The Importance of Sex Stratification in Autoimmune Disease Biomarker Research: A Systematic Review

Abstract

The immune system is highly dynamic and regulated by many baseline characteristic factors. As such, significant variability may exist among different patient groups suffering from the same autoimmune disease (AD). However, contemporary research practices tend to take the reductionist aggregate approach: they do not segment AD patients before embarking on biomarker discovery. This approach has been productive: many novel AD biomarkers have recently been discovered. Yet, subsequent validation studies of these biomarkers tend to suffer from a lack of specificity, sensitivity, and reproducibility which hamper their translation for clinical use. To enhance reproducibility in validation studies, an optimal discovery-phase study design is paramount: one which takes into account different parameters affecting the immune system biology. In this systematic review, we highlight need for stratification in one such parameter, i.e., sex stratification. We will first explore sex differences in immune system biology and AD prevalence, followed by reported sex-bias in the clinical phenotypes of two ADs—one which more commonly affects females: systemic lupus erythematosus, and one which more commonly affects males: ankylosing spondylitis. The practice of sex stratification in biomarker research may not only advance the discovery of sex-specific AD biomarkers but more importantly, promote reproducibility in subsequent validation studies, thus easing the translation of these novel biomarkers from bench to bedside to improve AD diagnosis. In addition, such practice will also promote deeper understanding for differential AD pathophysiology in males and females, which will be useful for the development of more effective interventions for each sex type.

Introduction

Autoimmune diseases (ADs) are a complex class of diseases resulting from the immune system failure to differentiate between self and foreign antigens (1). This misrecognition directs the immune system to attack self-antigens, which consequently modifies the biological functions of the affected tissues. Ultimately, tissue damage and dysfunctions ensue and present as clinical symptoms. However, the onset of clinical symptoms is often delayed and occurs following irreversible damage to the affected tissues or organ. There is a global urgency for the discovery of specific and sensitive biomarkers for an early detection of ADs. Additionally, the ideal AD biomarker(s) should also be surrogate for disease severity, progression to disability and response to therapy (2).

The discovery of such biomarkers is not straightforward. Currently, validated biomarkers do not yet fulfill this tall order (we list validated biomarkers from select ADs in Table S1 in Supplementary Material). The immune system biology is dynamic—it varies with genetic background, age, sex, and the environment (3–11). Thus, patients with varying characteristics may present with different clinical phenotype and biomarkers despite suffering from the same AD. Conventional biomarker research strategy has been reductionist and aggregated: they compare all AD patients and controls of mixed baseline characteristics. This approach, although suboptimal, has been productive, leading to the discovery of many novel AD biomarkers (2). Yet, validation and clinical translation of such novel biomarkers have proven to be challenging, possibly due to: (1) lack of control and patient group stratification and matching; (2) inappropriate biomarker validation strategy; and/or (3) techniques used in clinical trials (12, 13). In this review, we highlight the importance of sex stratification in AD biomarker research prior to the discovery-phase, by drawing attention to the fact that: (1) ADs display stronger female bias and (2) present with different disease trajectories in males and females. There are apparent sex differences in AD pathophysiology. These need to be recognized and hopefully over time, incorporated into AD research efforts, clinical diagnosis, and management for a better patient outcome.

Methods

Results

Males and Females Have Different Biological Landscapes

A report released by the Institute of Medicine in 2001, “Exploring the Biological Contributions to Human Health: Does Sex Matter?” describes in great detail the different factors that contribute to biological differences in males and females, and how these differences affect health and diseases in these two sexes (11). Beyond the overt differences in reproductive biology, males and females show differences in immune functions, brain organization, pain perception, gene dosing (for genes that escape X-chromosome inactivation) as well as metabolism, lifestyle, and physical performance, all of which may alter pharmacokinetic and pharmaco-dynamic variables in the two sexes (11). Males and females operate from different biological landscapes, be it in healthy, diseased, or recovering states.

To explain autoimmune sex dimorphism, it becomes necessary to first describe the cellular and hormonal interactions found in normal immune regulation and thereafter extrapolate these to autoimmune phenomena. In comparison to the innate immunity, the adaptive immune system is known to be significantly affected by sex. Adult females in general, show stronger immune responses than others, and these responses are partially modulated by sex hormones (3, 4, 6, 11). Other contributing parameters include genetic and environmental factors; we refer the readers to a string of excellent reviews for in-depth discussions of these factors (3–10). We summarize the sex dichotomy in normal immune system biology in Table 1 (3). All components of the innate immunity, such as the toll-like receptor pathway, antigen-presenting cells, dendritic cells, macrophages, granulocytes, and natural killer cells, show stronger activity in females. Despite the lower CD8+ T-cell count, the cytotoxicity of each of these cells is higher in females. As estrogen and progesterone levels wax and wane during the menstrual cycle, the balance between T_H1 and T_H2 system fluctuates. This balance and its interactions with other systems such as the T_H17, T_reg, and B-cells dictate the overall immune response. Disruptions to the equilibrium of these different systems lead to different AD pathologies and disease onsets in males and females (6).

ADs Show Stronger Female Bias

There are currently more than one hundred identified ADs, with 24 showing high prevalence (occurring in 1 per 10,000 people) (212). 71% of these common ADs (Figure 1 below, in bold) are more prevalent in females than males (>50% female prevalence), suggestive of a stronger female bias (213). However, these data were an aggregated one from “world,” and “USA” (213). In Table 2, we stratify some of these ADs by geographical location (as a proxy for ethnicity), in order to gain a better insight of each AD’s prevalence in different parts of the world. In addition, we include three ADs which have been reported to be more prevalent in males: idiopathic pulmonary fibrosis (IPF), ankylosing spondylitis (AS), and Guillain–Barré syndrome (GBS). Table 2 shows that female predominance prevails in all three systemic ADs. Regardless of the geography, females are more than thrice as likely as males to suffer from systemic ADs. For instance, Spanish women are 18.6 times more likely than men to suffer from Sjögren’s syndrome (SS). A similar trend is also observed with endocrine ADs: Grave’s disease and Hashimoto’s thyroiditis (HT). In India, the female to male ratio for HT is an astonishing 21.7 to 1. Another strong female bias (at least a 2:1 female to male ratio worldwide) is observed with some gastrointestinal and hepatic ADs (primary biliary cholangitis and autoimmune hepatitis), as well as a musculoskeletal AD (rheumatoid arthritis).

Figure 1

Although a strong female preponderance was observed with other ADs, these tend to vary with geographical locations. For example, antiphospholipid syndrome shows a female to male ratio of at least 3:1 worldwide, except in Spain and Italy, where it shows lower ratios (2.1:1 and 1.7:1, respectively). Immune thrombocytopenic purpura (ITP) was reported to have a 70% female prevalence in Denmark (213); however, the sex ratio is much lower in our dataset, ranging from 1.1:1 in the USA to 1.7:1 in France. Asian females seem to be more likely to get ITP than other ethnicities, with a female to male ratios ranging from 1.9:1 in India to 4.3:1 in Singapore. Other ADs reported include celiac disease (CoD) and ulcerative colitis (UC), which affected 57 and 65% of females, respectively (213). The female-to-male ratios for CoD and UC vary in our dataset, favoring males or females depending on geography. In Italy, UK, and India, males are more likely to suffer from CoD than females, whereas the reverse is true in Denmark and Sweden. In Asia, males are more likely to suffer from UC than in the Western world. AS and GBS show greater bias toward males, regardless of the geographical locations. In IPF, however, male predominance was observed all around the world except for the North Americas.

ADs Have Different Trajectories in Different Sexes

Autoimmune diseases are quintessentially immune system disorders. As the biology of the immune system varies between the two sexes, one would expect ADs to have different disease trajectories in males and females. Here, we utilize a female-biased AD: systemic lupus erythematosus (SLE), as well as a male-biased AD: ankylosing spondylitis (AS) to exemplify sex-bias in disease progression, complications, and mortality. SLE and AS data are stratified by clinical data, geography, and period of study, since older studies may suffer from delayed diagnoses in male SLE and female AS patients (Tables 3–6).

In SLE, clinical phenotypes show sex-bias. Alopecia, photosensitivity, malar rash, Raynaud’s phenomenon, musculoskeletal complications, oral ulcers as well as psychiatric disorders are female-biased (Table 3). In addition, females are more likely to suffer from relapses and a concurrent diagnosis for SS. Male-specific clinical phenotypes include discoid lesions, serositis, renal disease, seizure, and peripheral neuropathy, as well as cardiovascular complications. Males also tend to display constitutional symptoms and higher score in Systemic Lupus Erythematosus Disease Activity Index, indicative of a higher disease activity. Indeed, higher mortality has been reported in male patients vs female patients. Serology in SLE also shows some sex-bias: females SLE patients more frequently present with higher erythrocyte sedimentation rate (ESR) and test positive for anti-SSA/Ro while the male SLE patients more frequently test positive for lupus anticoagulant, anti-Sm, anti-dsDNA, and hypocomplementemia.

In AS, clinical phenotypes also show some degree of sex-bias. Male AS patients tend to have disease onset at younger age and present with higher CRP, more back pain, knee involvement, higher scores for BASRI (including BASRI-spinal and BASRI-hip), radiographic sacroilitis, higher modified Stoke Ankylosing Spondylitis Spinal Score, lower functional indices (occiput-to-wall and finger-to-floor distances), but higher SF-36 mental and physical scores. Female AS patients, on the other hand, present more with AS family history, higher Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) score, enthesitis, more numbers of swollen, tender joints and peripheral arthritis but higher ASQoL score. Notably, in a multivariate model, Lee et al. found that for a given level of radiographic damage, female AS patients have more functional limitations than their male counterparts (200).

