Cause Of Secondary Hyperparathyroidism Research Articles

Cardiovascular and fracture events analysis and intervention strategies in patients undergoing parathyroidectomy with secondary hyperparathyroidism.

Chronic kidney disease (CKD), especially end-stage renal disease (ESRD), is the most common cause of secondary hyperparathyroidism (SHPT), and SHPT is the most severe complication of ESRD. This study aimed to analyze the influencing factors of cardiovascular and fracture events in patients with SHPT which are the leading causes of death in patients with CKD, and provide a reference for selecting patients for whom surgery is more suitable. Patients who underwent parathyroidectomy (PTX) for SHPT at The First Affiliated Hospital, Zhejiang University School of Medicine from September 2021 to April 2024 were selected as the study object, with the inclusion and exclusion criteria as followed. They were divided into rural and urban residents for comparison as a cross-sectional study. The study evaluated the comorbidities, socioeconomic status, and postoperative complications diagnosed by radiography of patients undergoing surgery for SHPT. A total of 119 patients were included, among whom, 71 were from rural areas and 48 were from urban areas. Compared with urban residents, rural residents had poorer economic conditions, a longer interval from disease onset to PTX, and a higher incidence of cardiovascular and fracture events and concurrent nephrolithiasis, all of which were statistically significant. Multivariate analysis indicated that place of residence, age, and duration of uremia were independent risk factors of cardiovascular/fracture events. Medical staff in ESRD outpatient clinics should pay attention to patients with SHPT. ESRD patients should have better surveillance especially for rural, elder and poor phosphorus control patients, and promptly assess surgical intervention measures.

Opportunities to improve the diagnosis and treatment of primary hyperparathyroidism: retrospective cohort study.

Although primary hyperparathyroidism (PHPT) is readily diagnosed biochemically and can be cured with low-risk surgery, it is often underrecognized and undertreated. Our objectives were to characterize, within our health system, how often patients with hypercalcemia were evaluated for PHPT and how often patients with PHPT underwent definitive treatment with parathyroidectomy. Ambulatory patients aged 18 years or older seen at our health system between January 2018 and June 2023 with chronic hypercalcemia were identified from the medical record. After excluding causes of secondary hyperparathyroidism, the proportion of patients with parathyroid hormone (PTH) tests was calculated. Among patients with biochemical evidence of PHPT, the proportion of patients who underwent parathyroidectomy was calculated. Multivariable logistic regression was used to identify factors associated with an evaluation for PHPT and, separately, with parathyroidectomy. Of 7,675 patients with chronic hypercalcemia, 3,323 (43.3%) had a PTH test obtained within 6 months. An age between 40-49 vs. <30 years [(odds ratio (OR) =3.2; 95% confidence interval (CI): 1.8-5.6; P<0.001], a serum calcium level between 11.6-12.0 vs. <11.0 mg/dL (OR =3.9; 95% CI: 3.2-4.7; P<0.001), and osteoporosis (OR =3.1; 95% CI: 2.7-3.5; P<0.001) were associated with an evaluation for PHPT. Among those with PTH levels, 1,327 (39.9%) had PHPT but only 916 (69.0%) were recognized. Three hundred and forty-five (26.0%) patients with PHPT underwent parathyroidectomy. An increasing number of surgical indications was associated with parathyroidectomy (P<0.001), though overall rates remained less than 40%. Among indications for surgery, including age and serum total calcium level, only osteoporosis was associated with parathyroidectomy (OR =2.0; 95% CI: 1.4-2.8; P<0.001). In this study, more than half of patients with chronic hypercalcemia were not evaluated for PHPT. Among patients with biochemical evidence of PHPT, one-third were unrecognized and only one-in-four received curative treatment. Opportunities to improve the management of PHPT exist within our large integrated health system.

Secondary hyperparathyroidism: Update

Secondary hyperparathyroidism is a clinical condition characterized by an increase in the synthesis and secretion of parathyroid hormone (PTH). Its presentation will be conditioned by the development of stimuli such as hyperphosphatemia, hypocalcemia, vitamin D deficiency, and PTH resistance. The most common cause of secondary hyperparathyroidism is chronic kidney disease, a pathological condition in which all the afore mentioned stimuli converge. Secondary hyperparathyroidism is evidenced by an increase in the size of the parathyroid glands, favored by cellular hyperplasia and hypertrophy. At the bone level, there will be an increase in the quantity and activity of osteoblasts and osteoclasts, leading to bone with unusual structural characteristics. Symptoms related to the disease include itching, bone pain, concentration alteration, and depression. In the long term, patients have a higher risk of cardiovascular mortality. Therapeutic options include calcimimetics, phosphate binders, vitamin D supplements, and surgery.

