Thyroid Research and Practice

: 2012  |  Volume : 9  |  Issue : 3  |  Page : 102--104

Radiological manifestations of juvenile hypothyroidism

Prem P Patidar1, Rajeev Philip1, Ajit Toms2, Keshavkumar Gupta1,  
1 Department of Endocrinology, LLRM Medical College, Meerut, India
2 Department of Radiology, St Thomas Hospital, Changancherry, Kerala, India

Correspondence Address:
Prem P Patidar
G 10, PG Hostel, LLRM Medical College, Meerut, Uttar Pradesh- 250 004


Thyroid hormone is required for the normal growth and maturation of the skeleton. The action of thyroid hormone on skeleton is varied, including direct chondrocyte and osteoblast stimulation, as well as potentiating the action of growth hormone on the bone. Juvenile hypothyroidism is evolving as the most common form of thyroid dysfunction in the growing age, and it has different radiological manifestations from that of congenital hypothyroidism. We present the skeletal X-rays of a 24-year-old man with juvenile onset autoimmune hypothyroidism (duration of illness of approximately 16 years), who came for evaluation of short stature.

How to cite this article:
Patidar PP, Philip R, Toms A, Gupta K. Radiological manifestations of juvenile hypothyroidism.Thyroid Res Pract 2012;9:102-104

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Patidar PP, Philip R, Toms A, Gupta K. Radiological manifestations of juvenile hypothyroidism. Thyroid Res Pract [serial online] 2012 [cited 2021 Oct 28 ];9:102-104
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Thyroid hormone mediates growth and development of skeleton through its direct effects, as well as through permissive effects on growth hormone. [1] The classic findings of hypothyroidism in bone are all described in congenital hypothyroidism, where the thyroid hormone is inadequate before the formation of epiphysis. But, the effects of low thyroid hormone levels on a growing skeleton, after formation of epiphysis is less defined, and the data on these findings are scarce. Due to the popularity of congenital hypothyroidism screening programmes, the untreated congenital hypothyroid patient is a rarity. But the entity of juvenile hypothyroidism, where thyroid hormone becomes inadequate in childhood or adolescence, after the brain development is complete, is being recognised off late. Early autoimmune destruction of the thyroid gland is the commonest cause, [2] while cases due to iodine deficiency are also being reported. [3] The importance of recognising the radiological findings of juvenile hypothyroidism is that this condition profoundly impairs growth of the child, with skeletal deformities, and can mimic Perthes disease. [4] Also, the X-ray finding of juvenile hypothyroidism is different from that of congenital hypothyroidism. We present the skeletal X-rays of a 24-year-old man with juvenile onset hypothyroidism (duration of illness of approximately 16 years), who came for evaluation of short stature.

 Case Report

A 24-year-old male presented for evaluation of short stature. He had history of growth arrest, weight gain, puffiness of face and constipation since the age of 8 years. On examination his height was 124 cms, (less than 3 rd percentile), with disproportionate short stature, lower segment being shorter than upper segment and arm span 8 cms less than the height. He was obese with weight of 40 Kgs, and BMI of 26.1 Kg/m 2 . Other findings of hypothyroidism like loss of eyebrows, calf muscle hypertrophy, dry skin, and delayed relaxation of reflexes were also present. Investigations confirmed the diagnosis of autoimmune hypothyroidism, with T4: <1.0 μg/dl (5.01-12.4) T3: <0.25 ng/ml (0.6-1.81), TSH: 580. μiu/ml (0.35-5.50), anti TPO> 1300 units/ml (<60.00). His calcium profile - calcium, phosphorus, and alkaline phosphorus was also normal.

A skeletal screening was done to look for the effect of thyroid hormone deprivation on growth and skeletal maturation.

X-ray skull sellar view [Figure 1] showed an enlarged sella with hypoplastic maxillary and frontal sinuses. X-ray wrist left hand AP view [Figure 2] was done, which showed a bone age of 10 years (Tanner-Whitehouse 2 test) and delayed appearances of carpal bones, with the epiphysis of pisiform just appearing. Irregular ossification of growth plate was seen at ulna, and a sclerotic band was seen at the radial metaphysis. Soft tissue thickening was also appreciated. Also, the cortical bone was osteoporotic with pencil thin cortex, which is a finding described in hypothyroidism. X-ray of the lumbosacral vertebra, [Figure 3] showed bullet shaped L 1 vertebra and increased intervertebral disc spaces. Also, the vertebrae were osteoporotic. X-ray of pelvis [Figure 4] showed unfused epiphysis of femoral head, unfused apophysis and persistent triradiate cartilage. X-ray of the knee [Figure 5] revealed heterogeneous epiphysis with irregular ossification of growth plate.{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}


Thyroid hormone mediates the growth, development and maturation of the skeleton. It regulates chondrocyte proliferation, promotes differentiation of bone progenitor cells, induces mineralisation and promotes angiogenesis. It also stimulates production of type II and X collagen and alkaline phosphatase (ALP) promoting bone matrix formation and mineralisation. [5],[6] It also has a permissive role on the action of growth hormone by promoting GH secretion from pituitary, as well as GH dependent IGF-1 production in the bone.

When thyroid hormone is absent from birth, it leads to growth arrest, delayed bone age, and short stature. Ossification centers are defective, and they appear in an irregular and mottled pattern, with multiple foci that coalesce to give a porous or fragmented appearance known as stippled epiphyseal dysgenesis, most frequently noted in large cartilaginous centers, such as the head of the femur, head of humerus and the tarsal navicular bone. [7]

When hypothyroidism is acquired during the growing ages, as in juvenile hypothyroidism, the manifestations are different. Skeletal maturation, defined as the appearance of secondary centers of ossification, is predominantly affected, with delayed fusion of epiphysis, and delayed bone age. The epiphyseal centers are heterogeneous with irregular ossification. But the classical stippled epiphyseal dysgenesis, described with congenital hypothyroidism, does not occur. Changes in the upper lumbar vertebrae result in wedge-shaped anterior margins, and may lead to spondylolisthesis. [8] The metaphyseal end of long bones usually has a sclerotic band. [9]

Juvenile hypothyroidism decreases the activity of chondrocytes, osteoblastic cells as well as osteoclasts. Despite decrease in osteoblastic activity, trabecular bone volume [10] and bone mineral density [11] appear to be normal or slightly altered, because of the reduction in osteoclastic activity.

The major skeletal manifestations of hypothyroidism is summarised in [Table 1].{Table 1}


Juvenile hypothyroidism, impairing the skeletal maturation is evolving as a disease, more common than congenital hypothyroidism. The presentations may be varied including short stature, spondylolisthesis, delayed bone age and irregular ossification of epiphysis. Prompt recognition of the findings can lead to early and effective treatment, improving the skeletal defects.


Dr Renjit Philip, Consultant Radiologist, St Thomas Hospital, Changancherry, Dr Sanjay Saran Senior Resident, Department of Endocrinology, LLRM Medical College Meerut.


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