Thyroid Disorders in Children

Abstract

A 14-year-old girl presented with complaints of growth failure and poor development of secondary sexual characteristics. She also complained of occasional headache and for that a brain imaging was performed. The MRI of the brain showed a sellar–suprasellar mass and she was referred to the department of neurosurgery for surgical intervention. An endocrine consultation was sought prior to subjecting the patient to surgery. A detailed history was elucidated, which revealed that she had linear growth failure for the last 7–8 years. She also complained of lethargy, weakness, constipation, cold intolerance, dry skin, and decreased appetite. She studied till class seventh; however, later she dropped out because of progressive decline in her scholastic performance. There was history of poor development of secondary sexual characteristics; however the mother gave a history that the patient had a single episode of vaginal bleed at the age of 12 years. She had no history of visual field defect or diminution of visual acuity. She was residing in iodine-sufficient area and had no family history of autoimmune disorders. On examination, her height was 116 cm (−7 SDS, height age 6 years and target height 164 cm), weight 35 kg (weight age 10.5 years), pulse rate 64/min, regular and blood pressure 90/60 mmHg. Her facial features revealed pallor with yellowish hue, periorbital puffiness, and depressed nasal bridge. She did not have goiter. Her skin was dry and coarse with papillomatous projections (toad’s skin) and scalp hair was dry, thin, and brittle. Deep tendon reflexes were grossly delayed particularly the relaxation phase. She also had myoedema which was elicitable on flicking the biceps belly with thumb and index finger and showed a post-flicker mounding phase. She did not have a pseudohypertrophy of calf muscle. Other systemic examination was unremarkable. On investigations, hemoglobin was 8 g/dl with microcytic hypochromic anemia. Liver and renal function tests were normal. Serum cholesterol was 220 mg/dl, LDL-C 160 mg/dl, HDL-C 30 mg/dl, and triglyceride 220 mg/dl. Hormonal profile revealed, serum T₃ 0.3 ng/ml (N 0.8–2), T₄ 0.3 μg/dl (N 4.8–12.7), TSH 1024 μIU/ml (0.27–4.2), TPO >1200 IU/ml (N < 34), prolactin 50 ng/ml (N 4.7–23.3), LH 0.8 mIU/ml (N 2.4–12.6), FSH 8.6 mIU/ml (N 3.5–12.5), estradiol 15 pg/ml (N 12.5–166), and 0800h cortisol 170 nmol/L (N 171–536). Bone age was 6 years and there was no epiphyseal dysgenesis. CEMRI sella revealed a 1.5 × 1.8 cm homogeneously enhancing sellar–suprasellar mass, while the rest of the brain parenchyma was unremarkable. Ultrasound pelvis showed bilateral enlarged multicystic ovaries with small uterus and endometrial thickness of 1 mm. With this clinical and biochemical profile, she was diagnosed as a case of long-standing, untreated juvenile primary hypothyroidism of autoimmune origin (Hashimoto’s thyroiditis) with thyro-lactotrope hyperplasia and multicystic ovaries. She was initiated with L-thyroxine at a dose of 25 μg/day, with a weekly increase by 25 μg till a dose of 100 μg/day was attained. In addition, hydrocortisone was also added at a dose of 10 mg/day in divided doses. At 6 weeks of follow-up, serum T₄ was 6.6 μg/dl and TSH 15 μIU/ml. With initiation of treatment, she had polyuria which abated later. The dose of L-thyroxine was increased to 125 μg/day and hydrocortisone was withdrawn, and the repeat serum 0800h cortisol after 24h of omission of hydrocortisone was 390 nmol/L (Figs. 3.1 and 3.2).