Visual Failure During Replacement Therapy in Primary Hypothyroidism with Pituitary Enlargement

Stockigt, Jan R.; Essex, W. B.; West, Robert H.; Murray, Robin M.; Breidahl, H. D.

doi:10.1210/jcem-43-5-1094

Cited by 22 publications

(5 citation statements)

References 23 publications

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“…A systematic autopsy study of 64 patients with primary hypothyroidism (256) showed diffuse and nodular thyrotroph hyperplasia in, respectively, 69% and 25% of cases; in 12%, an entity called "tumorlet formation" (incomplete monomorphism, lack of destruction of reticulin network) " was described as an intermediate stage between nodular hyperplasia and adenoma; true adenomas were present in 12 + patients (older on average), with five of them staining for TSH. In reviewing the literature, we found other pathological reports, including autopsies (257)(258)(259)(260)(261)(262) and surgical cases A (263)(264)(265)(266)(267)(268)(269). Since the 1950s, much progress has been made in defining the different types of pituitary cells, with the in-A troduction of electron microscopy, specific staining (for thyrotrophs: alcian blue, aldehyde-thionin), and immunostaining (immunoperoxidase).…”

Section: Anatomic Pathologymentioning

confidence: 99%

“…Since the review article written by one of us (158), the reports have been enriched by better imaging and hormonal studies, including dynamic tests. For this article, we reviewed 210 published cases (83% females, 76% adults), very uneven in the depth of the analysis and the focus, depending on the year of publication and the specialty of the authors (257,259,260,(263)(264)(265)(266)(267)(268)(269).…”

Section: Clinical Featuresmentioning

confidence: 99%

“…Initial worsening of tumor-like symptoms was possible on thyroid hormone replacement (pseudotumor cerebri in children), with the appearance or progression of a visual field defect and/or papilledema in eight cases; four had decompressive surgery, which discovered two adenomas that did not stain for TSH (266,294), one hyperplasia (269), and one nodular hyperplasia (267); four were treated medically only, with complete resolution of the symptoms (292,320,352,355). The objective increase in pituitary volume was explained by a dissociation between a decrease of secretion and an increase of synthesis and storage of TSH, induced by the restoration of euthyroidism.…”

Section: E Treatmentmentioning

confidence: 99%

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Thyrotropin-Secreting Pituitary Tumors*

et al. 1996

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Section: Anatomic Pathologymentioning

confidence: 99%

Section: Clinical Featuresmentioning

confidence: 99%

Section: E Treatmentmentioning

confidence: 99%

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Thyrotropin-Secreting Pituitary Tumors*

et al. 1996

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“…As in the cases described by Melnyk & Greer (1965) and Herlant et al (1966), the presenting clinical syn¬ drome was that of hypothyroidism associated with menstrual disturbances, galactorrhoea and eleva¬ tion of serum Prl, which are not uncommon in primary hypothyroidism (Honbo et al 1980). Nor¬ malization of serum Prl and cessation of galactor¬ rhoea are known to occur with adequate replace¬ ment of thyroid homrone sometimes taking as long as 1 year (Stockigt et al 1976). Moderate elevations of serum Prl with persistence of amenorrhoea and galactorrhoea, after 1 year of thyroid replacement, in our patient, suggested before surgery a primary pituitary involvement, i.e., a Prl-secreting ade¬ noma.…”

Section: Discussionmentioning

confidence: 88%

TSH-containing pituitary adenoma associated with primary hypothyroidism manifested by amenorrhoea and galactorrhoea

Wajchenberg¹,

Tsanaclis²,

Marino³

1984

Acta Endocrinologica

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A 30 year old woman with primary hypothyroidism due to an ectopic (sublingual) thyroid, with a pituitary tumour invasive to the sphenoidal sinus presented with hyperprolactinaemia, amenorrhoea and galactorrhoea not corrected by long-term thyroid replacement. High basal TSH and TRH hyperresponsiveness were suppressed by thyroid therapy. After transsphenoidal removal of the tumour the Prl returned to normal. Light microscopy including differential staining and immunocytochemistry demonstrated that the tumour was composed of TSH cells. Ultrastructurally the adenoma cell contained small granules (90\p=n-\150nm) as described in TSH cells. This case provides evidence that a TSH cell adenoma probably arising from protracted overstimulation secondary to thyroid deficiency can induce hyperprolactinaemia. This did not appear to be produced directly by the adenoma nor was there any evidence of compression of the pituitary stalk. Samaan et al. (1977) and Katz et al. (1980) de¬ scribed adult patients with hypothyroidism asso¬ ciated with pituitary adenomas which were resected and proved to be TSH cell adenomas. We report a woman who had primary hypothyroidism asso¬ ciated with an ectopie (sublingual) thyroid and a pituitary adenoma presenting with amenorrhoea and galactorrhoea. Immunocytochemistry and ultrastructural examination was applied to the tum¬ our.A 30 year old woman was admitted to the hospital in January 1978 for menstrual irregularities since menarche and galactorrhoea for 1 year. Since the age of 2 months, when the diagnosis of hypothyoridism was made, the patient was placed on thyroid hormone re¬ placement taken regularly only until she was 10 years old.Menarche occurred at the age of 13 years. Because of reduction in the frequency of menses she was started on cyclic oral ethinyloestradiol 0.03 mg + levonorgestrel 0.1 mg at the age of 27 years, with normal withdrawal bleeding. On interruption of the oral steroids, for the last 18 months, she became amenorrhoeic. Galactorrhoea was found 1 year before admission and since then she had been treated with 120 µg i.-thyroxine and 30 µg I.-triiodothyronine (T, + T3) daily but galactorrhoea and amenorrhoea persisted. At the age of 22 years, with the patient off thyroid therapy, 2-and 24-h neck 131I uptake by aberrant thyroid tissue was 6.5 and 19%, respectively.The neck scintiscan revealed an ectopie thyroid (sublin¬ gual localization). No stigmata of hypothyroidism were found and the thyroid gland was not palpable. The breast had expressible milk. The remaining physical examination was normal. A lateral skull X-ray showed a slightly enlarged sella turcica with a double floor; hypocycloidal polytomography of the pituitary fossa indicated thinning of its floor and localized erosion at the left of the midline with a herniation of soft tissue into the sphenoidal sinus. CAT-scan of the skull confirmed the pre¬ sence of an intrasellar mass invading the left sphenoidal sinus. Pneumoencephalography did not show suprasellar extension of the tumour, and air did not enter the sel...

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“…We SINCE the first report of pituitary hyperplasia due to primary hypothyroidism by Niepce in 1851 [1], the disorder has been well described [2][3][4][5][6][7][8] . However, despite recent progress in imaging techniques, it is very difficult to distinguish between hyperplasia and TSH-producing adenoma of the pituitary, even when high-resolution contrast-enhanced computed tomography (CT) or gadolinium (Gd)-enhanced magnetic resonance imaging (MRI) was used [9].…”

Section: Introductionmentioning

confidence: 99%