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The rationale for using the thallium-technetium subtraction scan as a preoperative localizing study in previously untreated patients with primary hyperparathyroidism is presented. The concept of unilateral parathyroidectomy is also presented, and the role of preoperative localizing studies in this approach to parathyroid surgery is carefully analyzed.
BACKGROUND: Despite the fact that primary hyperparathyroidism (HPTH) is the result of a single adenoma in 85% to 92% of cases and is cured following the removal of this one gland, many surgeons continue to perform a complete bilateral neck exploration for patients with primary HPTH. The advent of the sestamibi scan now enables the identification of patients with a single adenoma. METHODS: The use of preoperative sestamibi scanning followed immediately by minimally invasive parathyroidectomy using intraoperative nuclear mapping allows cure for primary HPTH in properly selected patients. RESULTS: Reports have shown that preoperative sestamibi scanning has a sensitivity of approximately 90% and a specificity of almost 100% in identifying patients with a single adenoma. Intraoperative mapping allows a limited dissection to be performed under local anesthesia in an outpatient setting in approximately 80% of all patients with primary hyperparathyroidism. The details of this new technique - patient selection, timing, use of the intraoperative nuclear probe, and surgical exploration - are described. CONCLUSIONS: When selected appropriately, most patients with primary HPTH can be successfully treated through a minimally invasive technique.
The disappearance of plasma PTH after parathyroidectomy was assessed in patients with primary hyperparathyroidism and normal renal function, chronic renal failure or restored renal function (after transplantation). Plasma PTH levels were determined by renal cytochemical bioassay and by midregion and carboxyl-terminal RIAs. Baseline PTH levels were lower in each patient when assessed by bioassay than when determined by RIA, and the rate of hormone disappearance was faster when determined by bioassay than when measured by RIA. This difference was accentuated in chronic renal failure due to prolongation of the disappearance rates of midregion and carboxyl-terminal immunoreactivity. The half-life of bioassayable hormone in patients with chronic renal failure was prolonged less than 2-fold compared to the half-life in patients with normal or restored renal function. The results emphasize the discordance between levels of bioactive and immunoreactive hormone regardless of renal function, demonstrate that this discordance is augmented after acute reduction in circulating hormone, and show that it is further increased when kidney function is impaired. The studies also implicate extrarenal mechanisms as a major factor in the clearance of bioactive hormone in established renal failure.
The effects of decreasing serum levels of PTH after parathyroidectomy on circulating levels of 1 alpha,25-dihydroxyvitamin D [1,25-(OH)2D] and bone Gla protein (BGP) were studied in seven patients treated with chronic maintenance dialysis. Before surgery, all patients had extremely elevated levels of PTH, low normal or low levels of 1,25-(OH)2D, high levels of BGP, and histological signs of excess PTH action on bone. The fall in PTH levels after surgery resulted in a further decline in 1,25-(OH)2D concentrations and a reduction in circulating BGP levels. This fall in serum 1,25-(OH)2D and BGP levels was not related to serum calcium or phosphorus. Administration of 1,25-(OH)2D3 from 4-6 months after surgery did not significantly affect serum levels of BGP or PTH. These data indicate that 1,25-(OH)2D is still under regulatory control of PTH in patients without excretory kidney function. This might reflect some remaining endocrine activity of the kidneys in these dialyzed patients or extrarenal production of 1,25-(OH)2D. In addition, the data show that serum BGP levels in renal failure are elevated due not only to impaired clearance but also to PTH-mediated acceleration in bone turnover. Therapy with 1,25-(OH)2D3 in these patients resulted in supraphysiological serum 1,25-(OH)2D levels which did not stimulate BGP production.
Twenty of 31 consecutive ultrasound examined patients with primary hyperparathyroidism were selected for treatment with ultrasound-guided percutaneous injection of ethanol (96%) into biopsy-verified solitary parathyroid tumours following a strict protocol with regard to dose, number of treatments and a minimum of 6 months follow-up. Of 18 patients completing the above protocol, a biochemical improvement was observed in 12, of whom eight became normocalcaemic during the follow-up period of 6 months after the last treatment. An obvious clinical improvement was seen in eight of the patients. In four patients, a unilateral vocal cord paralysis was observed, but was permanent in only one patient. Progressive fibrosis of the parathyroid tumours following injections impeded the intraglandular dissemination of ethanol. Another problem noted was the inability of ultrasound to detect multiglandular involvement. We find ultrasound-guided chemical parathyroidectomy an attractive alternative to surgery in patients who are not well suited for surgical intervention. However, the technique has not been fully developed, and in the present study, possible improvements are indicated.
