Giovina De Rosa

Prospective study of bone loss in pre- and post-menopausal women on L-thyroxine therapy for non-toxic goitre.

Hyperthyroidism is associated with increased bone turnover and bone resorption, but the effects of suppressive doses of thyroxine in treating non‐toxic goitre remain unclear. We carried out a longitudinal study to evaluate the effect on bone of L‐thyroxine (L‐T4) therapy in women with non‐toxic goitre.

Thyroid carcinoma mimicking a toxic adenoma

A young woman with a thyroid papillary carcinoma behaving as an autonomously hyperfunctioning nodule is described. Only 17 similar patients have been seen in the past 25 years. It is emphasized that hyperthyroidism does not exclude malignant disease in hot nodules. This possibility suggests that all thyroid nodules, either cold or hot, require careful management. Therefore, in “at risk” cases, surgery could be the most useful treatment.

Primary papillary carcinoma arising from median ectopic thyroid in multinodular goitre

CARCINOMA ARISING from thyroglossal duct remnants is a rare entity [ 11. An interesting case of papillary thyroid carcinoma of the thyroglossal duct remnants, observed among 700 patients with thyroid carcinoma, is here reported and its particular features described. A 66-year-old woman, with a lo-year history of multinodular goitre, noticed a progressively growing mass in the midline of her neck 12 months ago. She had been in suppressive thyroid therapy for the last 7 years (L-thyroxine 2 pg/kg body weight resulting in suppressed thyroid stimulating hormone (TSH) response to thyrotropin releasing hormone (TRH). Free and total T4 and T3 were within normal range and TSH levels were undetectable. No uptake was detected over the midline neck mass in the 13tI thyroid scan, in which the thyroid gland appeared enlarged with a dishomogeneous distribution of the tracer. Ultrasonography revealed a diffuse enlargement of the thyroid gland, with mixed lesions and, above the gland, a solid lesion 2.0 cm in diameter with calcification. Cytopathological examination of the neck mass suggested a papillary proliferation. At surgery, a mass of diameter 2.2 cm just below the hyoid bone, was removed and a total thyroidectomy was performed. The mass was 3 cm above the upper margin of the thyroid gland and so was unconnected to it. Histological examination confirmed the presence of papillary carcinoma in the mass, whereas no evidence of neoplasm resulted in the thyroid gland. The interesting aspect of this case is the inability of the continuous, prolonged administration of thyroid hormone in protecting the patient from the occurrence of cancer. The case reported seems to contradict the belief that the growth of papillary carcinoma depends solely on TSH stimulation. This view stems from at least two kinds of observations: (i) that thyroid hyperplasia associated with elevated TSH levels in congenital goitrous patients untreated for many years can lead to malignant degeneration [2] and (ii) that differentiated tumours can show normal TSH receptors. This fact can explain their TSH dependent growth, whereas anaplastic cancer lacks high-affinity receptors and shows TSH-independent growth [3]. In conclusion the case described is consistent with a rare neoplastic localisation in the thyroglossal duct remnants and supports the possible+ven though unusual-development of cancer during suppressive therapy.

Autoimmune polyglandular syndrome, primary empty sella, and acute lymphocytic leukaemia

A young man is reported with an autoimmune polyglandular syndrome (APS) characterized by Addisons disease, primary hypothyroidism, primary hypogonadism, vitiligo, associated with primary empty sella and partial impairment of pituitary hormone secretion. Two years later the patient showed a null cell type acute lymphocytic leukaemia, immediately after surgery for an inguinal hernia. Pathogenetic mechanisms are postulated on the basis of HLA studies and lymphocytic typing.

ALTERNATION OF HYPO- AND HYPERCALCEMIA IN A PARATHYROIDECTOMIZED PATIENT WITH BREAST CANCER

We report the case of a 54-year-old female patient with postoperative hypoparathyroidism. Despite the fact that she was receiving calcitriol replacement therapy, following the appearance of bone metastases due to breast cancer she developed severe crises of hypo- and hypercalcemia.