This document summarizes laboratory and radiological findings in hyperparathyroidism. It notes that hyperparathyroidism is usually caused by a single parathyroid adenoma and results in excessive calcium excretion by the kidneys due to overproduction of PTH. Common clinical findings include bone loss, kidney stones, abdominal pain, and fatigue. Laboratory tests show elevated serum calcium, PTH, and alkaline phosphatase levels. Imaging like sestamibi scans and ultrasound can detect parathyroid adenomas, while DXA scans measure bone mineral density loss and X-rays show bone demineralization patterns. Management involves IV fluids, bisphosphonates, vitamin D, and calcimimetic drugs.

1. LABORATORY AND RADIOLOGICAL
FINDINGS IN HYPERPARATHYROIDISM

2. Hyperparathyroidism
• Hyperparathyroidism is a common cause of
hypercalcemia
• Prevalence of 1-4 cases per 1000 persons
• Most common in 7th decade and women(74%)
• Caused by hypersecretion of PTH usually by:
1. Single parathyroid adenoma(80%)
2. Hyperplasia of 2 or more parathyroid
glands(20%)
3. Carcinoma(≤1)

3. • Familial in 10% of cases
• Hyperplasia may arise in MEN types 1, 2A, 2B
• MEN1 has multiglandular hyperparathyroidism
as initial manifestation and ultimately occurs in
90%od affected individuals
• MEN2 has less frequent occurrence and is
milder
• Familial hyperparathyroidism can also occur in
hyperparathroidism-jaw tumor syndrome
• Rare autosomal dominant trait in which there is
association with ossifying fibromas of mandible,
maxilla and renal lesions

4. • Hyperparathyroidism results in excessive
excretion of calcium and phosphate by
kidneys
• PTH stimulates renal tubular reabsorption of
calcium; however in hyperparathyroidism causes
hypercalcemia and an increase in calcium in the
glomerular filtrate that overwhelms tubular
reabsorption capacity, resulting in hypercalciuria
• 5% of renal calculi are associated with this
• Excessive PTH can cause cortical
demineralization that is evident at wrist and
pelvis
• Chronic state can cause diffuse demineraliztion,
pathological fractures and cystic bone lesions;
osteitis fibrosa cystica

5. • In chronic renal disease hyperphosphatemia
and decreased renal production of 1,25-
dihydroxycholecalciferol initially produce a
decrease in ionized calcium
• Parathyroid glands are stimulated(secondary)
and may enlarge becoming
autonomous(tertiary)
• Renal disease here is called renal
osteodystrophy
• Parathyroid hyperplasia in uremia can result in
high serum PTH that lead to uremic vascular
calcification
• Hypercalcemia often occurs after kidney
transplant

6. • Parathyroid carcinoma is rare cause
• More common in patients with serum calcium
≥14mcg/dL
• 50% of parathyroid carcinoma are palpable

7. Clinical findings
• Mostly asymptomatic or mild symptoms
• Adenomas are small and deeply located, almost
never palpable
• Symptomatic patients have problems:
“Bones, stones, abdominal groans, psychic moans
with fatigue overtones”

8. Skeletal manifestations
• Loss of cortical bone
• Gain of trabecular bone
• Low bone density; particularly in wrist
• Asymptomatic vertebral fractures; post
menopausal women more prone
• Bone pain
• Arthralgia
• Brown tumors
• Cysts of jaw

9. Hypercalcemia manifestations
CNS
• Depression
• Constipation
• Bone and joint pain
• Paresthesia
• Muscular weakness
• Diminished deep tendon reflexes
• Malaise
• Fatigue
• Intellectual weariness
• Disorientation

10. Hypercalcemia manifestations
CVS
• Prolonged P-R interval
• Shortened Q-T interval
• Sensitivity to arrhythmic effects of digitalis
• Bradyarrhythmias
• Heart block
• Asystole

