无症状型原发性甲状旁腺功能亢进临床诊治

随着血钙和血甲状旁腺素检测以及颈部超声检查的普遍开展,越来越多的无症状型原发性甲状旁腺功能亢进（PHPT）病人得以诊断,其诊断和治疗逐渐受到人们的广泛关注。尽管关于无症状型PHPT的处理方法尚存在一定争议,但随着诊治经验的积累、较高论证强度临床研究的开展以及诊治指南的不断更新,针对无症状型PHPT的处理变得愈加规范。手术治疗、药物治疗与随访观察的合理选择是改善无症状型PHPT病人生存质量,获得最佳治疗效果的关键。     

原发性甲状旁腺功能亢进症的围手术期处理

目的：探讨围手术期处理对治疗原发性甲状旁腺功能亢进症（primary hyperparathyroidism,PHPT）的影响。方法：对近10年治疗26例PHPT的围手术期处理进行回顾性分析。结果：病人术前血清钙3．31mmol/L，5例出现高血钙危象（血清钙3．7－4．5mmol/L）。术后4d血清钙降低至最低点1．74mmol/L。血清甲状旁腺激素由术前1050．7pg/ml恢复至正常的17．12pg／ml。有2例由于未能及时治疗而死亡。全组累积死亡率为11．5％（3／26例）。分别为心搏骤停和左心功能不全。结论：重视围手术期的处理是PHPT治疗的重要环节；对高血钙危象的有效治疗必须尽早开始，以挽救病人生命。     

甲状旁腺腺瘤所致无症状原发性甲状旁腺功能亢进症24例诊治分析

目的探讨甲状旁腺腺瘤所致无症状原发性甲状旁腺功能亢进症（PHPT）的诊断和治疗。方法回顾性分析中国医科大学附属第一医院1990年1月至2013年4月期间收治的24例甲状旁腺腺瘤所致尤症状PHPT患者的临床资料。结果24例甲状旁腺腺瘤所致无症状PHPT患者中男9例,女15例;年龄（47．92±12．96）岁。均无骨关节疼痛、病理性骨折、泌尿系结石或胃肠道症状等典型PHPT的临床表现,均为体检和并存或误诊为甲状腺疾病时发现。24例患者术前血钙升高18例,正常6例;血磷降低7例,正常17例;16例术前行血甲状旁腺激素检测患者中11例升高,正常5例;22例患者术前测定血碱性磷酸酶升高9例,正常13例。血钙与甲状旁腺激素均正常者4例,其中1例为体检时超声发现甲状旁腺病变,3例为手术治疗甲状腺疾病术中探查发现。24例患者术前均行超声检查,15例行甲状旁腺ECT检查,14例行甲状旁腺增强CT检查,阳性率分别为66．67％（16／24）、93．33％（14／15）及78．57％（11／14）。15例术前定性定位检查获得明确诊断,5例定性或定位检查高度怀疑甲状旁腺病变,4例术前误诊为甲状腺病变。均行甲状旁腺腺瘤切除,其中甲状旁腺腺瘤位于左侧上位2例、左侧下位9例、有侧上位2例、右侧下位11例。肿瘤最大径为（2．22±0．88）cm。24例患者中13例合并甲状腺病变。本组患者术后有8例出现手足、口周麻木,给予静脉或口服补钙后缓解,其余患者均无自觉症状。术后血钙及甲状旁腺激素均有不同程度下降,术后2周均降至正常范围。结论甲状旁腺腺瘤所致无症状PHPT临床症状不典型,血清钙和甲状旁腺激素同步升高即可诊断,具有手术指征的患者应积极手术治疗。     

原发性甲状旁腺功能亢进症的诊断和治疗

目的 探讨原发性甲状旁腺功能亢进症(primary hyperparathyroidism，PHPT)的诊治方法。方法 回顾性分析90例PHPT的临床资料。结果 血钙大于2．65mmol／L，伴血PTH同步升高为定性诊断PHPT的主要依据。B超定位甲状旁腺腺瘤的特异性为95％，而^99mTc-MIBI的敏感性为100％。经双侧甲状旁腺探查发现下旁腺较上旁腺更易受累。良性病变1次手术成功率99％。结论 PHPT的定性诊断依据血钙和PTH的同步升高，结合颈部B超和MIBI能取得较为准确的术前定位。双侧颈部探查并切除甲状旁腺肿瘤安全有效。     

