Autoimmune polyglandular syndrome Type 2: the tip of an iceberg?

Betterle, Corrado; Lazzarotto, Francesca; Presotto, Fabio

doi:10.1111/j.1365-2249.2004.02561.x

Cited by 185 publications

(161 citation statements)

References 91 publications

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“…Hypoglycaemic episodes and a decreasing insulin requirement in a type 1 diabetic can be one of the earliest signs of the development of adrenal failure. Replacement of levothyroxin without simultaneous adrenal steroid replacement in a hypothyroid patient with Addison's disease can precipitate an adrenal crisis (73). Replacement of levothyroxin increases the cortisol turnover rate in the liver, and this may tax a failing adrenal gland.…”

Section: Treatmentmentioning

confidence: 99%

Polyglandular autoimmune syndromes

Kahaly

2009

European Journal of Endocrinology

206

106

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The polyglandular autoimmune syndromes (PAS) comprise a wide spectrum of autoimmune disorders and are divided into a very rare juvenile (PAS type I) and a relatively common adult type with (PAS II) or without adrenal failure (PAS III). First clinical manifestation of PAS I usually occurs in childhood, whereas PAS II mostly occurs during the third and fourth decades. PAS I is caused by mutations in the autoimmune regulatory (AIRE) gene on chromosome 21 and is inherited in an autosomal recessive manner. Mutations in the AIRE gene result in defect proteins which cause autoimmune destruction of target organs by disturbing the immunological tolerance of the patients. Genetic testing may identify patients with PAS I, but not those with PAS II/III. For PAS II/III, susceptibility genes are known which increase the risk for developing autoimmune disorders, but must not be causative. These are certain HLA genes, the cytotoxic T lymphocyte antigen gene, and the protein tyrosine phosphatase nonreceptor type 22 gene on chromosomes 6, 2 and 1 respectively. Actual diagnosis of PAS involves serological measurement of organ-specific autoantibodies and subsequent functional testing. Management of patients with PAS including their family relatives is best performed in centres with special expertise in autoimmune endocrine disorders.

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Section: Treatmentmentioning

confidence: 99%

Polyglandular autoimmune syndromes

Kahaly

2009

European Journal of Endocrinology

206

106

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“…The coexistence of and relationship between TD and DM have been addressed by many researchers (Wu, 2000;Betterle and Zanchetta, 2003;Betterle et al, 2004;Barker et al, 2005;Blois et al, 2010;Hage et al, 2011;Shaikh et al, 2014). The effects of these concurrent conditions on different systems of the body have been discussed only as retrospective studies on the basis of some naturally occurring clinical case records in humans, but the data were found lacking in the context of research trials into such a syndrome and its effects on reproductive health.…”

Section: Introductionmentioning

confidence: 99%

Effects of concomitant diabetes mellitus and hyperthyroidism on testicular and epididymal histoarchitecture and steroidogenesis in male animals

Korejo

Wei

Shah

2016

J. Zhejiang Univ. Sci. B

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This study evaluated the effects of comorbid disorders of diabetes and hyperthyroidism in the adult male mice. In total, 32 ICR strain mice were equally distributed into four groups: control (C), diabetic (D), diabetic-plushyperthyroid (DH), and hyperthyroid (H). Mice allocated for diabetes received a single intraperitoneal injection of streptozotocin (STZ) at 200 mg/kg body weight. At the onset of diabetes, one group of mice was concomitantly injected levothyroxine (LT4; 0.3 mg/kg body weight) and the other set of animals received the same treatment independently on a daily basis. The body weight, as well as the testicular and epididymal weights, was reduced markedly in D and DH mice. Higher trends of blood glucose levels were seen in the DH group, in comparison to euthyroid diabetic mice. Thyroid hormones could exert a transient effect on blood glucose homeostasis by altering the serum blood glucose level in diabetic patients. Histomorphometric analysis showed increased luminal sizes of seminiferous tubules, along with decreased epithelial height and atrophic changes in germinal stem cells in the testis of DH and H mice. Caput epididymis of DH mice showed extensive compaction of principal cells, loss of stereocilia, lipid vacuolization, and inflammatory infiltrations; however, damaged tubular integrity, packed clear cells, exfoliated cells, and round spermatids were profoundly noticed in the cauda epididymis. Hyperthyroidism elevated the serum testosterone levels in H and DH mice and produced critical damages to the histoarchitecture of the epididymis. Collectively, this experiment endeavored to mimic the polyglandular autoimmune syndrome, which will be helpful to better understand the reasons for male infertility in diabetic-cum-hyperthyroid patients.

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“…By analogy, chronic inflammations associated with autoimmune traits might result in cystic transformations of the female rete system. In some cases of autoimmune diseases, adjacent organs or tissues indirectly targeted by the autoimmune reaction are typically spared from the autoimmune attack (Betterle et al 2004). Therefore, it seems to be quite reasonable to educate those women, who suffer from autoimmune diseases, to pay close attention to their menstrual cycles and to participate in periodical gynecological monitoring for their future pregnancy planning.…”

Section: Qtl Analysis Mapping Of Ovarian Cystsmentioning

confidence: 99%

Quantitative trait locus analysis of ovarian cysts derived from rete ovarii in MRL/MpJ mice

et al. 2010

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MRL/MpJ (MRL) is a model mouse for autoimmune diseases that shows dermatitis, vasculitis, arthritis, and glomerulonephritis. In addition to these immune-associated disorders, we found that aged MRL mice develop ovarian cysts originating from the rete ovarii, which is lined by ciliated or nonciliated epithelium and considered remnants of mesonephric tubules. Ovarian cysts, which are reported to have several sources, are associated with female infertility, but information regarding the genetic etiology of ovarian cysts originating from the rete ovarii is rare. In this study, to elucidate the genetic background of development of ovarian cysts, we performed quantitative

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Autoimmune polyglandular syndrome Type 2: the tip of an iceberg?

Cited by 185 publications

References 91 publications

Polyglandular autoimmune syndromes

Polyglandular autoimmune syndromes

Effects of concomitant diabetes mellitus and hyperthyroidism on testicular and epididymal histoarchitecture and steroidogenesis in male animals

Quantitative trait locus analysis of ovarian cysts derived from rete ovarii in MRL/MpJ mice

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