The effect of surgery on Graves' orbitopathy (GO) is still controversial. Retrospective analyses of many authors (including our own group) demonstrated GO improvement after subtotal thyroid resection in up to 70% of operated patients, so the question arose whether total thyroidectomy could add anything to this pronounced positive effect on GO. We therefore performed a prospective randomized trial on 150 patients with Graves' disease (125 women, 25 men; mean thyroid volume 80.5 ml) comparing three surgical procedures (bilateral subtotal thyroid resection-total remnant < 4 ml; unilateral hemithyroidectomy with contralateral subtotal thyroid resection-remnant < 4 ml; total thyroidectomy) and their effect on postoperative GO changes, postoperative thyroid-stimulating hormone receptor (TSH-R) antibody titers, and postoperative complication rates. After a period of at least 6 months (6-36 months) GO had improved in 71% to 74% of all patients regardless of whether total or subtotal thyroidectomy was performed. TSH-R antibody titers showed no differences for the three surgical groups. Postoperative recurrent hyperthyroidism occurred in two patients with subtotal resections, and early postoperative hypoparathyroidism was more frequently detected in patients with total thyroidectomy than in those with subtotal thyroid resection (28% vs. 12%; p < 0.002). In respect to possible postoperative hypoparathyroidism and a lack of difference in postoperative GO changes, we do not advocate total thyroidectomy for patients with Graves' disease and Graves' orbitopathy but prefer radical subtotal thyroid resection with a remnant of less than 4 ml.
Various genetic loci harboring oncogenes, tumor suppressor genes, and genes for calcium receptors have been implicated in the development of parathyroid tumors. We have carried out loss of heterozygosity (LOH) studies in chromosomes 1p, 1q, 3q, 6q, 11q, 13q, 15q, and X in a total of 89 benign parathyroid tumors. Of these, 28 were sporadic parathyroid adenomas from patients with no family history of the disease, 41 were secondary parathyroid tumors, 5 were from patients with a history of previous irradiation to the neck, 12 were from patients with a family history of hyperparathyroidism, and 3 were parathyroid tumors related to multiple endocrine neoplasia type 1 (MEN1). In addition, we determined the chromosomal localization of a second putative calcium-sensing receptor, CaS, for inclusion in the LOH studies. Based on analysis of somatic cell hybrids and fluorescent in situ hybridization to metaphase chromsomes, the gene for CaS was mapped to chromosomal region 2q21-q22. The following results were obtained from the LOH studies: (1) out of the 24 tumors that showed LOH, only 4 had more than one chromosomal region involved, (2) in the tumors from uremic patients, LOH of chromosome 3q was detected in a subset of the tumors, (3) LOH of the MEN1 region at 11q13 was the most common abnormality found in both MEN1-related and sporadic parathyroid tumours but was not a feature of the other forms of parathyroid tumors, (4) LOH in 1p and 6q was not as frequent as previously reported, and (5) tumor suppressor genes in 1q and X might have played a role, particularly on the X chromosome, in the case of familial parathyroid adenomas. We therefore conclude that the tumorigenesis of familial, sporadic, and uremic hyperparathyroidism involves different genetic triggers in a non-progressive pattern.
Background: Subtotal parathyroidectomy (SPTX) and total parathyroidectomy with autotransplantation (TPTX and AT) are standard procedures in the treatment of renal autonomous hyperparathyroidism. In contrast to primary hyperparathyroidism, the persistence/recurrence rate is reported of up to 12.0%. Patients and methods: Between 1986 and 2000 we operated on 304 patients with renal autonomous hyperparathyroidism including 14 patients who were admitted after a primary operation in an outside hospital. Mean observation period was 51.4±38.9 months. Results: The overall persistence/recurrence rate in our patients was 9.0% (26/290). After SPTX, excluding patients with an incomplete operation, it was 3.7%, and after TPTX and AT it was 6.0%. Reasons for developing recurrent or persistent disease in these patients were removal of less than 3.5 glands (n=12), hyperplastic autograft (n=5), and supernumerary gland (n=4). After the first reoperation 7 patients (26.9%) had persistent or recurrent disease. Conclusions: An incomplete primary operation caused by missed cervical glands was the major reason for persistent (n=8) or recurrent (n=4) disease after different operative strategies in renal autonomous hyperparathyroidism.
Allelic loss of the retinoblastoma tumor suppressor gene has recently been shown to be highly specific for parathyroid carcinoma. It has been proposed that this genetic abnormality may have diagnostic and prognostic implications for parathyroid carcinoma, but to date no further studies are available to substantiate these findings. In the present study, three cases of atypical recurrent hyperparathyroidism were examined: a patient with parathyroid carcinoma and an autotransplanted adenoma that progressed into carcinoma, a patient with recurrent juvenile hyperparathyroidism, and a patient with severe recurrent secondary hyperparathyroid disease due to rapidly growing autotransplant. Six pairs each of sporadic parathyroid adenoma and secondary parathyroid disease were also studied for comparison. Allelic losses of RB and D13S71 at 13q14 was found in the parathyroid carcinoma and the corresponding autotransplant that had previously been considered benign tissue and in the case of recurrent juvenile hyperparathyroidism, but not in any of the other tumors. Our findings support the findings of the previous study that RB or 13q loss is specific for parathyroid tumors with increased aggressiveness and might be of clinical significance.
Mutations of the MEN1 gene do not play an important role in the pathogenesis of sporadic insulinomas. Therefore genetic screening is not cost effective in sporadic insulinoma patients without other indicators of MEN 1. Patients with primary HPT at a younger age and/or multiple gland disease should be screened for MEN1 gene mutations.
Background: To evaluate the current indications, resection strategies and short-term outcomes of surgery for benign goitre in a country with endemic goitre. Methods: Data of patients who underwent surgery for benign goitre were retrieved from the prospective StuDoQ/Thyroid registry and retrospectively analysed regarding the patient’s demographics, indications for surgery, surgical procedures, histology, and perioperative outcomes. Results: In a 15-month period, 12,888 patients from 83 departments underwent thyroid resections for benign conditions. Main indications for surgery were exclusion of malignancy (68%), compression symptoms (20.7%) and hyperthyroidism (9.7%). Preoperative fine needle aspiration cytology was performed in only 12.2% of patients with the indication “exclusion of malignancy”. Thyroidectomy (49.8%) or hemithyroidectomy (36.9%) were performed in 86.7% of patients. Minimally invasive or alternative surgical techniques were applied in only 2.2%. Intraoperative neuromonitoring was used in 98.4% of procedures, in 97.5% of patients at least one parathyroid gland was visualized, and in 15.3% of patients parathyroid tissue was autografted, respectively. The rates of unilateral and bilateral transient recurrent nerve palsy were 3.6% and 0.07% of nerves at risk, the rate of transitory hypoparathyroidism was 15.3%. The rates of postoperative bleeding and wound infections requiring reoperation were 1.4% and 0.07%, respectively. Conclusions: The indication “exclusion of malignancy” is made too liberally, and there is a strong attitude to perform complete thyroid resections. Postoperative hypoparathyroidism is the major complication after surgery for benign thyroid disease, thus requiring more awareness.
Patients with pHPT often present with neuropsychiatric symptoms and cognitive impairment. A successful parathyroid operation improves cognitive disorders in particular.
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