VITAMIN D

&
HYPERPARATHYROIDISM

-Dr.Apoorva.E
PG,DCMS
 VITAMIN-D AND ITS
METABOLISM
- Vitamin D is a fat soluble vitamin.

- It is the precursor of 1,25-

dihydroxycholecalciferol which is the active
form of vitamin D secreted by the kidney,
under the control of parathyroid hormone.

- Its deficiency causes rickets in children and

osteomalacia in adults.
SUNLIGHT AS A SOURCE
Sunlight in the ultraviolet
band
DIETARY SOURCES

Vitamin D3
CALCIUM HOMEOSTASIS SHOWING INTERACTION BETWEEN
PTH,VITAMIN D AND CALCIUM
HYPERPARATHYROIDISM

• Parathyroid glands are four glands located behind

the thyroid gland in the front of the neck.
• They produce a hormone called parathyroid
hormone (parathormone).
• PTH regulates serum calcium levels in the body.
• Hyperparathyroidism is the overproduction of
this hormone.
ACTION OF PTH
 CLASSIFICATION OF
HYPERPARATHYROIDISM
1. Primary
2. Secondary
3. Tertiary
 PRIMARY HYPERPARATHYROIDISM
• Excess secretion of PTH from one or more
parathyroid glands.
• Prevalence is 1 in 800,2-3times more common in
women,average age being 55years.
• Is associated with familial MEN syndromes
-MEN I: Primary hyperparathyroidism+pituitary
tumors+pancreatic tumors
-MEN IIa: Primary hyperparathyroidism+medullary
carcinoma of thyroid+pheochromocytoma
 ETIOLOGY
-Single adenoma in 90%
-Nodular hyperplasia in 5%
-Multiple adenomas in 4%
-Carcinoma in 1% .
 CLINICAL FEATURES
• The signs and symptoms of primary
hyperparathyroidism are those of hypercalcemia.
- Patients present with kidney
stones,nephrocalcinosis,diabetes insipidus
(polyuria and polydipsia).These ultimately lead
to renal failure.
- bone-related complications like osteitis fibrosa
(bone pain and pathological
fractures),osteoporosis,osteomalacia
and arthritis.
- gastrointestinal symptoms
of constipation,anorexia,nausea,vomiting,peptic
ulcers,acute pancreatitis.
- cardiovascular system involvement leading to
hypertension,bradycardia,shortened QT interval
and left ventricular hypertrophy.

- central nervous system symptoms include

lethargy,fatigue,depression,memory loss,
psychosis,ataxia,delirium and coma.

- other signs include proximal muscle

weakness,itching,band keratopathy of the eyes.
 DIAGNOSIS
• Serum calcium levels are elevated.
• Parathyroid hormone level is abnormally
high.
• There is hypophosphatemia and increase
in 24-hour urinary calcium excretion.
• DEXA scan shows skeletal involvement.
• Pathognomonic X-ray changes include salt and
pepper degranulation in the skull and subperiosteal
bone resorption in the phalanges.
• Imaging of renal tract (X-ray, ultrasound)
can demonstrate renal calculi.
• Localisation of parathyroid tumors by
technetium scan,ultrasound,CT of the neck
followed by FNAC.
 TREATMENT
1. Management of acute hypercalcemia by
rehydration with normal
saline,bisphosphonates,haemodialysis.
2. Medical line : -Monitor serum creatinine levels
and calcium levels every 6 months.DEXA scan
on an annual basis.
-Avoid thiazide diuretics.
-Maintain high oral fluid intake.
-Improving bone mineral density and achieving
calcium homeostasis by calcimimetics and HRT.
3. Surgery : -Is indicated in patients with
complications and in younger age group.
-Minimally invasive surgery to excise
solitary adenoma,
Subtotal parathyroidectomy in case of
diffuse hyperplasia are being done.
 SECONDARY HYPERPARATHYROIDISM
• It occurs when PTH secretion is increased to
compensate for prolonged hypocalcemia.
• It is seen in patients with chronic renal failure
where the failing kidneys do not convert
vitamin D to its active form and they do not
excrete phosphate.
Excess phosphate combines with calcium to
form calcium phosphate.
• Both processes lead to hypocalcemia,cause
hyperplasia of all parathyroid tissue and hence
secondary hyperparathyroidism.
• Secondary hyperparathyroidism can also
result from malabsorption of vitamin D
due to chronic pancreatitis,small bowel
disease,bariatric surgery.
• CLINICAL FEATURES : are mostly of renal
failure.If it is due to vitamin D
deficiency,limb deformities,pathological
fractures occur.
• INVESTIGATIONS : Serum calcium levels are
low.PTH levels are raised. Phosphate levels depend
on etiology (e.g. high in renal disease, low in
vitamin D deficiency).
Radiology shows evidence of bone disease.

• TREATMENT : Medical line is the mainstay.

The underlying condition needs to be treated
-correcting vitamin D deficiency.
-treatment of chronic kidney disease
(Calcium supplementation.
Treatment with vitamin D and its analogues.
Calcimimetics)
 TERTIARY HYPERPARATHYROIDISM
• In a small proportion of cases of secondary
hyperparathyroidism,continuous stimulation
of the parathyroids results in adenoma
formation and unregulated PTH secretion.
• Even correction of the underlying cause will
not stop excess PTH secretion i.e parathyroid
gland hypertrophy becomes irreversible.
• CLINICAL FEATURES : Symptoms and signs are
due to hypercalcemia so presentation is similar
to primary hyperparathyroidism.

• INVESTIGATIONS : Serum calcium and PTH

levels are raised.
Phosphate levels are often high.

• TREATMENT : Total or subtotal

parathyroidectomy is the recommended
treatment.
Autotransplantation of parathyroid tissue in the
forearm is also commonly carried out.
THANK YOU !!