Sex hormone status and osteoporosis in postmenopausal women with rheumatoid arthritis

Sambrook, P N; Eisman, John A.; Champion, G. David; Pocock, Nicholas

doi:10.1002/art.1780310805

Cited by 136 publications

(48 citation statements)

References 19 publications

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“…We discovered that women with pSS, sSS + SLE, and sSS + RA are androgen deficient [4]. Similarly, others have found that pSS [48], as well as SLE and RA [49-57], are associated with a significant decrease in serum levels of androgen precursors (i.e., DHEA [dehydroepiandrosterone] and DHEA sulfate). These circulating precursors are the primary substrate for androgen synthesis in peripheral tissues, and this intracrine production generates the vast majority of androgens in women [58, 59].…”

Section: Discussionmentioning

confidence: 99%

Meibomian Gland Dysfunction in Primary and Secondary Sjögren Syndrome

et al. 2018

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Purpose: We hypothesized that women with primary (pSS) and secondary Sjögren syndrome (sSS; with systemic lupus erythematosus [SLE] or rheumatoid arthritis [RA]) have meibomian gland dysfunction (MGD). We sought to test our hypothesis. Methods: Subjects with pSS, sSS + SLE, sSS + RA, and non-SS-related MGD were recruited from the Sjögren’s Syndrome Foundation or outpatient clinics at Tufts University School of Dental Medicine or Brigham and Women’s Hospital. The control population was recruited from the Greater Boston area. After providing written informed consent, the subjects underwent an eye examination and/or completed two questionnaires that assess symptoms of dry eye disease (DED). Results: Our results demonstrate that pSS and sSS patients have MGD. These subjects had meibomian gland orifice metaplasia, an increased number of occluded meibomian gland orifices, and a reduced quality of meibomian gland secretions. Further, patients with pSS, sSS + SLE, sSS + RA, and MGD had significant alterations in their tear film, lid margin, cornea, and conjunctiva. Symptoms of DED were increased ∼10-fold in all pSS, sSS, and MGD groups relative to controls. Conclusions: Our findings support our hypothesis and show that individuals with pSS, sSS + SLE, and sSS + RA have MGD. In addition, our study indicates that patients with pSS and sSS have both aqueous-deficient and evaporative DED.

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Section: Discussionmentioning

confidence: 99%

Meibomian Gland Dysfunction in Primary and Secondary Sjögren Syndrome

et al. 2018

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“…A decrease in serum levels of dehydroepiandrosterone sulfate (DHEAS) and DHEA is typical for noninfectious chronic inflammation where TNF and IL-6 have a predictive role for such changes 30,31 as in autoimmune disorders, including inflammatory bowel disease, 32 rheumatoid arthritis, 33,34 systemic lupus erythematosus, 35 and pemphigus. 36 These low levels are also seen in infectious diseases with chronic inflammation, such as tuberculosis, where DHEA prevents experimental infection in mice when given within the first few days or before M. tuberculosis inoculum.…”

Section: Patientsmentioning

confidence: 99%

Low Serum Levels of Dehydroepiandrosterone and Cortisol in Human Diffuse Cutaneous Leishmaniasis by Leishmania Mexicana

Galindo-Sevilla¹,

Soto²,

Mancilla³

et al. 2007

The American Journal of Tropical Medicine and Hygiene

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Abstract. Low levels of dehydroepiandrosterone (DHEA) and cortisol hormones produced by the suprarenal cortex have been associated with diseases involving chronic inflammation, low interferon (IFN)-␥, and high interleukin (IL)-6. Diffuse cutaneous leishmaniasis (DL), a long-lasting intracellular parasitic infectious disease, can spread unknown levels of DHEA and cortisol. Serum concentrations of both were measured in 5 patients with DL, in 15 patients with localized lesions produced by Leishmania (LL), and in 20 healthy volunteers. Leishmania mexicana mexicana was identified as the causal agent in patients with DL and LL. Hormone levels were lower in DL compared with controls and LL. Furthermore, we detected a lower percentage of IFN-␥-positive cells with higher levels of IL-6 and higher titers of antiLeishmania antibodies in patients with DL, whereas patients with LL were similar to controls. These data suggest that patients with DL may be good candidates for DHEA and cortisol supplementation.

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“…Corticosteroids impair bone formation directly through the inhibition of osteoblast activity [112] and indirectly by decreasing sex steroid secretion [113], decreasing intestinal calcium absorption [114], increasing urinary calcium excretion [115] and promoting bone resorption due to secondary hyperparathyroidism [116]. Prevention of corticosteroid-induced osteoporosis can be primary, at the onset of corticosteroid therapy, or secondary, after low bone density has developed.…”

Section: Vitamin D and Drug Therapymentioning

confidence: 99%