It is possible to assess bone resorption from a determination of urinary excretion of hydroxyproline, which is the specific amino-acid of collagen. As dietary collagen affects 24-hour urinary excretion of hydroxyproline, it has been stated that the urine should be collected under a gelatin-free diet. A new sampling method was described in the present paper for the determination of hydroxyproline in urine, which could eliminate the affection of dietary collagen by simple fasting. The method was useful for the evaluation of bone metabolism in patients with parathyroid disorders. 10 patients with primary hyperparathyroidism (3 skeletal types and 7 non-skeletal types), 3 patients with idiopathic hypoparathyroidism and 5 normal subjects were studied. It was found that the urinary excretion of hydroxyproline increased at night and diminished during the day in patients with primary hyperparathyroidism as well as in normal subjects, but this diurnal rhythm was not clear in a patient with idiopathic hypoparathyroidism. A pilot study revealed that 10 g gelatin administered orally did not affect the urinary excretion of hydroxyproline after a 12-hour fast. Therefore, 2-hour urine samples (700 h-900 h) were collected, and blood samples were drawn at 800 h after a 13-hour fasting from 1800 h on the previous day to 700 h in the morning studied. The urinary excretion of hydroxyproline was expressed as follows: HOP (microgram/ml)/Cr(mg/dl). The 2-hour urinary excretion of hydroxyproline thus determined was highly correlated with that determined in 24-hour urine collected under a gelatin-free diet (r = 0.995, p less than 0.001) and with the total serum alkaline phosphatase activity (r = 0.987, p less than 0.001). The levels of 2-hour urinary excretion of hydroxyproline in normal subjects were 0.18-0.28 in range, and those in patients with the skeletal type of primary hyperparathyroidism were high. However, the levels were not always higher than those in the patients with the non-skeletal type, in which cases the 2-hour excretion of hydroxyproline was higher than 0.50 except in one patient. The 9 patients with primary hyperparathyroidism who had elevated levels of the 2-hour urinary excretion of hydroxyproline showed tetany after parathyroidectomy.(ABSTRACT TRUNCATED AT 400 WORDS)
Total parathyroidectomy is required to cure neonatal primary hyperparathyroidism (NPH) as any parathyroid remnant quickly becomes hyperplastic, causing recurrent hypercalcaemia. We present a patient with NPH who had total removal of his eutopic parathyroid glands but continued to have parathyroid hormone secretion from presumed ectopic parathyroid tissue. Hypercalcaemia initially recurred but normal calcium homeostasis was established as the child grew older. We postulate that the underlying defect in NPH is decreased sensitivity to the serum ionic calcium feedback inhibition at the parathyroid receptor level and that this sensitivity can improve with age.
Calcium, parathyroid hormone, follicle-stimulating hormone, luteinizing hormone, and estradiol were measured in 15 postmenopausal women with primary hyperparathyroidism before and 1 year after parathyroidectomy. Normalization of serum calcium concentrations (from 2.87 to 2.29 mmol/l) was followed by a highly significant fall in serum LH and FSH concentrations. No significant alteration occurred in plasma estradiol concentration.
A series of 253 consecutive patients with proved primary hyperparathyroidism due to parathyroid tumours was reviewed. There were 68 (26.9%) men and 185 (73.1%) women, with a median age of 57 years (range 13-82 years). All patients, prior to successful parathyroidectomy, underwent one or more preoperative localization procedures such as: neck ultrasonography (US) in 191 (75.5%), (201)Tl/(99m)Tc-pertechnetate subtraction scintigraphy (TPS) in 144 (56.9%), CT scan in 92 (36.4%), (99m)Tc-sestamibi/(99m)Tc-pertechnetate subtraction scintigraphy (MPS) in 90 (35.6%), selective venous sampling (SVS) with parathyroid hormone (PTH) assay in 30 (11.9%), and magnetic resonance imaging (MRI) in 6 (2.4%) patients. The results were compared with operative and histological findings that showed 235 (92.9%) solitary parathyroid adenomas, 13 (5.1%) carcinomas and 5 (2.0%) double adenomas. Sensitivity and positive predictive value were 82.9% and 93.8% for US, 83.6% and 91.8% for TPS, 81.3% and 98.7% for CT scan, 85.1% and 96.1% for MPS, 65.4% and 80.9% for SVS, and 80.0% and 80.0% for MRI respectively. No different results (P=NS) were found using US, TPS, MPS or CT scan, whereas SVS and MRI sensitivity was lower (P<0.05). The combination of MPS and US was 94.0% sensitive (P<0.05) but when TPS, CT scan or MRI were also used overall sensitivity did not improve significantly (P=NS). In conclusion, MPS should be used as the starting preoperative localization procedure, while US and MPS together represent the most reliable noninvasive localization tool. If MPS and US are negative or not in agreement, further studies are not cost-effective and the patient should undergo bilateral neck exploration.