Discussion

In this systematic review, we summarize sex differences in immune system biology, AD prevalence, as well as clinical phenotypes of SLE and AS. Data accrued highlight female predominance in common ADs, although there exist geographical differences in some cases. These observed geographical differences are suggestive of potential contributions of genetics and environmental factors toward AD pathology.

In SLE, disease complications and serology seem to show sex-bias. Alopecia, for example, is exclusively observed in females just as serositis is exclusively seen in males. It is interesting how the serology in these males and females is reflective of sex-bias in clinical phenotypes. In The Genetic Profile Predicting the Phenotype (PROFILE) multiethnic cohort of 2,322 SLE patients, anti-Sm were significantly associated with antinuclear antibody, anti-double-stranded DNA (dsDNA), and clinical phenotypes, such as serositis, renal involvement, psychosis, vasculitis, Raynaud’s phenomenon, hemolytic anemia, leukopenia, lymphopenia, and arterial hypertension (214). Furthermore, double positive serology for anti-Sm and anti-dsDNA has been strongly associated with renal involvement (215–218) and higher disease activity (219). Most of these clinical phenotypes are male-specific SLE complications (Tables 3 and 4). Similarly, anti-SSA/Ro antibodies have been reported to be strongly associated with low C3 (hypocomplementemia) and clinical phenotypes such as photosensitivity, subacute cutaneous lupus erythematosus, cutaneous vasculitis (palpable purpura), hematological disorder (anemia, leukopenia, and thrombocytopenia) (220–227), as well as Jaccoud’s arthropathy (a type of arthritis) (228, 229). These phenotypes show female bias in our dataset (Tables 3 and 4). There are some clinical phenotypes such as mucocutaneous and hematological involvements, vasculitis, and association of anti-SSA/Ro with low C3 that differ between these correlation studies and our dataset. This may arise either from ethnic or age differences in the different study groups, or the size of the study groups. The trend for renal involvement persists in all of the studies we have analyzed; however, this clinical phenotype may or may not show a statistical difference for sex-bias owing to the low number of male SLE patients in some studies.

We also observed sex-bias in our dataset for AS clinical phenotypes: female AS patients present with enthesitis and higher BASDAI scores, while male patients present with higher BASRI scores. AS is clinically tested with HLA-B27, ESR, and CRP. While some studies suggested that high CRP is more significantly seen in male patients and high ESR with female patients, many other studies have not come to similar conclusions.

The findings from SLE and AS suggest that disease phenotypes differ between males and females. In some cases, these diseases arguably have higher activity in the sex having lower prevalence. Awareness of sex-bias in disease presentation is crucial for early diagnosis, as well as treatment strategies for ADs in different sexes. More importantly, such awareness may guide the development of improved study design strategies for biomarker discovery.

Future Direction and Conclusion

Timely diagnosis and treatment can be very effective for AD patients (230, 231) and biomarkers have great potential to enable it. Although AD biomarkers discovery is thriving, the same cannot be said of their clinical translation. Many biomarker projects fail at validation/replication stage (13) due to suboptimal sensitivity and specificity, as well as reproducibility in different studies (12). A few potential contributing factors to this observed failure include suboptimal infrastructure, study design, and execution in discovery-phase (12). Suboptimal study design includes small sample numbers, lack of patient history and subject matching (in terms of age, race, and sex) (12). Here we highlight the importance of sex stratification in biomarker discovery studies to promote reproducibility in replication/validation stage. Drawing example from SLE and AS, we note that differential clinical phenotypes exist in male and female patients. Different sexes may require different biomarkers for proper diagnosis of the same disease. From SLE serology we learn that some biomarkers are more frequently detected in one specific sex, and they show strong associations with sex-biased clinical phenotypes. Such specific associations may be missed when data from both sexes are aggregated.

In addition to enhancing sex-specific biomarker discovery and promoting reproducibility, a thorough understanding of sex differences in autoimmune milieu may guide disease prevention, diagnosis, and management. Our findings in Table 2 clearly demonstrate a higher prevalence ADs among females. Breast cancer screening mammography among women at average risk aged 50–74 has been shown to reduce breast cancer mortality by 30–40% (232). These findings suggest potential benefits of AD screenings specifically for women, for early AD detection and reduction of mortality rates through early intervention. Another plausible area of further study is to sex-stratify serological benchmarks for males and females, in light of varying cytokine levels and activity in different sexes as observed in Table 1. We have limited our scope in this review to SLE, AS and sex stratification. Further stratifications for improved patient segmentation and more specific biomarker discovery may include stratifications by age, ethnicities and disease stages.

References

• 1

  MacKayIRBurnetM. Sir, 1899–1985, Autoimmune Diseases: Pathogenesis, Chemistry and Therapy. Springfield, IL: Thomas (1963).

  • Google Scholar

• 2

  HueberWRobinsonWH. Proteomic biomarkers for autoimmune disease. Proteomics (2006) 6(14):4100–5.10.1002/pmic.200600017

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 3

  KleinSLFlanaganKL. Sex differences in immune responses. Nat Rev Immunol (2016) 16(10):626–38.10.1038/nri.2016.90

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 4

  FishEN. The X-files in immunity: sex-based differences predispose immune responses. Nat Rev Immunol (2008) 8(9):737–44.10.1038/nri2394

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 5

  NgoSTSteynFJMcCombePA. Gender differences in autoimmune disease. Front Neuroendocrinol (2014) 35(3):347–69.10.1016/j.yfrne.2014.04.004

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 6

  FairweatherDFrisancho-KissSRoseNR. Sex differences in autoimmune disease from a pathological perspective. Am J Pathol (2008) 173(3):600–9.10.2353/ajpath.2008.071008

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 7

  McCombePAGreerJMMackayIR. Sexual dimorphism in autoimmune disease. Curr Mol Med (2009) 9(9):1058–79.10.2174/156652409789839116

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 8

  KinderJMStelzerIAArckPCWaySS. Immunological implications of pregnancy-induced microchimerism, nature reviews. Immunology (2017) 17(8):483–94.10.1038/nri.2017.38

  • CrossRef
  • Google Scholar

• 9

  MarsonAHousleyWJHaflerDA. Genetic basis of autoimmunity. J Clin Invest (2015) 125(6):2234–41.10.1172/JCI78086

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 10

  FloreaniALeungPSGershwinME. Environmental basis of autoimmunity. Clin Rev Allergy Immunol (2016) 50(3):287–300.10.1007/s12016-015-8493-8

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 11

  WizemannTPardueMInstitute of Medicine (US) Committee on Understanding the Biology of Sex and Gender Differences. Exploring the Biological Contributions to Human Health: Does Sex Matter?Washington, DC: National Academies Press (US) (2001).

  • Google Scholar

• 12

  DruckerEKrapfenbauerK. Pitfalls and limitations in translation from biomarker discovery to clinical utility in predictive and personalised medicine. EPMA J (2013) 4(1):7.10.1186/1878-5085-4-7

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 13

  WillisJCLordGM. Immune biomarkers: the promises and pitfalls of personalized medicine. Nat Rev Immunol (2015) 15(5):323–9.10.1038/nri3820

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 14

  MurphyKP. Janeway’s Immunobiology. 8th ed. United States: Garland Science, Taylor & Francis Group, LLC (2012).

  • Google Scholar

• 15

  MurphyGIsenbergD. Effect of gender on clinical presentation in systemic lupus erythematosus. Rheumatology (2013) 52(12):2108–15.10.1093/rheumatology/ket160

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 16

  Muñoz-GrajalesCGonzálezLAAlarcónGSAcosta-ReyesJ. Gender differences in disease activity and clinical features in newly diagnosed systemic lupus erythematosus patients. Lupus (2016) 25(11):1217–23.10.1177/0961203316635286

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 17

  Yacoub WasefSZ. Gender differences in systemic lupus erythematosus. Gend Med (2004) 1(1):12–7.10.1016/S1550-8579(04)80006-8

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 18

  BoodhooKDLiuSZuoX. Impact of sex disparities on the clinical manifestations in patients with systemic lupus erythematosus: a systematic review and meta-analysis. Medicine (Baltimore) (2016) 95(29):e4272.10.1097/MD.0000000000004272

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 19

  JovaniVBlasco-BlascoMRuiz-CanteroMTPascualE. Understanding how the diagnostic delay of spondyloarthritis differs between women and men: a systematic review and metaanalysis. J Rheumatol (2017) 44(2):174–83.10.3899/jrheum.160825

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 20

  GutcherIBecherB. APC-derived cytokines and T cell polarization in autoimmune inflammation. J Clin Invest (2007) 117(5):1119–27.10.1172/JCI31720

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 21

  OchielDORossollRMSchaeferTMWiraCR. Effect of oestradiol and pathogen-associated molecular patterns on class II-mediated antigen presentation and immunomodulatory molecule expression in the mouse female reproductive tract. Immunology (2012) 135(1):51–62.10.1111/j.1365-2567.2011.03512.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 22

  WiraCRRossollRM. Antigen-presenting cells in the female reproductive tract: influence of sex hormones on antigen presentation in the vagina. Immunology (1995) 84(4):505–8.

