scholarly journals SAT-379 Giant Parathyroid Adenoma

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sima Saberi ◽  
Matthew J Wasco ◽  
Ramin Behjatnia ◽  
Beth Kimball

Abstract Giant parathyroid adenoma Background: Primary hyperparathyroidism is the most common cause of hypercalcemia. On ultrasound PTH adenomas are typically homogenous, hypoechoic, oval or bean-shaped with peripheral vascularity. Clinical Case: A 60 year old woman with a history of calcium oxalate nephrolithiasis presented with fatigue, worsening depression, body aches of 3 months duration. Labs showed a serum calcium 11.1 mg/dl (normal range 8.5–10.1 mg/dl), PTH 114.3 pg/ml (normal range 12–88 pg/ml), 25 OH Vitamin D 11 ng/ml (normal range above 29 ng/ml), alkaline phosphatase 137IU/L (normal range 27–120 IU/L), spot urine calcium 34.8 mg/dl, spot urine creatinine 92.1 mg/dl (estimated 24 hour urine calcium 415 mg/dl). She was started on Vitamin D 1000 IU daily. A PTH scan with SPECT/CT showed a right parathyroid adenoma and possible thyroid nodules. A neck ultrasound demonstrated a left 1.5 cm thyroid nodule and a right 3cm lesion. She underwent FNA of the left thyroid nodule and pathology was suggestive of a benign follicular nodule. She underwent parathyroid gland exploration with resection of the right lesion which was a 3.5 x 2.5 x 1.4 cm right superior 5.68 gm PTH adenoma. Postoperatively her serum calcium normalized to 10.1 mg/dl, PTH was 8.4 pg/ml, 25 OH vitamin D was 15 ng/ml. Her Vitamin D dose was increased. Clinical Lessons: A normal parathyroid gland typically weighs 30–60 mg and is 3–4 mm in size. The differential diagnosis for large parathyroid lesions is parathyroid carcinoma vs giant parathyroid adenoma. Although there is not a definitive size cutoff to define giant parathyroid adenomas, a size greater than 3.5 gm has been used (1). On ultrasound giant parathyroid adenomas are homogenous with smooth borders whereas parathyroid carcinomas are large lobulated heterogeneous hypoechoic lesions (2). A depth/width ratio on ultrasound may be the ultrasound parameter with greatest discriminatory capacity as a depth/width ratio greater than or equal to 1 had 94% sensitivity and 95% specificity for parathyroid carcinoma (2). Whether vitamin D deficiency is a risk factor for the development of large parathyroid glands is controversial as there has been conflicting data on this (1,3). Because there is no serum calcium level that distinguishes parathyroid carcinoma from a parathyroid adenoma neck ultrasound may be a helpful tool in evaluating these patients. References: 1. Spanhemier PM, Stoltze AJ, Howe JR, et al. Do giant PTH adenomas represent a distinct clinical entity? Surgery. 2013 Oct; 154(4):714–719. 2. Hara H, Igarashi A, Yano Y, et al. Ultrasonagraphic features of PTH carcinoma. Endocr J. 2001 April 48(2):213–217. 3. Rao DS, Honasoge M, Divine GW, et al. Effect of vitamin D nutrition on PTH adenoma weight: pathogenetic and clinical implications. J Clin Endocrinol Metab. 2000 Mar 85(3): 1054–1058.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Chellse Gazda ◽  
Jessica Abramowitz ◽  
Marconi Abreu