Serum parathormone, vitamin D and cardiovascular risk factors and markers: A pilot study

Background and aimsVitamin D deficiency is a common cause of secondary hyperparathyroidism, particularly in elderly people. The aim of this study was to evaluate the associations of serum vitamin D and parathormone (PTH) concentrations with blood pressure values and hypertension-mediated target organ damage (HMOD), including left ventricular (LV) hypertrophy and carotid plaque (CP). Methods and resultsWe enrolled consecutive patients admitted to the Hypertension Center of Federico II University Hospital in Naples, Italy. All patients underwent carotid doppler ultrasound and echocardiography, measurement of vitamin D and PTH levels and main clinical and laboratory parameters. A total of 126 patients (mean age 54 years, 68% males) were enrolled. Pearson's correlation analysis indicated that PTH levels directly correlated with age, diabetes, dyslipidemia, hypertension, fasting glucose, and LV mass, and inversely with glomerular filtration rate, LDL cholesterol, and vitamin D. Vitamin D levels correlated inversely with PTH, diabetes and CP. Multivariate regression models indicated that an increased LV mass was associated with the presence of obesity (β = 0.342; P = 0.001). Maximal intima-media thickness was significantly associated with older age (β = 0.303; P = 0.033). Combined presence of low vitamin D/high PTH levels were associated with more than 4-fold increased risk of having CP in both univariate (OR = 4.77, p = 0.0001) and multivariate regression analysis (OR = 4.52, p = 0.014). ConclusionIn a population at high cardiovascular risk, vitamin D and PTH levels were not directly associated with blood pressure values and HMOD. Secondary hyperparathyroidism due to vitamin D deficiency is associated with carotid atherosclerosis independently of other common cardiovascular risk factors.

THU474 Primary Hyperaldosteronism As A Cause Of PTH Elevation After Parathyroid Surgery

Abstract Disclosure: W. Thi: None. A. Rao: None. Background: Primary hyperaldosteronism can cause hypercalciuria, parathyroid hormone (PTH) elevation due to secondary hyperparathyroidism, and reduce bone mineral density. Screening for primary hyperaldosteronism can be done with serum aldosterone-renin ratio (ARR). We report a case of recurrent hyperparathyroidism after parathyroid surgery. Workup identified primary hyperaldosteronism as the cause of recurrent hyperparathyroidism. Treatment with spironolactone normalized PTH levels. Case Presentation: A 59-year-old African-American female in the Columbia VA Health Care System presented with hypertension, hypokalemia, bone density loss, and elevated PTH with normal calcium, one year after resection of a right inferior parathyroid adenoma to treat primary hyperparathyroidism. The patient had uncontrolled hypertension with hypokalemia while on losartan and amlodipine. Serum calcium was 9.4mg/dl(8.4-10.2mg/dl), PTH 89.4 pg/ml(29.2-79.9pg/ml), albumin 3.8g/dl(3.5-5G/dl), vitamin D 34 ng/ml(&amp;gt;28.9ng/ml), aldosterone 9ng/dl(&amp;lt;/=28ng/dl), plasma renin activity 0.28ng/ml/h(0.25-5.82ng/ml/h), ARR 32. Treatment of the patient with potassium supplements corrected the hypokalemia to 3.7mmol/L (5-5.1mm/l), and ARR was 94 with aldosterone 17 ng/dl and PRA 0.18 ng/ml/h and 24-hour urine calcium 304mg/24h(35-250mg/24h). Based on the laboratory values, and the absence of adrenal nodules during a CT scan, a diagnosis of primary hyperaldosteronism due to idiopathic hyperplasia of the adrenal was made. Spironolactone was started and PTH levels dropped down to 64.8pg/ml and serum calcium remained normal 5 months after treatment was initiated. Discussion: Primary Hyperaldosteronism causes extravascular fluid volume expansion with a reduction in proximal tubular sodium and calcium reabsorption. Increased calcium and sodium delivery to distal segments of the nephron leads to sodium reabsorption by mineralocorticoids without reabsorbing calcium, resulting in hypocalcemia with concomitant secondary hyperparathyroidism. Bone loss results from direct mineralocorticoid receptor-mediated effects of aldosterone on osteoblasts and osteoclasts and indirectly from high PTH levels to promote bone resorption. Treatment of primary hyperaldosteronism can reverse bone loss and reduce fracture risk rate within 18-36 months. This case suggests that primary hyperaldosteronism be considered a cause of secondary hyperparathyroidism and successfully treated with mineralocorticoid receptor antagonists. Presentation: Thursday, June 15, 2023

