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Herbert Chen - One of the best experts on this subject based on the ideXlab platform.
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Tertiary Hyperparathyroidism: Why the Delay?
Annals of surgery, 2020Co-Authors: Sophie Dream, Herbert Chen, Brenessa LindemanAbstract:OBJECTIVE To evaluate the reason for delay of surgical referral in Tertiary Hyperparathyroidism (THPT) and its impact on renal allograft function. BACKGROUND Persistent Hyperparathyroidism after renal transplant has been shown to negatively impact allograft function, yet referral for definitive treatment of THPT is often delayed. METHODS A retrospective review was performed of patients undergoing parathyroidectomy for THPT (n = 38) at a single institution from May 2016 to June 2018. The first elevated serum calcium after transplant and time to referral for parathyroid surgery were recorded. Baseline creatinine post-transplant and the most recent creatinine level were used to assess allograft function. RESULTS Thirty-eight patients were included, with mean age 53 ± 2 years and 66% male. Mean preoperative calcium and parathyroid hormone were 10.8 ± 0.1 mg/dL and 328 ± 48 pg/mL, respectively. THPT after renal transplant was diagnosed at a median of 15 days (range of 1-4892 days). Median time to parathyroidectomy referral was 320 days (range 16-6281 days). In over 50% of patients, the cited reason for referral to an endocrine surgeon was difficulty with cinacalcet - either cost, poor calcium control, and poor compliance or tolerance. In comparing renal function between patients referred early ( 278 days, n = 19) for parathyroidectomy, those referred early had an improvement in creatinine (27.6% vs -5%, P = 0.007). CONCLUSIONS Patients with THPT wait approximately a year, on average, before referral to an endocrine surgeon for curative parathyroidectomy; earlier referral was associated with improvement in serum creatinine.
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Radioguided parathyroidectomy for Tertiary Hyperparathyroidism.
The Journal of surgical research, 2015Co-Authors: Yash R. Somnay, Eric Weinlander, Amal Alfhefdi, David F. Schneider, Rebecca S. Sippel, Herbert ChenAbstract:Background Tertiary Hyperparathyroidism (3HPT) is defined as the persistent hyper-production of parathyroid hormone (PTH) and resulting hypercalcemia following renal transplantation. Here, we examine the utility of radioguided parathyroidectomy (RGP) in patients with 3HPT.
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Secondary and Tertiary Hyperparathyroidism, state of the art surgical management.
The Surgical clinics of North America, 2009Co-Authors: Susan C. Pitt, Rebecca S. Sippel, Herbert ChenAbstract:This article reviews the current surgical management of patients with secondary and Tertiary Hyperparathyroidism. The focus is on innovative surgical strategies that have improved the care of these patients over the past 10 to 15 years. Modalities such as intraoperative parathyroid hormone monitoring and radioguided probe utilization are discussed.
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Radioguided parathyroidectomy in patients with secondary and Tertiary Hyperparathyroidism.
Surgery, 2003Co-Authors: Peter F. Nichol, Eberhard Mack, Jesus A. Bianco, Allen Hayman, James R. Starling, Herbert ChenAbstract:Abstract Background To date there have been no reports on the feasibility of radioguided parathyroidectomy (RGP) in patients with secondary and Tertiary Hyperparathyroidism. Methods Twenty-three consecutive patients with secondary (n = 5) or Tertiary Hyperparathyroidism (n = 18) underwent RGP. Patients were injected with 10 mCi of technetium 99–sestamibi before surgery. All parathyroid glands were localized during operation with a neoprobe. Results The mean patient age was 50±3 years. The mean preoperative calcium and intact parathyroid hormone levels were 11.0±0.3 mg/dL and 400±107 pg/mL, respectively. Eighteen patients had 3- or 4-gland hyperplasia, 2 had double adenomas, 2 had forearm graft hyperplasia, 1 had 6-gland disease, and 3 had ectopic glands. All hyperplastic glands had ex vivo counts >20% of background (mean, 63%±6%), making frozen section unnecessary. When compared with 66 historical control subjects who underwent surgery without radioguidance for Tertiary Hyperparathyroidism, patients undergoing RGP had decreased operative times (96±8 minutes vs 151±15 minutes; P Conclusions RGP in patients with secondary and Tertiary Hyperparathyroidism is feasible, may reduce operative time, and permits omission of frozen section. Thus RGP appears to be a useful adjunct in the treatment of secondary and Tertiary Hyperparathyroidism.
