Glucocorticoid Dysregulations and Their Clinical Correlates

Marques, Andrea H.; Silverman, Milton; Sternberg, Esther M.

doi:10.1111/j.1749-6632.2009.04987.x

Cited by 140 publications

(110 citation statements)

References 154 publications

(278 reference statements)

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“…Cortisol is known to influence bone loss (Marques et al. 2009). Proinflammatory cytokines have been found to be associated with depressive disorders (Valkanova et al.…”

Section: Introductionmentioning

confidence: 99%

Bone density and depressive disorder: a meta‐analysis

Schweiger

Hüppe

et al. 2016

Brain and Behavior

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BackgroundThe aim of this study was to evaluate the evidence of low bone mineral density (BMD) in depression. Low BMD is a major risk factor for osteoporotic fractures and frailty.MethodsThe searched database was Pubmed, Meta‐analysis included human studies in men and women fulfilling the following criteria: (1) assessment of BMD in the lumbar spine, the femur or the total hip; (2) comparison of BMD between depressed individuals and the healthy control group; (3) measurement of BMD using dual‐energy X‐ray absorptiometry (DEXA); and (4) data on the mean, standard deviation, or standard error of BMD.ResultsTwenty‐one studies were identified, encompassing 1842 depressed and 17,401 nondepressed individuals. Significant negative composite weighted mean effect sizes were identified for the lumbar spine (d = −0.15, 95%CL −0.22 to −0.08), femur (d = −0.34, 95%CL −0.64 to −0.05), and total hip (d = −0.14, 95%CL −0.23 to −0.05) indicating low BMD in depression. Examining men and women shows low bone density in the lumbar spine and femur in women and low bone density in the hip in men. The differences between men and women with MDD and the comparison group tended to be higher when examined by expert interviewers. Low bone density was found in all age groups.ConclusionsBone mineral density is reduced in patients with depressive disorders. The studies provide little evidence for potential relevant mediating factors.

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“…Cortisol is known to influence bone loss (Marques et al. 2009). Proinflammatory cytokines have been found to be associated with depressive disorders (Valkanova et al.…”

Section: Introductionmentioning

confidence: 99%

Bone density and depressive disorder: a meta‐analysis

Schweiger

Hüppe

et al. 2016

Brain and Behavior

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“…GCR refers to a decrease in the sensitivity of immune cells to glucocorticoid hormones that normally terminate the inflammatory response (6)(7)(8)(9). Evidence for GCR in response to chronic stress has been found in parents of children with cancer (10), spouses of brain-cancer patients (11) and in persons reporting high levels of loneliness (5).…”

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confidence: 99%

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

Cohen

Janicki-Deverts

Doyle

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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782

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We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to downregulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.lymphocytes | receptor sensitivity | psychological stress | cortisol | hypothalamic-pituitary-adrenocortical axis

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“…Moreover, there are reports of the ACTH DEFICIENCY AND PAINLESS THYROIDITIS [47]. Glucocorticoids exert an important modulatory role on the immune system, and inappropriately low glucocorticoid levels predispose patients to autoimmune and inflammatory diseases [48]. Thus, hypoadrenocorticism-induced immunological changes could trigger the development of painless thyroiditis.…”

Section: Discussionmentioning

confidence: 99%

Isolated Adrenocorticotropin Deficiency Associated with Painless Thyroiditis: A Case Report and Review of the Literature

et al. 2012

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INTRODUCTIONAlthough isolated adrenocorticotropin (ACTH) deficiency (IAD) is a heterogeneous disorder with several etiologies, the majority of acquired cases are most likely due to an autoimmune process [1][2][3]. Painless thyroiditis, which is considered a variant form of Hashimoto's thyroiditis, is characterized by transient thyrotoxicosis that is sometimes followed by transient hypothyroidism and then recovery [4]. Although acquired IAD is not uncommonly associated with other autoimmune endocrine disorders, especially Hashimoto's thyroiditis [5,6], reported cases of IAD associated with painless thyroiditis are scarce. Herein, we report a case of IAD associated with painless thyroiditis and briefly review the literature. CASE REPORTA 53-year-old Japanese man was admitted to hospital with a 3-month history of transient headache followed by general fatigue, weight loss of 4 kg and myalgia. He had a history of ocular myasthenia gravis which had been in remission following thymectomy 30 years prior to admission. He had no family history of endocrine or autoimmune disorders. On admission, he was 157 cm in height and weighed 47 kg. His blood pressure was 108/68 mmHg, pulse was regular at 92 beats/min, and his temperature was 37.1℃. Ophthalmologic examinations, including visual acuity, visual field and ocular fundus revealed no abnormalities. A small diffuse goiter was palpable without tenderness. The heart, lungs and abdomen were not remarkable. The relaxation phase of the Achilles ten- Kurume Medical Journal, 59, 71-77, 2012 Summary: A 53-year-old Japanese man was admitted with a 3-month history of transient headache followed by general fatigue and weight loss. He had a history of ocular myasthenia gravis which had been in remission following thymectomy 30 years ago. He had a small diffuse goiter without tenderness, and was diagnosed as having painless thyroiditis with mild thyrotoxicosis on admission. Endocrinological studies showed he had isolated adrenocorticotropin deficiency. Magnetic resonance imaging of the pituitary gland revealed no abnormalities. His symptoms improved soon after replacement of glucocorticoid. After an episode of hypothyroidism, he spontaneously became euthyroid. It is likely that thyrotoxicosis uncovered adrenal insufficiency that had developed insidiously, and hypoadrenocorticism-induced immunological changes may have triggered the development of painless thyroiditis. Moreover, thymectomy might have facilitated the development of pituitary and thyroid autoimmunity.

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Glucocorticoid Dysregulations and Their Clinical Correlates

Cited by 140 publications

References 154 publications

Bone density and depressive disorder: a meta‐analysis

Bone density and depressive disorder: a meta‐analysis

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

Isolated Adrenocorticotropin Deficiency Associated with Painless Thyroiditis: A Case Report and Review of the Literature

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