  • Pubmed Abstract
  • Google Scholar

• 23

  LinAAWojciechowskiSEHildemanDA. Androgens suppress antigen-specific T cell responses and IFN-gamma production during intracranial LCMV infection. J Neuroimmunol (2010) 226(1–2):8–19.10.1016/j.jneuroim.2010.05.026

  • CrossRef
  • Google Scholar

• 24

  HuygenKPalflietK. Strain variation in interferon gamma production of BCG-sensitized mice challenged with PPD II. Importance of one major autosomal locus and additional sexual influences. Cell Immunol (1984) 85(1):75–81.10.1016/0008-8749(84)90279-X

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 25

  AmadoriAZamarchiRDe SilvestroGForzaGCavattonGDanieliGet alGenetic control of the CD4/CD8 T-cell ratio in humans. Nat Med (1995) 1(12):1279–83.10.1038/nm1295-1279

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 26

  FeldmanCHHirakiLTLiuJFischerMASolomonDHAlarconGSet alEpidemiology and sociodemographics of systemic lupus erythematosus and lupus nephritis among US adults with Medicaid coverage, 2000–2004. Arthritis Rheum (2013) 65(3):753–63.10.1002/art.37795

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 27

  TanTCFangHMagderLSPetriMA. Differences between male and female systemic lupus erythematosus in a multiethnic population. J Rheumatol (2012) 39(4):759–69.10.3899/jrheum.111061

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 28

  JiJSundquistJSundquistK. Gender-specific incidence of autoimmune diseases from national registers. J Autoimmun (2016) 69:102–6.10.1016/j.jaut.2016.03.003

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 29

  ChicheLJourdeNUlmannCManciniJDarqueABardinNet alSeasonal variations of systemic lupus erythematosus flares in southern France. Eur J Intern Med (2012) 23(3):250–4.10.1016/j.ejim.2011.12.006

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 30

  YongJLCKillingsworthMCLaiK. Renal biopsy pathology in a cohort of patients from southwest Sydney with clinically diagnosed systemic lupus erythematosus. Int J Nephrol Renovasc Dis (2013) 6:15–26.10.2147/IJNRD.S34357

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 31

  LiuSSYeDLouJFanZYeDQ. No evidence for a genetic association of IRF4 with systemic lupus erythematosus in a Chinese population. Z Rheumatol (2014) 73(6):565–70.10.1007/s00393-013-1279-6

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 32

  MokCCLauCSChanTMWongRW. Clinical characteristics and outcome of southern Chinese males with systemic lupus erythematosus. Lupus (1999) 8(3):188–96.10.1191/096120399678847605

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 33

  ShimJSSungYKJooYBLeeHSBaeSC. Prevalence and incidence of systemic lupus erythematosus in South Korea. Rheumatol Int (2014) 34(7):909–17.10.1007/s00296-013-2915-9

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 34

  OhtaANagaiMNishinaMTomimitsuHKohsakaH. Age at onset and gender distribution of systemic lupus erythematosus, polymyositis/dermatomyositis, and systemic sclerosis in Japan. Mod Rheumatol (2013) 23(4):759–64.10.1007/s10165-012-0733-7

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 35

  NanniniCJebakumarAJCrowsonCSRyuJHMattesonEL. Primary Sjögren’s syndrome 1976–2005 and associated interstitial lung disease: a population-based study of incidence and mortality. BMJ Open (2013) 3(11): e003569.10.1136/bmjopen-2013-003569

  • CrossRef
  • Google Scholar

• 36

  EatonWWRoseNRKalaydjianAPedersenMGMortensenPB. Epidemiology of autoimmune diseases in Denmark. J Autoimmun (2007) 29(1):1–9.10.1016/j.jaut.2007.05.002

  • CrossRef
  • Google Scholar

• 37

  SerorRGottenbergJEDevauchelle-PensecVDubostJJLe GuernVHayemGet alEuropean league against rheumatism Sjogren’s syndrome disease activity index and European league against rheumatism Sjogren’s syndrome patient-reported index: a complete picture of primary Sjogren’s syndrome patients. Arthritis Care Res (2013) 65(8):1358–64.10.1002/acr.21991

  • CrossRef
  • Google Scholar

• 38

  Diaz-LopezCGeliCCorominasHMalatNDiaz-TornerCLlobetJMet alAre there clinical or serological differences between male and female patients with primary Sjogren’s syndrome?J Rheumatol (2004) 31(7):1352–5.

  • Google Scholar

• 39

  Downie-DoyleSBayatNRischmuellerMLesterS. Influence of CTLA4 haplotypes on susceptibility and some extraglandular manifestations in primary Sjogren’s syndrome. Arthritis Rheum (2006) 54(8):2434–40.10.1002/art.22004

  • CrossRef
  • Google Scholar

• 40

  MisraRHissariaPTandonVAggarwalAKrishnaniNDabadghaoS. Primary Sjogren’s syndrome: rarity in India. J Assoc Physicians India (2003) 51:859–62.

  • Pubmed Abstract
  • Google Scholar

• 41

  TsuboiHAsashimaHTakaiCHagiwaraSHagiyaCYokosawaMet alPrimary and secondary surveys on epidemiology of Sjögren’s syndrome in Japan. Mod Rheumatol (2014) 24(3):464–70.10.3109/14397595.2013.843765

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 42

  ZhaoYLiYWangLLiX-FHuangC-BWangG-Cet alPrimary Sjögren syndrome in Han Chinese: clinical and immunological characteristics of 483 patients. Medicine (2015) 94(16):e667.10.1097/MD.0000000000000667

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 43

  RaghuGWeyckerDEdelsbergJBradfordWZOsterG. Incidence and prevalence of idiopathic pulmonary fibrosis. Am J Respir Crit Care Med (2006) 174(7):810–6.10.1164/rccm.200602-163OC

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 44

  RaghuGChenSYYehWSMaroniBLiQLeeYCet alIdiopathic pulmonary fibrosis in US Medicare beneficiaries aged 65 years and older: incidence, prevalence, and survival, 2001–11. Lancet Respir Med. (2014) 2(7):566–72.10.1016/S2213-2600(14)70101-8

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 45

  HyldgaardCHilbergOMullerABendstrupE. A cohort study of interstitial lung diseases in central Denmark. Respir Med (2014) 108(5):793–9.10.1016/j.rmed.2013.09.002

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 46

  FerraraGCarlsonLPalmAEinarssonJOlivestenCSkoldM. Idiopathic pulmonary fibrosis in Sweden: report from the first year of activity of the Swedish IPF-registry. Eur Clin Respir J (2016) 3:31090.10.3402/ecrj.v3.31090

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 47

  Pedraza-SerranoFLópez de AndrésAJiménez-GarcíaRJiménez-TrujilloIHernández-BarreraVánchez-MuñozGSet alRetrospective observational study of trends in hospital admissions for idiopathic pulmonary fibrosis in Spain (2004–2013) using administrative data. BMJ Open (2017) 7(2):e013156.10.1136/bmjopen-2016-013156

  • CrossRef
  • Google Scholar

• 48

  GribbinJHubbardRBLe JeuneISmithCJWestJTataLJ. Incidence and mortality of idiopathic pulmonary fibrosis and sarcoidosis in the UK. Thorax (2006) 61(11):980–5.10.1136/thx.2006.062836

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 49

  BehrJKreuterMHoeperMMWirtzHKlotscheJKoschelDet alManagement of patients with idiopathic pulmonary fibrosis in clinical practice: the INSIGHTS-IPF registry. Eur Respir J (2015) 46(1):186–96.10.1183/09031936.00217614

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 50

  MoodleyYGohNGlaspoleIMacanshSWaltersEHChapmanSet alAustralian Idiopathic Pulmonary Fibrosis Registry: vital lessons from a national prospective collaborative project. Respirology (2014) 19(7):1088–91.10.1111/resp.12358

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 51

  SongJWHongSBLimCMKohYKimDS. Acute exacerbation of idiopathic pulmonary fibrosis: incidence, risk factors and outcome. Eur Respir J (2011) 37(2):356.10.1183/09031936.00159709

  • CrossRef
  • Google Scholar

• 52

  NatsuizakaMChibaHKuronumaKOtsukaMKudoKMoriMet alEpidemiologic survey of Japanese patients with idiopathic pulmonary fibrosis and investigation of ethnic differences. Am J Respir Crit Care Med (2014) 190(7):773–9.10.1164/rccm.201403-0566OC

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 53

  GelberACMannoRLShahAAWoodsALeENBoinFet alRace and association with disease manifestations and mortality in scleroderma: a 20-year experience at the Johns Hopkins Scleroderma Center and review of the literature. Medicine (2013) 92(4):191–205.10.1097/MD.0b013e31829be125

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 54

  Hoffmann-VoldAMMidtvedtOMolbergOGarenTGranJT. Prevalence of systemic sclerosis in south-east Norway. Rheumatology (Oxford) (2012) 51(9):1600–5.10.1093/rheumatology/kes076

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 55

  Lo MonacoABruschiMLa CorteRVolpinariSTrottaF. Epidemiology of systemic sclerosis in a district of northern Italy. Clin Exp Rheumatol (2011) 29(2 Suppl 65):S10–4.