11. Hypercalcemia manifestations
Renal
• Polyuria
• Polydipsia
• Nephrogenic diabetes insipidus
• Calcium nephrolithiasis

12. Hypercalcemia manifestations
GI
• Anorexia
• Abdominal pain
• Weight loss
• Constipation
• Constipation
• Pancreatitis
MISC
• Pruritis
• Precipitation of Ca in cornea; band keratopathy
• Precipitation in extravascular tissue and arteries
causing small vessel thrombosis and skin necrosis

13. Laboratory findings
• Hypercalcemia with serum adjusted total
calcium ≥10.5 mg/dL
Adjusted total calcium=measured serum
calcium in mg/dL +[0.8x(4-patient’s serum
albumin in g/dL)]
• Serum ionized calcium in hyperproteinemic
states and hyperparathyroidism is >5.4mg/dL

14. • Low serum phosphate <2.5mg/dL due to loss in
urine
• In secondary renal disease serum phosphate is high
• Alkaline phosphatase is elevated if bone
disease present
• Plasma chloride and uric acid levels elevated
• Vitamin D deficiency
• Low serum 25-OH vitamin D levels <20mcg/L
aggravate bone manifestation
• Elevated serum level of intact PTH confirm
diagnosis (normal 10-65ng/L)
• 24hour urine for calcium and creatinine done to
screen for familial benign hypocalciuric
hypercalcemia; Ca <50mg/24hours

15. • Patients with low bone density and elevated PTH
but normal serum Ca must be evaluated for
causes of secondary hyperparathyroidism
• In absence of secondary hyperparthyroisim but
raised PTH and normal serum Ca patients are
said to have normocalcemic
hyperparathyroidism

16. Imaging
• Preoperative sestamibi-iodine subtraction scanning
• Involve injecting a small amount of special radioactive
material into a vein and taking an X-ray image of the
chest, neck, and head
• Accuracy rate of about 80 to 95%
• Neck ultrasound can locate parathyroid adenoma
• Adenomas appear as well-defined hypoechoic lesions
with potential cystic or necrotic areas.
• Ultrasonography offers the advantage of depicting
potential concomitant thyroid disease, present in 40%
of patients
• Helps in limiting the invasiveness in surgery

17. • CT and MRI of neck are helpful for ectopic
parathyroid glands
• CT scanning of kidneys to determine calcium
containing stones
• Bone density measurement by dual energy x-
ray absorptiometry(DXA) to see the bone loss
• DXA of lumbar spine, pelvis and distal radius

18. • X-rays to show bone demineralization;
subperiosteal resorption; radial aspects of fingers
• About 30-50% of the bone density must be lost to
show changes on radiographs.
• Loss of lamina dura of teeth
• Mottling of skull; salt and pepper appearance
• Pathological fractures
• Articular cartilage calcification
• In patients with renal osteodystrophy ectopic
calcifications around joints or soft tissue
• Radiographic changes show osteopenia, osteitis
fibrosa, osteosclerosis
• Osteosclerosis of vertebral bodies; rugger jersey
spine

23. Brown tumors
• Brown tumors are well-circumscribed lytic
lesions of bone that represent the osteoclastic
resorption of a confluent area of bone with
fibrous replacement.
• The lesions may be single or multiple, with
expansion of overlying bone, usually occur in
cortical bone.
• Common sites include the mandible, clavicle,
ribs, pelvis, and femur.

28. Distal femur shows scalloped defects along
the inner margin of the cortex, which
denote endosteal resorption.

29. Humerus- osseous expansion and
lucency of the proximal humerus.
Radiograph of the mid femoral diaphysis -
eccentric (arrowheads) and central
positions (arrow) of the lesions.

31. Management
• IV fluids
• Bisphosphonates; pamidronate, zoledronic acid
• Vitamin D and vitamin D analogs; calcitriol,
paricalcitrol, doxercalciferol
• Cinacalcet; calcimimetic agent

32. THANK YOU