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Long-Term Follow-Up of Patients With Tertiary Hyperparathyroidism Treated by Resection of a Single or Double Adenoma
Annals of surgery, 2002Co-Authors: Peter F. Nichol, Eberhard Mack, James R. Starling, Jason J. Klovning, Bryan N. Becker, Herbert ChenAbstract:Tertiary Hyperparathyroidism occurs in patients with chronic renal failure who have undergone a successful kidney transplant. The development of Tertiary Hyperparathyroidism is thought to arise from a resetting of the homeostatic response mechanism of the parathyroid tissue secondary to prolonged alterations in serum calcium and phosphate in patients with renal failure. Although Tertiary Hyperparathyroidism is not a common disease process in the renal transplant population (1.6–3% in some series), 1–4 it can cause significant problems, including pathologic fractures, joint disease, renal calculi, mental status changes, muscle weakness, and peptic ulcer disease as well as pancreatitis. 4–10 Surgery remains the only curative therapy for Tertiary Hyperparathyroidism. 1,3,11,12 The standard surgical approach to patients with Tertiary Hyperparathyroidism has been either subtotal parathyroidectomy or total parathyroidectomy with autotransplantation. This surgical strategy is based on the belief that Tertiary Hyperparathyroidism is generally the result of hyperplasia of all four (or more) glands. However, several reports indicate that up to 29% of patients with Tertiary Hyperparathyroidism may have disease limited to one or two glands. 4,13–22 Although some surgeons recommend subtotal or total parathyroidectomy with autotransplantation for fear of recurrent disease in these patients, others propose resection of only the enlarged glands after a formal neck exploration. 1,3,4 To determine whether resection of a single or double adenoma in patients with Tertiary Hyperparathyroidism results in equivalent long-term cure rates, we reviewed our experience.
Andrew Arnold - One of the best experts on this subject based on the ideXlab platform.
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mutational analysis of cdkn1b a candidate tumor suppressor gene in refractory secondary Tertiary Hyperparathyroidism
Kidney International, 2008Co-Authors: Kelly Lauter, Andrew ArnoldAbstract:Most patients with refractory secondary/Tertiary Hyperparathyroidism have monoclonal parathyroid tumors. Inactivating mutations of CDKN1B, encoding the p27 cyclin-dependent kinase inhibitor, were reported to cause Hyperparathyroidism in a multiple endocrine neoplasia type 1-like syndrome. Further, there was decreased expression of CDKN1B in parathyroid tumors of patients with chronic kidney disease. We sequenced the entire coding region and splice sites of CDKN1B in 50 parathyroid tumors from 35 patients to see if inactivating mutations could cause monoclonal tumorigenesis in refractory secondary/Tertiary Hyperparathyroidism. No frameshift, nonsense, or other clearly inactivating mutations were found, nor was there evidence of homozygous deletion or loss of heterozygosity. The absence of clonal inactivating mutations suggests that CDKN1B is not a classical tumor-suppressor gene in secondary/Tertiary parathyroid tumors.
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Mutational analysis of CDKN1B, a candidate tumor-suppressor gene, in refractory secondary/Tertiary Hyperparathyroidism
Kidney international, 2008Co-Authors: Kelly Lauter, Andrew ArnoldAbstract:Most patients with refractory secondary/Tertiary Hyperparathyroidism have monoclonal parathyroid tumors. Inactivating mutations of CDKN1B, encoding the p27 cyclin-dependent kinase inhibitor, were reported to cause Hyperparathyroidism in a multiple endocrine neoplasia type 1-like syndrome. Further, there was decreased expression of CDKN1B in parathyroid tumors of patients with chronic kidney disease. We sequenced the entire coding region and splice sites of CDKN1B in 50 parathyroid tumors from 35 patients to see if inactivating mutations could cause monoclonal tumorigenesis in refractory secondary/Tertiary Hyperparathyroidism. No frameshift, nonsense, or other clearly inactivating mutations were found, nor was there evidence of homozygous deletion or loss of heterozygosity. The absence of clonal inactivating mutations suggests that CDKN1B is not a classical tumor-suppressor gene in secondary/Tertiary parathyroid tumors.
Kelly Lauter - One of the best experts on this subject based on the ideXlab platform.
