Acromegaly in PregnancyAn Overview of the Key Issues
Bibliographic record
Abstract
Acromegaly in pregnant women is an uncommon clinical problem.However, today, due to earlier diagnosis, women present with this concern at a younger age.In patients with pre-existing acromegaly, there may be difficulty conceiving, there are concerns regarding maternal and fetal outcomes, and there are no good data to fully assess the risk:benefit ratio of the various therapies that could be used during pregnancy.Acromegaly diagnosed for the first time during pregnancy is another clinical problem.Acromegaly is a rare disease with an annual incidence of three to four per million people, 1 characterized by excessive production of growth hormone (GH) from somatotroph cells in the pituitary gland, almost always from an adenoma.Acromegaly in pregnancy is even more rare and limited data are available, mainly as a consequence of the reduced fertility often found in women with pre-existing pituitary disease. Pituitary Changes in Normal PregnancyMagnetic resonance imaging (MRI) scans performed during pregnancy demonstrate a gradual increase in maternal pituitary volume over the course of gestation, with an increased final weight (660-760 mg) as well as a volume increase of 30 % above the pre-gestational volume.2,3 This enlargement results in a homogeneous upward convexity of the superior surface of the gland when visualized radiologically, and the gland reaches 12 mm in height a few days post-partum.It usually does not increase more than 2.6 mm.The pituitary gland increases in all dimensions, with an average increase of 136 %. 2 Rare reports exist of impingement on the optic chiasm, with resulting visual field changes, in women who have otherwise normal pregnancies.4 The pituitary stalk remains unchanged and is in the midline.These changes usually regress after delivery. Effect of Acromegaly on Fertility in WomenMenstrual irregularity is a common and early finding in acromegaly.Potential causes are impairment of the hypothalamic-pituitary-gonadal axis from anatomic compromise due to tumor mass effect, or hyperprolactinemia secondary to stalk compression (i.e., interference with dopamine action) or prolactin co-secretion.5 Prolactin-like effects of GH, specifically spillover, may contribute to the menstrual irregularity observed in acromegaly.6 In addition, recent evidence also suggests that there is a direct effect of GH and insulin-like growth factor 1 (IGF-1) on ovarian function.6 Hyperandrogenemia may result in a polycystic ovary syndrome (PCOS)-like pattern.7 Furthermore, previous surgery or radiotherapy may impair normal pituitary gonadotropin secretion.Correction of hyperprolactinemia may be necessary to restore normal ovulation in these patients.Recent advances in ovulation induction and medical or AbstractAcromegaly in pregnancy is a rare occurrence and the literature regarding its diagnosis and management is limited.Normal pregnancies have a physiologic increase in growth hormone due to the production of a variant form by the placenta.Conventional assays are unable to differentiate pituitary from placental growth hormone and, as a result, making a diagnosis of acromegaly or assessing biochemical control in pregnancy is a challenge.While risks to the patient and fetus exist, they are mainly limited to complications associated with insulin resistance-which, if present, should be monitored and treated.Tumor enlargement may occur if therapy is discontinued at the start of pregnancy, but this is usually not the case and most have an uneventful pregnancy.Consequently, definitive diagnosis or treatment can often be delayed until after delivery-although, when indicated, treatment with dopamine agonists or somatostatin analogs is a reasonable option.To date, there are no data to suggest adverse outcomes with these agents; however, limited evidence is available and they should only be used in severely symptomatic acromegalics or those with symptomatic tumor enlargement.Transsphenoidal surgery is associated with an increased rate of pre-term labor and fetal loss, and should be considered only in emergency situations such as pituitary apoplexy.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.002 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.002 | 0.001 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.002 | 0.002 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.002 | 0.003 |
| Insufficient payload (model declined to judge) | 0.002 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".