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|Year : 1977 | Volume
| Issue : 4 | Page : 197-200
Primary hyperparathyroidism due to (chief-cell hyperplasia- (a review with a case illustration)
Department of Thoracic Surgery, Rajendra Medical College, Ranchi., India
H N Verma
Department of Surgery, Patna Medical College and Hospital, Patna-800 004
Source of Support: None, Conflict of Interest: None
A 37 year old man presented with multiple pathological fractures, mental symptoms and features o f renal insufficiency without renal stones and nephrocalcinosis. This was found to be a case of primary hyperparathyroidism due to chief cell hyperplasia. Three parathyroids were removed leaving behind the right superior gland. The patient had temporary symptomatic improvement with the healing of the fractures of metacarpals. There was no union of fractures of necks of femora. The symptoms reappeared and the patient died of renal failure more than a year after operation.
Severe renal impairment is therefore the most important single complication in advanced osseous lesions. Even if parathyroidectomy is done in such advanced cases probably no permanent clinical improvement may be expected. Better results in these cases might be observed by early diagnosis of the disease and adequate surgery. It is hence suggested that in a case of parathyroid hyperplasia one should aim at excision o f 31- parathyroid glands, i.e., near total parathyroidectomy, to avoid recurrence of disease.
|How to cite this article:|
Verma H N. Primary hyperparathyroidism due to (chief-cell hyperplasia- (a review with a case illustration). J Postgrad Med 1977;23:197-200
| :: Introduction|| |
Primary hyperparathyroidism is a rare and interesting condition. Below we describe a patient with primary hyperpara-thyroidism due to chief cell hyperplasia.
| :: Case report|| |
G.L., a 37 year old Hindu male from West Bengal, was admitted into the Orthopaedic Ward of R.M.C. Hospital, Ranchi on 24-1-1970. He complained of backache, bone pains, difficulty in walking, anorexia and weight loss for 1 year. Initially, he was thought to have spinal tuberculosis and was treated accordingly. On 9-2-1970, he developed mental symptoms including confusion, hallucinations, nervousness, agitation and tremors of hands and feet. At this stage, a diagnosis of "Motor type of polyneuropathy" was made and he was treated with corticosteroids and with vitamin B 1 and B 12 . The patient did not respond to this treatment. On 21-4-1970, he was suspected to have primary hyperparathyroidism and was then transferred to the Surgical Ward of the hospital. On examination at this stage, he was wasted, anemic, obviously ill-looking and was in agonising pain. His pulse. temperature and blood pressure were normal. There was limitation of movements of both hips. Systemic examination was negative. A skeletal survey showed (a) reabsorption of both femoral necks with pathological fractures and decalcification of pelvic bone see [Figure 1] on page 196B; (b) demineralization with fractures of the lower end of tibia and fibula; (c) loss of lamina dura of teeth see [Figure 2] on page 196B ; (d) multiple rib fractures and fluffy shadows in the chest see [Figure 3] on page 196B; (e) generalized demineralization with subperiosteal erosion of hands with fractures of the bases of 2nd metacarpals on both hands see [Figure 4] on page 198A ; (f) typical fuzzy appearance of both tables of the skull with ground glass appearance see [Figure 5] on page 198A ; (g) demineralization of the lateral end of the left clavicle and of the upper end of the left humerus with a fracture of the neck of the left scapula see [Figure 6] on page 198A ; similar decalcification was seen in other bones
There was no evidence of renal calculi. His serum calcium level varied between 10.8 mg% and 11.8 mg% and the serum phosphorus level between 3.22 mg and 4.3 mg%. Serum albumin was 3.64 gm% and serum globulin, 3.0 gm%. Blood urea was 34 mg%. Serum alkaline phosphatase varied between 6.6 and 16.5 K.A. Units and the serum acid phosphatase was 7.0 K.A units. His hemoglobin was 9.0 gm%. Total and differential white cell count was normal, The urine showed a trace of protein, 2-4 pus cells per field and a lot of amorphous phosphate.