SAT216 Multiple Reasons Of Secondary Hyperthyroidism And Unexpected Results

Abstract Disclosure: I. Dzherieva: None. N. Volkova: None. S. Brovkina: None. I. Reshetnikov: None. L. Gritsenko: None. T. Mamedova: None. U. Ismailov: None. Background: Revealing the cause of secondary hyperparathyroidism might be a difficult problem especially if a patient has a few diseases to lead to this condition. Clinical Case: A 52-year-old-man was referred to our service for revealing the cause of weakness which started after COVID 19. When the patient was treated by rivaroxaban there was an unusual feature such as a hemoptysis, so the medicine was canceled. In medical history only the Achilles tendovaginitis was performed. The patient plays football twice a weak regularly, does not smoke, does not use drags. The physical examination showed nothing special. An arterial blood pleasure was 120/80 mm Hg, Body Mass Index was 25,4 kg/m2. Laboratory workup showed high erythrocyte sedimentation rate (ESR)(33mm/hr), leukocytosis (11000mm3) and a normocytic anemia(Hb 115 g/l),hematuria (16650 RBCsper hpf). Creatinine was 163µmol/L, glomerular filtration rate (GFR) was 43 ml/min/1.73m 2 , total serum calcium corrected for the patient's albumin concentration was 2.47 mM/L (2.15-2.50 mM/L), parathyroid hormone (PTH-intact) was 130 pg/mL (10-65 pg/mL),the level of 25-hydroxyvitamin D was 14.4 ng/mL(30.0-100.0 ng/mL). Chest radiograph findings were as follows: bilateral irregular, nodular, and patchy opacities. After vitamin D deficiency correction level of PTH-intact became normal (65 ng/mL). Serological tests : antinuclear antibody [ANA] and double-stranded DNA [dsDNA], ANCA were performed. Antineutrophil cytoplasmic antibody (ANCA) test result revealed perinuclear ANCA related to myeloperoxidase with the level more than 80 IgG. According to this finding Microscopic polyangiitis was diagnosed. Conclusion: This case has shown that sometimes there are two reasons for development of secondary hyperthyroidism and only successive actions help to choose right way for diagnosis. Presentation: Saturday, June 17, 2023

Normocalcemic Primary Hyperparathyroidism. A Case Report and Literature Review

Normocalcemic primary hyperparathyroidism (PHP) has been proposed to be a new phenotype of the disease. It is characterized by persistently high levels of parathyroid hormone (PTH) and normal calcium levels. Since there are no known causes of secondary hyperparathyroidism or PTH elevation, the exact biological mechanism is not known. It could be the first stage of the disease or a unique situation marked by resistance of the kidneys and bones to the effects of PTH. This is a disease that is getting more and more common. It is often found when evaluating perimenopausal women with low bone mass or when evaluating or following up on patients with osteoporosis. Normocalcemic PHP has a diverse and varied phenotype that ranges from cases with no usual PHP symptoms to cases with symptoms and specific complications. The method to diagnosing secondary hyperparathyroidism should focus on ruling out all possible causes, especially vitamin D deficiency (25-OH vitamin D levels less than 30ng/mL) and kidney function impairment (glomerular filtration rate less than 60 mL/min, as measured by CKD- EPI). Not much is known about its past in the wild. Some people get hypercalcemia, but more than 75% of them don't. There don't seem to be any ways to predict who will get hypercalcemia, so measuring total and adjusted calcium levels once a year is recommended. Even though measuring ionic calcium is a part of what it means to have Normocalcemic PHP and is recommended by some writers during follow-up, there are a number of real problems with it that should be kept in mind.

