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 SOURCESunlight 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+pituitarytumors+pancreatic tumors

-MEN IIa: Primary hyperparathyroidism+medullarycarcinoma of thyroid+pheochromocytoma

ETIOLOGY

-Single adenoma in 90%

-Nodular hyperplasia in 5%

-Multiple adenomas in 4%

-Carcinoma in 1% .

• The signs and symptoms of primary hyperparathyroidism are those of hypercalcemia.

CLINICAL FEATURES

- 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,osteomalaciaand arthritis.

- gastrointestinal symptoms of constipation,anorexia,nausea,vomiting,pepticulcers,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 subperiostealbone 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,causehyperplasia 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,pathologicalfractures 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.

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