Elevated Serum Parathyroid Hormone Research Articles

Reference values of parathyroid hormone in very low birth weight infants.

The primary goal was to estimate reference values of parathyroid hormone (PTH) in very low birth weight infants without severe neonatal morbidity. A secondary objective was to assess the relationship between PTH serum levels and selected laboratory markers of bone metabolism. Ninety two infants with birth weight less than 1500g met the inclusion criteria of the study. Serum levels of PTH, 25-hydroxyvitamin-D [25(OH)D], C3-epi-25(OH)D, total calcium, phosphorus, and alkaline phosphatase, and urinary levels of calcium, phosphorus, and creatinine were examined on day 14 and subsequently every 2weeks until discharge. Of the total 167 serum samples examined for PTH levels in infants without 25(OH)D deficiency the estimated range was 0.9-11.9 pmol/l (8.5-112.3 pg/mL). During the first month, no statistically significant correlation was observed between PTH level and that of 25(OH)D, C3-epimers of 25(OH)D, S-Ca, S-P, or ALP, nor with urinary excretion of calcium and phosphorus. From the second month of life, there was a moderately significant correlation between PTH and 25(OH)D (Rho = -0.40, P =< .001), between PTH and calcium/creatinine ratio (Rho = -0.56, P = < .001), and between PTH and phosphorus/creatinine ratio (Rho = 0.51, P = < .001). The physiological range for PTH levels for preterm neonates without 25(OH)D deficiency was estimated as 0.9-11.9 pmol/l (8.5-112.3 pg/mL). It seems that elevation of serum PTH above this range can be considered as hyperparathyroidism in very low birth weight infants.

Abstract LB153: Spatial transcriptomics of mouse parathyroid gland cells expressing an activating variant of gcm2

Abstract Tumors of one or multiple parathyroid glands and elevated serum calcium and parathyroid hormone (PTH) are the common characteristics of primary hyperparathyroidism (PHPT). Genes associated with familial PHPT (hereditary parathyroid tumors) include - MEN1, CDKN1B, CDC73, RET, MAX and GCM2. The glial cells missing 2 (GCM2) gene functions as a transcription factor that is essential for parathyroid gland development. Heterozygous germline missense variants located within the C-terminal conserved inhibitory domain (CCID) of GCM2 have been reported in a subset of patients with familial PHPT. In functional assays, these missense variants enhance the transcriptional activity of GCM2, suggesting that GCM2 could act as a proto-oncogene in parathyroid neoplasia. A recurrent germline activating missense variant of GCM2, p.Y394S in patients with familial PHPT has been reported in various publications. To study the direct contribution of this missense variant in parathyroid neoplasia, we used the CRISPR/Cas9 system to generate a heterozygous germline knock-in of p.Y392S in the mouse Gcm2 gene (which corresponds to the human variant p.Y394S in GCM2). In GCM2-binding site mediated luciferase reporter assays, the mouse Gcm2 variant p.Y392S also exhibited the transcription enhancing effect that was observed for the human GCM2 p.Y394S variant. However, mice with this variant (Gcm2 +/Y392S) did not show obvious parathyroid tumors. Because the mouse Gcm2 variant p.Y392S exhibited enhanced transcriptional activity, we performed spatial transcriptomics of parathyroid glands from wildtype (WT) and Gcm2 +/Y392S mice to examine differentially expressed transcripts in parathyroid cells with the p.Y392S variant of Gcm2. Using the 10X Genomics Visium platform, spatially resolved RNA-seq analysis was performed on parathyroid gland cells of WT and Gcm2 +/Y392S mice specifically marked by the expression of Pth and Gcm2. Spatial transcriptomics and Pathway analysis was performed to evaluate transcripts with more than 2-fold increased expression in parathyroid cells from the p.Y392S variant of Gcm2 compared to WT. Further investigation of these genes and pathways in mouse and human parathyroid cells can provide insights into the functional consequences of GCM2 activating variants and the pathophysiology of parathyroid tumorigenesis. Citation Format: Priyanka Bolel, Jeremie O. Pina, Fabio R. Faucz, Lee S. Weinstein, Sunita K. Agarwal. Spatial transcriptomics of mouse parathyroid gland cells expressing an activating variant of gcm2 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(7_Suppl):Abstract nr LB153.