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mutational analysis of cdkn1b a candidate tumor suppressor gene in refractory secondary Tertiary Hyperparathyroidism
Kidney International, 2008Co-Authors: Kelly Lauter, Andrew ArnoldAbstract:Most patients with refractory secondary/Tertiary Hyperparathyroidism have monoclonal parathyroid tumors. Inactivating mutations of CDKN1B, encoding the p27 cyclin-dependent kinase inhibitor, were reported to cause Hyperparathyroidism in a multiple endocrine neoplasia type 1-like syndrome. Further, there was decreased expression of CDKN1B in parathyroid tumors of patients with chronic kidney disease. We sequenced the entire coding region and splice sites of CDKN1B in 50 parathyroid tumors from 35 patients to see if inactivating mutations could cause monoclonal tumorigenesis in refractory secondary/Tertiary Hyperparathyroidism. No frameshift, nonsense, or other clearly inactivating mutations were found, nor was there evidence of homozygous deletion or loss of heterozygosity. The absence of clonal inactivating mutations suggests that CDKN1B is not a classical tumor-suppressor gene in secondary/Tertiary parathyroid tumors.
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Mutational analysis of CDKN1B, a candidate tumor-suppressor gene, in refractory secondary/Tertiary Hyperparathyroidism
Kidney international, 2008Co-Authors: Kelly Lauter, Andrew ArnoldAbstract:Most patients with refractory secondary/Tertiary Hyperparathyroidism have monoclonal parathyroid tumors. Inactivating mutations of CDKN1B, encoding the p27 cyclin-dependent kinase inhibitor, were reported to cause Hyperparathyroidism in a multiple endocrine neoplasia type 1-like syndrome. Further, there was decreased expression of CDKN1B in parathyroid tumors of patients with chronic kidney disease. We sequenced the entire coding region and splice sites of CDKN1B in 50 parathyroid tumors from 35 patients to see if inactivating mutations could cause monoclonal tumorigenesis in refractory secondary/Tertiary Hyperparathyroidism. No frameshift, nonsense, or other clearly inactivating mutations were found, nor was there evidence of homozygous deletion or loss of heterozygosity. The absence of clonal inactivating mutations suggests that CDKN1B is not a classical tumor-suppressor gene in secondary/Tertiary parathyroid tumors.
Etienne Sochett - One of the best experts on this subject based on the ideXlab platform.
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Prolonged high‐dose phosphate treatment: a risk factor for Tertiary Hyperparathyroidism in X‐linked hypophosphatemic rickets
Clinical endocrinology, 2003Co-Authors: Outi Mäkitie, Sang Whay Kooh, Etienne SochettAbstract:Summary objective X-linked hypophosphatemic rickets is characterized by renal phosphate wasting, hypophosphatemia and defective bone mineralization. Treatment with oral phosphate (Pi) and calcitriol improves skeletal changes but associates with secondary Hyperparathyroidism and nephrocalcinosis. Tertiary Hyperparathyroidism is a rare complication of the treatment. The aim of the present study was to identify treatment-related factors that might be associated with the transition of secondary Hyperparathyroidism to Tertiary Hyperparathyroidism in patients with X-linked hypophosphatemic rickets. design Thirteen patients with X-linked hypophosphatemic rickets and secondary or Tertiary Hyperparathyroidism were included in the study. Their hospital records were reviewed and compared for onset, duration and dosage of treatment, and for age of diagnosis and degree of secondary Hyperparathyroidism. results Two patients developed Tertiary Hyperparathyroidism and 11 patients secondary Hyperparathyroidism during the treatment. Patients with Tertiary Hyperparathyroidism had, on average, earlier onset and longer duration of treatment, higher dose of Pi and longer duration of treatment with very high Pi doses (> 100 mg/kg/day) compared to the 11 patients with secondary Hyperparathyroidism. However, variation of all parameters was great with considerable overlap. Very high S-PTH levels ≥ 42 pmol/l were observed in those who later developed Tertiary Hyperparathyroidism. conclusions Prolonged very high dose oral Pi treatment is a major risk factor for the development of Tertiary Hyperparathyroidism in X-linked hypophosphatemic rickets.
