Major hormonal changes emerge during pregnancy. The pituitary gland is one of the most affected organs with altered anatomy and physiology. The pituitary gland is enlarged as a result of lactotroph hyperplasia. Due to physiological changes in the pituitary and target hormone levels, binding globulins, and placental hormones, hormonal evaluation becomes more complex in pregnant women. As a consequence of physiological hormonal changes, the evaluation of pituitary functions in pregnant women is quite different from that done in the prepregnant state. Pituitary adenomas may cause problems by their hormone secretion that affects the mother and the fetus besides causing an increased risk of tumor growth. Furthermore, diagnosis, course, and treatment of pituitary diseases point out differences. The changes in anatomy and physiology of the pituitary gland during pregnancy are reviewed. Pituitary disorders namely Cushing's disease; acromegaly; prolactinoma; TSH-secreting, gonadotropin-producing, and clinically nonfunctioning adenomas; craniopharyngioma; and Sheehan's syndrome, which is one of the most common causes of hypopituitarism, lymphocytic hypophysitis, and hypopituitarism, in relation to pregnancy are discussed. Being aware of all this information will prevent any serious problems which mother and child will be exposed to.
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- Abstract: acromegalic x
- Abstract: acromegaly x
- Abstract: ACTH x
- Abstract: adeoncarcinoma x
- Abstract: craniopharyngioma x
- Abstract: Cushing x
- Abstract: empty sella x
- Abstract: glucocorticoids x
- Abstract: gonadotropin x
- Abstract: growth hormone x
- Abstract: hyperpituitarism x
- Abstract: insulinoma x
- Abstract: Nelson x
- Abstract: neuroendocrine x
- Abstract: paraganglioma x
- Abstract: pheochromocytoma x
- Abstract: pituitary x
- Abstract: prolactinoma x
- Abstract: Sheehan x
- Abstract: TSH x
Z Karaca, F Tanriverdi, K Unluhizarci and F Kelestimur
Makoto Otsuki, Hidetaro Mori, Shigeaki Baba and Naohisa Hiroshige
Different doses of thyrotrophin-releasing factor (TRF) were administered by three different routes (intravenous, subcutaneous and oral) to 87 normal subjects in order to standardize the "TRF test" for the pituitary TSH reserve. The results were: 1) Intravenous single injection may be suitable as a routine TRF test because of the stability of TSH response to TRF and the reliability of TRF administration. 2) The maximum TSH increases were dose-related between 50 and 400 μg, so that we can recommend the use of 50 μg of TRF as a screening test for TSH secretion. 3) Oral administration and slow intravenous infusion of TRF with estimation of thyroxine levels can be useful as an indirect test of pituitary TSH reserve when TSH assays are not available. According to these results, the TRF test was performed in patients with hypothalamic-pituitary disorders. A normal increase in plasma TSH occurred in 10 out of 20 patients with operated pituitary chromophobe adenoma following the administration of 50 or 100 μg of TRF. Two patients showed no rise in plasma TSH after receiving 50 or 100 μg of TRF but a normal rise after receiving 400 or 600 μg of TRF. Little or no rise in the plasma TSH levels occurred following the administration of 100 μg TRF in pituitary chromophobe adenoma and Sheehan's syndrome who had a long standing pituitary insufficiency and secondary hypothyroidism. However, some cases with craniopharyngioma and pinealoma, accompanied with a low level of thyroid function, showed a normal TSH responses to 50 μg of TRF. Since the pituitary of these cases remained intact from tumour invasion, they should be assumed to have tertiary (hypothalamic) hypothyroidism. Of particular interest is the fact that the patients with suprahypophyseal tumour surprisingly showed a supernormal TSH response to 50 μg of TRF.
Fahrettin Keleştimur, Peter Jonsson, Senay Molvalilar, Jose Manuel Gomez, Christoph J Auernhammer, Ramiz Colak, Maria Koltowska-Häggström and Miklos I Goth
Objective: Sheehan’s syndrome occurs as a result of ischaemic pituitary necrosis due to severe postpartum haemorrhage. It is one of the most important causes of hypopituitarism, and hence growth hormone deficiency (GHD), in developing countries. However, little is known about the effects of growth hormone (GH) replacement therapy in patients with Sheehan’s syndrome.