原发性甲状旁腺功能亢进的诊断与治疗

原发性甲状旁腺功能亢进症（primaryhyperpa-rathyroidism,PHPT）是由于病变的甲状旁腺组织合成和分泌过多的甲状旁腺激素（PTH）引起高血钙、低血磷及高尿钙的一种多系统疾病。     

甲状旁腺功能亢进症的诊断和治疗

目的探讨原发性甲状旁腺功能亢进症(PHPT)和继发性甲状旁腺功能亢进症(SHPT)的诊断及治疗方法。方法回顾性分析我院19年间收治的15例PHPT和26例SHPT患者的临床资料,诊断依靠血清学、影像学、99mTc-MIBI及临床表现;按病情不同行手术和非手术治疗。结果 41例患者的血清甲状旁腺激素(PTH)均升高,PHPT的血钙水平升高,SHPT的血钙水平降低。彩超、99mTc-MIBI定位诊断准确率分别为73.17%和85.71%。行手术治疗的15例PHPT和3例SHPT患者术后均无复发;非手术治疗的23例SHPT患者均能缓解病情进展。结论 PTH和血钙是HPT定性诊断的主要依据,定位诊断首选彩超、99mTc-MIBI。PHPT以外科手术治疗为主;SHPT以非手术治疗为主,非手术治疗无效者可行手术治疗。     

原发性甲状旁腺功能亢进症的外科诊治

目的： 探讨原发性甲状旁腺功能亢进症（PHPT）的外科诊治经验。 方法：回顾性分析2002—2012年间收治的86例PHPT患者的临床资料。 结果：首发症状表现为骨骼系统病变45例,泌尿系统症状21例,消化道症状14例;无症状者6例。术前86例患者平均血钙浓度（3.13±0.46）mmol/L,甲状旁腺素（PTH）中位浓度864.6 pmol/mL。B超检出率90.3%,99mTc-MIBI检出率95.0%,CT检出率78.6%。58例单纯单发甲状旁腺瘤（其中包括异位甲状旁腺腺瘤5例）行单侧颈部探查术;11例双侧甲状旁腺腺瘤,15例单发甲状旁腺腺瘤合并双侧结节性甲状腺肿,2例甲状旁腺增生行双侧颈部探查术。术后成功随访80例,时间3个月至6年,所有患者均无复发。 结论：血钙、血PTH是PHPT定性诊断的主要依据,B超、99mTc-MIBI是PHPT主要定位手段。手术治疗是最有效的方法,单侧颈部探查术是常用术式。     

继发性甲状旁腺功能亢进高磷血症的治疗

继发性甲状旁腺功能亢进（SHPT）是指由于机体内存在刺激甲状旁腺的因素,特别是低血钙、低血镁和高血磷,腺体受刺激后增生、肥大,分泌过多的甲状旁腺素（PTH）,代偿性维持正常血钙、血磷水平。     

原发性甲状旁腺功能亢进的外科治疗及评价

随着人们对甲状旁腺疾病认识的不断深入,临床诊断原发性甲状旁腺功能亢进（primary hyperparathyroidism,PHPT）的病例日趋增多。PHPT是导致血钙升高的最常见原因之一。由于甲状旁腺自身过度分泌甲状旁腺素从而引起血清钙水平升高,并导致全身多个系统出现损害,其中包括神经肌肉、消化道、心血管、关节及软组织、泌尿及骨骼系统。外科手术是治疗PHPT的重要手段,手术成败的关键在于术前精确定位,术中仅切除病变旁腺组织而保留正常旁腺组织,同时不破坏正常旁腺组织血供并保护周围重要组织,特别是喉返神经。     

骨型甲状旁腺功能亢进症临床分析

１９９３年１月～９月，我科收治经手术病理证实的骨型甲状旁腺功能亢进症患者６例，其临床特点为起病缓慢，均有多发固定部位骨痛，ｘ线检查呈全身骨质疏松，多发性溶骨性改变，同时血清钙和血清碱性磷酸酶升高，甲状旁腺激素升高更有意义。本组４例被误诊为骨肿瘤，骨关节病误行骨科手术。作者认为临床医师如能提高对本病的认识和鉴别诊断的知识，不仅可以早期发现、早期治疗。且可避免误诊、误治。     

