Parathyroid gland (hypo-parathyroid tetany, primary and secondary hyperparathyroidism) in children
1. Osmonova Gulnaz Zhenishbaevna
2. Gaurav Rajendra Gadge
(1. Teacher, Dept. of Hospital Therapy, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic)
(2. Student, International Medical Faculty, Osh State University, Osh, Kyrgyz Republic)
Abstract
Parathyroid gland disorders in children, though relatively uncommon, are clinically significant due to their profound effects on calcium–phosphorus metabolism and neuromuscular function. Hypoparathyroidism leads to hypocalcemia and tetany, while hyperparathyroidism—primary or secondary—results in hypercalcemia or compensatory parathyroid hormone (PTH) elevation, respectively. Early recognition is crucial to prevent life-threatening complications such as seizures, cardiac arrhythmias, skeletal deformities, and renal damage.
Keywords: Parathyroid hormone, hypocalcemia, hypercalcemia, tetany, hypoparathyroidism, hyperparathyroidism, children, calcium metabolism
Introduction
The parathyroid glands play a vital role in maintaining calcium and phosphorus homeostasis through secretion of parathyroid hormone (PTH). PTH regulates bone resorption, renal calcium reabsorption, phosphate excretion, and vitamin D activation. Disorders of the parathyroid gland in children can disrupt these mechanisms, leading to neuromuscular, skeletal, renal, and cardiovascular complications.
Pediatric parathyroid disorders include:
• Hypoparathyroidism (with hypocalcemic tetany)
• Primary hyperparathyroidism
• Secondary hyperparathyroidism
Objectives
1. To describe the etiopathogenesis of parathyroid gland disorders in children
2. To outline the clinical features of hypoparathyroidism and hyperparathyroidism
3. To explain diagnostic and differential diagnostic approaches
4. To discuss treatment, prevention, and long-term medical follow-up
Methods
This review is based on:
• Standard pediatric endocrinology textbooks
• Clinical guidelines for calcium–phosphate disorders
• Analysis of laboratory, imaging, and clinical diagnostic methods
• Comparative evaluation of treatment protocols used in pediatric practice
Results
1. Hypoparathyroidism and Hypocalcemic Tetany
Etiopathogenesis
• Congenital absence or hypoplasia of parathyroid glands (e.g., DiGeorge syndrome)
• Autoimmune destruction
• Post-surgical damage (thyroid or neck surgery)
• Genetic defects in PTH synthesis or action
• Functional hypoparathyroidism due to severe hypomagnesemia
Pathophysiology:
↓ PTH → ↓ serum calcium → ↑ serum phosphate → increased neuromuscular excitability → tetany
Clinical Features
• Neonatal or childhood onset
• Neuromuscular irritability:
• Positive Chvostek’s sign and Trousseau’s sign
• Cardiac manifestations: prolonged QT interval
• Dental enamel hypoplasia, delayed tooth eruption
Diagnosis
• ↓ Serum calcium
• ↑ Serum phosphate
• ↓ or absent PTH
• Normal or low vitamin D
• ECG: prolonged QT interval
Differential Diagnosis
• Vitamin D deficiency (rickets)
• Pseudohypoparathyroidism
• Hypomagnesemia
• Chronic kidney disease
• Acute pancreatitis
Treatment
• Acute tetany:
• Intravenous calcium gluconate
• Long-term:
• Oral calcium supplements
• Active vitamin D (calcitriol)
• Magnesium supplementation if deficient
Prevention and Follow-up
• Early screening in high-risk neonates
• Regular monitoring of calcium, phosphate, and renal function
• Growth and neurodevelopment assessment
2. Primary Hyperparathyroidism
Etiopathogenesis
• Parathyroid adenoma (most common)
• Parathyroid hyperplasia
• Rarely parathyroid carcinoma
• Genetic syndromes (MEN type 1, MEN type 2A)
Pathophysiology:
↑ PTH → ↑ bone resorption → ↑ serum calcium → ↓ phosphate
Clinical Features
• Often asymptomatic in early stages
• Bone pain, fractures
• Muscle weakness, fatigue
• Polyuria, polydipsia
• Nephrolithiasis
• Abdominal pain, constipation
• Neuropsychiatric symptoms (irritability, poor concentration)
Diagnosis
• ↑ Serum calcium
• ↓ Serum phosphate
• ↑ PTH
• ↑ Alkaline phosphatase
• Imaging: neck ultrasound, sestamibi scan
Differential Diagnosis
• Familial hypocalciuric hypercalcemia
• Vitamin D intoxication
• Malignancy-associated hypercalcemia
• Thyrotoxicosis
Treatment
• Surgical removal of adenoma or hyperplastic gland
• Preoperative hydration and correction of hypercalcemia
• Postoperative monitoring for hypocalcemia (hungry bone syndrome)
Prevention and Follow-up
• Genetic counseling in familial cases
• Regular monitoring of calcium and renal function
• Bone mineral density assessment
3. Secondary Hyperparathyroidism
Etiopathogenesis
• Chronic kidney disease (most common)
• Vitamin D deficiency or malabsorption
• Inadequate calcium intake
Pathophysiology:
↓ Calcium or ↓ vitamin D → compensatory ↑ PTH → parathyroid hyperplasia
Clinical Features
• Signs of underlying disease
• Bone deformities (renal osteodystrophy)
• Growth retardation
• Muscle weakness
Diagnosis
• Normal or low calcium
• ↑ Phosphate (in renal disease)
• ↑ PTH
• ↓ Vitamin D levels
Differential Diagnosis
• Primary hyperparathyroidism
• Hypoparathyroidism
• Nutritional rickets
Treatment
• Treat underlying cause
• Vitamin D supplementation
• Calcium supplementation
• Phosphate binders (in CKD)
• Calcimimetics in severe cases
Prevention and Follow-up
• Adequate nutrition and vitamin D intake
• Early management of chronic kidney disease
• Periodic monitoring of calcium–phosphate balance
Discussion
Parathyroid gland disorders in children present diagnostic challenges due to overlapping symptoms and biochemical findings. Hypocalcemia may present acutely with tetany, while hyperparathyroidism often evolves insidiously. Early biochemical screening and appropriate imaging are essential. Long-term follow-up is critical to prevent complications affecting growth, skeletal development, renal function, and neurocognitive outcomes.
Clinical Presentation and Diagnostic Challenges
Hypoparathyroidism often presents dramatically in neonates and infants with hypo calcemic tetany or seizures, whereas older children may exhibit subtle neuromuscular irritability or neuropsychiatric manifestations. Chronic hypocalcemia may lead to basal ganglia calcifications, cataracts, and dental abnormalities, underscoring the importance of early diagnosis and sustained management.
References
1. Kliegman RM, et al. Nelson Textbook of Pediatrics. Elsevier
2. Sperling MA. Pediatric Endocrinology. Saunders
3. Jameson JL, et al. Harrison’s Principles of Internal Medicine
4. European Society for Paediatric Endocrinology (ESPE) Guidelines
5. UpToDate: Disorders of Calcium and Phosphorus Metabolism in Children