Neonatal Severe Hyperparathyroidism: A Case Report

Background: Neonatal severe hyperparathyroidism is an extremely rare condition that presents in the first few months of life. Recognition at the early stage followed by prompt surgical intervention are of vital importance for survival. Hypotonia, respiratory distress, lethargy and delay in growth and development occur in association with the elevated serum parathormone levels and hypercalcemia. Definitive therapy involves total parathyroidectomy. Case Description: We are presenting a case with Neonatal severe hyperparathyroidism, who underwent total parathyroidectomy. The patient had been followed up with medical therapy until. Parathormone levels rapidly declined following total parathyroidectomy and the patient was discharged with full recovery. Literature Review: Sestamibi scintigraphy might fail to show an ectopic parathyroid gland. In such conditions, on table confirmation of parathyroid glands by frozen section and Intraoperative parathormone monitoring is vital at this point. Persistently elevated parathormone levels might suggest a remnant parathyroid tissue at the surgical site or an ectopic parathyroid gland that should be excised. Clinical Relavance: Neonatal severe hyperparathyroidism is a life-threatening disease. In the present case surgery performed at the early is life-saving due to the failure of medical therapy to control the disease.

Renal Dysfunction in Primary Hyperparathyroidism is associated with nephrolithiasis, elevated serum calcium-phosphate product and parathormone levels.

Baseline renal dysfunction predicts mortality in primary hyperparathyroidism (PHPT). However, it remains controversial whether renal insufficiency in PHPT is due to disease severity alone or other risk factors. This study aimed to explore the association of clinico-biochemical variables with renal dysfunction [estimated glomerular filtration rate (eGFR) < 60 ml/min/m2] in PHPT. A total of 112 patients of PHPT were selected and divided into following subgroups: renal dysfunction (n = 28) and normal renal function (n = 84). Demographic characteristics, traditional risk factors, phenotypes of PHPT based on target organ involvement, and biochemical parameters were compared between these subgroups. Patient subgroups of PHPT with and without renal dysfunction had similar age, frequency of diabetes, and hypertension. Renal dysfunction was more prevalent in males (p < 0.05). Compared to normal renal function subgroup, individuals with renal dysfunction had higher serum levels of calcium, phosphate, alkaline phosphatase, intact parathormone (all p < 0.05), while having lower hemoglobin levels (p < 0.05) and higher nephrolithiasis rates (p < 0.05). Multiple regression analysis revealed that nephrolithiasis, serum calcium-phosphorous product (CaxP), parathormone levels were positively associated with baseline renal dysfunction (all p < 0.01). A baseline PTH > 456 pg/mL and CaxP > 30.0 mg2/dl2 could discriminate renal dysfunction from normal renal function with sensitivity and specificity of 75% and 74.5% and 92.6% and 74.4%, respectively. Renal dysfunction was associated with presence of nephrolithiasis, elevated serum CaxP and PTH levels in our cohort with predominantly symptomatic PHPT, indicating an association with the underlying disease itself. Serum CaxP may additionally be appraised during risk assessment in PHPT.

C-Cell Hyperplasia and Cystic Papillary Thyroid Carcinoma in a Patient with Type 1B Pseudohypoparathyroidism and Hypercalcitoninaemia: Case Report and Review of the Literature.