  • Pubmed Abstract
  • Google Scholar

• 56

  MoinzadehPFonsecaCHellmichMShahAAChighizolaCDentonCPet alAssociation of anti-RNA polymerase III autoantibodies and cancer in scleroderma. Arthritis Res Ther (2014) 16(1):R53–53.10.1186/ar4486

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 57

  StricklandGPaulingJCavillCShaddickGMcHughN. Mortality in systemic sclerosis—a single centre study from the UK. Clin Rheumatol (2013) 32(10):1533–9.10.1007/s10067-013-2289-0

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 58

  TolédanoCGainMKettanehABaudinBJohanetCChérinPet alAldolase predicts subsequent myopathy occurrence in systemic sclerosis. Arthritis Res Ther (2012) 14(3):R152–152.10.1186/ar3888

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 59

  NikpourMHissariaPByronJSahharJMicallefMPaspaliarisWet alPrevalence, correlates and clinical usefulness of antibodies to RNA polymerase III in systemic sclerosis: a cross-sectional analysis of data from an Australian cohort. Arthritis Res Ther (2011) 13(6):R211–211.10.1186/ar3544

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 60

  BasappaKReddyKN. Period prevalence of systemic sclerosis (morphoea) in tertiary care hospital in India: an update. Am J Pharmtech Res (2013) 3(6): 368–74.

  • Google Scholar

• 61

  PradhanVRajadhyakshaANadkarMPanditPSurvePLecerfMet alClinical and autoimmune profile of scleroderma patients from Western India. Int J Rheumatol (2014) 2014:6.10.1155/2014/983781

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 62

  YeungHTakeshitaJMehtaNNKimmelSEOgdieAMargolisDJet alPsoriasis severity and the prevalence of major medical co-morbidities: a population-based study. JAMA Dermatol (2013) (10):1173–9.10.1001/jamadermatol.2013.5015

  • CrossRef
  • Google Scholar

• 63

  TakeshitaJGelfandJMLiPPintoLYuXRaoPet alPsoriasis in the U.S. Medicare population: prevalence, treatment, and factors associated with biologic use. J Invest Dermatol (2015) 135(12):2955–63.10.1038/jid.2015.296

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 64

  DanielsenKWilsgaardTOlsenAOEggenAEOlsenKCassanoPAet alElevated odds of metabolic syndrome in psoriasis: a population-based study of age and sex differences. Br J Dermatol (2015) 172(2):419–27.10.1111/bjd.13288

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 65

  Morales Suárez-VarelaMReguera-LealPGrantWBRubio-LópezNLlopis-GonzálezA. Vitamin D and psoriasis pathology in the Mediterranean region, Valencia (Spain). Int J Environ Res Public Health (2014) 11(12):12108–17.10.3390/ijerph111212108

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 66

  KochMBaurechtHRiedJSRodriguezESchlesingerSVolksNet alPsoriasis and cardiometabolic traits: modest association but distinct genetic architectures. J Invest Dermatol (2015) 135(5):1283–93.10.1038/jid.2015.8

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 67

  LanganSMSeminaraNMShinDBTroxelABKimmelSEMehtaNNet alPrevalence of metabolic syndrome in patients with psoriasis: a population-based study in the United Kingdom. J Invest Dermatol (2012) 132(3 Pt 1):556–62.10.1038/jid.2011.365

  • CrossRef
  • Google Scholar

• 68

  PlunkettAMerlinKGillDZuoYJolleyDMarksR. The frequency of common nonmalignant skin conditions in adults in central Victoria, Australia. Int J Dermatol (1999) 38(12):901–8.10.1046/j.1365-4362.1999.00856.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 69

  SakaiRMatsuiSFukushimaMYasudaHMiyauchiHMiyachiY. Prognostic factor analysis for plaque psoriasis. Dermatology (2005) 211(2):103–6.10.1159/000086437

  • CrossRef
  • Google Scholar

• 70

  NerichVMonnetEEtienneALouafiSRameeCRicanSet alGeographical variations of inflammatory bowel disease in France: a study based on national health insurance data. Inflamm Bowel Dis (2006) 12(3):218–26.10.1097/01.MIB.0000206540.38834.8c

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 71

  VeghZBurischJPedersenNKaimakliotisIDuricovaDBortlikMet alIncidence and initial disease course of inflammatory bowel diseases in 2011 in Europe and Australia: results of the 2011 ECCO-EpiCom inception cohort. J Crohns Colitis (2014) 8(11):1506–15.10.1016/j.crohns.2014.06.004

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 72

  JessTRiisLVindIWintherKVBorgSBinderVet alChanges in clinical characteristics, course, and prognosis of inflammatory bowel disease during the last 5 decades: a population-based study from Copenhagen, Denmark. Inflamm Bowel Dis (2007) 13(4):481–9.10.1002/ibd.20036

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 73

  AsakuraKNishiwakiYInoueNHibiTWatanabeMTakebayashiT. Prevalence of ulcerative colitis and Crohn’s disease in Japan. J Gastroenterol (2009) 44(7):659–65.10.1007/s00535-009-0057-3

  • CrossRef
  • Google Scholar

• 74

  Rubio-TapiaALudvigssonJFBrantnerTLMurrayJAEverhartJE. The prevalence of celiac disease in the United States. Am J Gastroenterol (2012) 107(10):1538–44; quiz 1537, 1545.10.1038/ajg.2012.219

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 75

  DixitRLebwohlBLudvigssonJFLewisSKRizkalla-ReillyNGreenPH. Celiac disease is diagnosed less frequently in young adult males. Dig Dis Sci (2014) 59(7):1509–12.10.1007/s10620-014-3025-6

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 76

  JainAKSircarSJainMAdkarSWaghmareC. Inflammatory bowel disease in central India: a single centre experience over five years. Trop Doct (2012) 42(4):198–9.10.1258/td.2012.120105

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 77

  NgSCTangWChingJYWongMChowCMHuiAJet alIncidence and phenotype of inflammatory bowel disease based on results from the Asia-Pacific Crohn’s and colitis epidemiology study. Gastroenterology (2013) 145(1):158–65.e2.10.1053/j.gastro.2013.04.007

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 78

  SalehMNFisherMGrotzingerKM. Analysis of the impact and burden of illness of adult chronic ITP in the US. Curr Med Res Opin (2009) 25(12):2961–9.10.1185/03007990903362388

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 79

  DaneseMDLindquistKGleesonMDeusonRMikhaelJ. Cost and mortality associated with hospitalizations in patients with immune thrombocytopenic purpura. Am J Hematol (2009) 84(10):631–5.10.1002/ajh.21500

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 80

  BoyleSWhiteRHBrunsonAWunT. Splenectomy and the incidence of venous thromboembolism and sepsis in patients with immune thrombocytopenia. Blood (2013) 121(23):4782–90.10.1182/blood-2012-12-467068

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 81

  FrederiksenHMaegbaekMLNorgaardM. Twenty-year mortality of adult patients with primary immune thrombocytopenia: a Danish population-based cohort study. Br J Haematol (2014) 166(2):260–7.10.1111/bjh.12869

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 82

  Grimaldi-BensoudaLNordonCMichelMViallardJFAdoueDMagy-BertrandNet alImmune thrombocytopenia in adults: a prospective cohort study of clinical features and predictors of outcome. Haematologica (2016) 101(9):1039–45.10.3324/haematol.2016.146373

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 83

  WindeGSchmidKWLugeringNFischerRBrandtBBernsTet alResults and prognostic factors of splenectomy in idiopathic thrombocytopenic purpura. J Am Coll Surg (1996) 183(6):565–74.

  • Pubmed Abstract
  • Google Scholar

• 84

  SchoonenWMKuceraGCoalsonJLiLRutsteinMMowatFet alEpidemiology of immune thrombocytopenic purpura in the General Practice Research Database. Br J Haematol (2009) 145(2):235–44.10.1111/j.1365-2141.2009.07615.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 85

  SeymourLANourseJPCrooksPWocknerLBirdRTranHet alThe presence of KIR2DS5 confers protection against adult immune thrombocytopenia. Tissue Antigens (2014) 83(3):154–60.10.1111/tan.12295

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 86

  NourseJPLeaRCrooksPWrightGTranHCatalanoJet alThe KIR2DS2/DL2 genotype is associated with adult persistent/chronic and relapsed immune thrombocytopenia independently of FCGR3a-158 polymorphisms. Blood Coagul Fibrinolysis (2012) 23(1):45–50.10.1097/MBC.0b013e32834d7ce3

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 87

  ChoiPYGordonJEHarveyMChongBH. Presentation and outcome of idiopathic thrombocytopenic purpura in a single Australian centre. Intern Med J (2012) 42(7):841–5.10.1111/j.1445-5994.2012.02740.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 88

  ZhouHFuRWangHZhouFLiHZhouZet alImmune thrombocytopenia in the elderly: clinical course in 525 patients from a single center in China. Ann Hematol (2013) 92(1):79–87.10.1007/s00277-012-1567-2

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 89

  ChengGSalehMNMarcherCVaseySMayerBAivadoMet alEltrombopag for management of chronic immune thrombocytopenia (RAISE): a 6-month, randomised, phase 3 study. Lancet (2011) 377(9763):393–402.10.1016/S0140-6736(10)60959-2

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 90

  RaoKRaoGPatilNBalajiORaoNRRaoJet alA clinical study of patients with idiopathic thrombocytopenic purpura. Asian J Pharm Clin Res (2017) 10(7):373–77.10.22159/ajpcr.2017.v10i7.18775

  • CrossRef
  • Google Scholar

• 91

  KuehYK. Adult idiopathic thrombocytopenic purpura (ITP) – a prospective tracking of its natural history. Singapore Med J (1995) 36:367–70.

