الفهرس 
Historical ReviewOnly 14 pages are availabe for public view
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Abstract
The parathyroid glands are usually four small, yellowish-brown ovoid or lentiform structures measuring about 6 mm long, 3-4 mm across, and 1-2 mm from back to front each weighing about 50 mg commonly related to the posterior lobar borders of the thyroid gland and its capsule.
They are developed from the endoderm of the third (the inferior one) and fourth (the superior one) branchial pouches about the fifth week of gestation. The inferior one is attached more to the thymus gland and more liable for migration and abnormal position, while the superior is more fixed in position and more related to the thyroid gland.
Histologically they are formed of chief cells, oxyphil cells and clear cells. The discovery of its anatomy was relatively recently in 1849 by Sir Richard Owen of London zoo and by Ivar Viktor Sandström of Sweden in 1880. Its function is described few decades later by group of imminent Surgeons, pathologist and physiologist. Its main function is the secretion of the parathyroid hormone, the so called the Collip’s hormone in reference to J. B. Collip (1925) the scientist who first isolate it.
This hormone together with the hormone calcitonin secreted by the parafollicular cells of the thyroid and the activated form of VD control the calcium and phosphate levels in the blood. Its major target cells are in the bones and kidneys and indirectly affect intestinal absorption through activation of vitamin D.
The secretion of the Parathyroid Hormone is controlled mainly by the serum level of ionized calcium. The extracellular concentrations of ionized calcium act in a negative feedback mechanism to stimulate or to shut down the secretion of PTH.
On the bone, it stimulates osteoclasts to reabsorb bone mineral, liberating calcium into blood. In the intestine, it indirectly enhances and facilitates the absorption of calcium from the small intestine, by stimulating the production of the active form of vitamin D in the kidney. In the kidneys, it suppresses calcium loss in urine.
Hyperfunction of the parathyroid gland is referred to as hyperparathyroidism. This can be primary which is commonly met in aged people particularly females. It can be due to generalized hyperplasia of the four parathyroid glands, which rarely sporadic but commonly familial (10% of cases) associated with other endocrinal diseases. Alternatively, it can be due to solitary adenoma, which is commonly sporadic (single adenoma in 79%, multiple adenomas in 5%), parathyroid hyperplasia is less often (15%) and rarely parathyroid carcinoma (1%). Secondary HPT due to low serum calcium level and tertiary due the continuous stimulation of the parathyroid glands by persistent low level of serum calcium.
Since its discovery in 1925 to until relatively recently, primary hyperparathyroidism (PHPT) was regarded as an uncommon rare disorder. However, since the advent of automated biochemical testing in the mid-1970s, many primary hyperparathyroidism with asymptomatic hypercalcemia were discovered.
It was traditionally taught as a disease of “Painful Bones and brown cystic tumours of the bone, renal stones and calcinosis, abdominal groans, and psychic moans”
The sole diagnostic mean for primary hyperparathyroidism is high serum calcium, high PTH (or high normal) and the high urinary calcium. The later differentiate it from Familial Hypocalciuric Hypercalcemia(FHH). Other diagnostic means includes; good medical history, drug history, history for other endocrinal diseases, for cancer, measuring serum phosphate, serum chloride, calculation of serum chloride/ phosphate ratio.
The other investigation assessing the magnitude of the disease includes serum alkaline phosphatase, serum creatinine, urinary calcium level, and bone mineral density by dual energy X-ray absorptiometry or DXA scan. Plain x-ray to the skeleton to diagnose osteoporosis, cystic changes in the bone, also plain x-ray abdomen to spot renal stone, nephrocalcinosis, and chest x-ray to eliminate lung carcinoma to be a cause of hypercalcaemia.
Localizing studies are mainly used for preoperative localization of the accused gland particularly in ectopic and recurrent cases. They include; Preoperative methylene blue, Selective venous sampling with PTH assay, Selective Arteriogram, Thallium/technetium subtraction scanning, Nuclear medicine scanning with radiolabeled sestamibi, Ultrasonography of the neck, Computed tomography, Magnetic resonance imaging.
Measure to assess the completeness of the surgical procedure performed while the patient is still under anaesthesia includes intraoperative measurement of iPTH, measurement of total serum calcium (TSC) has been proposed but found not useful.
For treating PHPT controversy and debates did occur on two main issues. The first issue on when contemplating on surgery whether to do complete bilateral neck exploration or unilateral limited one, the present status with advent of the sophisticated localizing measures is in favour of unilateral exploration the so-called targeted parathyroidectomy. The second issue whether to treat the so called asymptomatic group by surgery or by frequent monitoring and by medical drugs such as hormonal therapy for osteoporosis or drugs such as Calcimimetics drugs or bisphosphonates.
The National Institutes of Health (NIH) convened for this issue on three occasions to solve this debate, on 1990, 2002 and 2008. After reviewing the experience of many endocrinologist and reviewing the natural history of the disease, they confirmed that in the untreated group there is increased risk of osteoporosis, fractures, disturbed glucose metabolism, disturbed Lipid metabolism, Cardio-vascular morbidity and of Neuropsychological abnormalities. It was concluded that surgery is the ideal treatment for symptomatic PHPT with overt clinical signs and symptoms, also surgery has gained support and recommendation even to the asymptomatic ones since it reduces the liability of osteopenia, the incidence of disturbed glucose metabolism and dyslipidaemia and atherogenic index, and cardiovascular complication particularly left ventricular hypertrophy and reduces the incidence of premature death.
Although surgery affords a cure rate more than 95%, yet it requires the availability of an experienced surgeon in the field of parathyroid surgery, imagining facilities for localization of the tumour to minimise the surgical procedure to make it less invasive, and facilities for intraoperative iPTH determination to assess the success of the surgical procedure and assess the possibility of its further extension.
In the absence of these facilities, bisphosphonate such as zoledronic acid is a good alternative since reoperation carries an increased risk of injury to the recurrent laryngeal nerves and to the residual normal parathyroid tissue particularly if the pathology is in an ectopic gland difficult to localize. However, in spite of this advantage for bisphosphonates yet its use has its limitation and contraindication.
In fact, Surgery and bisphosphonate may be combined in the treatment of: Hypercalcemic crisis in such cases the patient has to be treated initially by saline hydration loop diuretics and then bisphosphonate to normalise the high calcium level to make the patient safe for surgery, and in the treatment of persistent postoperative osteopenia after parathyroidectomy.