The patient was judged unfit for general anaesthesia and hence the neck was explored by a collar incision under local anaesthesia with careful dissection. The four parathyroid glands were individually isolated and found to be hyperplastic. They were removed leaving behind the right superior gland. The patient's condition was satisfactory at the end of the operation and his voice was intact. During the post-operative period, he was treated with Vitamin D 1 , calcium and a broad-spectrum antibiotic. Histopathological examination of the removed parathyroid glands showed chief cell hyperplasia see [Figure 7] on page 198B.
In the early post-operative period, the general condition of the patient improved. He felt cheerful and the mental symptoms including confusion, hallucinations and nervousness disappeared. His serum calcium levels on 24-8-70,14-9-70, and 5-10-70 were 9.4 mg%, 9.7 mg% and 10.2 mg% respectively. Urine examination showed a trace of albumin and a few pus cells. The tremors of the hands and feet persisted with lesser severity. This was thought to be of functional in origin. X-ray of hands and pelvis on 17-9-70 showed some improvement in the rarefied areas and union of the fracture of the 2nd metacarpals see [Figure 8] on page 198B). There was no evidence of healing of fractures of both necks of femora. Further follow-up for six months showed a gradual improvement in the patient's general condition but later, it deteriorated. His previous mental symptoms re-appeared. His serum calcium rose gradually to 13.3 mg% by 24-9-1971. The pain in the bones and loss of appetite returned and fractures of both femoral necks failed to unite. At the end, he developed severe urinary infection with copious albuminuria and the passage of epithelial casts and pus cells. On 24-9-71 he became disoriented and stuporous and developed uraemic features. He died on 27-9-71. An autopsy could not be done.
| :: Discussion|| |
Primary hyperplasia is found in approximately 5% in all cases of hyperparathyroidism. Cope et a1  reported only 8 cases of primary chief cell hyperplasia out of 206 cases of primary hyperparathyroidism. Pyrah et al  found only 2 cases of chief cell hyperplasia out of 68 cases of primary hyperparathyroidism. Straus et al  at the University of Chicago Hospital reported only 6 cases of primary hyperplasia of chief cell type out of 58 patients suffering from hyperparathyroidism. Primary hyperparathyroidism with advanced bony changes without apparent renal involvement was recorded in 4 out of 53 cases of McGeown and Morrisson.  Seventeen such cases were found by Pyrah et al  out of sixty-eight patients. Dent and Harper  regarded the osseous and renal lesions as two separate clinical entities, The present case had advanced bony lesions without renal stone or nephrocalcinosis. The case had bilateral fracture neck of femur similar to one recorded by McGeown and Morrison. 
Although the patient had no obvious renal stone or nephrocalcinosis he showed features of renal damage. There was evidence of pyelonephritis with copious albuminuria and passage of epithelial casts. The severe impairement of renal function in worst type of osseous lesions, often in absence of any form of renal calcification, is believed to be due to microscopic damage to the renal tubules and their blockage by calcific debris (Pyrah et al  )
Edvall,  after reviewing 20 patients, found that the parathormone has two effects on the kidney: (a) a functional change which is reversible after surgery, and (b) on organic tubular lesion which is irreversible and persists after the operation. He believed that the renal disturbances were mainly caused directly by the excessive amount of circulating parathormone in absence of renal calculi or nephrocalcinosis. Hellstorm and IveMark  also showed that the incidence of such renal impairment was higher than that of renal calculi in patients with advanced osseous lesions. Our patient also developed renal failure in the later stage and died of uraemia. The severe irreversible impairment of renal function in this patient could have been due to microscopic tubular damage. Karcher  reviewed 499 cases of hyperparathyroidism with 33 postoperative deaths, the most common cause of which was renal failure.