Hypercalcitoninaemia has been described in patients with pseudohypoparathyroidism (PHP) type 1A and 1B. Elevated calcitonin levels are thought to result from impaired Gsα receptor signaling, leading to multiple hormone resistance. Evidence on the risk of medullary thyroid carcinoma (MTC) or C-cell hyperplasia in PHP patients with hypercalcitoninaemia is lacking. A 43-year-old Caucasian man was referred to our endocrinology clinic for chronic hypocalcemia associated with elevated serum parathormone levels and a single cystic thyroid nodule. The patient did not show skeletal deformities, and screening for concomitant hormone resistances was negative, except for the presence of elevated serum calcitonin levels. The workup led to a molecular diagnosis of sporadic PHP1B. Fine needle aspiration of the thyroid nodule was not diagnostic. The calcium stimulation test yielded an abnormal calcitonin response. Given the scarcity of data on the risk of thyroid malignancy in PHP and calcium stimulation test results, total thyroidectomy was performed. Histological examination revealed cystic papillary thyroid cancer in a background of diffuse C-cell hyperplasia. To our knowledge, we are the first to describe a rare form of thyroid cancer combined with C-cell hyperplasia in a patient with PHP and hypercalcitoninaemia. In the present case, a mere receptor resistance might not fully explain the elevated calcitonin levels, suggesting that hypercalcitoninaemia should be carefully evaluated in PHP patients, especially in the case of concomitant thyroid nodules. Further studies on larger cohorts are needed to elucidate this topic.

흉선에서 발생한 이소성 부갑상선 선종 1예

Primary hyperparathyroidism (PHPT) is a common endocrine disorder with elevated serum parathyroid hormone levels. In most cases, the disease involves a single parathyroid adenoma, followed by parathyroid hyperplasia. Parathyroid glands are rare, but can be present in a variety of locations because it migrates long distance during fetal period. Therefore, the incidence of ectopic parathyroid adenoma is rare and it is not easy to diagnose ectopic parathyroid adenomas and to specify the location before surgery. Recently, we diagnosed ectopic parathyroid adenoma at the thymus and treated successfully. So, we report this case with literature review.

A Novel Adult Case of Recurrent Acute Pancreatitis Caused by Hypercalcemia With Concurrent Manifestation of Posterior Reversible Encephalopathy Syndrome Revealing Undiagnosed Primary Hyperparathyroidism due to an Underlying Parathyroid Adenoma.

Hypercalcemia-induced posterior reversible encephalopathy syndrome (PRES) is a rare entity primarily associated with iatrogenic vitamin D/calcium overdose, malignancy, or, infrequently, primary hyperparathyroidism. We present a novel case of an adult male from rural India who experienced recurrent acute pancreatitis caused by hypercalcemia with concurrent manifestation of PRES. Diagnostic evaluation revealed markedly elevated serum calcium levels and parathyroid hormone concentrations, consistent with primary hyperparathyroidism. Imaging studies identified a parathyroid adenoma near the right thyroid lobe, subsequently surgically excised. This case underscores the importance of considering primary hyperparathyroidism as an underlying cause of PRES, especially in the absence of acute arterial hypertension or autonomic dysfunction. Early recognition and intervention are essential in mitigating the morbidity and mortality of PRES.

OR23-01 The Nonredundant Role Of Beta-Amyloid In Mediating Tonic PTH Secretion In Physiological And Pathological States