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prolonged high dose phosphate treatment a risk factor for Tertiary Hyperparathyroidism in x linked hypophosphatemic rickets
Clinical Endocrinology, 2003Co-Authors: Outi Mäkitie, Sang Whay Kooh, Etienne SochettAbstract:Summary objective X-linked hypophosphatemic rickets is characterized by renal phosphate wasting, hypophosphatemia and defective bone mineralization. Treatment with oral phosphate (Pi) and calcitriol improves skeletal changes but associates with secondary Hyperparathyroidism and nephrocalcinosis. Tertiary Hyperparathyroidism is a rare complication of the treatment. The aim of the present study was to identify treatment-related factors that might be associated with the transition of secondary Hyperparathyroidism to Tertiary Hyperparathyroidism in patients with X-linked hypophosphatemic rickets. design Thirteen patients with X-linked hypophosphatemic rickets and secondary or Tertiary Hyperparathyroidism were included in the study. Their hospital records were reviewed and compared for onset, duration and dosage of treatment, and for age of diagnosis and degree of secondary Hyperparathyroidism. results Two patients developed Tertiary Hyperparathyroidism and 11 patients secondary Hyperparathyroidism during the treatment. Patients with Tertiary Hyperparathyroidism had, on average, earlier onset and longer duration of treatment, higher dose of Pi and longer duration of treatment with very high Pi doses (> 100 mg/kg/day) compared to the 11 patients with secondary Hyperparathyroidism. However, variation of all parameters was great with considerable overlap. Very high S-PTH levels ≥ 42 pmol/l were observed in those who later developed Tertiary Hyperparathyroidism. conclusions Prolonged very high dose oral Pi treatment is a major risk factor for the development of Tertiary Hyperparathyroidism in X-linked hypophosphatemic rickets.
D. C. Aronson - One of the best experts on this subject based on the ideXlab platform.
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Outcome of Total Parathyroidectomy and Autotransplantation as Treatment of Secondary and Tertiary Hyperparathyroidism in Children and Adults
World Journal of Surgery, 2010Co-Authors: A. J. Kievit, J. G. M. Tinnemans, M. M. Idu, J. W. Groothoff, S. Surachno, D. C. AronsonAbstract:Background Treatment safety and effectiveness of total parathyroidectomy and autotransplantation for secondary and Tertiary Hyperparathyroidism have been extensively proven in adults; the evidence for children, however, is scarce. Children and adolescents cannot simply be seen as young adults in the case of chronic kidney disease and Hyperparathyroidism. The aim of this retrospective study was therefore, to evaluate whether parathyroidectomy with forearm autograft is as effective and safe in children and adolescents as in adults. Methods A group of 64 adults and 8 children and adolescents treated for secondary or Tertiary Hyperparathyroidism were retrieved from our database. The outcomes were compared on patient demographics, operation results, and blood parameters consisting of parathyroid hormone (PTH) and calcium levels. Our results were compared with all currently available articles on parathyroidectomy in children with secondary or Tertiary Hyperparathyroidism ( n = 11). Results For adults, preoperative mean serum calcium was 2.67 ± 0.29 mmol/l and mean parathyroid hormone (PTH) level was 120 ± 86 pmol/l. For children, preoperative mean serum calcium was 2.62 ± 0.20 mmol/l and mean parathyroid hormone (PTH) level was 80 ± 38 pmol/l. Postoperative calcium and parathyroid hormone levels for adults dropped to 2.39 ± 0.23 mmol/l and 30 ± 53 pmol/l, respectively. Postoperative calcium and parathyroid hormone levels for children dropped to 2.41 ± 0.16 mmol/l and 26 ± 33 pmol/l, respectively. The effectiveness of parathyroidectomy with autotransplantation was 75% in children and 72% in adults. Thus, effectiveness did not differ significantly between children and adults. Conclusions Combining the results of our own study with a literature review on pediatric parathyroidectomy, we conclude that parathyroidectomy and forearm autograft is as effective a treatment for secondary and Tertiary Hyperparathyroidism in children and adolescents as it is in adults.
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Outcome of Total Parathyroidectomy and Autotransplantation as Treatment of Secondary and Tertiary Hyperparathyroidism in Children and Adults
World journal of surgery, 2010Co-Authors: A. J. Kievit, J. G. M. Tinnemans, M. M. Idu, J. W. Groothoff, S. Surachno, D. C. AronsonAbstract:Background Treatment safety and effectiveness of total parathyroidectomy and autotransplantation for secondary and Tertiary Hyperparathyroidism have been extensively proven in adults; the evidence for children, however, is scarce. Children and adolescents cannot simply be seen as young adults in the case of chronic kidney disease and Hyperparathyroidism. The aim of this retrospective study was therefore, to evaluate whether parathyroidectomy with forearm autograft is as effective and safe in children and adolescents as in adults.