Design: The demographic background characteristics of 91 GH-deficient patients with Sheehan’s syndrome (mean age ± s.d., 46.3 ± 9.4 years) were compared with those of a group of 156 GH-deficient women (mean age ± s.d., 51.5 ± 13.1 years) with a non-functional pituitary adenoma (NFPA). The baseline characteristics and the effects of 2 years of GH replacement therapy were also studied in the 91 patients with Sheehan’s syndrome and an age-matched group of 100 women with NFPA (mean age ± s.d. 44.5 ± 10.2 years).
Results: All patients were enrolled in KIMS (Pfizer International Metabolic Database). Patients with Sheehan’s syndrome were significantly younger at pituitary disorder onset, diagnosis of GHD and at entry into KIMS than patients with NFPA (P < 0.01), and had significantly lower insulin-like growth factor I levels (P < 0.001). At baseline, quality of life (QoL) was significantly (P < 0.05) reduced in patients with Sheehan’s syndrome compared with those with NFPA (P < 0.001). With regard to treatment effects, lean body mass increased significantly (P < 0.05), QoL improved significantly (P < 0.05) and total and low-density lipoprotein-cholesterol decreased significantly (P < 0.05) in patients with Sheehan’s syndrome after 1 year of GH replacement therapy. Similar significant changes in QoL and lipid profiles occurred in patients with NFPA after 2 years of GH replacement. Blood pressure remained unchanged in patients with Sheehan’s syndrome, but decreased significantly (P < 0.01) in the group with NFPA after 1 year, before returning to pretreatment levels at 2 years.
Conclusions: In conclusion, patients with Sheehan’s syndrome have more severe GHD compared with individuals with NFPA. GH replacement therapy in patients with Sheehan’s syndrome may have beneficial effects on QoL, body composition and lipid profile.
Kunihiko Hanew, Atsushi Utsumi, Akira Sugawara, Yasuyuki Shimizu and Kaoru Yoshinaga
The sources of TSH, which was excessively released by sulpiride (dopamine D2 receptor antagonist), were studied in 15 female patients with PRL-secreting adenoma (18-43 years). Sequential 3-day administration of sulpiride (100 mg, im) was given to 12 patients with prolactinoma and 6 normal female subjects (19-24 years). Patients with prolactinoma showed much greater TSH responses than normal subjects on the first day. However, TSH responses to sulpiride disappeared on the 2nd and 3rd day in both groups. In contrast, plasma PRL responses to the 1st sulpiride administration were smaller in patients with prolactinoma than in normal subjects, and the response disappeared following the 2nd administration in both groups. When TRH (500 μg, iv) was administered 120 min after the 3rd sulpiride injection, TSH and PRL increments were not different from those before the sulpiride injection in both patients with prolactinoma (N=6) and normal subjects (N=6) Further, combined administration of sulpiride and TRH in 5 patients with prolactinoma clearly enhanced the TSH and PRL responses compared with the single administration of each agent. These results suggest that there may be two readily releasable pituitary TSH and PRL pools, i.e. one dopamine-related and the other TRH-related, in patients with prolactinoma and normal female subjects.
Risto Pelkonen, J. Salmi and B.-A. Lamberg
The relationship between the TSH and prolactin (Prl) responses to TRH has been investigated in 36 patients with prolactinoma, in 12 patients with symptomless autoimmune thyroiditis (SAT) and in 10 patients with Graves' disease in remission (GD). Autoimmune thyroiditis in combination with prolactinoma was found in 3 patients. The TSH -response was exaggerated in 4 prolactinoma patients without autoimmune thyroiditis. Moreover, in the patients with prolactinoma and intact function of the non-tumours pituitary gland the mean TSH increment was higher than in the controls. In patients with SAT, on the other hand, the Prl-response to TRH was significantly greater than that in the controls and in patients with GD.