Abstract Disclosure: C. Tu: None. Z. Cheng: None. K.A. Pena: None. N. Szeto: None. J.A. Sosa: None. J. Vilardaga: None. J. Koh: None. W. Chang: None. Understanding the mechanisms driving parathyroid hormone (PTH) hypersecretion in primary hyperparathyroidism (PHPT) is essential for better management of this common endocrinopathy. Prior studies showed that reduced Ca2+-sensing receptor (CaSR) expression and the subsequent increases in heterodimerization of the CaSR with the type B γ-aminobutyric acid receptor 1 (GABAB1R) are causally linked to PTH hypersecretion in PHPT mouse models (Nat Metab 2:243-255). We further showed that expression of the putative GABAB1R ligands, amyloid precursor protein (APP) and its proteolytic product, β-amyloid (Aβ1-42), is significantly upregulated in adenomas of PHPT patients associated with vitamin D insufficiency/deficiency when compared to normal donor controls. The current study aims to delineate the actions of Aβ1-42 in promoting tonic PTH secretion and its interactions with vitamin D receptor (VDR) signaling in parathyroid glands (PTGs) in basal and PHPT states. We show that Aβ1-42 (200 nM) stimulated tonic PTH secretion in cultures of normal human PTGs without shifting the calcium/PTH secretion setpoint (Ca2+-setpoint). In contrast, conditional knockout (KO) of the App gene in the parathyroid cell (PTC) of PTCAppΔflox/Δflox mice significantly reduced serum PTH levels (KO: 64±13 pg/ml vs Control: 109±12 pg/ml; p&amp;lt;0.05, n=8) despite hypocalcemia, indicating hypoparathyroidism. In PTGs cultured from the PTCAppΔflox/Δflox mice, supplementation of Aβ1-42 dose-dependently (EC50=5.6 nM, p&amp;lt;0.001) increased PTH secretion without altering the Ca2+-setpoint. However, the stimulatory effects of Aβ1-42 on tonic PTH secretion were completely abrogated in the PTGs with concurrent deletions of App, Casr and Gabbr1 genes, supporting a direct action of Aβ1-42 on CaSR and/or GABAB1R. The latter notion is further supported by the ability of Aβ1-42 to stimulate cAMP production in cells co-expressing CaSR and GABAB1R. PTC-specific deletion of the Vdr gene in the PTCVdrΔflox/Δflox mice led to elevated serum PTH levels in vivo and increased tonic PTH secretion with unaffected Ca2+-setpoint in PTGs in vitro. Concurrent ablation of the App gene completely normalized serum PTH levels in the PTCVdrΔflox/Δflox mice and prevented PTH hypersecretion in their PTGs in culture. These findings support a critical role of the APP-derived Aβ1-42 in mediating tonic PTH secretion in the normal physiological state and suggest a new mechanism driving PTH hypersecretion in PHPT due to vitamin D deficiency. Presentation: Saturday, June 17, 2023

A case of right parathyroid adenoma and its management

A 33 year old female patient presented with history of body and joint pain with easy fatiguability unable to perform her routine daily activities since 2 months. She also gave history of recurrent urinary tract infections, pain abdomen, loss of appetite and loss of weight. Examination of neck showed no palpable mass. Laboratory data revealed elevated serum calcium levels and parathyroid hormone levels. Contrast enhanced computed tomography of neck showed well-defined soft tissue density lesion measuring 2.6×1.9×1.6 cm in the postero inferior aspect of right lobe of thyroid suggestive of right parathyroid adenoma. Parathyroid imaging (SPECT) 99mTc-MIBI showed focal increased tracer uptake in relation to inferior aspect of right lobe of thyroid gland. NCCT KUB showed bilateral non obstructive renal calculi with medullary nephrocalcinosis. Patient underwent surgical resection under general anesthesia and histopathology confirmed parathyroid adenoma. Following surgery, parathyroid hormone and calcium levels gradually returned to normal levels. Parathyroid adenoma shows excellent prognosis with complete surgical resection.

Natural Orifice Approach to Parathyroid Surgery: An Anesthesiologist’s Challenge

ABSTRACT Endocrine surgeries pose unique challenges to the anesthesiologists, so is the case in primary hyperparathyroidism due to hypercalcemia. A 29-year-old male, operated case of intertrochanteric femur neck fracture following trivial fall, had history of frequent muscle cramps and fatiguability post operatively and swelling in right side of front of neck. On investigating, his thyroid function tests were normal, elevated serum calcium, alkaline phosphatase and parathormone, and decreased phosphate. After ultrasound of neck and abdomen, the patient was diagnosed with primary hyperparathyroidism and posted for peroral endoscopic parathyroidectomy under general anesthesia. Induction was done with propofol and succinylcholine video-direct laryngoscopy-guided nasal intubation was done to avoid the pathological fracture of cervical spine; maintained on isoflurane, fentanyl and titrated doses of vecuronium; extubated smoothly and shifted to intensive care unit. Thorough perioperative monitoring of electrolytes including calcium was done. Adequate preoperative assessment, preparation, monitoring the signs and symptoms of hypo/hypercalcemia, and maintaining normocalcemia during perioperative period determines the success of anesthetic management.

