Growth Hormone Cell Antibodies and Partial Growth Hormone Deficiency in a Girl With Turner's Syndrome

Bottazzo, G. F.; McIntosh, C.; Stanford, William L.; Preece, M A

doi:10.1111/j.1365-2265.1980.tb03126.x

Cited by 64 publications

(32 citation statements)

References 8 publications

(3 reference statements)

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“…Autoantibodies to GH-secreting cells were first detected by Bottazzo et al (84) in a patient with Turner's syndrome, partial GH deficiency and a familial history of autoimmune polyendocrinopathy (Schmidt's syndrome in the mother). These antibodies have also been detected in only three out of 397 prepubertal subjects with idiopathic short stature (29) and in one out of four patients with idiopathic GH deficiency (28).…”

Section: Etiopathogenesismentioning

confidence: 99%

Lymphocytic hypophysitis: a rare or underestimated disease?

Bellastella

Bizzarro²,

Coronella³

et al. 2003

Eur J Endocrinol

197

205

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Lymphocytic hypophysitis (LYH) is an uncommon autoimmune disease in which the pituitary gland is infiltrated by lymphocytes, plasma cells and macrophages and its function is usually impaired. It has to be suspected in pregnant women and in women with recent delivery presenting with hyperprolactinemia, headache, visual field alterations and changes of one or more pituitary hormone secretions with secondary impairment of related peripheral target glands, especially when associated with other autoimmune endocrine or non-endocrine disorders. It can also occur less frequently in prepubertal or post-menopausal women and in men. Headache, visual field impairment and more rarely diplopia are due to extrasellar pituitary enlargement with optic chiasma compression and/or to invasion of cavernous sinuses. Among the 'isolated' pituitary hormone deficiencies, ACTH deficit is usually the earliest and most frequent hormonal impairment and in rare cases can induce an acute secondary hyposurrenalism as the first sign of the disease, with high mortality in affected patients. Histopathological findings from pituitary biopsy show lymphoplasmacytic infiltrate with lymphoid aggregates surrounding atropic acini of pituitary cells; immunohistochemical analysis shows numerous mast cells randomly distributed and also localized in the vicinity of capillaries, suggesting a possible influence on capillary permeability and angiogenesis, thus favoring the inflammatory and immunological aggression against pituitary cells. Nuclear magnetic resonance imaging shows uniform sellar floor depression and an extrasellar symmetrical pituitary enlargement, usually displacing the optic chiasma, which shows a rapid homogeneous enhancement after gadolinium also involving the adjacent dura (dural tail). Antipituitary antibodies have been detected in several patients with LYH but their role needs to be clarified. Since a possible spontaneous remission can occur, a careful follow-up is required in subclinical patients without important hyposurrenalism or symptomatic extrasellar expansion. Medical (immunosuppressive, replacement and antiprolactinemic) and neurosurgical (decompression) treatments are needed in clinical symptomatic patients.

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Section: Etiopathogenesismentioning

confidence: 99%

Lymphocytic hypophysitis: a rare or underestimated disease?

Bellastella

Bizzarro²,

Coronella³

et al. 2003

Eur J Endocrinol

197

205

View full text Add to dashboard Cite

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“…Autoantibodies to adenohypophysial cell antigens were first revealed in women during the postpartum period, and antibodies persisting for 6-12 months after labour were associated with the development of pituitary insufficiency in 25% of cases compared with 4% in women who did not show these antibodies (Engleberth & Jezkova 1965). Antipituitary antibodies were later found in patients with different disorders: Turner's syndrome (Bottazzo et al 1980), primary empty sella syndrome (ESS), various kinds of pituitary deficiency, idiopathic panhypopituitarism, prolactinoma, inactive pituitary tumour (Komatsu et al 1988, Sauter et al 1990), Cushing's disease (Sherbaum et al 1987) and hypogonadism (Barkan et al 1985).…”

Section: Introductionmentioning

confidence: 99%

Antibodies to pituitary surface antigens during various pituitary disease states

Keda¹,

Krjukova²,

Иловайская³

et al. 2002

Journal of Endocrinology

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Autoantibodies to cell surface antigens of human somatotropinoma (ASAS), human prolactinoma (ASAP) and rat adenohypophysis (ASARA) were assayed in the serum of patients with pituitary diseases associated with GH deficiency (GHD), such as pituitary dwarfism and primary empty sella syndrome (ESS), and in the serum of patients with hyperprolactinaemia of different etiologies: idiopathic hyperprolactinaemia, prolactinoma and ESS. The investigation was carried out with a cellular variant of an ELISA. Among children with GHD, the highest percentage of antibody-positive patients was found in the group with idiopathic isolated GHD (89% of ASAS + patients and 30% of ASARA + patients vs 33·3% and 0% respectively in the group with idiopathic combined pituitary hormone deficiency, and 33·3% and 9% in patients with pituitary hypoplasia associated with isolated GHD or combined pituitary hormone deficiency). Among hyperprolactinaemic patients, the highest ASAP and ASARA frequency was observed in patients with idiopathic hyperprolactinaemia (67·7% and 41·9% respectively) where it was twice as high as in the group of patients with prolactinoma.

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“…They were always directed against PRL cells as shown by a four-layer indirect immunofluorescent tech nique using rabbit antihormone antisera al ready described [ 13]. Later a second pituitary antibody reacting specifically with the growth hormone-producing cells was identified [14] in 3 children with growth defects. Some sera either from polyendocrine or from patients with partial deficiencies were found positive on other cells, but these cells could not be identified in this study.…”

Section: Detection Of Antibodies To Anterior Pituitary Cellsmentioning

confidence: 99%