The Eucalcemic Patient With Elevated Parathyroid Hormone Levels.

Primary hyperparathyroidism (PHPT) is classically characterized by hypercalcemia with elevated or inappropriately normal parathyroid hormone (PTH) levels. Elevated PTH levels in the presence of normal calcium levels are not infrequently found during the evaluation of metabolic bone disorders or kidney stone disease. This can be caused by secondary hyperparathyroidism (SHPT) or normocalcemic primary hyperparathyroidism (NPHPT). NPHPT is due to autonomous parathyroid function whereas SHPT is caused by a physiologic stimulation to PTH secretion. Many medical conditions and medications can contribute to SHPT, and differentiation between SHPT and NPHPT may be difficult. Cases are presented to illustrate examples. In this paper, we review the distinction between SHPT and NPHPT as well as end organ effects of NPHPT and outcomes of surgery in NPHPT. We suggest that the diagnosis of NPHPT be made only after careful exclusion of causes of SHPT and consideration of medications that can increase PTH secretion. Further, we advise a conservative approach to surgery in NPHPT.

Vitamin D Deficiency Reduces Postthyroidectomy Protracted Hypoparathyroidism Risk. Is Gland Preconditioning Possible?

Hypoparathyroidism is the most frequent complication after total thyroidectomy (PT-hypoPTH). After 1 year, most patients recover parathyroid function; however, the implicated physiologic dynamics remain unknown. Vitamin D deficiency (VDD) is the main cause of secondary hyperparathyroidism. Whether this compensatory hyperparathyroidism could influence parathyroid function recovery (PFR) in the setting of PT-hypoPTH has not been studied. This work aimed to evaluate the effect of preoperative VDD on PFR. A retrospective study was conducted with a prospectively maintained database including patients undergoing a total thyroidectomy between May 2014 and June 2019. Preoperative vitamin D (25(OH)D) less than 20 mg/mL was defined as VDD. Intact PTH less than 14 pg/mL on postoperative day 1 was defined as PT-hypoPTH. Transient PT-hypoPTH displayed PFR within the first year (early recovery: < 30 days; protracted recovery: > 30 days) whereas definite PT-hypoPTH did not. Survival analysis evaluated the effect of preoperative VDD on PFR, and a binary logistic regression model identified associated factors. A total of 397 patients were identified. The observed rates of transient, protracted, and definite PT-hypoPTH were 32.9%, 15.1%, and 5.2%, respectively. Rates of VDD were higher in the early-recovery PT-hypoPTH group (55.2% vs 31.5%; P = .01). Preoperative VDD was associated with faster PFR (19 vs 35 days; P = .03) and behaved as a protective factor for protracted PT-hypoPTH (odds ratio 0.47; 95% CI, 0.25-0.881; P = .016) in the multivariable analysis. Preoperative VDD could act as a preconditioning factor of the parathyroid glands prior to the surgical aggression exerted against them during surgery aiding PFR. Basic research studies and prospective clinical trials are needed to explain the underlying physiological mechanisms and to provide further evidence to improve clinical management.

The Role of Scintigraphy and Hybrid Single-Photon Emission Tomography in Comparison with Laboratory Data in a Comprehensive Examination of Patients with Secondary Hyperparathyroidism