Abstract #1404780: Implementing a Screening Protocol for Endocrinopathies in Patients with Secondary Hemochromatosis due to Sickle Cell Anemia

Sickle cell disease (SCD) is an autosomal recessive hemoglobinopathy characterized by hemolytic anemia, intermittent small vessel occlusion, and organ dysfunction. Red blood cell transfusions are a therapeutic mainstay in SCD, which can lead to iron overload and endocrine disease. However, due to diagnostic difficulties and lack of data, there is not a wide consensus in approach. This has led to many practitioners screening for endocrinopathies only once patients are symptomatic. In this study, we implemented a standardized protocol for screening of iron overload and certain endocrinopathies in a single-study cohort of patients with SCD to assess viability in real-world practice and to detect disease prior to significant burden. We studied 19 patients diagnosed with SCD or sickle-cell trait (SCT) at a single institution. Patients had serum testing for ferritin and a metabolic panel at usual clinical visits. Iron overload was diagnosed with serum ferritin levels of at least 1000 ng/mL. If iron overload was detected, additional testing for 25-Hydroxyvitamin D (OHD), Thyroid Stimulating Hormone (TSH), Parathyroid Hormone (PTH), and Insulin-Like Growth Factor-1 (IGF-1) was obtained. Nineteen patients (12 men and 7 women) were included with a mean age of 32 years old. Twelve patients and seven patients were diagnosed with SCD and SCT, respectively. The average ferritin levels of SCD and SCT patients were 4874 and 270 ng/mL, respectively. Nine patients had ferritin levels greater than 1000 ng/mL, eight of which were diagnosed with SCD, one was diagnosed with SCT, and seven of which were prescribed iron chelation therapy. Of these nine patients, the average random glucose was 103 ng/mL. The average serum calcium corrected for albumin levels was 9.3 ng/mL. Seven of eight patients were found to have low 25-OHD levels with two of four patients showing elevated serum PTH. One of six patients had abnormal thyroid testing, with an elevated TSH and normal free thyroxine. Three of five patients showed abnormal IGF-1 testing, with low IGF-1 levels and low IGF-1 binding protein levels. This study successfully implemented a protocol for screening for endocrinopathies in a cohort of SCD and SCT patients at a single institution. We showed evidence that many patients with iron overload demonstrated abnormalities in 25-OHD, PTH, TSH, and IGF-1. The few studies that have been done to analyze this topic have shown findings of growth failure, osteopenia, hypogonadism, hypothyroidism, and glucose intolerance in SCD and SCT patients. This study did not explore bone disease or sex hormone function due to difficulty in performing these tests and obtaining insurance payor coverage. An additional limitation includes low sample size. However, this study replicates real-world care for these patients due to these barriers, making these methods easily translatable to other clinical settings. Our findings suggest implementation of a standardized protocol for iron overload and endocrinopathy screening in SCD and SCT patients is not only viable but could also detect disease before symptom onset when intervention is more effective.

Serum Calcium, 25-Hydroxyvitamin D, and Parathyroid Hormone Levels in Relation to Aneurysmal Subarachnoid Hemorrhage.

Elevated serum calcium (S-Ca), 25-hydroxyvitamin D (S-25OHD), and parathyroid hormone (S-PTH) levels have been associated with risk of aneurysmal subarachnoid hemorrhage (SAH) in observational studies. However, whether these associations are causal is unclear. The objective of the present study was to determine whether genetically predicted S-Ca, S-25OHD, and S-PTH levels are causally associated with aneurysmal SAH using a Mendelian randomization design. Analyses were performed using summary-level data for genetic variants associated with S-Ca, S-25OHD, and S-PTH concentrations. Summary data for aneurysmal SAH were adopted from a genome-wide association study (GWAS) on intracranial aneurysm (n = 79,429 individuals, 69% of the cases had aneurysmal SAH). The inverse variance-weighted approach was adopted as the primary analyses. For sensitivity analyses, the weighted median and MR-Egger approaches were adopted. Genetically predicted S-Ca and S-PTH levels were associated with aneurysmal SAH in the primary analyses. The odds ratios (ORs) of aneurysmal SAH were 1.96 (95% CI: 1.003-3.812; P = 0.049) and 1.495 (95% CI: 1.058-2.114; P = 0.023) for one SD increase of genetically predicted S-Ca and S-PTH levels, respectively. Genetically predicted S-25OHD concentration was not associated with aneurysmal SAH (per 1 SD increase in S-25OHD: OR = 0.92; 95% CI, 0.78-1.09; P = 0.332). Sensitivity analysis yielded similar results, and no evidence of pleiotropy was observed. Our results indicated that higher genetically predicted S-Ca and S-PTH levels may increase the risk of aneurysmal SAH.

