ESPE Abstracts (2019) 92 P3-209

Pituitary Hyperplasia as a Complication of Severe Hypothyroidism due to Hashimoto's Thyroiditis Could Impair Pituitary Function

Domenico Corica1, Francesca Granata2, Karol Galletta2, Malgorzata Wasniewska1

1Department of Human Pathology of Adulthood and Childhood "G. Barresi", Unit of Pediatrics, University of Messina, Messina, Italy. 2Department of Biomedical, Dental, Morphological and Functional Imaging Sciences, Unit of Radiology, University of Messina, Messina, Italy

Introduction: Long-standing primary hypothyroidism is an unusual cause of pituitary hyperplasia (PH) in children, sometimes difficult to distinguish on CT or MRI from primary pituitary tumors. Loss of thyroxine feedback determines overproduction of thyrotropin releasing hormone (TRH) and subsequent TSH-releasing cells hyperplasia in the anterior pituitary. Levothyroxine replacement therapy has been shown to usually determine regression of PH.

We report the case of 11-years-old girl with PH in which growth arrest was the only symptom of a severe primary hypothyroidism due to Hashimoto's thyroiditis (HT).

Case Report: A 11-years-old, Caucasian, prepubertal girl referred to Outpatient Clinic because of complete statural growth arrest in the last year as unique clinical feature. To exclude the intracranial expansive pathology, brain MRI was immediately performed and revealed anterior pituitary enlargement (pituitary volume 648.9 mm3). Hormonal evaluation documented: markedly elevated TSH (319 µUI/ml) and very low FT4 (2.79 pmol/L) associated with positive antibodies to thyroglobulin and thyroid peroxidase (289 UI/ml and 4580 UI/ml, respectively), suggesting HT also confirmed by thyroid ultrasound (normal thyroid volume, diffuse hypoechogenicity and increased parenchymal vascularization). Other basal hormonal evaluation demonstrated slight hyperprolactinemia (497 mUI/ml, normal range 102-496) and low concentrations of cortisol (5.3 pg/ml, 7.3-32), IGF-1 (88.5 ng/ml; 146-462) with subnormal GH secretion (GH peaks 6 ng/ml and 7 ng/ml in clonidine and glucagon stimulation tests, respectively). Gonadotropins (FSH 2.15 mUI/ml, LH <0.3 mUI/ml) and estradiol (< 5 pg/ml) were in prepubertal range. Screening for celiac disease was negative. Levothyroxine treatment (2 mcg/kg/day) was immediately started.

Six month after the beginning of levothyroxine, patient presented increased growth velocity (4.4 cm, 0.42 SD), onset of puberty (Tanner stage B2), normalization of thyroid (TSH 0.60 µUI/ml, FT4 18.7 pmol/L) and pituitary function (cortisol 11.87 ug/ml, IGF-1 182.8 ng/ml, GH peak 10.52 ng/ml, prolactin 88.6 uUI/ml, estradiol 42.30 pg/ml, FSH 4.01 mUI/ml, LH 0.88 mUI/ml). PH regression was also documented by MRI (218.4 mm3).

Conclusions: PH due to primary hypothyroidism should be considered in the differential diagnosis of statural growth arrest. PH may cause temporary deficit of the pituitary tropins secretion, in particular, GH secretion impairment might be due to TRH-induced transdifferentiation of somatotroph into thyrotroph cells, as previously demonstrated in murine model.

In patients with pituitary enlargement, thyroid function tests are important to recognize PH secondary to primary hypothyroidism so as to avoid unnecessary surgery.

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