Objective:to estimate the possibilities and determine the diagnostic value of scintigraphy and single-photon emission computed tomography combined with computed tomography (SPECT/CT) in the assessment of the functional state of parathyroids in comparison with laboratory data in patients with secondary hyperparathyroidism (SHPT). Material and methods.The study consistently included 64 patients with the established diagnosis of SHPT due to the acquired vitamin D deficiency or with terminal chronic kidney disease (CKD), with the presence of ultrasound data and laboratory tests of calcium-phosphoric exchange indicators. Neck and mediastum nuclear study with 99mTc-methoxy-isobutyl-isonitrile (MIBI) was performed in the planar two-phase scintigraphy mode according to the standard protocol with an estimation of parathyroid visualization intensity, as well as in SPECT/CT performed 1 hour after MIBI injection. Results. In the group of patients with CKD as a cause of SHPT (n = 14), the most pronounced increase of parathyroid hormone (PTH) level (210.8 ± 103.0 vs. 107.0 ± 40.2 pg/ml in patients with vitamin D deficiency (n = 50, p &lt; 0.001)) and phosphorus (mean 1.39 ± 0.51 mmol/l), as well as excess of normal levels of alkaline phosphatase (407.7 ± 338.1 units/l) were noted. In patients with vitamin D deficiency, impaired parathyroids according to SPECT/CT data was visualized in 8 % of cases, and in patients with CKD in 14.3 %. No significant differences in the mean levels of vitamin D in patients with (n = 46) and without (n = 4) modified parathyroids according to scintigraphy were detected: 26.06 ± 13.19 vs. 25.82 ± 18.80 ng/ml, respectively (p = 0.97). Differences in PTH and calcium levels were not observed: 91.3 ± 39.2 vs. 89.2 ± 29.5 pg/ml (p = 0.90), 2.53 ± 0.21 vs. 2.58 ± 0,15 mmol/l (p = 0.64), respectively. Conclusion.The neck SPECT/CT is a key method of topical imaging of impaired parathyroids in preoperative preparation of patients with SHPT caused by CKD. The method may have a diagnostic value in treatment-resistant patients with vitamin D deficiency and upper-normal PTH and calcium levels in terms of detection of the nodular form of parathyroid hyperplasia. The implementation of SPECT/CT after 1 hour after MIBI injection increases the sensitivity of the study.

Occult Renal Calcifications in Patients with Normocalcemic Primary Hyperparathyroidism and Their Association with the Parathyroid Hormone-Vitamin D Axis.

Normocalcemic primary hyperparathyroidism (NPHPT) is characterized by elevated serum levels of parathyroid hormone (PTH) with persistently normal serum calcium concentrations after excluding secondary causes of hyperparathyroidism. Urolithiasis and/or nephrocalcinosis may occur in hypercalcemic PHPT, but little is known about these complications in NPHPT. Objectives. To identify occult urolithiasis and nephrocalcinosis in asymptomatic patients with NPHPT and evaluate biochemical markers as risk predictors for the development of renal calcification (RC). Methods. Cross-sectional analysis of 34 patients with no history of urolithiasis and/or nephrocalcinosis. The diagnosis of NPHPT was as follows: elevated serum PTH (reference range: 15–65 pg/mL), normal albumin-corrected serum calcium, normal urinary calcium excretion, serum 25(OH)D >30 ng/mL, eGFR (CKD-EPI) > 60 mL/min/1.73 m2, without intestinal disease, and not on medications such as thiazide diuretics, lithium, bisphosphonates, or denosumab. Patients were categorized according to the presence or absence of RC identified by renal imaging. Their clinical and biochemical characteristics were then compared. Results. The patients had a mean age of 67.97 ± 10.45 years, predominantly postmenopausal women (88.2%); serum PTH, 119.67 ± 64.44 pg/mL; 25(OH)D, 39.00 ± 8.88 ng/dL; 1.25(OH))2D, 74.53 ± 26.37 pg/mL; corrected serum calcium, 9.34 ± 0.62 mg/dL; and 24-hour urinary calcium, 134.87 ± 79.68 mg/day. RC was identified in 26.5% of the patients. There was no difference in anthropometric and clinical parameters, renal function, 25(OH)D, and urinary pH in patients with or without RC. Patients with RC had higher PTH values (176.22 vs. 99.32 pg/mL, P = 0.001), 1.25(OH) 2D (96.83 vs. 62.36 pg/mL, P = 0.005), and 24-hour urinary calcium (181.9 vs. 117.94 mg/day, P = 0.037). Conclusion. Occult renal calcifications are common in NPHPT and are associated with increased serum PTH, 1.25(OH))2D, and 24 h urinary calcium.

