In rare cases, a parathyroid adenoma can mimic the signs and symptoms of rickets or contribute to ricket-like changes in the body. Parathyroid adenomas are benign tumors that develop in the parathyroid glands, which are responsible for regulating calcium and phosphate levels in the body. When an adenoma overproduces parathyroid hormone (PTH), it can disrupt the normal balance of calcium and phosphate, leading to ricket-like manifestations. Here are some ways in which a parathyroid adenoma can mimic rickets: 1) bone demineralization: excessive production of PTH by a parathyroid adenoma can cause increased bone resorption, resulting in bone demineralization. This can lead to weakened bones, similar to the under mineralization seen in rickets; 2) skeletal deformities: parathyroid adenomas causing hyperparathyroidism can lead to skeletal deformities, such as bowing of the long bones or other abnormalities, resembling the bone deformities seen in rickets; 3) growth delay: hyperparathyroidism resulting from a parathyroid adenoma can disrupt normal growth and development, causing growth delay in children; 4) vitamin D deficiency: in some cases, parathyroid adenomas can lead to vitamin D deficiency. Vitamin D is deficiency of vitamin D can contribute to ricket-like changes, as observed in rickets; 5) electrolyte imbalances: hyperparathyroidism caused by a parathyroid adenoma can disrupt the balance of calcium and phosphate in the body, leading to abnormal serum levels. These electrolyte imbalances can contribute to the development of ricket-like changes. If ricket-like changes are suspected, it is important to thoroughly evaluate the underlying cause. This typically involves conducting blood tests to assess calcium, phosphate, PTH, and vitamin D levels, as well as imaging studies to identify the presence of a parathyroid adenoma. Treatment of the adenoma usually involves surgical removal, which can help restore normal parathyroid function and resolve the ricket-like symptoms. Primary hyperparathyroidism (PHPT), a rare disorder in pediatric age, with an estimated incidence of 2-5 cases in 100,000 live births. A 17-year-old male patient was brought to the orthopaedics out patient department (OPD) with complaints of joint pain and deformity since 2 year which were increasing over the period of time with no history of trauma. On examination there were X-ray changes seen like mimicking rickets which were physeal widening, epiphyseal cupping and fraying, metaphyseal fraying and splaying, looser zones (pseudo fractures), bowed or distorted long bones, and delayed bone age.

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Corresponding author
Hardik Patel, Department of Orthopedics, Datta Meghe Institute of Medical Sciences(DU), Sawangi, Wardha, Maharashtra, India (hardikpatekbjmc@gmail.com)