原发性甲状旁腺功能亢进症临床分析（附138例报告）

目的 总结原发性甲状旁腺功能亢进症的诊治体会。方法 回顾性分析本院普通外科2015年1月至2017年11月经手术治疗的138例原发性甲状旁腺功能亢进症病人的临床资料。结果 138例病人,男30例,女108例,均行手术治疗,其中甲状旁腺危象5例,1例行急诊手术治疗。切除病变甲状旁腺150枚。术后病理检查显示：123枚（82.0%）为甲状旁腺腺瘤,9枚（6.0%）为甲状旁腺增生,4枚（2.7%）为甲状旁腺癌,10枚（6.6%）为甲状旁腺囊肿,4枚（2.7%）为甲状旁腺非典型腺瘤。术后第1天甲状旁腺素（parathyroid hormone, PTH）均降至正常,血钙下降。其中48例术后出现低血钙症状,经补充活性维生素D和葡萄糖酸钙,恢复正常。无喉返神经损伤等并发症发生。结论 血钙和PTH可作为原发性甲状旁腺功能亢进的初步诊断方法。甲状旁腺切除术是有效治疗手段。术前准确定位有助于缩小探查范围。对于甲状旁腺危象,给予水化利尿及双膦酸盐降钙治疗、及时早期行甲状旁腺切除术,可取得良好治疗效果。     

Primary hyperparathyroidism associated with hypocalcemia in a patient presenting with kidney disease

Elevated serum parathyroid hormone (PTH) level together with hypocalcemia in chronic kidney disease usually suggests secondary hyperparathyroidism. However, primary hyperparathyroidism should also be considered, especially if concomitant vitamin D deficiency is suspected. We report a case of parathyroid adenoma associated with hypocalcemia and metabolic bone disease in a patient presenting with kidney disorder. The patient was successfully treated by parathyroidectomy that was preceded and followed by intensive calcium and vitamin D supplementation.     

Parathyroidectomy for tertiary hyperparathyroidism associated with X-linked dominant hypophosphatemic rickets

BACKGROUND: X-linked dominant hypophosphatemic rickets (XLHR) is a hereditary metabolic bone syndrome that is only beginning to be understood and is rarely associated with progression to irreversible tertiary hyperparathyroidism. We report our surgical experience with 6 patients with XLHR who underwent parathyroidectomy for associated autonomous parathyroid hyperfunction. HYPOTHESIS: Parathyroidectomy can successfully treat tertiary hyperparathyroidism in the setting of XLHR, although an understanding of expected operative findings and postoperative complications is essential. DESIGN: The study group comprised 6 patients with XLHR identified from our endocrine surgery database. Presentation, surgical procedure, parathyroid pathologic findings, and subsequent outcome are outlined. RESULTS: There were 4 women and 2 men. All were exposed to long-term vitamin D and phosphate supplementation therapy. All had persistently elevated preoperative levels of parathyroid hormone and serum calcium. The patients were treated as follows: 3 had total parathyroidectomy, 2 had 3 parathyroid glands identified and resected, and 1 had 2 abnormal parathyroid glands resected with 2 normal-appearing parathyroid glands left in situ. One patient subsequently required completion parathyroidectomy for recurrent disease. Pathologic examination results revealed hyperplasia of all resected parathyroid glands in 4 of 6 patients. One patient had a single adenoma with 3-gland hyperplasia, and 1 patient had a double adenoma. The principal complication of this procedure was profound symptomatic hypocalcemia requiring intravenous calcium infusion. Hungry bone syndrome was also observed in most subjects. Long-term, all patients achieved normocalcemia. CONCLUSION: Tertiary hyperparathyroidism is a rare but recognized complication of XLHR. Parathyroidectomy effectively treats this complication caused by autonomous parathyroid hyperfunction, but profound postoperative hypocalcemia necessitates careful management.     

Renal Tubular Acidosis after Jejunoileal Bypass for Morbid Obesity: role of secondary hyperparathyroidism

The effect of calcium infusion was studied in patients with renal tubular acidosis (RTA) and secondary hyperparathyroidism. Both developed after jejunoileal bypass operation (JIB) for morbid obesity. In three of four cases the acidification defect was abolished, probably due to a decrease of serum parathyroid hormone. As we found RTA in 9% (95% confidence limits 2-21%) of our patients, screening for acidosis is recommended in obesity patients after malabsorptive operations. RTA can be verified through an ammonium loading test. Before deciding on reestablishing bowel continuity due to RTA, we suggest that patients be evaluated for secondary hyperparathyroidism and vitamin D deficiency by measurement of serum calcium, parathyroid hormone and vitamin 1.25(OH)₂D₃, and any calcium and vitamin D deficiency be corrected. An intravenous calcium loading test can predict the outcome of oral calcium and vitamin D supplementation. If RTA can be abolished through correction of calcium homeostasis, reoperation may be avoided. Before deciding on re-establishing bowel continuity in JIB patients with RTA, we therefore suggest that patients be evaluated for secondary hyperparathyroidism and any calcium deficiency be corrected.     