Parathyroid Carcinoma with Low Values of Elevated Parathyroid Hormone: A Case Report

Parathyroid Carcinoma (PC) is a rare endocrine malignancy, accounting for &lt;1% of sporadic Primary Hyperparathyroidism (PHPT) cases. A preoperative and even intraoperative diagnosis of PC is rarely reported due to its close resemblance to parathyroid adenoma with respect to symptoms- hypercalcaemia, renal stones and/or failure, osteoporosis, and cardiac/neurocognitive dysfunction. The mean serum calcium in PC is reported to be greater than 14 mg/dL along with serum Parathyroid Hormone (PTH) levels often above 1000 pg/mL. When serum PTH levels are 10 times the upper limit of the normal, it is considered diagnostic of PC. Surgical en-bloc resection without capsular breach is the only definitive cure for PC. The present case report included two patients who presented with features of single parathyroid glandular enlargement, hypercalcaemia, its consequences and with normal ionised calcium, but relatively low levels of elevated serum PTH (&lt;300 pg/mL). They were operated and identified postoperatively as having PC. This rare presentation of PC where the preoperative serum PTH values were lower than usually seen in carcinoma, should alert endocrinologists and surgeons that lower levels of elevated serum PTH do not primarily exclude the possibility of carcinoma.

Differences in Phosphate and Parathyroid Hormone Concentrations over the Day among Patients on Hemodialysis.

Elevated serum phosphate and parathyroid hormone (PTH) concentrations are associated with cardiovascular events, bone disease, and mortality in patients on maintenance hemodialysis. Although circadian changes are known in people with CKD, it is unknown whether differences occur in these parameters over the course of a day in people receiving hemodialysis. We used clinical data from Fresenius Medical Care US dialysis clinics to determine how the time of day when measurements were collected (hemodialysis treatment start time) may be associated with serum phosphate and PTH concentrations. We used harmonic regression to assess these associations while accounting for demographic data and treatment parameters. A total of 96,319 patients receiving maintenance hemodialysis were included in this analysis. Patients had a mean age of 64±14 years, 43% were women, and dialysis start times ranged from 3:00 am to 7:59 pm. The mean serum phosphate concentration was 5.2±1.5 mg/dl, and the median PTH was 351 pg/ml (interquartile range [IQR], 214-547). In fully adjusted models, serum phosphate had a nadir at 11:00 am of 4.97 (IQR, 4.94-5.01) mg/dl and a peak at 7:00 pm of 5.56 (IQR, 5.50-5.62) mg/dl. Serum PTH had a nadir at 9:00 am of 385 (IQR, 375-395) pg/ml and a peak at 7:00 pm of 530 (IQR, 516-547) pg/ml. Among patients receiving maintenance hemodialysis, concentrations of PTH and phosphate before a dialysis session vary with the time of day that these values are measured. Consideration of whether these values were obtained at peak or nadir times of the day may be important in treatment decisions.