Parathyroid Surgery Outcome at King Salman Armed Forces Hospital

Introduction: The aim of this study is to review the surgical outcome of parathyroidectomy at one institution over nine years in form of methods of diagnosis, type of surgery, postoperative complications and histopathology findings. Methods: This is a retrospective study from a single institution (King Salman North West Armed Forced Hospital (KSAFH), Tabuk, Saudi Arabia). All cases underwent parathyroidectomy from 1/1/2010 until 31/12/2018 were retrieved from the archives of the department of surgery. Data were extracted from the patients’ charts. They included demographical data, presence of comorbidities, laboratory and radiological investigations, type of surgery, postoperative complications and histopathology findings. Inclusion criteria include patients older than 13 years old. Exclusion criteria include patients younger than 13 years old, hyperparathyroidism cured with medication, patients unwilling to give informed consent and patients with serious underlying medical conditions that restrict diagnostic testing or therapy such as congestive cardiac failure. Results: A total of 30 patients underwent parathyroidectomy at KSAFH. 20 out of 30 patients were female (66.7%). The mean age was 35 - 45 years old. Diabetes mellitus was found in 5 patients (16.7%), while hypertension was seen in 10 patients (33.3%). 6 patients (20%) had end stage renal disease (ESRD). The data showed 24 patients with primary hyperparathyroidism (80%), 5 patients with secondary hyperparathyroisim (16.7%) and one patient with tertiary hyperparathyroidism (3.3%). Our study demonstrated that 23 patients underwent partial parathyroidectomy (76.6%), while 7 patients underwent total parathyroidectomy (23.3%). According to the method used for diagnosis of hyperparathyroidism, blood tests were used in 27 patients (90%), Sestamibi parathyroid scan in 26 patients (86.6%), ultrasound scanning in 28 patients (93.3%) and bone scan in 9 patients (30%). Sensitivity of Sestamibi scan in primary hyperparathyroidism (91.7%) and (66%) for secondary hyperparathyroidism. Mean operative time was 79 minutes. Mean hospital stay was 4 days. Postoperative ccomplications included hypocalcemia in 9 patients (30%), wound infection was (0%), hematoma formation in 2 patients (6.67%), seroma formation in 1 patient (3.33%), vascular injury (0%) and recurrence rate in 2 patients (6.67%). Histopathology findings included parathyroid adenoma in 22 patients (73.3%), parathyroid hyperplasia in 6 patients (20%) and parathyroid carcinoma in 2 patients (6.7%). Rate of cure was 93.3%. Conclusions: Hyper-parathyroidism is more common in female patients than male patients. High sensitivity for sestamibi scan in primary hyperparathyroidism. ESRD is the most common cause of secondary hyperparathyroidism. Most common complication is hypocalcemia. High rate of cure following parathyroid surgery.

Bone and primary hyperparathyroidism.

Primary hyperparathyroidism (PHPT) is a disease caused by excessive and inappropriate secretion of parathyroid hormone resulting in hypercalcemia. It is usually diagnosed incidentally in case of hypercalcemia, osteoporosis or, more rarely, renal involvement such as lithiasis. The clinical presentation reflects hypercalcemia and involves several organs, mainly the cardiovascular system, bone, and kidneys. However, most patients with PHPT are asymptomatic. The diagnosis is biological, obvious when serum calcium and parathyroid hormone levels are high, but difficult when one of these two values is normal. The diagnosis of normocalcemic PHPT is possible only after ruling out all causes of secondary hyperparathyroidism. Parathyroid imaging does not contribute to the positive diagnosis but guides surgery and rules out an associated thyroid abnormality. Parathyroid surgery is the gold standard treatment. Parathyroid surgery is indicated in the presence or risk of complications, and it is the only treatment that prevents fractures. Pharmaceutical treatments have only limited effects on complications and are limited to cases where surgery is contraindicated. After parathyroid surgery, the use of bisphosphonates must be avoided as they seem to interfere with the parathyroidectomy's fracture-preventing effects. In the absence of surgical indication, medical monitoring of patients includes assessment of laboratory values, bone density, and renal function.

Brown Tumor Causing Thoracic Compressive Myelopathy

Brown tumors are nonneoplastic bony lesions resulting from primary, secondary or tertiary hyperparathyroidism. Primary hyperparathyroidism is caused by parathyroid adenomas or parathyroid hyperplasia while chronic renal failure is a common cause of secondary hyperparathyroidism. Elevated parathyroid hormone levels cause increased osteoclastic activity, bone resorption and reactive fibroblastic proliferation leading to the formation of Brown tumor. Although Brown tumors are more commonly seen in the maxilla and mandible, it can occur in the long, flat bones or any bone. It is less commonly seen in the spine. In this report, we discuss the presentation, management, difficulties with histopathological diagnosis, and follow-up of a Brown tumor in a 55-year-old gentleman undergoing renal dialysis who presented with thoracic compressive myelopathy. Our patient underwent a T4 laminectomy, tumor debulking, and T2–T6 instrumented posterior fusion. Based on histopathological examination of the tissue specimen and raised serum parathyroid hormone levels, we arrived at a diagnosis of Brown tumor. Our review of the literature revealed 62 cases of vertebral Brown tumor resulting in neurologic symptoms. The lesion was more common in females (58%), those aged between 40 and 49 years (26%), and in the thoracic spine (51.6%). Early surgical intervention and management of the underlying cause of hyperparathyroidism lead to sustained symptomatic improvement. Brown tumor should be considered in the differential diagnosis of expansile vertebral lesions in the presence of hyperparathyroidism or chronic kidney disease. Treatment of the underlying hyperparathyroidism and decompression of the neural structures with or without stabilization is recommended.