The significance of these findings is not obvious but they suggest that TRH may be involved in the development of prolactin secreting adenomata.
Conrad M. Swartz, Victor S. Wahby and Ruth Vacha
Abstract. Applying the principles of chemical kinetics to the time course of TSH concentrations after TRH infusion, individual values for total TSH release from the pituitary, TSH elimination and release rates, and latency for TSH release were found for 40 patients. Justification for using the observed peak TSH elevation as a consistent reflection of the total TSH release was provided by the high correlation between these two (r = 0.97, P < 0.001). Kinetic modeling indicated that the most consistent reflection of total pituitary TSH response is the TSH elevation over baseline 35 min after TRH (with the peak expected 30 min post-TRH), rather than the area under the curve.
Ildo Nicoletti, Paolo Filipponi, Leone Fedeli, Franca Ambrosi, Camillo Giammartino, Fabrizio Spinozzi and Fausto Santeusanio
Abstract. In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the effect of low-dose DA infusion on TRH stimulated TSH secretion in normally cycling women and in patients with pathological hyperprolactinaemia. The effect of long-term bromocriptine therapy on TSH dynamics was also evaluated in a selected group of hyperprolactinaemic women.
Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values after TRH administration than 75 healthy controls. Furthermore, the TSH rises induced by the DA-synthesis inhibitor α-methyl-p-tyrosine (AMPT, 500 mg orally) were enhanced in both prolactinoma and 'idiopathic hyperprolactinaemia' patients as compared with controls. There was a positive correlation between the TRH- and AMPT-induced TSH rises in the hyperprolactinaemic group.
Low-dose DA infusion (0.1 μg/kg min) reduced TSH response to TRH in both regularly cycling women and patients with hyperprolactinaemic amenorrhoea. Long-term bromocriptine therapy (2.5 mg tid over 60– 150 days) not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had presented exaggerated TSH responses to the basal TRH test.
These findings confirm that DA plays a physiological role in the inhibition of TSH release, probably at the level of the anterior pituitary. The fact that both low-dose DA infusion and long-term bromocriptine treatment effectively reduced TSH release in hyperprolactinaemic patients seems to indicate that endogenous DA inhibition of pituitary thyrotrophs is reduced rather than enhanced in pathological hyperprolactinaemia.
Friedrich W. Erhardt and Peter C. Scriba
Homogenates of human pituitaries were centrifuged at 30 000 × g and the supernatant chromatographed on Sephadex G-100. Approximately 1 % of the radioimmunologically measured total activity of TSH was eluted in the void volume. Rechromatography of this material on Sephadex G-200 usually showed TSH-activity at Kav = 0.5 (regular TSH), Kav = 0 (void volume-TSH) and at Kav = 0.3 ("big"-TSH). "Big"-TSH was extracted from the corresponding fractions by affinity-chromatography with solid phase anti-TSH. It was eluted with 5 mol/l ammonium thiocyanate and further characterized:
1. The molecular weight was approximately 200 000 by comparison with bovine catalase on Sephadex G-200.
2. Immunoidentity as compared with standard-TSH (M. R. C. 68/38) was shown by parallel dilution curves in the radioimmunoassay.
3. Concanavalin-A-Sepharose adsorbed "big"-TSH, which could be eluted with α-methyl-D-mannoside, indicating the glycoprotein nature of "big"-TSH.
4. On polyacrylamide-gel-electrophoresis pH 7.5, "big"-TSH migrated faster (R F = 0.32) than regular TSH (R F = 0.1), indicating a more negatively charged molecule.
5. "Big"-TSH, in contrast to regular TSH, was remarkably stable against 6 mol/l guanidine hydrochloride, suggesting a covalently linked (aggregate) structure.
6. 1 % mercaptoethanol destroyed the immunological activity of both regular and "big"-TSH.
7. "Big"-TSH was digested by trypsin, under mild conditions, to radioimmunologically active products with molecular weights between "big"- and regular TSH, but practically no regular TSH was formed.
8. "Big"-TSH and guanidine-treated "big"-TSH, as well as regular TSH and TSH from the void volume of Sephadex G-200 columns, exhibited biological activity in a cytochemical bioassay in good agreement with the respective immunological activities.
