes in sexual behavior, including the adoption of safe sex practices, associated with the survival of AIDS patients with immunogenetic markers of rapid disease progression. 27 AIDS patients were interviewed, with genetic predisposition to rapid progression to AIDS. Genes were typified through the polymerase chain reaction. In spite of the presence of immunogenetic factors, associated with individual predisposition to a rapid evolution of the disease, changes in sexual behavior, including safe sex practices and antiretroviral therapy, may be related to greater survival. This suggests that counseling, detection of risk attitudes and health education, focusing on positive health behavior, are tools nursing must use with HIV-positive patients, with a view to better quality of life and greater survival among these individuals, even among those with genetic predisposition to rapid disease progression.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Immunogenetic and clinical characterization of slowly progressive IDDM.

OBJECTIVE: To examine the clinical and immunogenetic heterogeneity of IDDM. RESEARCH DESIGN AND METHODS: We divided 207 IDDM patients into groups based on the interval from clinical onset to initiation of insulin therapy: group A (< 3 mo, acute clinical-onset group, n = 134), group B (3-12 mo, intermediate group, n = 31), and group C (> or = 13 mo, slowly progressive group, n = 42). Immunogenetic and clinical markers were compared between group A and group C. RESULTS: The mode age of onset was higher in group C (52 yr) than group A (10 yr). Group C had a higher prevalence of islet cell antibodies (42.9%, 18 of 42) than group A (25.4%, 34 of 134, P = 0.05). Serum C-peptide immunoreactivity assayed by radioimmunoassay in response to a 100-g oral glucose tolerance test was significantly higher in group C than in group A. Group C patients were also more likely to have a family history of NIDDM (26.1%, 11 of 42) among their first-degree relatives than group A patients (11.2%, 15 of 134, P = 0.039). The prevalences of family history of IDDM and endocrine autoimmune diseases were not different between groups C and A. The frequency of complications of endocrine autoimmune disease was not different between group A (6.7%, 9 of 134) and group C (2.3%, 1 of 42). Significant associations with two class I major histocompatibility complex antigens (HLA-A24 and -Bw54) and one class II antigen (HLA-DR4) were observed in group A. Group A patients were associated with three diabetogenic HLA-DQ haplotypes including DQA1*0301-DQB1*0401, DQA1*0301-DQB1*0302, and DQA1*0301-DQB1*0303. In contrast, group C lacked the association with class I antigens, although HLA-DR4 and HLA-DQA1*0301-DQB1*0401 were more common in this group than in control subjects. CONCLUSIONS: These results indicate that the clinical subtype with slowly progressive course (slowly progressive IDDM) has distinct findings including late-age onset, high prevalence of islet cell antibodies, preserved beta-cell function, and high family history of NIDDM. An additive effect of class I and class II major histocompatibility complex antigens is suggested as an explanation for the acute clinical manifestations and more severe beta-cell destruction in group A patients.

Adolescent↗
PubMed2000

Gliadin antibodies in adult insulin-dependent diabetes--autoimmune and immunogenetic correlates.

Gliadin antibody (GA) tests used in screening for coeliac disease (CD) frequently yield positive GA results without accompanying CD in cases of diabetes mellitus type 1 (DM-1). To enlighten this phenomenon we screened 848 DM-1 patients for IgA- and IgG-GA. Subsequently, 16 out of 19 high titre GA patients (6 with CD) were compared with 37 low titre DM-1 patients matched for sex, age and disease duration, for autoimmune and immunogenetic markers. Chronic thyroiditis and thyroid peroxidase (TPO) antibody positivity were more frequent in the GA-positive than in the GA-negative sub-group (38 vs. 2.7%, p = 0.003, and 69 vs. 27%, p < 0.00, respectively). The tissue transglutaminase (tTg) IgA titres correlated with CD but not with GA. tTg IgG titres were lower in GA-positive individuals (p = 0.0012). GA-positivity correlated with a higher titre of factor XIII IgA antibodies (p < 0.001). GA-positive DM-I patients were characterised by a distinct immunogenetic profile; the risk of HLA DQB1*02 was lower among GA-positive patients than among GA-negatives (OR 0.4, preventive fraction 0.43). All CD patients were HLA DRB1*03-DQB1* 02-positive, but none of the five patients with normal biopsies. GA-positive patients instead had HLA DRB1*13 in 37.5% as compared to 8.6% in GA-negative (OR 6.4, etiologic fraction 0.32). Thus, the occurrence of positive GA in DM-1 is correlated to TPO antibody positivity, thyroiditis and factor XIII IgA antibodies, but inversely correlated to tTg IgG, and seems to be associated with another HLA haplotype than that previously found to be associated with CD.

Addison Disease↗
PubMed1994

Poultry immunogenetics: which way do we go?

A major goal in poultry immunogenetics is the enhancement of innate immunoresponsiveness and resistance to disease. This may be pursued by studying either single genes or polygenic traits. The MHC is perhaps the best-characterized family of host genes that modulates response to a variety of antigens and pathogenic challenges. The association of different MHC alleles with disease resistance has been known for decades. But only recently has analysis at the DNA level opened new avenues of understanding and new opportunities for application of genetic variation in the MHC with immunoresponsiveness. An alternate approach to molecular analysis is selection for a desired phenotype controlled by polygenes. Several studies have illustrated the successful alteration of immunoresponsiveness by genetic selection for antibody production. Recently, a selection program based upon multiple traits of immune response was conducted. Results of this project demonstrated that selection on multiple immune-response traits altered immunophysiology, MHC allelic frequencies, and disease resistance. Several areas for future pursuits in poultry immunogenetics research are proposed.

Animal Husbandry↗
PubMed2000

Immunogenetics of peripheral arteriopathies.

Takayasu's arteritis (TA) and thrombangiitis obliterans (Buerger's disease) are idiopathic, inflammatory arteriopathies with strong indications for the involvement of autoimmunity and host genetic factors in their immunopathogenesis. The exact etiology of these arteriopathies still remains unknown even after almost nine decades of their description. A series of immunogenetic studies conducted worldwide seeking to define genetic factors in governing immune response in these diseases have yielded conflicting results on the involvement of HLA molecules. While an association of HLA-B5 or its molecular subtypes with Takayasu's arteriitis has been emphasized in patients from Japan, Korea and India, no such association has been reported in Mexican and North American patients. On the other hand, a limited data is available on the association of HLA antigens with Buerger's disease. In this article, we provide an overview of the immunogenetics of Buerger's disease and Takayasu's arteriitis in the context of studies in North Indian patients and those in other ethnic groups. Our studies indicate a positive association of Takayasu's arteriitis with the HLA-B5 molecule with no preferential association with its two major subtypes. In Buerger's disease, we have observed a strong positive association with HLA-DRB1*1501 consistent with the findings in Japanese patients. These results suggest an important role of HLA linked factors in governing susceptibility to both arteriopathies.

Adult↗