This patient had severe mental symptoms including confusion, hallucination, nervousness and tremors. They were relieved temporarily after the operation but reappeared later when serum calcium rose. Eitinger  reported a female patient with hyperparathyroidism in whom psychiatric and neurological changes were the main presenting features. Bogdenoff and others  reported a female patient aged 58 years, with gross psychiatric abnormalities and depression which improved temporarily following surgery but in whom the symptom's recurred after some months. These mental symptoms are possibly due to hypercalcemia and deposition of calcium phosphate salt in the brain.
In the present case, only three parathyroids were removed and right superior parathyroid was left behind to avoid hypoparathyroidism. In the early postoperative period, the patient improved remarkably, but later on there was a gradual deterioration in his condition with a gradual rise in the serum calcium level. The mental symptoms recurred and the features of renal insufficiency appeared. This may be attributed to (i) inadequate surgery or to (ii) advanced osseous lesions with irreversible renal damage. Churchill and Cope  advocated removal of 3 enlarged glands completely and a subtotal removal of 4th leaving behind amount of gland weighing 50 to 150 mg. Even after careful resection it is easy to leave too much of the parathyroid tissue. There is, therefore, less certainty of complete cure in a case of hyperplasia than in a case of an adenoma. Castleman and Cope  reported that none of their 11 cases of primary hyperplasia had been completely cured by subtotal resection.
| :: Acknowledgements|| |
I wish to thank Dr. B. Singh, Superintendent, Rajendra Medical College Hospital, Ranchi for permission to report this case.
I am thankful to Prof. J. Sharan, Prof. of Pathology and Prof. N. D. Basu, Prof. of Radiology for their invaluable technical assistance. I am grateful to Dr. Surendra Sinha, Physician-incharge for referring this case.
| :: References|| |
|1.||Bogdonoff, M. D., Woods, A. H., White, J. E. and Engel, E. L.: Hyperparathyroidism, Amer. J. Med., 21: 583-591, 1956. |
|2.||Castleman, B. and Cope, O.: Bull. Hosp. Jt. Diseases, 12: 368, 1951, as quoted by Pyrah et al.  |
|3.||Churchill, E. D. and Cope, O.: Parathyroid tumors associated with hyperparathyroidism. Surg. Gynec. Obst.. 58: 253271, 1.934. |
|4.||Cope, O., Keynes, W. M., Roth, S. I. and Castleman, B.: Primary Chief cell hyperplasia of the parathyroid glands-a new entity in surgery of hyperparathyroidism. Ann. Surg., 148: 375-388, 1958. |
|5.||Dent, C. E. and Harper, C. M.: Plasma alkaline phosphatase in normal adults and in patients with primary hyperparathythyroidism. Lancet, 1: 559-563, 1962. |
|6.||Edvall, C. A.: Acta. Chir. Scandinav. Supplement No. 229, 1958, as quoted by Pyrah et al.  |
|7.||Eitinger, L.: Nord. Med., 14: 1581. 1942, as quoted by Pyrah et al.  |
|8.||Hellstrom, J. and Ivemark, B. I.: Acta. Chir. Scand. Supplement No. 294, I, 1962, as quoted by Pyrah et al.  |
|9.||Karchar, H.: Ergebn. Chir. Orthop., 140: 92, 1958, as quoted by Pyrah et al.  |
|10.|| McGeown, M. G. and Morrison, E.: Hyperparathyroidism. Postgrad. Med. J., 35: 330-337, 1959. |
|11.||McGeown, M. G. and Morrison, E.: "The Parathyroids" Recent Advances in Surgery. Editor: Taylor, S., 6th Edition, J. and Churchill Ltd., London, 1964, pp. 406-424. |
|12.||Pyrah, L. N., Hodgkinson, A. and Anderson, C. K.: Primary Hyperparathyroidism. Brit. J. Surg., 53: 245-316, 1966. |
|13.||Strauss, F. H. and Paloyem, E.: The pathology of hyperparathyroidism. Surg. Clin. N. Amer., 49: 27-42, 1969. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]