Abstract Introduction: Parathyroid carcinoma is rare and represents <1% of patients diagnosed with hyperparathyroidism (1). Clinical Cases: We present two cases of incidentally diagnosed parathyroid carcinoma during parathyroidectomy for primary hyperparathyroidism. A 69-year-old female was referred for hypercalcemia of 10.7 mg/dL (normal range 8.4-10.2). She had bone pain, fatigue, and mild depression. She was taking triamterene-hydrochlorothiazide, vitamin D 2000 international units daily, and 1 caltrate daily. Her thiazide diuretic was discontinued, and a repeat calcium was 9.5 mg/dL with a PTH of 79 pg/mL (normal range 14-64). Vitamin D and renal function were normal. A 24 hour urine calcium was elevated at 706 mg/24 hours (normal range 100-321). A bone density revealed osteopenia. Based on the high urine calcium, a thyroid ultrasound was completed and showed an enlarged right parathyroid gland. Intraoperatively, the surgeon found a superior parathyroid gland adherent to the local soft tissues with recurrent laryngeal nerve entrapment. The right superior parathyroid and right thyroid lobe were resected. Pathology demonstrated an infiltrating parathyroid carcinoma. Postoperative monitoring has included: calcium, creatinine, PTH and neck ultrasound every six months without evidence of recurrence. A 79-year-old man was referred for an approximate 18-month history of hypercalcemia. He had a prior kidney stone and constipation. He was not on calcium supplementations or thiazides. On lab testing calcium was 11.0 mg/dl with prior levels of 11.7 mg/dl. PTH was 246 pg/ml and vitamin D was 20.1 ng/ml (normal range 30-80). Imaging was obtained for parathyroid localization. A neck ultrasound and nuclear medicine study showed a right inferior parathyroid adenoma. A bone density revealed osteoporosis. Intraoperatively, the surgeon found a bilobed parathyroid extending intrathyroidal and adherent to the recurrent laryngeal nerve. The right inferior parathyroid, right thyroid lobe, and isthmus were resected. Pathology was consistent with parathyroid carcinoma. The patient had recurrent laryngeal nerve damage with persistent hoarseness postoperatively. Clinical Lessons: Patients with parathyroid carcinoma typically present with symptomatic hypercalcemia with mean levels of 13.5-14 mg/dL and mean PTH values 8.7 times the upper limit of normal (1). Given the rarity of the condition, there are no guidelines for surveillance (1). These cases highlight atypical, mild, and early presentations of an unusual and typically aggressive disease and serve as an example of how to monitor for recurrence. Reference: 1- Stack BC, Bodenner DL. Medical and Surgical Treatment of Parathyroid Diseases An Evidence-Based Approach. Switzerland: Springer, Cham; 2017.http://link.springer.com/chapter/10.10 07/978-3-319-26794-4_31#enumeration. Accessed November 3, 2019.


2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Ankur Mishra ◽  
David Newman

Context.Severe hypercalcemia is a life-threatening condition. Atypical parathyroid adenoma and parathyroid carcinomas are uncommon causes which can be difficult to differentiate.Objective.We report a case of a 36-year-old male with very high serum calcium due to a possible atypical parathyroid adenoma versus parathyroid carcinoma.Case Illustration.A serum calcium level of 23.2 mg/dl was noted on admission. He was initially treated with IV hydration, pamidronate, and salmon calcitonin to lower his calcium levels. He also underwent a surgical en bloc resection of parathyroid mass. Pathology showed a mixed picture consistent with possible atypical adenoma versus parathyroid carcinoma. However, due to the possible involvement of the recurrent laryngeal nerve, parathyroid carcinoma was more likely. Also after operation the patient developed hungry bones syndrome and his calcium was replaced vigorously. He continues to be on calcium, vitamin D, and calcitriol supplementation.Results.A review of the literature was conducted to identify previous studies pertaining to parathyroid adenomas and parathyroid cancer.Conclusion.We thereby conclude that hypercalcemia requires very careful monitoring especially after operation. Also it can be very difficult to distinguish between atypical parathyroid adenomas and parathyroid carcinomas as in our case and no clear cut guidelines yet exist to differentiate the two based on histology.


Author(s):  
Federica Saponaro ◽  
Elena Pardi ◽  
Laura Mazoni ◽  
Simona Borsari ◽  
Liborio Torregrossa ◽  
...  

Abstract Context Atypical parathyroid adenomas (APAs) are neoplasms with uncertain malignant potential but lack unequivocal histological signs of malignancy. Objective To retrospectively evaluate the clinical and biochemical profiles of patients with APA, the outcome after parathyroidectomy (PTX), and the presence of CDC73 germline and somatic mutations. Design Monocentric study on consecutive patients undergoing PTX for primary hyperparathyroidism (PHPT) between June 2000 and December 2020. Patients Fifty-eight patients with a confirmed histopathological diagnosis of APA. Age and sex-matched controls with parathyroid adenoma (PA) were also included. Results Fifty-four patients had sporadic PHPT and four familial isolated hyperparathyroidism (FIHP). Thirty-four patients (59%) had a symptomatic disease. Serum calcium and PTH levels were significantly higher in symptomatic compared to asymptomatic patients (P=0.048 and 0.008, respectively). FIHP patients were younger than the sporadic counterpart (30±17yr vs. 55±13 yrs). APA patients had significantly higher serum calcium and PTH levels and lower 25(OH)D concentration, BMD and T-score at 1/3 distal radius compared to those with PA. Four of 56 APA patients displayed a CDC73 germline mutation. No somatic CDC73 mutation was identified in 24 tumor specimens. The mean follow-up after surgery was of 60±56.4 months. All but six patients (90%), five with apparently sporadic PHPT and one with FIHP, were cured after surgery. Conclusions The large majority of patients with APA, despite a moderate/severe phenotype, have a good prognosis. Germline CDC73 mutation-positive patients had a higher rate of persistent/recurrent disease. CDC73 gene alterations do not seem to have a relevant role in the tumorigenesis of sporadic APA.


