Exacerbation of Rheumatoid Arthritis after Removal of Adrenal Adenoma in Cushing's Syndrome.

Yakushiji, Fumiatsu; Kita, Masako; Hiroi, Naoki; Ueshiba, Hajime; Monma, Issei; Miyachi, Yukitaka

doi:10.1507/endocrj.42.219

Cited by 44 publications

(21 citation statements)

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“…However, there are several case reports of exacerbation of autoimmune hypothyroidism or Graves' disease following partial hypophysectomy or adrenalectomy (5 -9). There is also evidence of the onset of rheumatoid arthritis (26,27) and systemic lupus erythematosus (28) after surgical treatment of CD. The main pituitary-dependent hormone that influences immune reactions is cortisol, which inhibits most aspects of the immune response, including proliferation of lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Primary thyroid disorders in endogenous Cushing's syndrome

Nièpomniszcze

Pitoia

Katz

et al. 2002

European Journal of Endocrinology

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Objective: To study the prevalence of primary thyroid disorders in patients who underwent endogenous hypercortisolism. Design: Retrospective evaluation of 59 patients with Cushing's syndrome (CS) who had, at least, a record of thyroid palpation by expert endocrinologists and basal measurements of TSH by second generation assays. When available, tri-iodothyronine and thyroxine serum levels, TRH-TSH tests and anti-thyroid antibodies were also analyzed. There were two age-and gender-matched control groups. The 'goiter control group' comprised 118 healthy subjects who underwent thyroid palpation. The 'antibody control group' was composed of 40 individuals who attended the blood bank of our hospital. Antibodies against thyroperoxidase and measurements of TSH were analyzed in their blood samples. Methods: Available files of 83 CS patients admitted to our endocrine unit from 1985 to 1998 were examined. Fifty-nine patients (52 women and 7 men) with a mean age of 36.2 years (range 14 -61 years) met the above requirements. Diagnosis of hypercortisolism had been established by a standard 1-mg overnight dexamethasone suppression test and urinary free cortisol (UFC). Etiological diagnosis involved dynamic testing, measurements of ACTH levels and imaging techniques. After treatment, all but one of the patients were cured or controlled of their hypercortisolism. This was established by the finding of subnormal serum cortisol concentrations and/or subnormal 24-h UFC levels. Primary thyroid disorders were defined by the presence of one or more of the following diagnostic criteria: (i) goiter, (ii) positive anti-thyroid antibodies and/or (iii) primary thyroid function abnormalities. Results: Eighteen (30.5%) patients had goiter (diffuse in 78% and nodular in 22%), 14 (23.7%) had primary subclinical hypothyroidism and 5 (8.4%) had hyperthyroidism. In 41 patients evaluated for antithyroid antibodies, it was found that 23 (56.1%) had positive titers. In a group of patients in which thyroid autoantibodies were measured both before and after resolution of hypercortisolism, prevalences of positive titers were 26.7% and 86.7% respectively ðP ¼ 0:001Þ: The overall frequency of primary thyroid abnormalities in our patients with Cushing's syndrome was 55.9%. Conclusions: Patients with endogenous Cushing's syndrome exhibit a remarkably high prevalence of primary thyroid disease. Resolution of hypercortisolism seems to trigger the development of autoimmune thyroid disorders in presumably predisposed subjects.

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Section: Discussionmentioning

confidence: 99%

Primary thyroid disorders in endogenous Cushing's syndrome

Nièpomniszcze

Pitoia

Katz

et al. 2002

European Journal of Endocrinology

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“…Particularly, exacerbation of coeliac disease (73) and rheumatoid arthritis (74), and development of sarcoidosis (75) and lupus erythematosus (76) were reported in patients with different forms of CS after correction of hypercortisolism. The most frequently autoimmune diseases reported after remission of CS are thyroid immune diseases, mainly including autoimmune thyroiditis (77,78) and Graves's disease (79).…”

