Primary hypothyroidism presenting as multiple ovarian cysts in an adult woman: A case report

Abstract

A 21-year-old woman was referred because of abdominal pain. On physical examination, her abdomen was distended up to the umbilical region. Ultrasound and computer tomography of the abdomen revealed bilateral multiple ovarian cysts. Laboratory studies revealed increased liver function, total cholesterol and creatine phosphokinase. Further clinical investigations determined that the patient suffered from primary hypothyroidism due to autoimmune thyroiditis. The cysts resolved spontaneously after the simple replacement of a thyroid hormone. Some reports have been published of primary hypothyroidism presenting as ovarian cysts and precocious puberty in prepubertal girls. However, the case presented herein indicates that an ovarian tumor as a result of hypothyroidism may also occur in adult females. To avoid inadvertent surgery to remove an ovarian tumor, it is essential that a patient with multiple ovarian cysts and hypothyroidism be properly managed, as the simple replacement of a thyroid hormone could resolve the ovarian cysts.

An unusual presentation of acquired hypothyroidism: the Van Wyk–Grumbach syndrome

“…Girls with this syndrome have breast development, follicular cysts and menstruation in the absence of pubic or axillary hair, which depends on adrenal androgens (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22). Histopathological analysis of resected ovaries and ovarian cysts shows cystic follicles and little if any luteinisation.…”

“…Surgery should only be indicated if there is ovarian torsion or if the cystic enlargement does not regress with treatment (4, 6, 9, 11). The peripubertal phase, where low FSH levels prevail, could be vulnerable to FSH receptor stimulation by TSH (18,24,27) with cases very rarely being reported outside of this age group (18,21,22). A dose-dependent response of the FSH receptor to TSH is assumed as only very few children, all with extremely high TSH levels, are affected.…”

“…Positive thyroid peroxidase antibodies confirmed autoimmune thyroiditis; TPO antibody titre was 378 kU/l (normal range 0-35 kU/l). Further blood tests highlighted a raised prolactin at 1310 mU/l, deficient vitamin D (16.2 nmol/l) and a suppressed parathyroid hormone (PTH) of 7 ng/l (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29), in the presence of normal calcium and phosphate. She had a raised white blood cell count of 14.9 gG/l, raised ESR and severe, hyporegenerative, microcytic anaemia (Table 2).…”

“…Biochemically, low free thyroxine (T 4 ) is combined with raised levels of thyroid stimulating hormone (TSH), prolactin and oestradiol. Typically, luteinising hormone-releasing hormone (LHRH) stimulation shows an FSH-dominated prepubertal response with suppressed luteinising hormone (LH), confirming gonadotropin-releasing hormone (GnRH)-independent precocious pseudopuberty (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22). Most cases in the literature are secondary to autoimmune thyroid disease but there are some case reports where the syndrome is secondary to unrecognised congenital hypothyroidism (5,10,12).…”

“…Most cases in the literature are secondary to autoimmune thyroid disease but there are some case reports where the syndrome is secondary to unrecognised congenital hypothyroidism (5,10,12). It is important to recognise this syndrome as symptoms regress with thyroid hormone replacement and patients spontaneously enter true puberty at an appropriate time (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22).…”