Multicystic ovarian disease secondary to hypothyroidism in a prepubertal girl

Abstract

We present a case of bilateral ovarian enlargement with multiple ovarian cysts associated with hypothyroidism in a prepubescent female. The patient was managed conservatively with hormonal therapy.

Keywords: Hypothyroidism, Multicystic, Ovary, Ultrasonography

How to cite this article:
Gupta S P, Mittal A, Mehta V, Mahendru R. Multicystic ovarian disease secondary to hypothyroidism in a prepubertal girl. Ann Trop Med Public Health 2011;4:107-9

 

How to cite this URL:
Gupta S P, Mittal A, Mehta V, Mahendru R. Multicystic ovarian disease secondary to hypothyroidism in a prepubertal girl. Ann Trop Med Public Health [serial online] 2011 [cited 2017 Nov 14];4:107-9. Available from: https://www.atmph.org/text.asp?2011/4/2/107/85762

 

Introduction

The association of cystic ovarian enlargement with primary hypothyroidism is not widely recognised in medical literature. At present the exact mechanism leading to ovarian cyst formation in patient in primary hypothyroidism remains uncertain. Identification of hypothyroidism in these girls obviates the need for extensive investigation and surgical management as they can be managed conservatively with proper hormonal treatment of hypothyroidism.

Case Report

A 10-year-old female child presented with lethargy, fatigue, lack of concentration and poor performance at school, increasing obesity, and growth retardation. For last one week she complained of pain in pelvic area. She had not attained menarche and there were no signs of precocious puberty. On clinical examination, the patient was slightly obese, had stunted growth for her age, and weak deep tendon reflexes. Her weight was 34.5 kg. Per abdominal examination was normal. She was referred for ultrasonography (USG) of the abdomen and pelvis for pelvic pain, which showed enlargement of both the ovaries, with multiloculated cysts present bilaterally. The right ovary measured 8 × 7 × 7 cm and the left ovary was 7 × 7 × 7 cm [Figure 1]. The uterus was normal for her age. With the possibility of hypothyroidism suggested by the clinical findings, USG of the thyroid was done. This showed both lobes of the thyroid as well as the isthmus to be smaller in size than normal, with the parenchyma having an altered echotexture and areas of hypoechogenicity within [Figure 2]. No mass lesion was seen in the thyroid. No cervical lymphadenopathy was present on ultrasonography. Radiographs of the chest and skull were normal. Laboratory examination showed decreased T 3 (0.25 ng/ml) and T 4 (1 ng/dl), with a markedly raised TSH (791.42 IU/ml). The serum levels of the rest of the hormones were as follows: Prolactin 86.2 μg/l (normal: 4.7-23.3 μg/l), luteinizing hormone (LH) 0.596 IU/l (normal: 2.4-12.6 IU/l), follicle stimulating hormone (FSH) 13.3 IU/l (normal: 3.5-12.5 IU/l), and 17-b-estradiol 1232.1 pmol/l (normal: 45.9-642.4 pmol/l). To identify the cause of the hypothyroidism, we checked the antibody levels; this showed the anti-TPO (thyroid peroxisomal antibodies) level to be 184.32 IU/ml (normal: <34 IU/ml). Thus, the cause was established to be autoimmune thyroiditis, which was supported by the USG finding of altered echotexture of the thyroid gland. Skiagram of the skull was normal with normal pituitary fossa. In view of the known association between hypothyroidism and ovarian cysts/enlargement, we started treatment for hypothyroidism and followed up the patient with periodic USG to check for regression in the size of the ovaries and the ovarian cysts.

Figure 1: USG shows gross enlargement of both ovaries. Multiple cysts are present in both ovaries, with internal echoes seen in the larger cysts

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Figure 2: USG shows both lobes of the thyroid to be reduced in size, with altered echotexture and hypoechogenicity

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At 5 months, USG showed regression in the size of the cysts in both the ovaries [Figure 3]. Her weight had decreased to 28 kg. Thyroid function tests also showed improvement, with normalization of T 3 and T 4 and reduction in TSH after 3 months. By 1 year she showed marked improvement in her symptoms, with complete resolution of the ovarian cysts [Figure 4] and normalization of thyroid function (T 3 0.62 ng/ml, T 4 5.2 ng/dl, and TSH 8.2 IU/ml); the other endocrine tests were also normal. The patient continues to be on regular follow-up.