Perioperative indicators of hypocalcemia in total thyroidectomy: the role of vitamin D and parathyroid hormone

Background

Hypocalcemia is a common complication of thyroidectomy. The aim of this study was to identify risk factors for this problem.

Methods

This prospective analysis included 111 patients undergoing total or completion thyroidectomy. Preoperative vitamin D levels and postoperative day 1 parathyroid hormone levels were analyzed for their predictive effects on postoperative hypocalcemia.

Results

Patients with ionized calcium <4.4 mg/dL had significantly lower mean parathyroid hormone levels than normocalcemic patients (13.0 vs 28.4 pg/mL, P < .001). Parathyroid hormone levels were also significantly lower in symptomatic patients (11.0 vs 28.4 pg/mL, P < .001). Preoperative vitamin D level, body mass index, gender, and pathologic findings were not associated with low calcium levels or symptoms of hypocalcemia.

Conclusions

Younger age and low postoperative parathyroid hormone levels are predictive of symptomatic hypocalcemia. A parathyroid hormone level outside of the reference range may indicate a need for more aggressive postoperative calcium supplementation and treatment with activated vitamin D. Older patients with normal postoperative parathyroid hormone levels may be safely discharged with appropriate calcium supplementation.     

Primärer Hyperparathyreoidismus

Introduction

Normocalcemic hyperparathyrinemia, i.e. elevated parathyroid hormone (PTH) levels after parathyroidectomy in patients with primary hyperparathyroidism (pHPT) may occur in the course of postoperative recovery without the development of persistence or relapse.

Materials, methods and results

Intraoperative and long-term (7 year) postoperative PTH and calcium levels after curative parathyroidectomy are demonstrated on the basis of a case report of a 62-year-old female patient with severe pHPT and pronounced osseous and renal manifestations. The intraoperative PTH gradient displayed a decrease from 1072 pg/ml to 13 pg/ml (normal range 11–67 pg/ml) followed by an increase of up to 287pg/ml. The hyperparathyoid values decline to subnormal levels on administration of calcium and vitamin D and increase again after tapering these medications. The inverse calcium/PTH correlation in the course of the 7-year observation period suggests an intact feed-back mechanism. Preoperative PTH screening was performed in 316 consecutive normocalcemic thyroid patients to evaluate the rate of incidental hyperparathyroidism in patients with normal serum calcium levels. Of these patients 31 (9.8%) with normocalcemia (average 2.28 mmol/l, normal range 2.1–2.7 mmol/l) exhibited increased PTH levels averaging 84.2 pg/ml. A parathyroid adenoma was found intraoperatively as the cause for normocalcemic pHPT in only 1 of these 31 patients.

Discussion and conclusions

A review of the literature revealed that late postoperative elevated parathyroid hormone levels after successful pHPT surgery occur in 21.5%. Multiple causes are discussed, e.g. reactive hyperparathyroidism in cases of relative hypocalcemia, hungry bone syndrome, vitamin D deficiency, renal dysfunction and ethnic or lifestyle differences. In mild cases of postoperative hyperparathyrinemia observation of the patient may be sufficient. In cases of reactive hyperparathyroidism due to hypocalcemia, administration of calcium is indicated, in symptomatic patients, additional administration of vitamin D or calcitriol is necessary. Vitamin D deficiency per se needs adequate substitution. In cases of ongoing hyperparathyrinemia an interdisciplinary diagnostic and therapeutic approach is required.     

Hypercalcemic hyperparathyroidism and hypophosphatemic osteomalacia complicating neurofibromatosis

Summary Neurofibromatosis is sometimes complicated by impaired renal tubular reabsorption of phosphate, hypophosphatemia, and osteomalacia. Hyperparathyroidism has also been reported in patients with neurofibromatosis. When hypercalcemia and elevated levels of parathyroid hormone are found in osteomalacia, however, it may be difficult to determine if the hyperparathyroidism was primary or tertiary. We describe a patient with neurofibromatosis, hypercalcemic hyperparathyroidism, hypophosphatemic osteomalacia, vitamin D deficiency, and clear-cell hyperplasia of all four parathyroid glands. Serial biomechanical, bone biopsy, and densitometric studies confirmed that treatment with ergocalciferol, calcium, and phosphate supplements significantly improved the osteomalacia but caused increased parathyroid overactivity. After subtotal parathyroidectomy, the parathyroid hormone concentration became normal and the bone mineral content increased at the spine and hip, but inappropriate phosphaturia persisted. The findings indicate that hyperparathyroidism, osteomalacia, and vitamin D deficiency adversely affect each other.     

