• Increased PTH
• PTH increases Ca²⁺ levels in blood
• Hormonal disorder:
  • Increased serum PTH
  • Increased alkaline phosphatase
  • Multiple bone lesions + osteoclastic multinucleate cells

Etiology/clinical subtypes:

1. Primary

• Benign tumors (75-80%) (adenoma)
• Gland hyperplasia (10-15%)
• Malignant tumors (<5%) (adenocarcinoma)

2. Secondary:

• Renal failure – compensatory reaction to low Ca²⁺ levels – therefore deceased kidney function – decreased vitamin D metabolism and decreased Ca²⁺ absorption and metabolism from blood
• Vitamin D deficiency
• Malabsorption

3. Hereditary: AD trait – mutation in HRPT2 (endocrine tumor suppressor gene) chromosome 1

• *Ectopic glandular tissue
• Short stature
• Distorted face
• Mental retardation
• Cardiac defects

Clinical:

1. Brown tumor (Brown color due to hemorrhage)
2. Kidney stones
3. Metastatic calcification
4. Osteoporosis
5. Fibroblastic/giant cell tumors of bone
6. Neural dysfunction due to fluctuating Ca²⁺ levels
7. Serum Ca²⁺ level increased > 16-17 mg/dl
8. Increased alkaline phosphatase

Symptoms:

• Pain
• Renal dysfunction
• Fatigue
• Weakness
• Brittle bones
• Bone swellings
• Nausea
• Arrythemia
• Parathyroid crisis
• Coma

Radiology:

• Loss of lamina dura
• “Pepper pot skull” = osteopenia → stippling patterns
• Radiolucent cyst like areas
• Multiloculated appearance
• Subperiosteal resorption

Histology:

• High osteoclastic activity: Demineralization of bone – starts at subperiosteal and endosteal surface of cortex – replaced with fibrous CT – containing microcysts (osteitis fibrosa cystica)
• Brown tumor: Vascular intrabony lesions (sinusoids filled with blood) + osteoclastic giant cells)

Management:

1. Surgery – Parathyroidectomy
2. Palliative care
3. Hormonal replacement and vitamins

Picture