After calcitonin injection, parathyroidectomy, or both, in young growing rats, broadening of the proximal femoral metaphysis with lack of normal concavity of the medial and lateral contours was observed radiographically. Histologically, this abnormal modelling was associated with retarded osteocytic osteolysis. Further manifestations of decelerated resorption included retention and extension of the chondroid core in the secondary spongiosa, retention of cartilage in the cortex and a large increase in the number of cementing lines.
Xenografts of mouse tail skin to the rib cages of normal and sham-parathyroidectomized rats caused an increase in plasma calcium concentration and concomitant increase in bone marrow mitosis. Neither was elicited in aparathyroid rats and graft survival was prolonged in these animals. No hypercalcaemic episode was associated with the delayed hypersensitivity response induced by painting rat ears with oxazolone. Compared with the response in sham-parathyroidectomized rats, that in parathyroidectomized rats was enhanced although both responses were less than that in normal rats. Parathyroidectomy of parental donors did not affect the ability of their splenic lymphocytes to mount a graft-versus-host response in F1 hybrid recipients. When sham-operated and aparathyroid parents were sensitized with F1 hybrid lymphocytes no differences were observed in a subsequent graft-versus-host response in F1 recipients. However, when aparathyroid F1 recipients were employed a marked reduction in the graft-versus-host reaction was observed. Thus the clonal expansion of cells with specific reactivity to certain antigens in secondary lymphoid tissue, which is driven by those same specific antigens, is not affected or only moderately affected by the parathyroid status of the animal. However, the more general increase in lymphocyte numbers promoted by non-specific mitogenic lymphokines is markedly impaired in the hypocalcaemic parathyroidectomized rat. Furthermore, the parathyroid gland is essential for the development of a hypercalcaemic episode which follows antigenic challenge and causes cell proliferation in primary lymphoid tissues. This surge of mitosis could serve to replenish the depleted pools of virgin T and B lymphocytes in the secondary lymphoid tissue which occur as a result of their response to antigens.
A histophatologic study of uraemic arterial lesions was performed in rats. They were made uraemic by 5/6 kidney resection, and the aorta and peripheral arteries were examined after intervals of up to 36 weeks. The characteristics of the arterial lesions were necrosis of medial smooth muscle cells and, in some cases, calcification of the media. The changes appeared first in the aorta, but after long uraemic periods also in peripheral arteries. The incidence and severity of necrosis and of calcification were assessed separately. Parathyroidectomy largely prevented the development of calcification, and to a lesser degree also smooth muscle cell necrosis. The results suggest that secondary hyperparathyroidism plays an important part in the development of uraemic arterial disease.
We investigated the influence of parathyroidectomy (PTX) on blood pressure (BP) and hindlimb vascular reactivity to noradrenaline (NA) and vasopressin (AVP) in male spontaneously hypertensive (SHR) and normotensive Wistar Kyoto rats (WKR). Three groups of SHR and WKR, respectively, were investigated: Sham-operated (SO) rats on a normal calcium intake (0.95%), SO rats on moderately elevated calcium intake (1.6% calcium diet) and PTX rats on the 1.6% calcium diet. At the end of the experiment (3 months), directly or indirectly measured BP was significantly lower in the PTX-SHR group on the 1.6% calcium diet than in SO-SHR on the same diet. In WKR groups, no changes of BP were recorded. Hindlimb perfusion with oxygenated Tyrode's solution for cumulative dose response curves with NA (0.1-1000 x 10(-6) M) and AVP (0.5-500 x 10(-9) M) showed no differences between PTX and SO groups. Maximal pressures and ED50 for agents used were significantly higher in SHR than WKR groups (p less than 0.05). The results support the hypothesis that the parathyroid glands contribute to high blood pressure in SHR. However, the antihypertensive action of PTX was not mediated by a change in hindlimb vascular reactivity.