Normocalcemic non-renal hyperparathyroidism

Parathyroid hormone (PTH) is produced by the parathyroid glands, which are the main regulators of calcium and phosphorus metabolism. Hyperparathyroidism is a clinical condition associated with an increase in serum PTH content. The state of parathyroid glands depends very much on the amount of vitaminD, magnesium and boron in the blood because, according to official data, substantiated by a number of scientific studies, the majority of the world population (80%) has a lack/deficiency of vitamin D. This fact explains the high prevalence of thyroid diseases (hyperplasia, adenoma, hyperparathyroidism) and associated pathology. Previous studies have shown that a deficiency/lack of vitaminD was found in 85–94% of Ukraine population. A deficiency/lack of vitamin D compensatorily stimulates an increase in PTH synthesis. Doctors very rarely determine the level of PTH, which prolongs the progression of hyperparathyroidism, and they detect it only with severe associated changes in other systems. Hyperparathyroidism occurs when one or more of the parathyroid glands become hyperactive, gradually leading to elevated serum parathyroid hormone levels and hypercalcemia. The diagnostic criteria for hyperparathyroid conditions are very vague, which is confusing and leads to unnecessary surgeries instead of simple vitamin D and boron therapy. Normocalcemic primary hyperparathyroidism is a diagnosis of exclusion, and it can be considered only after careful assessment of the causes of secondary hyperparathyroidism, including that associated with a lack of vitamin D. The most common form of hyperparathyroidism is normocalcemic non-renal hyperparathyroidism. Prophylactic use of vitamin D in the correct individualized doses (25(OH)D range of 100–150 nmol/l or 40–60 ng/ml) should reduce the risk of parathyroid pathology but only 10% of the population receives such therapy, others do not know that it is useful. The only way to eliminate the gradual progression of parathyroid disorders is to administer individual prophylactic or therapeutic doses of vitaminD.

72 SEASONAL VARIATION IN HYPERPARATHYROIDISM IN OLDER IRISH ADULTS

Abstract Background Vitamin D deficiency is common in Ireland, varies by season and can result in secondary hyperparathyroidism. High Parathyroid Hormone (PTH) levels due to low vitamin D status are associated with increased bone turnover and lower bone mineral density, especially at cortical sites such as the hip. Given the variation in vitamin D status by time of year, our study aimed to examine for seasonal differences in hyperparthyroidism in older adults. Methods Study participants were from a large cross-sectional study of older Irish adults recruited from hospital outpatient services and GP practices. Exclusion criteria were: eGFR&amp;lt; 30ml/min and elevated serum calcium (&amp;gt;2.5 mmol/l) in order to avoid primary hyperparathyroidism or elevated serum PTH due to advanced renal impairment. Hyperparathyroidism was defined as a PTH level &amp;gt; 65 ng/ml. The relationship between hyperparathyroidism and season was examined in regression models adjusting for potential factors affecting PTH. Results There were 4324 participants, mean age 73.8 +/- 7.9 years, 65.4% were female. Hyperparathyroidism was more prevalent in Spring versus Autumn (17.4 vs 11.4 %, P = 0.0002). The increased prevalence remained after adjusting for age, gender, body mass index, timed up and go, dairy intake, eGFR, and smoking (OR 1.6, 1.2- 2.0, P=0.0003). This also corresponded to the seasonal variation in vitamin D status with deficiency (25(OH)D &amp;lt; 30 nmol/l) highest in Spring (23.3%) and lowest in Autumn (16.8%). Conclusion We found that hyperparathyroidism fluctuates with season in an inverse relationship with vitamin D. Overall, high PTH levels were 60% more likely in Spring versus Autumn. This emphasises the importance of maintaining adequate vitamin D status all year round. While we adjusted for dairy intake, we did not have accurate measures of total dietary calcium intake which could also vary seasonally and be a contributory factor.

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39-Year-Old Woman With Severe Weakness

Normocalcaemic primary hyperparathyroidism: is nephrolithiasis more common than osteoporosis?