  • Google Scholar

• 92

  PhitayakornRMorales-GarciaDWandererJLubitzCCGazRDStephenAEet alSurgery for Graves’ disease: a 25-year perspective. Am J Surg (2013) 206(5):669–73.10.1016/j.amjsurg.2013.07.005

  • CrossRef
  • Google Scholar

• 93

  CarleAPedersenIBKnudsenNPerrildHOvesenLRasmussenLBet alEpidemiology of subtypes of hyperthyroidism in Denmark: a population-based study. Eur J Endocrinol (2011) 164(5):801–9.10.1530/EJE-10-1155

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 94

  KrassasGETziomalosKPontikidesNLewyHLaronZ. Seasonality of month of birth of patients with Graves’ and Hashimoto’s diseases differ from that in the general population. Eur J Endocrinol (2007) 156(6):631–6.10.1530/EJE-07-0015

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 95

  GaujouxSLeenhardtLTrésalletCRouxelAHoangCJublancCet alExtensive thyroidectomy in Graves’ disease. J Am Coll Surg (2006) 202(6):868–73.10.1016/j.jamcollsurg.2006.02.031

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 96

  KhongJJFinchSDe SilvaCRylanderSCraigJESelvaDet alRisk factors for Graves’ orbitopathy; the Australian thyroid-associated orbitopathy research (ATOR) study. J Clin Endocrinol Metab (2016) 101(7):2711–20.10.1210/jc.2015-4294

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 97

  GuoTHuoYNZhuWXuFLiuCLiuNet alGenetic association between IL-17F gene polymorphisms and the pathogenesis of Graves’ Disease in the Han Chinese population. Gene (2013) 512(2):300–4.10.1016/j.gene.2012.10.021

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 98

  StaiiAMirochaSTodorova-KotevaKGlinbergSJaumeJC. Hashimoto thyroiditis is more frequent than expected when diagnosed by cytology which uncovers a pre-clinical state. Thyroid Res (2010) 3:11–11.10.1186/1756-6614-3-11

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 99

  TjiangHLahootiHMcCorquodaleTParmarKRWallJR. Eye and eyelid abnormalities are common in patients with Hashimoto’s thyroiditis. Thyroid (2010) 20(3):287–90.10.1089/thy.2009.0199

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 100

  ZhangLLiHJiQ-HZhuY-XWangZ-YWangYet alThe clinical features of papillary thyroid cancer in Hashimoto’s thyroiditis patients from an area with a high prevalence of Hashimoto’s disease. BMC Cancer (2012) 12(1):610.10.1186/1471-2407-12-610

  • CrossRef
  • Google Scholar

• 101

  SahooJPSelviambigapathyJKamalanathanSNegiVSSridharMGKarSSet alThe Serological and biochemical markers of adrenal cortex and endocrine pancreas dysfunction in patients with Hashimoto’s thyroiditis: a hospital-based pilot study. Ind J Endocrinol Metab (2017) 21(4):540–4.10.4103/ijem.IJEM_72_17

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 102

  CostacouTFriedLEllisDOrchardTJ. Sex differences in the development of kidney disease in individuals with type 1 diabetes mellitus: a contemporary analysis. Am J Kidney Dis (2011) 58(4):565–73.10.1053/j.ajkd.2011.05.025

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 103

  GaleEAGillespieKM. Diabetes and gender. Diabetologia (2001) 44(1):3–15.10.1007/s001250051573

  • CrossRef
  • Google Scholar

• 104

  KyvikKONystromLGorusFSonginiMOestmanJCastellCet alThe epidemiology of type 1 diabetes mellitus is not the same in young adults as in children. Diabetologia (2004) 47(3):377–84.10.1007/s00125-004-1331-9

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 105

  HuxleyRRPetersSAMishraGDWoodwardM. Risk of all-cause mortality and vascular events in women versus men with type 1 diabetes: a systematic review and meta-analysis. Lancet Diabetes Endocrinol (2015) 3(3):198–206.10.1016/S2213-8587(14)70248-7

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 106

  SpeightJBrowneJLHolmes-TruscottEHendrieckxCPouwerF. Diabetes MILES – Australia (management and impact for long-term empowerment and success): methods and sample characteristics of a national survey of the psychological aspects of living with type 1 or type 2 diabetes in Australian adults. BMC Public Health (2012) 12:120.10.1186/1471-2458-12-120

  • CrossRef
  • Google Scholar

• 107

  BhadadaSKKochharRBhansaliADuttaUKumarPRPoornachandraKSet alPrevalence and clinical profile of celiac disease in type 1 diabetes mellitus in north India. J Gastroenterol Hepatol (2011) 26(2):378–81.10.1111/j.1440-1746.2010.06508.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 108

  KawasakiEEguchiK. Is type 1 diabetes in the Japanese population the same as among Caucasians?Ann N Y Acad Sci (2004) 1037:96–103.10.1196/annals.1337.014

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 109

  Parikh-PatelAGoldEBWormanHKrivyKEGershwinME. Risk factors for primary biliary cirrhosis in a cohort of patients from the united states. Hepatology (2001) 33(1):16–21.10.1053/jhep.2001.21165

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 110

  GershwinMESelmiCWormanHJGoldEBWatnikMUttsJet alRisk factors and comorbidities in primary biliary cirrhosis: a controlled interview-based study of 1032 patients. Hepatology (2005) 42(5):1194–202.10.1002/hep.20907

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 111

  CorpechotCChretienYChazouilleresOPouponR. Demographic, lifestyle, medical and familial factors associated with primary biliary cirrhosis. J Hepatol (2010) 53(1):162–9.10.1016/j.jhep.2010.02.019

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 112

  PrinceMIDuckerSJJamesOFW. Case–control studies of risk factors for primary biliary cirrhosis in two United Kingdom populations. Gut (2010) 59(4):508.10.1136/gut.2009.184218

  • CrossRef
  • Google Scholar

• 113

  SoodSGowPJChristieJMAngusPW. Epidemiology of primary biliary cirrhosis in Victoria, Australia: high prevalence in migrant populations. Gastroenterology (2004) 127(2):470–5.10.1053/j.gastro.2004.04.064

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 114

  WangLZhangF-CChenHZhangXXuDLiY-Zet alConnective tissue diseases in primary biliary cirrhosis: a population-based cohort study. World J Gastroenterol (2013) 19(31):5131–7.10.3748/wjg.v19.i31.5131

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 115

  IkedaFOkamotoRBabaNFujiokaSShojiBYabushitaKet alPrevalence and associated factors with esophageal varices in early primary biliary cirrhosis. J Gastroenterol Hepatol (2012) 27(8):1320–8.10.1111/j.1440-1746.2012.07114.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 116

  WongRJGishRFrederickTBzowejNFrenetteC. The impact of race/ethnicity on the clinical epidemiology of autoimmune hepatitis. J Clin Gastroenterol (2012) 46(2):155–61.10.1097/MCG.0b013e318228b781

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 117

  WernerMPrytzHOhlssonBAlmerSBjornssonEBergquistAet alEpidemiology and the initial presentation of autoimmune hepatitis in Sweden: a nationwide study. Scand J Gastroenterol (2008) 43(10):1232–40.10.1080/00365520802130183

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 118

  BobergKMAadlandEJahnsenJRaknerudNStirisMBellH. Incidence and prevalence of primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis in a Norwegian population. Scand J Gastroenterol (1998) 33(1):99–103.10.1080/00365529850166284

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 119

  GronbaekLVilstrupHJepsenP. Autoimmune hepatitis in Denmark: incidence, prevalence, prognosis, and causes of death. A nationwide registry-based cohort study. J Hepatol (2014) 60(3):612–7.10.1016/j.jhep.2013.10.020

  • CrossRef
  • Google Scholar

• 120

  PrimoJMerinoCFernandezJMolesJRLlorcaPHinojosaJ. [Incidence and prevalence of autoimmune hepatitis in the area of the Hospital de Sagunto (Spain)]. Gastroenterol Hepatol (2004) 27(4):239–43.10.1016/S0210-5705(03)70452-X

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 121

  MuratoriPCzajaAJMuratoriLPappasGMaccarielloSCassaniFet alGenetic distinctions between autoimmune hepatitis in Italy and North America. World J Gastroenterol (2005) 11(12):1862–6.10.3748/wjg.v11.i12.1862

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 122

  VogelAStrassburgCPMannsMP. Genetic association of vitamin D receptor polymorphisms with primary biliary cirrhosis and autoimmune hepatitis. Hepatology (2002) 35(1):126–31.10.1053/jhep.2002.30084

  • CrossRef
  • Google Scholar

• 123

  NguJHBechlyKChapmanBABurtMJBarclayMLGearryRBet alPopulation-based epidemiology study of autoimmune hepatitis: a disease of older women?J Gastroenterol Hepatol (2010) 25(10):1681–6.10.1111/j.1440-1746.2010.06384.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 124

  HaiderASKayeGThomsonA. Autoimmune hepatitis in a demographically isolated area of Australia. Intern Med J (2010) 40(4):281–5.10.1111/j.1445-5994.2009.02041.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 125

  MiyakeYIwasakiYKobashiHYasunakaTIkedaFTakakiAet alAutoimmune hepatitis with acute presentation in Japan. Dig Liver Dis (2010) 42(1):51–4.10.1016/j.dld.2009.04.009

  • CrossRef
  • Google Scholar

• 126

  PengMLiYZhangMJiangYXuYTianYet alClinical features in different age groups of patients with autoimmune hepatitis. Exp Ther Med (2014) 7(1):145–8.10.3892/etm.2013.1363

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 127

  ChoudhuriGSomaniSKBabaCSAlexanderG. Autoimmune hepatitis in India: profile of an uncommon disease. BMC Gastroenterol (2005) 5(1):27.10.1186/1471-230X-5-27

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 128

  LeeYMTeoEKNgTMKhorCFockKM. Autoimmune hepatitis in Singapore: a rare syndrome affecting middle-aged women. J Gastroenterol Hepatol (2001) 16(12):1384–9.10.1046/j.1440-1746.2001.02646.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 129