Figure 3: Follow-up USG done 3 months after treatment shows reduction in size of the ovaries; one cyst is still seen in the right ovary

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Figure 4: Follow-up USG done after 1 year shows marked reduction in the size of both ovaries, with resolution of all the cysts

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Discussion

Multicystic ovarian disease with hypothyroidism has been previously described in literature. [1],[2],[3],[4],[5],[6]] The pathophysiology of this entity is unclear. Various mechanisms have been proposed as the cause of the ovulatory dysfunction and the multiple ovarian cysts, including altered estrogen metabolism, hypothalamo-pituitary axis dysfunction, and altered prolactin metabolism. [1] At high levels TSH can have FSH- and LH-like activity and thus cause cyst formation in the ovaries. [2] In some cases there would seem to be hypersecretion of more than one tropic hormone by the pituitary in response to deficiency of only one endocrine gland; for example, thyroid deficiency may stimulate gonadotrophin release and hence FSH and LH secretion, resulting in symptoms of precocious puberty. There may or may not be enlargement of the pituitary gland in response to an end organ deficiency. [3] Enlargement of the pituitary gland or pituitary adenoma have been described in hypothyroidism and some of these patients had ovarian enlargement and multiple ovarian cysts. [4] However, there was no enlargement of the pituitary gland in our patient. As mentioned earlier, ovarian enlargement in the presence of severe hypothyroidism can be due to stimulation of FSH receptors by the unusually high TSH levels which is known to have weak FSH-like activity. [5] In addition, some investigators have proposed that these patients may have a mutation that increases the sensitivity of FSH receptors to TSH. [6],[7] This seems to be the likely mechanism of action in our case.

Our patient had the typical symptoms of hypothyroidism along with delay in growth and sexual development but no evidence of hyperpituitarism. Other authors have also described improvement of symptoms in such patients, with normalization of thyroid function tests and resolution of ovarian cysts, after treatment for hypothyroidism. [1],[4] Our patient was put on thyroid replacement therapy and showed dramatic response, with complete resolution of the ovarian cysts and her symptoms. No surgical intervention was undertaken, as has been documented by other authors. [3],[8]

Conclusion

Whenever enlarged ovaries with multiple ovarian cysts are found in a prepubescent female, the possibility of hypothyroidism should be kept in mind. Correct diagnosis is extremely important as these patients can be successfully treated with thyroid hormone replacement therapy and an unwarranted surgical intervention can be avoided.

References

 

1. Hansen KA, Tho SP, Hanly M, Moretuzzo RW, McDonough PG. Massive ovarian enlargement in primary hypothyroidism. Fertil Steril 1997;67:169-71.
2. Evers JL, Rolland R. Primary hypothyroidism and ovarian activity evidence for an overlap in the synthesis of pituitary glycoproteins. Case report. Br J Obstet Gynaecol 1981;88:195-202.
3. Riddlesberger MM Jr, Kuhn JP, Munschauer RW. The association of juvenile hypothyroidism and cystic ovaries. Radiology 1981;139:77-80.
4. Yamashita Y, Kawamura T, Fuzikawa R, Mochizuki H, Okubo M, Arita K. Regression of both pituitary and ovarian cysts after administration of thyroid hormone in a case of primary hypothyroidism. Intern Med 2001;40:751-5.
5. Anasti JN, Flack MR, Froehlich J, Nelson LM, Nisula BC. A potential novel mechanism for precocious puberty in juvenile hypothyroidism. J Clin Endocrinol Metab 1995;80:276-9.
6. Vasseur C, Rodien P, Beau I, Desroches A, Gerard C, de Poncheville L, et al. A chorionic gonadotropin-sensitive mutation in the follicle-stimulating hormone receptor as a case of familial gestational spontaneous ovarian hyperstimulation syndrome. N Engl J Med 2003;349:753-9.
7. Smith G, Olalunbosun O, Delbaere A, Pierson R, Vassart G, Coslagliola S. Ovarian hyperstimulation syndrome due to a mutation in the follicle-stimulating hormone receptor. N Engl J Med 2003;349:760-6.
8. Bassam T, Ajlouni K. A case of ovarian enlargement in severe primary hypothyroidism and review of literature. Ann Saudi Med 2006;26:66-8.

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/1755-6783.85762

Figures

[Figure 1], [Figure 2], [Figure 3], [Figure 4]

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