Author(s):  
Thomas Bardin ◽  
Tilman Drüeke

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.


2005 ◽  
Vol 25 (4) ◽  
pp. 362-366 ◽  
Author(s):  
Nirav Shah ◽  
Judith Bernardini ◽  
Beth Piraino

Background Peritoneal dialysis (PD) patients are at risk for 25(OH) vitamin D deficiency due to effluent loss in addition to traditional risk factors. Objectives To measure 25(OH) vitamin D deficiency in prevalent PD patients, to evaluate a replacement dose, and to determine the effects of correction. Methods 25(OH) vitamin D levels were drawn on prevalent PD patients. Patients deficient in 25(OH) vitamin D were given ergocalciferol, 50 000 IU orally once per week for 4 weeks. Patients scored muscle weakness, bone pain, and fatigue on a scale of 0 (none) to 5 (severe). Serum calcium, phosphate, parathyroid hormone (PTH), and 25(OH) vitamin D, and 1,25(OH)2 vitamin D levels were obtained before and after treatment. Results 25(OH) vitamin D levels were measured in 29 PD patients. Deficiency (<15 ng/mL) was found in 28/29 (97%); 25/29 (86%) had undetectable levels (<7 ng/mL). One course of ergocalciferol corrected the deficiency in all but 1 patient, who required a second course. Scores for muscle weakness and bone pain fell from pre- to posttreatment ( p < 0.001). 1,25(OH)2 vitamin D levels rose post ergocalciferol (from 20 to 26 pg/mL, n = 20, p = 0.09). Serum calcium, phosphate, and PTH levels did not change with ergocalciferol. Conclusions Most PD patients had marked 25(OH) vitamin D deficiency, which was readily and safely corrected with one course of 50000 IU ergocalciferol, having no effect on serum calcium, phosphorus, or PTH, but complaints of muscle weakness and bone pain decreased. A prospective, placebo-controlled double-blinded study is needed to determine whether replacement of 25(OH) vitamin D is beneficial in PD patients.


2020 ◽  
Vol 34 (1-2) ◽  
pp. 15-18
Author(s):  
Umar Amin Qureshi ◽  
Abdus Sami Bhat ◽  
Muzaffar Jan ◽  
Uruj Qureshi

Purpose: Late onset neonatal hypocalcemia (LNH) is defined as hypocalcemia detected after day 3 of life. Its occurrence in babies fed with cow’s milk is well understood. Since the advent of modern-day formulas, the incidence has however decreased. Methods: A prospective descriptive study (January 2017 to December 2017) of LNH seizures in neonates was conducted. LNH was defined as the total serum calcium of less than 7 mg/dL in preterm or less than 8 mg/dL in term newborns after 72 h of life. Results: 14 neonates were presented with myoclonic and focal seizures due to late hypocalcemia. All were formula fed. Their mean serum calcium, phosphorus, alkaline phosphatase, magnesium, 25-OH vitamin D, intact PTH levels were 4.93 mg/dL, 9.19 mg/dL, 244 U/L, 1.2 mg/dL, 30 nmol/L, 38.6 pg/mL, respectively. Mean maternal vitamin D levels were 43 nmol/L. Mean hospital stay was 4 days. Clinical response to treatment was brisk in those who were able to shift to total breast feeding early. Conclusions: LNH in formula-fed and vitamin D deficient babies is not uncommon. Emphasis should be laid on exclusive breast feeding even in vitamin D deplete mothers. However, mothers at risk should be supplemented with vitamin D during pregnancy.


Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1632 ◽  
Author(s):  
Adekunle Dawodu ◽  
Khalil M. Salameh ◽  
Najah S. Al-Janahi ◽  
Abdulbari Bener ◽  
Naser Elkum