Normocalcaemic primary hyperparathyroidism (NPHPT) is often under-recognised in clinical practice. To determine the prevalence and clinical significance of NPHPT in an unselected sample in an acute hospital setting. Patients aged >18 years who had measurement of an elevated serum parathyroid hormone (PTH ≥ 7 pmol/L) during 12 months from 1 January 2017 to 31 December 2017 were retrospectively studied. NPHPT was defined by the presence of elevated serum PTH with normal albumin-corrected serum calcium on two or more occasions after excluding secondary causes. Patients were followed up for 2 years. Relevant data were collected by review of electronic medical records. Of the 2593 patients who had PTH measured during the study period, 1278 had serum PTH ≥ 7 pmol/L. Hypercalcaemic primary hyperparathyroidism (PHPT) was diagnosed in 174 patients. Secondary causes for elevated serum PTH were identified in 993 patients: 815 (chronic kidney disease - estimated glomerular filtration rate < 60 mL/min/1.73 m2 or renal transplant), 98 (vitamin D deficiency - 25(OH)D < 50 nmol/L), 28 (gastric bypass surgery), 38 (medications), 13 (malabsorption or post-thyroidectomy) and 1 (hypercalciuria). Data were incomplete for 80 patients. The prevalence of NPHPT with and without the exclusion of hypercalciuria was 0.19% (5) and 0.39% (10) respectively. The prevalence of nephrolithiasis in NPHPT was higher than PHPT (100% vs 15% among five patients (P < 0.001) and 50% vs 15% among 10 patients (P = 0.014)). The prevalence of osteoporosis was not significantly different between NPHPT and PHPT (20% vs 45% among five patients (P = 0.389) and 30% vs 45% among 10 patients (P = 0.518)). These findings give further credence to the diagnosis of NPHPT as a clinical entity. Nephrolithiasis may be a greater problem than osteoporosis in NPHPT compared with PHPT. This needs prospective evaluation.

Case series of diagnosis and surgery challenges in parathyroid carcinoma.

IntroductionParathyroid carcinoma (PC) is a rare malignancy that accounts for 1 % of cases of hyperparathyroidism. Data regarding PC in Indonesia are scarce, which poses challenges to diagnosis and treatment. This study aims to describe a series of PC cases from a tertiary health care center over 12 years.Presentation of casesRetrospective data of six patients with hyperparathyroidism diagnosed with PC between 2008 and 2020 were reviewed. Clinical presentation, diagnosis, management, and short-term outcomes of PC were analyzed. All six PC patients were diagnosed postoperatively. Four of the patients presented with symptomatic hypercalcemia, and two presented with neck swelling. Elevated serum parathyroid hormone was observed in five patients. Only two patients had imaging results corresponding to PC characteristics. Ipsilateral parathyroidectomies were performed on 5 patients where invasion and metastasis are not evident. Four frozen section samples suggested PC, and two suggested parathyroid adenoma. Further histopathologic examination confirmed a diagnosis of PC in all patients. No metastasis to the adjacent lymph nodes or distant target organs was found during surgery.DiscussionPreoperative diagnosis of PC remains challenging. Suspicion of PC is appropriate in the presence of severe hypercalcemia, elevated parathyroid hormone level, and a mass observed either during imaging or intraoperatively.ConclusionIpsilateral parathyroidectomy seems to be feasible compared to total resection in order to preserve function and structure. Incomplete excision may lead to an increased risk of recurrence, emphasizing the importance of routinely following up on PC cases.

Vitamin D Deficiency Mimicking Pseudohypoparathyroidism Type II in an Adolescent Boy: A Case Report

Background: Vitamin D deficiency in children is common and usually characterized by hypocalcemia, hypophosphatemia, and elevated serum parathyroid hormone level. However, vitamin D deficiency can be associated with parathyroid hormone resistance in the kidneys which may cause hyperphosphatemia instead, mimicking thus pseudohypoparathyroidism type II. The exact pathogenesis for parathyroid hormone resistance remains unclear, and the distinction between the two conditions remains difficult. We describe the case of an adolescent who presented with seizures and was found to have biochemical features consistent with pseudohypoparathyroidism, likely related to vitamin D deficiency. Case Report: A 13-year-old previously healthy adolescent presented with seizures. He experienced back pain during the previous month prior to the presentation. He did not have features of Albright hereditary osteodystrophy. His laboratory studies were significant for hypocalcemia, hyperphosphatemia, elevated serum alkaline phosphatase level, elevated parathyroid hormone level, and a deficient vitamin D level. Magnetic resonance imaging of the spine revealed multiple compression fractures. The child was treated with intravenous calcium and vitamin D administration with rapid improvement and his seizures resolved. Conclusion: Hypocalcemia from vitamin D deficiency can mimic pseudohypoparathyroidism type II. The principles of treatment for hypocalcemia in both conditions are similar and patients require timely intervention with close follow-up to ensure the resolution of symptoms. Patients with resolution of symptoms after adequate treatment may not require further evaluation for other types of pseudohypoparathyroidism.