  GathunguGZhangCKZhangWChoJH. A two-marker haplotype in the IRF5 gene is associated with inflammatory bowel disease in a North American cohort. Genes Immun (2012) 13(4):351–5.10.1038/gene.2011.90

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 130

  MustalahtiKCatassiCReunanenAFabianiEHeierMMcMillanSet alThe prevalence of celiac disease in Europe: results of a centralized, international mass screening project. Ann Med (2010) 42(8):587–95.10.3109/07853890.2010.505931

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 131

  RonnblomAHolmstromTTanghojHWandersASjobergD. Celiac disease, collagenous sprue and microscopic colitis in IBD. Observations from a population-based cohort of IBD (ICURE). Scand J Gastroenterol (2015) 50(10):1234–40.10.3109/00365521.2015.1041152

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 132

  CookHBBurtMJCollettJAWhiteheadMRFramptonCMChapmanBA. Adult coeliac disease: prevalence and clinical significance. J Gastroenterol Hepatol (2000) 15(9):1032–6.10.1046/j.1440-1746.2000.02290.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 133

  NijhawanSKatiyarPNagaichNSaradavaVNijhawanMGuptaGet alPrevalence of associated disorders in Indian patients with celiac disease. Ind J Gastroenterol (2013) 32(5):330–4.10.1007/s12664-013-0345-y

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 134

  WuJXiaBvon BlombergBMZhaoCYangXWCrusiusJBet alCoeliac disease: emerging in China?Gut (2010) 59(3):418–9.10.1136/gut.2009.197863

  • CrossRef
  • Google Scholar

• 135

  CarterETMcKennaCHBrianDDKurlandLT. Epidemiology of ankylosing spondylitis in Rochester, Minnesota, 1935–1973. Arthritis Rheum (1979) 22(4):365–70.10.1002/art.1780220408

  • CrossRef
  • Google Scholar

• 136

  Kaipiainen-SeppanenOAhoK. Incidence of chronic inflammatory joint diseases in Finland in 1995. J Rheumatol (2000) 27(1):94–100.

  • Pubmed Abstract
  • Google Scholar

• 137

  HaglundEBremanderABPeterssonIFStrombeckBBergmanSJacobssonLTet alPrevalence of spondyloarthritis and its subtypes in southern Sweden. Ann Rheum Dis (2011) 70(6):943–8.10.1136/ard.2010.141598

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 138

  TrontzasPAndrianakosAMiyakisSPantelidouKVafiadouEGarantziotouVet alSeronegative spondyloarthropathies in Greece: a population-based study of prevalence, clinical pattern, and management. The ESORDIG study. Clin Rheumatol (2005) 24(6):583–9.10.1007/s10067-005-1106-9

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 139

  OldroydJSchachnaLBuchbinderRStaplesMMurphyBBondMet alAnkylosing spondylitis patients commencing biologic therapy have high baseline levels of comorbidity: a report from the Australian Rheumatology Association Database. Int J Rheumatol (2009) 2009:268569.10.1155/2009/268569

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 140

  XiangY-JDaiS-M. Prevalence of rheumatic diseases and disability in China. Rheumatol Int (2008) 29(5):481.10.1007/s00296-008-0809-z

  • CrossRef
  • Google Scholar

• 141

  AggarwalRMalaviyaAN. Clinical characteristics of patients with ankylosing spondylitis in India. Clin Rheumatol (2009) 28(10):1199–205.10.1007/s10067-009-1227-7

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 142

  HukudaSMinamiMSaitoTMitsuiHMatsuiNKomatsubaraYet alSpondyloarthropathies in Japan: nationwide questionnaire survey performed by the Japan Ankylosing Spondylitis Society. J Rheumatol (2001) 28(3):554–9.

  • Pubmed Abstract
  • Google Scholar

• 143

  GonzalezAMaradit KremersHCrowsonCSNicolaPJDavisJMIIITherneauTMet alThe widening mortality gap between rheumatoid arthritis patients and the general population. Arthritis Rheum (2007) 56(11):3583–7.10.1002/art.22979

  • CrossRef
  • Google Scholar

• 144

  HumphreysJHVerstappenSMMHyrichKLChippingJRMarshallTSymmonsDPM. The incidence of rheumatoid arthritis in the UK: comparisons using the 2010 ACR/EULAR classification criteria and the 1987 ACR classification criteria. Results from the Norfolk Arthritis Register. Ann Rheum Dis (2013) 72(8):1315–20.10.1136/annrheumdis-2012-201960

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 145

  WilsonFCIcenMCrowsonCSMcEvoyMTGabrielSEKremersHM. Time trends in epidemiology and characteristics of psoriatic arthritis over 3 decades: a population-based study. J Rheumatol (2009) 36(2):361–7.10.3899/jrheum.080691

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 146

  MadlandTMApalsetEMJohannessenAERosseboBBrunJG. Prevalence, disease manifestations, and treatment of psoriatic arthritis in Western Norway. J Rheumatol (2005) 32(10):1918–22.

  • Pubmed Abstract
  • Google Scholar

• 147

  HadjimichaelOVollmerTOleen-BurkeyMNorth American Research Committee on Multiple Sclerosis. Fatigue characteristics in multiple sclerosis: the North American Research Committee on Multiple Sclerosis (NARCOMS) survey. Health Qual Life Outcomes (2008) 6(1):100.10.1186/1477-7525-6-100

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 148

  BentzenJMeulengracht FlachsEStenagerEBrønnum-HansenHKoch-HenriksenN. Prevalence of multiple sclerosis in Denmark 1950—2005. Mult Scler J (2010) 16(5):520–5.10.1177/1352458510364197

  • CrossRef
  • Google Scholar

• 149

  El AdssiHDebouverieMGuilleminF. Estimating the prevalence and incidence of multiple sclerosis in the Lorraine region, France, by the capture–recapture method. Mult Scler J (2012) 18(9):1244–50.10.1177/1352458512437811

  • CrossRef
  • Google Scholar

• 150

  HammondSRde WyttCMaxwellICLandyPJEnglishDMcLeodJGet alThe epidemiology of multiple sclerosis in Queensland, Australia. J Neurol Sci (1987) 80(2):185–204.10.1016/0022-510X(87)90154-7

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 151

  O’GormanCBukhariWToddAFreemanSBroadleySA. Smoking increases the risk of multiple sclerosis in Queensland, Australia. J Clin Neurosci (2014) 21(10):1730–3.10.1016/j.jocn.2014.01.009

  • CrossRef
  • Google Scholar

• 152

  ChengQChengXJJiangGX. Multiple sclerosis in China—history and future. Mult Scler (2009) 15(6):655–60.10.1177/1352458509102921

  • CrossRef
  • Google Scholar

• 153

  OsoegawaMKiraJFukazawaTFujiharaKKikuchiSMatsuiMet alTemporal changes and geographical differences in multiple sclerosis phenotypes in Japanese: nationwide survey results over 30 years. Mult Scler (2008) 15(2):159–73.10.1177/1352458508098372

  • CrossRef
  • Google Scholar

• 154

  PanditLKundapurR. Prevalence and patterns of demyelinating central nervous system disorders in urban Mangalore, South India. Mult Scler (2014) 20(12):1651–3.10.1177/1352458514521503

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 155

  GuptillJTMaranoAKruegerASandersDB. Cost analysis of myasthenia gravis from a large U.S. insurance database. Muscle Nerve (2011) 44(6):907–11.10.1002/mus.22212

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 156

  MantegazzaRBaggiFAntozziCConfalonieriPMorandiLBernasconiPet alMyasthenia gravis (MG): epidemiological data and prognostic factors. Ann N Y Acad Sci (2003) 998:413–23.10.1196/annals.1254.054

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 157

  Guy-CoichardCNguyenDTDelormeTBoureauF. Pain in hereditary neuromuscular disorders and myasthenia gravis: a national survey of frequency, characteristics, and impact. J Pain Symptom Manage (2008) 35(1):40–50.10.1016/j.jpainsymman.2007.02.041

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 158

  GattellariMGoumasCWorthingtonJM. A national epidemiological study of myasthenia gravis in Australia. Eur J Neurol (2012) 19(11):1413–20.10.1111/j.1468-1331.2012.03698.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 159

  SuzukiYUtsugisawaKSuzukiSNaganeYMasudaMKabasawaCet alFactors associated with depressive state in patients with myasthenia gravis: a multicentre cross-sectional study. BMJ Open (2011) 1(2):e000313.10.1136/bmjopen-2011-000313

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 160

  SinghalBBhatiaNUmeshTMenonS. Myasthenia gravis: a study from India. Neurol India (2008) 56(3):352–5.10.4103/0028-3886.43455

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 161

  HuangXLiuWBMenLNFengHYLiYLuoCMet alClinical features of myasthenia gravis in southern China: a retrospective review of 2,154 cases over 22 years. Neurol Sci (2013) 34(6):911–7.10.1007/s10072-012-1157-z

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 162

  AlshekhleeAHussainZSultanBKatirjiB. Guillain-Barre syndrome: incidence and mortality rates in US hospitals. Neurology (2008) 70(18):1608–13.10.1212/01.wnl.0000310983.38724.d4

  • CrossRef
  • Google Scholar

• 163

  SipilaJOSoilu-HanninenM. The incidence and triggers of adult-onset Guillain-Barre syndrome in southwestern Finland 2004–2013. Eur J Neurol (2015) 22(2):292–8.10.1111/ene.12565