Appropriate Cutoff for 25OHD Levels in the Diagnosis of Normocalcemic Primary Hyperparathyroidism (NPHPT): A Systematic Review

Introduction: The Fourth International Workshop in 2014 delineated guidelines for the diagnosis of NPHPT which include ruling out secondary causes of hyperparathyroidism, and recommended cutoffs for 25 vitamin D (25OHD) to be ≥20ng/mL. Keeping in mind that the exact levels to optimize 25OHD in hyperparathyroid states are unknown, we aim to review possible variation in the prevalence of NPHPT if 25OHD cutoffs were to be raised to rule out vitamin D deficiency with more specificity. Methods: A PubMed search was conducted with key words “normocalcemic primary hyperparathyroidism” to review studies about NPHPT and 25OHD status. 533 articles were found, and 127 articles were identified by title/abstract screening with year of publication between 2014 to 2020. Ten studies were identified for the systematic review based on full text review for relevance. Results: Studies have been conducted in various countries across all continents to characterize NPHPT further. 5/10 studies used 25OHD cutoff of ≥20ng/mL and 4 studies had a cutoff of ≥30ng/mL and 1 study looked into the difference in prevalence with both cutoffs. All 3 studies from Italy used the higher cutoff. Rosario et al from Brazil reported a decrease in prevalence of NPHPT from 6.8% (25OHD≥20ng/mL) to 0.74% by supplementing those subjects to 25OHD ≥30ng/mL without any increase in serum calcium or parathyroid hormone (PTH) levels.1 Wang et al found that when total 25OHD levels were kept between 30–40 ng/mL, free 25OHD levels were actually lower compared to normal subjects.2 Conclusion: The levels of 25OHD that would define deficiency in NPHPT remain undetermined and both >20 ng/mL and >30ng/mL have been studied as cutoffs. It is well known that vitamin D insufficiency (25D 20-30ng/mL) drives up PTH and supplementation to 30-40ng/mL is required to reduce such effects. Wang et al suggest that free 25OHD levels correlate better with PTH as compared to total 25OHD and maybe a more reliable marker of 25OHD status. We suggest that a diagnostic criterion of ≥30ng/mL would be more appropriate in ruling out 25OHD deficiency in this special population. The role of free 25OHD levels in PHPT needs further evaluation.

How should normocalcemic primary hyperparathyroidism be managed? Comparison with classical hypercalcemic form

Aim: Normocalcemic primary hyperparathyroidism (N-PHPT) is a different variant of primary hyperparathyroidism characterized by normal serum calcium (Ca) concentrations and elevated parathormone (PTH) levels in the absence of secondary causes of hyperparathyroidism. However, the clinical course and therapeutic approaches of this entity have been not fully demonstrated. We aimed to determine the clinicopathological characteristics and surgical outcomes of patients with N-PHPT, comparing with patients who had hypercalcemic PHPT (H-PHPT). Materials and Methods: A total of 185 patients who underwent parathyroidectomy for PHPT were included in the study. The patients were classified as N-PHPT and H-PHPT. The two groups were then compared between each other in terms of all demographic, clinical, and surgical features. Results: One hundred and fifty-one (81.6%) patients had a diagnosis of H-PHPT while 34 (18.4%) patients were normocalcemic. Both groups were similar in age, preoperative vitamin D level, preoperative PTH level, and type of surgery (p > 0.05). Preoperative Ca level was significantly different between the groups (p 0.05). Conclusion: N-PHPT patients had similar demographic and clinical features in comparison to those with H-PHPT, indicating that the surgical decision in patients with N-PHPT should be similar with H-PHPT cases.