Section: Autoimmune Diseasesmentioning

confidence: 99%

Cushing's syndrome: aftermath of the cure

Pivonello¹,

Martino²,

Leo³

et al. 2007

Arq Bras Endocrinol Metab

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Cushing's syndrome (CS) is a chronic and systemic disease caused by endogenous or exogenous hypercortisolism, associated with an increase of mortality rate due to the clinical consequences of glucocorticoid excess, especially cardiovascular diseases. After cure, usually obtained by the surgical removal of the tumor responsible for the disease, the normalization of cortisol secretion is not constantly followed by the recovery of the clinical complications developed during the active disease, and it is often followed by the development of novel clinical manifestations induced by the fall of cortisol levels. These evidences were mostly documented in patients with pituitary-dependent CS, after surgical resection of the pituitary tumor. Indeed, despite an improvement of the mortality rate, metabolic syndrome and the consequent cardiovascular risk have been found to partially persist after disease remission, strictly correlated to the insulin resistance. Skeletal diseases, mainly osteoporosis, improve after normalization of cortisol levels but require a long period of time or the use of specific treatment, mainly bisphosphonates, to reach the normalization of bone mass. A relevant improvement or resolution of mental disturbances has been described in patients cured from CS, although in several cases, cognitive decline persisted and psychological or psychiatric improvement was erratic, delayed, or incomplete. On the other hand, development or exacerbation of autoimmune disorders, mainly thyroid autoimmune diseases, was documented in predisposed patients with CS after disease remission. The totality of these complications persisting or occurring after successful treatment contribute to the impairment of quality of life registered in patients with CS after disease cure. A síndrome de Cushing (SC) é uma desordem sistêmica crônica causada por hipercortisolismo endógeno ou exógeno, associada a um aumento da taxa de mortalidade devido às conseqüências clínicas do excesso de glicocorticóides, especialmente a doença cardiovascular. Após a cura, usualmente obtida pela remoção cirúrgica do tumor responsável pela desordem, a normalização da secreção de cortisol não é sistematicamente seguida da recuperação das complicações clínicas desenvolvidas durante a fase ativa da doença, e é freqüentemente seguida pelo surgimento de novas manifestações clínicas induzidas pela queda dos níveis de cortisol. Estas evidências foram, na sua maioria, documentadas em pacientes com SC de origem hipofisária, após a ressecção cirúrgica do tumor na hipófise. Na verdade, a despeito de uma melhoria na taxa de mortalidade, a sín-drome metabólica e seu conseqüente risco cardiovascular têm se mostrado parcialmente persistentes após a remissão da doença, em estrita relação com a resistência à insulina. Anormalidades esqueléticas, especialmente a osteoporose, melhoram após a normalização dos níveis de cortisol, mas requerem um longo tempo ou o uso de tratamento especí-fico, principalmente bisfosfonatos, para se obter a normalização da massa óssea. Um...

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“…Treatment of RA patients with metyrapone (which blocks the synthesis of endogenous glucocorticoids in the adrenal cortex), results in a flare of disease activity (Panayi, 1992). In patients with Cushing's syndrome, adrenalectomy has resulted in the development of RA and autoimmune thyroid disease (Takasu et al 1990;Yakushiji et al 1995). In pre-clinical studies in rodents, adrenalectomy results in an earlier onset of disease and an increase in severity of adjuvant-induced arthritis (AA) and experimental allergic encephalomyelitis (EAE) (Mason et al 1990;Harbuz et al 1993b).…”

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confidence: 99%

Neuroendocrine Function and Chronic Inflammatory Stress

Harbuz

2002

Experimental Physiology

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The HPA axis and the response to acute stress The end-point of the activation of the HPA axis is the release of glucocorticoids (cortisol in man, corticosterone in rodents) from the adrenal cortex into the general circulation. The synthesis and release of glucocorticoids are controlled by ACTH released from the anterior pituitary gland. ACTH is synthesised from the precursor proopiomelanocortin (POMC) mRNA. The release of ACTH is regulated by the corticotrophin releasing factors corticotrophin-releasing factor(1-41) (CRF) and arginine vasopressin (AVP), which are released from the median eminence and synthesised in the parvocellular cells of the paraventricular nucleus (PVN). Under normal conditions approximately 50 % of these CRF neurons contain AVP; the remainder contain CRF but no vasopressin. CRF and AVP exert a synergistic action on the release of ACTH. The PVN acts as a co-ordinating centre receiving signals from many brain areas to regulate the response to stress. The glucocorticoids are able to regulate their own synthesis by negative feedback mediated by two corticosteroid receptors, the type II (glucocorticoid) receptor, which is found in the pituitary, PVN and other brain areas such as the hippocampus, and the type I receptor, which is found in the hippocampus. The hippocampus has a tonic inhibitory input to the PVN. In response to acute stress, the HPA axis is activated evoking the release of CRF and AVP into the The factors regulating susceptibility and severity of autoimmune diseases are poorly understood. That neuroendocrine factors are critical modulators in this regard is self-evident. For example, there are major gender differences in susceptibility with women at greater risk than men of, for example, rheumatoid arthritis (RA) and multiple sclerosis (MS). The hypothalamo-pituitary-adrenal (HPA) axis has rightly attracted a considerable amount of attention. Of particular interest has been the hypothesis that susceptibility to autoimmune disease may be related to an impaired responsiveness of the HPA axis; that is, an inability to mount an appropriate cortisol response with which to down-regulate the immune system might allow the immune system to rampage unchecked and attack self. This hypothesis links regulation of the release from the adrenal gland of the potent anti-inflammatory glucocorticoids to the disease process. Endogenous glucocorticoids are crucial for the regulation of the severity of the disease process. The hypothesis proposing a link between a hyporesponsive HPA axis and susceptibility to disease is compelling. However, evidence from a number of sources has suggested that this may not be the entire story and alterations in the activity of the HPA axis have not been consistently observed in patients with RA. This review will concentrate on recent findings concerning the HPA axis in determining susceptibility to, and in regulating the severity of, inflammatory processes in autoimmune disease. These studies have revealed that a single exposure to endotoxin can confer protection to sub...

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Exacerbation of Rheumatoid Arthritis after Removal of Adrenal Adenoma in Cushing's Syndrome.

Cited by 44 publications

References 5 publications

Primary thyroid disorders in endogenous Cushing's syndrome

Primary thyroid disorders in endogenous Cushing's syndrome

Cushing's syndrome: aftermath of the cure

Neuroendocrine Function and Chronic Inflammatory Stress

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