  • CrossRef
  • Google Scholar

• 164

  ForsbergAde Pedro-CuestaJWiden HolmqvistL. Use of healthcare, patient satisfaction and burden of care in Guillain-Barre syndrome. J Rehabil Med (2006) 38(4):230–6.10.1080/16501970600582997

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 165

  BenedettiMDPugliattiMD’AlessandroRBeghiEChioALogroscinoGet alIncidence study of Guillain-Barre syndrome in Italy. The ITANG Study. Neuroepidemiology (2015) 45(2):90–9.10.1159/000438752

  • CrossRef
  • Google Scholar

• 166

  WebbAJBrainSAWoodRRinaldiSTurnerMR. Seasonal variation in Guillain-Barre syndrome: a systematic review, meta-analysis and Oxfordshire cohort study. J Neurol Neurosurg Psychiatry (2015) 86(11):1196–201.10.1136/jnnp-2014-309056

  • CrossRef
  • Google Scholar

• 167

  PouwelsSde BoerALeufkensHGMWeberWEJCooperCvan StaaTPet alRisk of fracture in patients with Guillain-Barré syndrome. Osteoporos Int (2014) 25(7):1845–51.10.1007/s00198-013-2442-2

  • CrossRef
  • Google Scholar

• 168

  BlumSReddelSSpiesJMcCombeP. Clinical features of patients with Guillain-Barre syndrome at seven hospitals on the East Coast of Australia. J Peripher Nerv Syst (2013) 18(4):316–20.10.1111/jns5.12045

  • CrossRef
  • Google Scholar

• 169

  DhadkeSVDhadkeVNBangarSSKoradeMB. Clinical profile of Guillain Barre syndrome. J Assoc Physicians India (2013) 61(3):168–72.

  • Pubmed Abstract
  • Google Scholar

• 170

  ChengQWangDSJiangGXHanHZhangYWangWZet alDistinct pattern of age-specific incidence of Guillain-Barre syndrome in Harbin, China. J Neurol (2002) 249(1):25–32.10.1007/PL00007844

  • CrossRef
  • Google Scholar

• 171

  MitsuiYKusunokiSArimuraKKajiRKandaTKuwabaraSet alA multicentre prospective study of Guillain-Barre syndrome in Japan: a focus on the incidence of subtypes. J Neurol Neurosurg Psychiatry (2015) 86(1):110–4.10.1136/jnnp-2013-306509

  • CrossRef
  • Google Scholar

• 172

  PretePEMajlessiAGilmanSHamidehF. Systemic lupus erythematosus in men: a retrospective analysis in a Veterans Administration Healthcare System population. J Clin Rheumatol (2001) 7(3):142–50.10.1097/00124743-200106000-00003

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 173

  RivestCLewRAWelsingPMSanghaOWrightEARobertsWNet alAssociation between clinical factors, socioeconomic status, and organ damage in recent onset systemic lupus erythematosus. J Rheumatol (2000) 27(3):680–4.

  • Pubmed Abstract
  • Google Scholar

• 174

  de CarvalhoJFdo NascimentoAPTestagrossaLABarrosRTBonfaE. Male gender results in more severe lupus nephritis. Rheumatol Int (2010) 30(10):1311–5.10.1007/s00296-009-1151-9

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 175

  MillerMHUrowitzMBGladmanDDKillingerDW. Systemic lupus erythematosus in males. Medicine (Baltimore) (1983) 62(5):327–34.10.1097/00005792-198309000-00005

  • CrossRef
  • Google Scholar

• 176

  GarciaMAMarcosJCMarcosAIPons-EstelBAWojdylaDArturiAet alMale systemic lupus erythematosus in a Latin-American inception cohort of 1214 patients. Lupus (2005) 14(12):938–46.10.1191/0961203305lu2245oa

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 177

  MongkoltanatusJWangkaewSKasitanonNLouthrenooW. Clinical features of Thai male lupus: an age-matched controlled study. Rheumatol Int (2008) 28(4):339–44.10.1007/s00296-007-0442-2

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 178

  KeskinGTokgozGDuzgunNDumanMKinikliGOlmezUet alSystemic lupus erythematosus in Turkish men. Clin Exp Rheumatol (2000) 18(1):114–5.

  • Google Scholar

• 179

  StefanidouSBenosAGalanopoulouVChatziyannisIKanakoudiFAslanidisSet alClinical expression and morbidity of systemic lupus erythematosus during a post-diagnostic 5-year follow-up: a male:female comparison. Lupus (2011) 20(10):1090–4.10.1177/0961203311403640

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 180

  OthmaniSLouzirBGroup d’etude du lupus. [Systemic lupus erythematosus in 24 tunisian males: clinico-biological analysis and clinical course]. La Revue de medecine interne (2002) 23(12):983–90.10.1016/S0248-8663(02)00684-7

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 181

  FengJ-BNiJ-DYaoXPanH-FLiX-PXuJ-Het alGender and age influence on clinical and laboratory features in Chinese patients with systemic lupus erythematosus: 1,790 cases. Rheumatol Int (2010) 30(8):1017–23.10.1007/s00296-009-1087-0

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 182

  GomezJSuarezALopezPMozoLDiazJBGutierrezC. Systemic lupus erythematosus in Asturias, Spain: clinical and serologic features. Medicine (2006) 85(3):157–68.10.1097/01.md.0000224711.54886.b1

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 183

  PatwardhanMPradhanVRajadhyakshaAUmareVRajendranVSurvePet alClinical and serological features of male systemic lupus erythematosus patients from Western India. Ind J Rheumatol (2012) 7(4):204–8.10.1016/j.injr.2012.09.002

  • CrossRef
  • Google Scholar

• 184

  VoulgariPVKatsimbriPAlamanosYDrososAA. Gender and age differences in systemic lupus erythematosus. A study of 489 Greek patients with a review of the literature. Lupus (2002) 11(11):722–9.10.1191/0961203302lu253oa

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 185

  PamukONAkbayFGDonmezSYilmazNCalayirGBYavuzS. The clinical manifestations and survival of systemic lupus erythematosus patients in Turkey: report from two centers. Lupus (2013) 22(13):1416–24.10.1177/0961203313499956

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 186

  FontJCerveraRNavarroMPallaresLLopez-SotoAVivancosJet alSystemic lupus erythematosus in men: clinical and immunological characteristics. Ann Rheum Dis (1992) 51(9):1050–2.10.1136/ard.51.9.1050

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 187

  JacobsenSPetersenJUllmanSJunkerPVossARasmussenJMet alA multicentre study of 513 Danish patients with systemic lupus erythematosus. I. Disease manifestations and analyses of clinical subsets. Clin Rheumatol (1998) 17(6):468–77.10.1007/BF01451282

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 188

  FaeziSTHosseini AlmodarresiMAkbarianMGharibdoostFAkhlaghiMJamshidiAet alClinical and immunological pattern of systemic lupus erythematosus in men in a cohort of 2355 patients. Int J Rheum Dis (2014) 17(4):394–9.10.1111/1756-185X.12268

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 189

  BorbaEFAraujoDBBonfaEShinjoSK. Clinical and immunological features of 888 Brazilian systemic lupus patients from a monocentric cohort: comparison with other populations. Lupus (2013) 22(7):744–9.10.1177/0961203313490432

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 190

  MolinaJFDrenkardCMolinaJCardielMHUribeOAnayaJMet alSystemic lupus erythematosus in males. A study of 107 Latin American patients. Medicine (1996) 75(3):124–30.10.1097/00005792-199605000-00002

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 191

  AlonsoMDMartinez-VazquezFRiancho-ZarrabeitiaLDiaz de TeranTMiranda-FilloyJABlancoRet alSex differences in patients with systemic lupus erythematosus from Northwest Spain. Rheumatol Int (2014) 34(1):11–24.10.1007/s00296-013-2798-9

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 192

  KohWHFongKYBoeyMLFengPH. Systemic lupus erythematosus in 61 Oriental males. A study of clinical and laboratory manifestations. Br J Rheumatol (1994) 33(4):339–42.10.1093/rheumatology/33.4.339

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 193

  AzizahMRAinolSSKongNCNormaznahYRahimMN. Gender differences in the clinical and serological features of systemic lupus erythematosus in Malaysian patients. Med J Malaysia (2001) 56(3):302–7.