Oral changes in secondary to chronic kidney disease hyperparathyroidism

The most common cause of secondary hyperparathyroidism is a chronic kidney disease. The imbalance between calcium, phosphorus and vitamin D3 in the course of secondary hyperparathyroidism may affect an oral health. The changes are presented in jaw bones as a loss of bone density, focuses of demineralization or even large tumors deforming facial region – brown tumors, ossifying fibromas and aneurismal bone cysts. There is also a higher frequency of dental caries, periodontal disease and fungal infections. Secondary hyperparathyroidism in the young age may cause teeth development disorders and dental abnormalities. Dental treatment in patient with secondary hyperparathyroidism can be a challenge for a dentist, so the strict cooperation with an attending physician is needed, as well as to introduce dental prophylactic procedures as soon as possible. In addition, due to the occurrence of characteristic changes in the oral cavity, the dentist may play an important role in the primary detection of secondary hyperparathyroidism.

Parathormone, bone alkaline phosphatase and 25-hydroxyvitamin D status in a large cohort of 1200 children and teenagers

ABSTRACT Objectives: 25-Hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH) and bone alkaline phosphatase (BALP) are biomarkers of calcium/phosphate metabolism and bone turnover. Although vitamin D deficiency is a well-known cause of secondary hyperparathyroidism, few studies have considered vitamin D status when establishing reference ranges. In this study, we report PTH levels according to the vitamin D status and BALP levels in a large cohort of 1200 children. Additionally, we provide PTH pediatric reference values according to 25(OH)D status as well as BALP pediatric reference ranges. Methods: Serum samples from 1200 children (equally distributed from 5 months to 20 years old) who underwent blood sampling for allergy exploration were used to quantify 25(OH)D, PTH and BALP. Results: The percentage of vitamin D deficient children (<20 ng/ml) progressively increased during childhood starting from 7% in the 0 to 2 year-old subgroup to a mean of at least 50% among teenagers. PTH levels inversely mirrored 25(OH)D concentrations for all age and gender subgroups, and 25(OH)D deficient subgroups presented higher PTH levels than their non-deficient counterparts. In the non-deficient 25(OH)D population, PTH levels were the highest at 11 years old for girls and 14 years old for boys. BALP results were slightly increased during childhood and showed a constant decrease during teenage years starting from 12 years old for girls and 14 years old for boys. Conclusion: Our results highlight the inverse relationship between PTH and 25(OH)D in children and the need for a well characterized 25(OH)D population to establish pediatric reference ranges for PTH.

MON-339 Secondary Hyperparathyroidism Due to Decrease 1 Alpha Hydroxylase Activity

•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 <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

Normocalcemic Hyperparathyroidism: Study of its Prevalence and Natural History.

ContextNormocalcemic hyperparathyroidism (NPHPT) is characterized by persistently normal calcium levels and elevated parathyroid hormone (PTH) values, after excluding other causes of secondary hyperparathyroidism. The prevalence of the disease varies greatly and the data on the natural history of this disease are sparse and inconclusive.ObjectivesThe objectives of this study are to describe the prevalence of NPHPT and its natural history in a referral population and to compare the variability of serum calcium with a group of patients with primary hyperparathyroidism (PHPT).DesignA retrospective study was conducted over 5 years.SettingThe setting for this study was a metabolic bone referral center.PatientsA total of 6280 patients were referred for a bone mineral density measurement (BMD).Main Outcome MeasuresThe prevalence and natural history of NPHPT and variability of calcium were the main outcome measures.ResultsWe identified NPHPT patients using data from the day of the BMD measurement. We excluded patients with low estimated glomerular filtration rate (eGFR) or vitamin D, or with no measurements available. Based on the evaluation of their medical files, we identified 11 patients with NPHPT (prevalence 0.18%). Only 4 patients had consistent normocalcemia throughout their follow-up, with only 2 also having consistently high PTH. None had consistently normal eGFR or vitamin D.Intermittent hypercalcemia was present in 7 of the 11 NPHPT patients. The mean adjusted calcium was found to be significantly lower in the NPHPT group compared with the PHPT group but higher than the control group. PTH was similar for NPHPT and PHPT. These 2 groups had similar variability in serum calcium.ConclusionsNPHPT patients often have episodes of hypercalcemia. We believe that NPHPT is a mild form of PHPT.