In view of continuing reports of high prevalence of severe vitamin D deficiency and low rate of infant vitamin D supplementation, an alternative strategy for prevention of vitamin D deficiency in infants warrants further study. The aim of this randomized controlled trial among 95 exclusively breastfeeding mother–infant pairs with high prevalence of vitamin D deficiency was to compare the effect of six-month post-partum vitamin D3 maternal supplementation of 6000 IU/day alone with maternal supplementation of 600 IU/day plus infant supplementation of 400 IU/day on the vitamin D status of breastfeeding infants in Doha, Qatar. Serum calcium, parathyroid hormone, maternal urine calcium/creatinine ratio and breast milk vitamin D content were measured. At baseline, the mean serum 25-hydroxyvitamin D (25(OH)D) of mothers on 6000 IU and 600 IU (35.1 vs. 35.7 nmol/L) and in their infants (31.9 vs. 29.6) respectively were low but similar. At the end of the six month supplementation, mothers on 6000 IU achieved higher serum 25(OH)D mean ± SD of 98 ± 35 nmol/L than 52 ± 20 nmol/L in mothers on 600 IU (p < 0.0001). Of mothers on 6000 IU, 96% achieved adequate serum 25(OH)D (≥50 nmol/L) compared with 52%in mothers on 600 IU (p < 0.0001). Infants of mothers on 600 IU and also supplemented with 400 IU vitamin D3 had slightly higher serum 25(OH)D than infants of mothers on 6000 IU alone (109 vs. 92 nmol/L, p = 0.03); however, similar percentage of infants in both groups achieved adequate serum 25(OH)D ≥50 nmol/L (91% vs. 89%, p = 0.75). Mothers on 6000 IU vitamin D3/day also had higher human milk vitamin D content. Safety measurements, including serum calcium and urine calcium/creatinine ratios in the mother and serum calcium levels in the infants were similar in both groups. Maternal 6000 IU/day vitamin D3 supplementation alone safely optimizes maternal vitamin D status, improves milk vitamin D to maintain adequate infant serum 25(OH)D. It thus provides an alternative option to prevent the burden of vitamin D deficiency in exclusively breastfeeding infants in high-risk populations and warrants further study of the effective dose.


2003 ◽  
Vol 88 (12) ◽  
pp. 5644-5649 ◽  
Author(s):  
Dolores M. Shoback ◽  
John P. Bilezikian ◽  
Stewart A. Turner ◽  
Laura C. McCary ◽  
Matthew D. Guo ◽  
...  

Abstract Calcimimetics increase the sensitivity of the calcium-sensing receptor (CaR) to circulating serum calcium, reducing the secretion of PTH and the serum calcium concentration. We evaluated the calcimimetic cinacalcet, a novel therapy for the management of primary hyperparathyroidism. In this randomized, double-blind, dose-finding study, patients (n = 22) with primary hyperparathyroidism were given cinacalcet (30, 40, or 50 mg) or placebo twice daily for 15 d and observed for an additional 7 d. Serum calcium, plasma PTH, and 24-h and fasting urine calcium were measured. Baseline mean serum calcium was 10.6 mg/dl for the combined cinacalcet-treated patients (normal range, 8.4–10.3 mg/dl), compared with 10.4 mg/dl for the placebo group. Mean PTH at baseline was 102 pg/ml (normal range, 10–65 pg/ml) for the combined cinacalcet-treated patients, compared with 100 pg/ml in the placebo group. Serum calcium normalized after the second dose on d 1 and remained normal through d 15 in all cinacalcet dose groups. Maximum decreases in PTH of over 50% occurred 2–4 h after dosing in all cinacalcet-treated groups. The fasting and 24-h urine calcium to creatinine ratios were similar in the cinacalcet and placebo groups. This study demonstrates that cinacalcet safely normalized serum calcium and lowered PTH concentrations without increasing urinary calcium excretion in the study subjects, indicating the potential benefit of cinacalcet as a medical treatment for primary hyperparathyroidism.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mohamed K M Shakir ◽  
Vijay Kiran ◽  
Zachary Bloomer ◽  
Terry Shin ◽  
Vinh Q Mai ◽  
...  