  • Pubmed Abstract
  • Google Scholar

• 194

  RenauAIIsenbergDA. Male versus female lupus: a comparison of ethnicity, clinical features, serology and outcome over a 30 year period. Lupus (2012) 21(10):1041–8.10.1177/0961203312444771

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 195

  AndradeRMAlarconGSFernandezMApteMVilaLMReveilleJD. Accelerated damage accrual among men with systemic lupus erythematosus: XLIV. Results from a multiethnic US cohort. Arthritis Rheum (2007) 56(2):622–30.10.1002/art.22375

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 196

  HwangJLeeJAhnJKParkE-JChaH-SKohE-M. Clinical characteristics of male and female Korean patients with systemic lupus erythematosus: a comparative study. Korean J Intern Med (2015) 30(2):242–9.10.3904/kjim.2015.30.2.242

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 197

  CooperGSParksCGTreadwellELSt ClairEWGilkesonGSCohenPLet alDifferences by race, sex and age in the clinical and immunologic features of recently diagnosed systemic lupus erythematosus patients in the southeastern United States. Lupus (2002) 11(3):161–7.10.1191/0961203302lu161oa

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 198

  WardMMStudenskiS. Clinical manifestations of systemic lupus erythematosus. Identification of racial and socioeconomic influences. Arch Intern Med (1990) 150(4):849–53.10.1001/archinte.1990.00390160099020

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 199

  WangYFXuYXTanYYuFZhaoMH. Clinicopathological characteristics and outcomes of male lupus nephritis in China. Lupus (2012) 21(13):1472–81.10.1177/0961203312458467

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 200

  LeeWReveilleJDDavisJCLearchTJWardMMWeismanMH. Are there gender differences in severity of ankylosing spondylitis? Results from the PSOAS cohort. Ann Rheum Dis (2007) 66(5):633–8.10.1136/ard.2006.060293

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 201

  Ortega CastroRFont UgaldePCastro VillegasMCCalvo GutierrezJMunoz GomarizEZarco MontejoPet alDifferent clinical expression of patients with ankylosing spondylitis according to gender in relation to time since onset of disease. Data from REGISPONSER. Reumatol Clin (2013) 9(4):221–5.10.1016/j.reuma.2012.09.008

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 202

  JungYOKimIKimSSuhCHParkHJParkWet alClinical and radiographic features of adult-onset ankylosing spondylitis in Korean patients: comparisons between males and females. J Korean Med Sci (2010) 25(4):532–5.10.3346/jkms.2010.25.4.532

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 203

  ShahlaeeAMahmoudiMNicknamMHFarhadiEFallahiSJamshidiAR. Gender differences in Iranian patients with ankylosing spondylitis. Clin Rheumatol (2015) 34(2):285–93.10.1007/s10067-013-2439-4

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 204

  HebeisenMNeuenschwanderRSchererAExerPWeberUTamborriniGet alResponse to tumor necrosis factor inhibition in male and female patients with ankylosing spondylitis: data from a Swiss Cohort. J Rheumatol (2018) 45(4):506–12.10.3899/jrheum.170166

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 205

  WebersCEssersIRamiroSStolwijkCLandeweRvan der HeijdeDet alGender-attributable differences in outcome of ankylosing spondylitis: long-term results from the outcome in Ankylosing Spondylitis International Study. Rheumatology (Oxford) (2016) 55(3):419–28.10.1093/rheumatology/kev340

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 206

  RoussouESultanaS. Spondyloarthritis in women: differences in disease onset, clinical presentation, and bath ankylosing spondylitis disease activity and functional indices (BASDAI and BASFI) between men and women with spondyloarthritides. Clin Rheumatol (2011) 30(1):121–7.10.1007/s10067-010-1581-5

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 207

  Ibn YacoubYAmineBLaatirisAHajjaj-HassouniN. Gender and disease features in Moroccan patients with ankylosing spondylitis. Clin Rheumatol (2012) 31(2):293–7.10.1007/s10067-011-1819-x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 208

  TournadreAPereiraBLhosteADubostJJRistoriJMClaudepierrePet alDifferences between women and men with recent-onset axial spondyloarthritis: results from a prospective multicenter French cohort. Arthritis Care Res (Hoboken) (2013) 65(9):1482–9.10.1002/acr.22001

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 209

  de CarvalhoHMBortoluzzoABGoncalvesCRda SilvaJAXimenesACBertoloMBet alGender characterization in a large series of Brazilian patients with spondyloarthritis. Clin Rheumatol (2012) 31(4):687–95.10.1007/s10067-011-1890-3

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 210

  LandiMMaldonado-FiccoHPerez-AlaminoRMaldonado-CoccoJACiteraGArturiPet alGender differences among patients with primary ankylosing spondylitis and spondylitis associated with psoriasis and inflammatory bowel disease in an iberoamerican spondyloarthritis cohort. Medicine (2016) 95(51):e5652.10.1097/MD.0000000000005652

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 211

  BaraliakosXListingJvon der ReckeABraunJ. The natural course of radiographic progression in ankylosing spondylitis: differences between genders and appearance of characteristic radiographic features. Curr Rheumatol Rep (2011) 13(5):383–7.10.1007/s11926-011-0192-8

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 212

  A.A.R.D. Association. Autoimmune Disease List. (2017). Available from: https://www.aarda.org/diseaselist/ (accessed June 20, 2017)

  • Google Scholar

• 213

  HayterSMCookMC. Updated assessment of the prevalence, spectrum and case definition of autoimmune disease. Autoimmun Rev (2012) 11(10):754–65.10.1016/j.autrev.2012.02.001

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 214

  Arroyo-ÁvilaMSantiago-CasasYMcGwinGCantorRSPetriMRamsey-GoldmanRet alClinical associations of anti-Smith antibodies in PROFILE: a multi-ethnic lupus cohort. Clin Rheumatol (2015) 34(7):1217–23.10.1007/s10067-015-2941-y

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 215

  ReveilleJD. Predictive value of autoantibodies for activity of systemic lupus erythematosus. Lupus (2004) 13(5):290–7.10.1191/0961203303lu1015oa

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 216

  VilaLMMolinaMJMayorAMPeredoRASantaellaMLVilaS. Clinical and prognostic value of autoantibodies in puerto Ricans with systemic lupus erythematosus. Lupus (2006) 15(12):892–8.10.1177/0961203306069352

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 217

  AlbaPBentoLCuadradoMJKarimYTungekarMFAbbsIet alAnti-dsDNA, anti-Sm antibodies, and the lupus anticoagulant: significant factors associated with lupus nephritis. Ann Rheum Dis (2003) 62(6):556–60.10.1136/ard.62.6.556

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 218

  JanwityanuchitSVerasertniyomOVanichapuntuMVatanasukM. Anti-Sm: its predictive value in systemic lupus erythematosus. Clin Rheumatol (1993) 12(3):350–3.10.1007/BF02231577

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 219

  Martinez-CorderoEMartinez-MirandaENegrete-GarciaMCPadillaAAguilar LeonDE. Anti-dsDNA and Sm autoantibodies in systemic lupus erythematosus. Clin Rheumatol (1992) 11(3):341–5.10.1007/BF02207190

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 220

  MondCBPetersonMGERothfieldNF. Correlation of anti-Ro antibody with photosensitivity rash in systemic lupus erythematosus patients. Arthritis Rheum (1989) 32(2):202–4.10.1002/anr.1780320213

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 221

  McCauliffeD. Cutaneous diseases in adults associated with anti-Ro/SS-A autoantibody production. Lupus (1997) 6(2):158–66.10.1177/096120339700600211

  • CrossRef
  • Google Scholar

• 222

  FukudaMVLoSCde AlmeidaCSShinjoSK. Anti-Ro antibody and cutaneous vasculitis in systemic lupus erythematosus. Clin Rheumatol (2008) 28(3):301.10.1007/s10067-008-1043-5

  • CrossRef
  • Google Scholar

• 223

  AlexanderELArnettFCProvostTTStevensM. Sjögren’s syndrome: association of anti-ro(ss-a) antibodies with vasculitis, hematologic abnormalities, and serologic hyperreactivity. Ann Intern Med (1983) 98(2):155–9.10.7326/0003-4819-98-2-155

  • CrossRef
  • Google Scholar

• 224

  KurienBTNewlandJPaczkowskiCMooreKLScofieldRH. Association of neutropenia in systemic lupus erythematosus (SLE) with anti-Ro and binding of an immunologically cross-reactive neutrophil membrane antigen. Clin Exp Immunol (2000) 120(1):209–17.10.1046/j.1365-2249.2000.01195.x

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 225

  MaddisonPMogaveroHProvostTTReichlinM. The clinical significance of autoantibodies to a soluble cytoplasmic antigen in systemic lupus erythematosus and other connective tissue diseases. J Rheumatol (1979) 6(2):189–95.

  • Pubmed Abstract
  • Google Scholar

• 226

  ChungJKKimMKWeeWR. Prognostic factors for the clinical severity of keratoconjunctivitis sicca in patients with Sjögren’s syndrome. Br J Ophthalmol (2012) 96(2):240–5.10.1136/bjo.2011.202812

  • CrossRef
  • Google Scholar

• 227

  HarleyJBAlexanderELBiasWBFoxOFProvostTTReichlinMet alAnti-Ro (SS-A) and Anti-La (SS-B) in patients with Sjögren’s syndrome. Arthritis Rheum (1986) 29(2):196–206.10.1002/art.1780290207

  • CrossRef
  • Google Scholar

• 228

  FranceschiniFCrettiLQuinzaniniMLodi RizziniFCattaneoR. Deforming arthropathy of the hands in systemic lupus erythematosus is associated with antibodies to SSA/Ro and to SSB/La. Lupus (1994) 3(5):419–22.10.1177/096120339400300510

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 229

  Simmons-O’BrienEChenSWatsonRAntoniCPetriMHochbergMet alOne hundred anti-Ro (SS-A) antibody positive patients: a 10-year follow-up. Medicine (1995) 74(3):109–30.10.1097/00005792-199505000-00001

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 230

  DoriaAZenMCanovaMBettioSBassiNNalottoLet alSLE diagnosis and treatment: when early is early. Autoimmun Rev (2010) 10(1):55–60.10.1016/j.autrev.2010.08.014

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 231

  HennesEMZeniyaMCzajaAJParésADalekosGNKrawittELet alSimplified criteria for the diagnosis of autoimmune hepatitis. Hepatology (2008) 48(1):169–76.10.1002/hep.22322

  • CrossRef
  • Google Scholar

• 232

  KerlikowskeKGradyDRubinSMSandrockCErnsterVL. Efficacy of screening mammography. A meta-analysis. JAMA (1995) 273(2):149–54.10.1001/jama.1995.03520260071035

  • Pubmed Abstract
  • CrossRef
  • Google Scholar