S. Filetti, B. Rapoport, D. C. Aron, F. C. Greenspan, C. B. Wilson and W. Fraser
Studies were performed on pituitary adenoma tissue obtained from a patient with hyperthyroidism secondary to inappropriate thyrotrophin (TSH) secretion. Cells dispersed enzymatically were established in primary monolayer culture for a period of 39 days. Intact TSH and TSH-subunit release into the culture medium declined over the initial 20 days, followed by a rebound in TSH and β-TSH production until the time of subculture at day 39. In vitro α-TSH production declined more slowly than did TSH and β-TSH, but did not recover in parallel with intact TSH. Production of α-TSH by cultured cells, at different times, was 20–80-fold greater than that of β-TSH. In the pituitary tissue α-TSH content (112 ng/mg tissue) was 8.6-fold greater than the β-TSH concentration (13 ng/mg tissue), but similar to intact TSH content (105 ng/mg tissue). In serum, the α-TSH concentration (6.5 ng/ml) was lower than in most previously reported patients with thyrotrophic adenomata. TSH bioactivity in tumour tissue (approximately 600 ng/mg tissue) was greater than the immunoreactive TSH concentration. LH, FSH and prolactin were undetectable in tumour tissue, and in the culture medium throughout the period of cell culture. Exposure of thyrotroph monolayers to 10−6 m TRH for 4 h led to 32%-– 600% increases in TRH release, depending on the day of culture and the cell flask utilized. The α-TSH response to TRH paralleled that of intact TSH, β-TSH being unmeasureable. Incubation of cell monolayers for 4 h in 5 × 10−7 m dopamine decreased TSH and α-TSH secretion into the medium. In contrast, exposure of cells to T3 at concentrations as high as 10−6 m did not affect TSH secretion. Surprisingly, TRH (10−7 m to 2 × 10−6 m) inhibited cultured thyrotroph cAMP content by about 50%; cGMP levels were unaffected.
This study, the first to examine secretory function of human thyrotrophic tumour cells in vitro, confirms the disproportionate production of α-TSH by these tumours, even though this may not be apparent from the level of the α-subunit in serum. The data indicate that TSH secretion by thyrotroph tumour cells, at least from this particular patient, remains sensitive to TRH stimulation and dopamine inhibition, but insensitive to inhibition by T3. Not all TSH bioactivity is reflected by the immunoassayable TSH concentration, suggesting that the tumour may be producing variants of normal TSH that nevertheless retain biological activity. Finally, the data suggest that, at least in this particular tumour, TRH stimulation of TSH secretion is not mediated by cAMP as a second messenger.
The release of radiolabelled thyroid hormone into the circulation in low iodine fed mice has been used extensively as a bioassay for thyroid stimulating hormone (TSH). However, the specificity of several bioassays of pituitary hormones have been subject to question. Consequently, the validity of the assay endpoint for TSH in the mouse was re-evaluated with respect to the effect of luteinizing hormone (LH) whose chemical composition closely resembles that of TSH. Mice, prepared for bioassay of TSH received injections of purified LH or α or β subunits of LH. Identical doses of LH and LH subunits were quantified by LH and TSH radioimmunoassays and the results compared with those obtained by the bioassay. Microgram quantities of LH and subunits of LH elicited appreciable responses in the TSH bioassay but produced only negligible effects in the TSH radioimmunoassay. The response of the TSH bioassay of LH and α or β subunits of LH was 40–56% that obtained with LH radioimmunoassay. However, the pituitary concentrations obtained by TSH bioassay when compared with those obtained by radioimmunoassays for TSH, LH, or growth hormone (GH) paralleled closely the TSH radioimmunoassay data, although in terms of quantitative estimates, there was a 15-fold discrepancy between the TSH assays. Estimations of pituitary concentrations of LH lead to the conclusion that, at the doses normally employed, most crude rat pituitary extracts do not contain sufficient quantities of LH to alter significantly bioassayable (McKenzie) estimates of TSH.