Abstract IntroductionHypercalciuria is generally considered to be the most common identifiable metabolic risk factor for calcium nephrolithiasis. Important renal manifestations of primary hyperparathyroidism (PHPT) include asymptomatic nephrolithiasis, hypercalciuria, nephrocalcinosis, and chronic renal insufficiency. However renal papillary necrosis (RPN) occurring in PHPT has not been reported previously. We report a 50-year-old woman who manifested RPN associated with hypercalciuria and normocalcemic PHPT. Case ReportA 50-year-old Caucasian woman was evaluated in 2006 for hypercalcemia. She had no history of nephrolithiasis, fractures, or symptoms of hypercalcemia. Laboratory: serum calcium 11.8 mg/dL, ionized calcium 6.3 mg/dL, phosphorus 1.8 mg/dL, intact PTH 98 pg/mL (ref 15–65), urine calcium 543 mg/24 hrs (ref &lt;235). Renal ultrasound showed no evidence of nephrocalcinosis or nephrolithiasis. A parathyroid scan was consistent with a left superior parathyroid adenoma. Patient underwent parathyroidectomy and became normocalcemic with normal serum PTH levels postoperatively. One year later she was diagnosed with a left sided bronchial carcinoid tumor. Surveillance Gallium-68 PET/CT scan done 2 years later was negative for any metastases. Twelve years later she reported to our clinic for follow up. She had no symptoms of hypercalcemia, fractures, nephrolithiasis, history of pyelonephritis, diabetes mellitus, analgesic use, or hypertension. Serum calcium was 9.1 mg/dL, serum phosphorous 3.8mg/dL, PTH 82 pg/mL, 25-OH vitamin D 34 ng/mL, 1,25-vitamin D 38 pg/mL, and a urorisk panel was normal except for a 24-hour urine calcium of 410 mg. However renal ultrasound showed bilateral RPN and this diagnosis was also confirmed by a CT scan. A urinalysis showed only microalbuminuria with no red cells. She had no history of any analgesic drug abuse, pyelonephritis, sickle cell disease, or diabetes mellitus. A glucose tolerance test was completely normal. Discussion RPN is characterized by coagulative necrosis of the renal medullary pyramids and papillae brought on by several associated disorders and toxins that exhibit synergism toward the development of ischemia. Although the initial kidney US was normal, a repeat US done 12 years later showed evidence of RPN. This finding along with hypercalciuria and a diagnosis of normocalcemic PHPT suggests that RPN may be associated with hypercalciuria and normocalcemic PHPT. Furthermore she had no other risk factors for RPN. Additional studies with large number of patients are needed to confirm the association between these 2 disorders.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Maimoona Bahlol ◽  
Alan Scott Sacerdote ◽  
Gul Bahtiyar

Abstract •Our patient is a 63-year-old African American female with medical history significant for hypertension, class 1 obesity, osteoarthritis of knees who initially presented to the adult ambulatory clinic on 9/19/2013 with complaints of body aches and bone pain. Labs were remarkable for a serum calcium level of 9.8 mg/dl, serum phosphorous of 4.7 mg/dl, and serum parathyroid hormone level of 166 pg/ml (15-65 pg/ml), normal GFR and serum vitamin 25-OH D of 62. A DEXA scan was performed which showed mild osteopenia wof 1.0 (0.8-1.8), serum 1,25 - OH vitamin D of &lt;8 pg/ml, normal alpha and beta carotene level, negative endomysial antibodies and normal magnesium level. A diagnosis of secondary hyperparathyroidism with unclear etiology was made. Same treatment was continued and a follow up in 3 months with repeat labs was advised. Repeat PTH went up to 281pg/ml but serum calcium and phosphate remained normal. Based on normal serum 25 OH vitamin D and low 1, 25 OH vitamin D, patient was started on calcitriol 0.25 mg daily. On next follow up in 3 months PTH decreased to 203pg/ml and 1, 25 OH vitamin D level normalized (35pg/ml). MEN was excluded with normal serum free metanephrine and gastrin levels. On subsequent visits DEXA scan normalized and PTH further trended downward to 101.7 pg/ml. Patient was discharged from endocrine clinic back to the PCP. • •Patient continued to follow up in adult medicine clinic but calcitriol fall off of patient’s medication list likely due to an error. Patient was off of calcitriol for 6 months but continue to take calcium vitamin D.PTH trended up to 186pg/ml and then to 350pg/ml. A referral to endocrinology was made again and a parathyroid sestamibi scan was obtained which did not reveal any abnormal uptake. Serum calcium, phosphate, magnesium and vitamin OH 25 vitamin D remained normal. •Patient was started back on calcitriol 0.5 mg daily and PTH again started to trend downward. The last PTH was down to 82 on March 20th 2019 with normal serum calcium, phosphate, magnesium and eGFR. The final diagnosis was secondary hyperparathyroidism due to decrease 1 alpha hydroxylase activityith a T score of −1.5 at left forearm. A diagnosis of primary hyperparathyroidism was made by the PCP and patient was started on calcium vitamin D and Fosamax and was referred to endocrinology for further evaluation. • •Further testing in the endocrine clinic revealed 24-hour urine calcium of 49 mg (100-300) and urine creatinine. This case report concludes that low 1-alpha hydroxylase activity should be considered as a cause of secondary hyperparathyroidism in a patient with normal GFR and 25-OH vitamin D level


Sign in / Sign up

Export Citation Format

Share Document