Gender Differences in Autoimmune Diseases: Estrogen Increases Calcineurin Expression in Systemic Lupus Erythematosus

Rider, Virginia; Foster, Raymond T.; Evans, Marilyn; Suenaga, Ronsuke; Abdou, Nabih I.

doi:10.1006/clin.1998.4604

Cited by 61 publications

(42 citation statements)

References 48 publications

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“…In the present study, majority of patients were females (83%) whereas only 17% were males. The male to female ratio was 1:5 and this female preponderance is well documented in the literature 3 .…”

Section: Discussionsupporting

confidence: 61%

A Clinico-Pathological Study of Cutaneous Lupus Erythematosus

Chandran¹

2017

jmscr

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Section: Discussionsupporting

confidence: 61%

A Clinico-Pathological Study of Cutaneous Lupus Erythematosus

Chandran¹

2017

jmscr

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“…Clinical features included: hypertension, skin lesions, arthritis, serositis, and hematologic disorder. These complications were selected because their occurrence was related with the biological effects of estrogen, and their frequency in lupus were varied conspicuously in different genders [10, 11, 31, 32, 33, 34]. Recently, it has been proved that estrogen plays an important role in angiogenesis of vascular endothelial cells besides its effects on the immune system [35, 36, 37, 38], pathologic characteristics of glomerular capillary thrombi, necrosis, sclerosis, and glomerular crescent formations, as well as interstitial arterial vasculitis, were used to analyze the relationship between ER genotype and pathological lesions.…”

Section: Discussionmentioning

confidence: 99%

Sex Differences in Estrogen Receptor Gene Polymorphism and Its Association with Lupus Nephritis in Chinese

Liu

Cheng

Gong

et al. 2002

Nephron

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Background/Aims: Lupus nephritis (LN) is a clinical heterogeneous autoimmune disease and genetic factors contribute to the development of LN. One of the most striking characteristics in LN is the high prevalence among childbearing women, as well as that its clinical manifestation differs in women and men, suggesting the role of sex hormones in its pathogenesis. Methods: ThePvuII and XbaI restriction fragment length polymorphism (RFLP) of estrogen receptor (ER) gene were analyzed in 245 biopsy-proven LN patients (58 males and 187 females) and 172 normal controls (101 males and 71 females) by PCR-RFLP. The clinical and pathological features of 49 male and 152 female LN patients with different genotypes were analyzed. Results: It was found that genotype PpXx, ppxx and Ppxx were three major genotypes of ER gene in both of lupus patients and control groups. The distribution of ER gene polymorphism was quite different in lupus patients of different genders. The frequency of the PpXx genotype in male LN patients was significantly higher than both the gender matched normal controls (p < 0.05) and the female LN patients (p < 0.05), while no difference was shown in the frequency of PpXx genotype between female LN patients and gender matched controls. Interestingly, skin rashes and arthritis were found more common in the patients with PpXx genotype. The frequency of hematological abnormalities and hypertension were higher in patients with ppxx genotype (p < 0.05), while capillary thrombi and glomerular sclerosis were more frequently complicated in the patients with ppxx genotype. In addition, the renal vasculitis and interstitial injury were more frequent in those with Ppxx genotype (p < 0.01). Conclusion: The distribution of ER gene polymorphism in LN patients is distinct with different gender. The PpXxgenotype of ER gene may be associated with the susceptibility of SLE in male. ER gene polymorphism is probably one of the genetic factors contributing to the development of clinical heterogeneity and sexually dimorphic manifestations of LN.

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“…Since oestrogen is a key regulator of molecules involved in inflammation, and circulating oestradiol is highest during the peak time of SLE onset, oestradiol could contribute to the development, progression or severity of SLE [16,17]. Oestrogen stimulates T cell activation markers [18,19] and regulates molecules that promote inflammation (reviewed in [20]). In animal models of SLE, female mice develop an earlier aggressive disease that is ameliorated by ovariectomy and/or androgen therapy [21].…”

Section: Diseasementioning

confidence: 99%

“…Altered metabolism may contribute to increased oestrogen sensitivity in some patients. However, SLE T cells in culture respond with increased sensitivity to the poorly metabolized 2-fluoro-oestradiol [18], suggesting that altered metabolism is not the only mechanism responsible for the differential action of oestrogen in SLE T cells.…”

Section: Diseasementioning

confidence: 99%