hyperparathyroidism investigations and management

1. DR MOHAMMED SHAHID

2.  BLOOD: Hypercalcemia
Hypophosphatemia
ALP- increased
 URINE: Hypercalciuria
Hyperphosphaturia
 HPE: single adenoma-mc,
pale, clear-chief cells
 ECG: short QT interval
 USG & Tc99 SESTAMIBI SCAN

3.  24hr urinary calcium:
• Differentiates pHPT from familial hypocalciuric
hypercalcemia
 Phosphate excretion test:
• PTHdecreases net tubular phosphorous
reabsorptionphosphaturia.
 Phosphorous loading test:
• In case of poor intake or poor absorption, there is normal
phosphorous excretion
• Oral phosphorous (2-3g over 3days)  decreases tubular
phosphorous reabsorption phosphaturia

4.  Cortisone suppression test:
• Administration of steroids (150mg cortisone per day for
10days)  no effect on hypercalcemia of
hyperparathyroidism in contrast to sarcoidosis, multiple
myeloma, hypervit D
 Urinary Hydroxyproline: markedly raised. attributed to
increased bone turnover and collagen degradation.
 Isotope studies:
• Se-75 (selenomethionine) scan detects abnormal
parathyroid tissue
 RIA: radiolabelled antibodies directed against PTH. More
specific.

5.  M/C : generalized osteopenia
 Bone resorption- subperiosteal, intracortical,
trabecular, endosteal, subchondral, subligamentous, or
subtendinous.
 Bone sclerosis
 Brown tumors
 Chondrocalcinosis
 Soft tissue calcification and vascular calcification.

6. •M/c -Radial aspects of the
middle phalanges.
•Phalangeal tufts.
•Distal end of the clavicle
•Medial tibial & humeral
metaphysis.
•Medial femoral neck
•Superior & inferior margins
of ribs.

7. Spotty de-ossification- salt & pepper appearance

8. •Iliac side of SI joint.
•DIP joint(m/c- ring &
little fingers).
•MCP joint.
•Clavicular side of AC
joint.

9. Scalloping along the cortex
M/c in long bones

10. •Expansile lytic lesion with
well defined non sclerotic
margin
•Replacement of bone by
vascularized fibrous tissue-
osteoclastic activity

11. •m/c in secondary
hyperparathyroidism
• horizontal, bandlike
("rugger jersey")
sclerosis.

12. Ca PTH P ALP
PHPT
SECONDARY
HPT (CKD)
(soft
tissue
deposition)
MILK ALKALI /N N
MALIGNANCY /N
PAGET’S N N N
RICKETS

13.  Acute hypercalcemia -rehydration with normal saline,
reduced calcium intake, haemodialysis.
 Loop diuretics
 Avoid thiazide diuretics.
 Monitor serum creatinine levels
and calcium levels every 6 months.
 DEXA scan on an annual basis.

14.  Calcimimetics: mimics calcium by stimulating calcium
sensors -> less PTH release.
• Side effects: joint and muscle pain, diarrhea, nausea, and
respiratory infection.
 Bisphosphonates: decreases osteoclastic bone resorption,
osteo protective.
• Side effects: low blood pressure, fever and vomiting.

15.  Surgery :
- Symptomatic hyperparathyroidism
-Asymptomatic hyperparathyroidism with:
◦ 24-hour urinary calcium > 400 mg
◦ serum calcium > 1 mg/dl above upper limit of normal
◦ Creatinine clearance > 30% below normal for patient's age
◦ Bone density > 2.5 SD below peak (i.e., T-score of -2.5)
◦ People age < 50
 Minimally invasive surgery - solitary adenoma,
 Subtotal parathyroidectomy - diffuse hyperplasia.

16.  “Hungry Bone Syndrome”- postoperative, prolonged (>4days),
profound hypocalcemia (<8.4 mg/dL) -osteoblastic activity.
 Can also present in men metastatic prostate cancer.
 Presents with hypocalcemic tetany.
 Rx- bolus 10% ca. gluconate 10-20 mL in 50-100 mL of 5%-D IV
over 5-10 minutes(100 to 200 mg of elemental calcium.)
 Continuous infusion- 100cc of 10% ca.gluconate in 1L of
5%D (1 mg/mL of elemental calcium.)
 Start at 50 ml/hr and follow Ca, phosphorus, and magnesium
levels titrating every 4-6 hours.

17. SECONDARY HYPERPARATHYROIDISM:
 Correcting vitamin D deficiency.
 Treatment of chronic kidney disease (Calcium
supplementation)
TERTIARY HYPERPARATHYROIDISM:
 Total or subtotal parathyroidectomy.
 Autotransplantation
PATHOLOGICAL/STRESS FRACTURES:
 immediate immobilisation – treat the primary cause.
 Bisphosphonate therapy

18. THANK YOU