Late Calcium Metabolic Consequences of Jejuno-ileal Bypass

Seventeen patients with previous jejuno-ileal bypass operation (JIB) for obesity were included in a follow-up study 11 to 19 years after JIB. Evaluation of calcium-parathyroid hormone axis was performed by a highly sensitive two-site IRMA assay for serum intact parathyroid hormone and serum ionized calcium. Evidence of a varying degree of secondary hyperparathyroidism was found. The observed hyperparathyroidism was of clinical significance in a subpopulation characterized by increased bone turnover and reduced bone mineral content. As a consequence, the calcium metabolism with special attention to the parathyroid function must be carefully monitored in JIB patients. Serum ionized calcium alone and vitamin D metabolites do not identify patients at risk of bone loss.     

Parathyroid growth and suppression in renal failure

In advanced uremia, parathyroid hormone (PTH) levels should be controlled at a moderately elevated level in order to promote normal bone turnover. As such, a certain degree of parathyroid hyperplasia has to be accepted. Uremia is associated with parathyroid growth. In experimental studies, proliferation of the parathyroid cells is induced by uremia and further promoted by hypocalcemia, phosphorus retention, and vitamin D deficiency. On the other hand, parathyroid cell proliferation might be arrested by treatment with a low-phosphate diet, vitamin D analogs, or calcimimetics. When established, parathyroid hyperplasia is poorly reversible. There exists no convincing evidence of programmed parathyroid cell death or apoptosis in hyperplastic parathyroid tissue or of involution of parathyroid hyperplasia. However, even considerable parathyroid hyperplasia can be controlled when the functional demand for increased PTH levels is removed by normalization of kidney function. Today, secondary hyperparathyroidism can be controlled in patients with long-term uremia in whom considerable parathyroid hyperplasia is to be expected. PTH levels can be suppressed in most uremic patients and this suppression can be maintained by continuous treatment with phosphate binders, vitamin D analogs, or calcimimetics. Thus modern therapy permits controlled development of parathyroid growth. When nonsuppressible secondary hyperparathyroidism is present, nodular hyperplasia with suppressed expression of the calcium-sensing receptor (CaR) and vitamin D receptor (VDR) has been found in most cases. An altered expression of some autocrine/paracrine factors has been demonstrated in the nodules. The altered quality of the parathyroid mass, and not only the increased parathyroid mass per se, might be responsible for uncontrollable hyperparathyroidism in uremia and after kidney transplantation.     

Does routine blood bone biochemistry predict vitamin D insufficiency in elderly patients with low-velocity fractures?

PURPOSE: Vitamin D deficiency impairs bone mineralisation and can predispose individuals to fractures. This study aimed at testing whether measurement of plasma calcium, alkaline phosphatase, and phosphate levels could detect vitamin D insufficiency. METHODS: During a 10-week winter period from December 2000 to February 2001, all elderly patients presenting to a general hospital in Brighton--British seaside town--with a fracture of the proximal femur and without known bone mineralisation problems were invited to participate in the study. RESULTS: 23 (63.9%) of the 36 eligible patients had insufficient levels of vitamin D, with a plasma concentration of less than 30 nmol/L. The mean parathyroid hormone level was 56 pg/mL (range, 12-193 pg/mL). 11 of the 36 patients had an elevated level of parathyroid hormone were insufficient in vitamin D. The mean plasma concentration of calcium was 2.30 mmol/L (range, 2.05-2.98 mmol/L). The mean phosphate level was 0.98 mmol/L (range, 0.40-1.79 mmol/L), and the mean alkaline phosphatase level was 91 IU/L (range, 46-127 IU/L). There was poor correlation between vitamin D insufficiency and plasma calcium, alkaline phosphatase, or phosphate levels. CONCLUSION: Plasma calcium, alkaline phosphatase, and phosphate testing cannot detect vitamin D insufficiency. We recommend that vitamin D and calcium supplementation be considered for patients with low-energy hip fractures.