We retrospectively reviewed 32 patients who underwent parathyroidectomy at our hospital for the last fourteen years. 1) Clinical appearance of primary hyperparathyroidism was in younger age in women. 2) In previous history or at the time of PTX, 9 patients had malignant tumors including 6 thyroid cancers, 36% of the patients with out bone related symptoms had a remarkable decrease in bone mineral content. 3) After PTX, none of patients had recurrent urolithiasis and bone mineral content of all patients was significantly increased in a short time. In addition, upper GI complaints were improved, or hypertension was partially normalized. However, renal insufficiency remained unchanged. 4) In preoperative localization study, Ultrasound sonography (US) demonstrated the best accuracy rate of 88% when only one gland was involved. US was able to detect multiple gland involvement only in 20% of 5 cases. 5) Hypercalciuria was recognized as one of the risk factors of stone formation in patients with primary hyperparathyroidism.
Grave hypercalcemia may complicate primary hyperparathyroidism. This clinical condition is potentially life-threatening, if it is untreated. The emergency therapy consist in rehydratation, stimulation of diuresis and somministration of biphosphonates. A urgent surgery is required if conservative therapy is not successful. The Authors herein present a consecutive series of 6 cases with acute hypercalcemic crisis due primary hyperparathyroidism, successful treated with urgent parathyroidectomy after conservative treatment.
Impacts of total parathyroidectomy and autotransplantation on bone histology were evaluated in secondary hyperparathyroidism. Low turnover bone disease accompanied with fibrous tissue developed at 4 weeks after surgery, and osteoclasts disappeared. In addition, fibrous tissue also disappeared at 12 weeks. Even though serum PTH level indicated quite low in some cases, bone resorption exceeded bone formation at 1 years after surgery. So we should pay special attention to the decrease in bone mineral density in the long term in these cases.
A possible interaction between d-1 propranolol and hyperparathyroid plasma ultrafiltrate on guinea pig auricles has been studied in "in vitro" experiments. Plasma ultrafiltrates have been samples in two patients on chronci haemodialysis before (pre-PTx) and after (post-PTx) parathyroidectomy. A significant inhibition of propranolol depressant activity on cardiac contractile strength has been observed in the presence of pre-PTx plasma ultrafiltrates. On the contrary, no such inhibition was noted in the presence of post-PTx plasma ultrafiltrates.
It has recently been suggested that selective parathyroidectomy modifies drug-induced acute renal failure. In the present study, we tested whether parathyroid hormone (PTH) could play a role in the pathogenesis of cisplatin (CP) nephrotoxicity. Parathyroidectomized rats (PTX) with normal blood calcium, were injected with two different doses of CP (group Ia: 10 mg/kg and group Ib: 6 mg/kg) and their renal functions were evaluated after 72 hours (group 1 a) and 120 h (group 1 b), respectively. All animals exhibited a milder course of acute renal failure when compared to sham-PTX CP treated rats, with lower serum creatinines (SCr) (group Ia: 1.99 +/- 0.14 vs 2.91 +/- 0.56 mg/dl, p less than 0.05) (group Ib: 1.45 +/- 0.08 vs 1.80 +/- 0.09 mg/dl, p less than 0.05) and blood urea (BUN) (group Ia: 76 +/- 5 vs 115 +/- 19 mg/dl, p less than 0.05) (group Ib: 70 +/- 9 vs 88 +/- 10 mg/dl p less than 0.05). Furthermore, the i.p. administration of PTH (50 I.U. twice daily for 9 days) to normal rats treated with CP (6 mg/kg) aggravated the CP-induced ARF as compared to vehicle injected animals (SCr 2.23 +/- 0.16 vs 1.63 +/- 0.19 mg/dl, p less than 0.05 and BUN 153 +/- 22 vs 97 +/- 20 mg/dl, p less than 0.05). Treatment with the calcium channel blocker verapamil (4 mg/kg) nine days before and three days after CP (4 mg/kg) administration, had no significant effect on cisplatin nephrotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)