bluuebunny/crossref_metadata_2025_split huggingface dataset:
SAT216 Multiple Reasons Of Secondary Hyperthyroidism And Unexpected Results
Authors: Dzherieva Irina , Volkova Natalia , Brovkina Snezhana , Reshetnikov Igor , Gritsenko Lyubov , Mamedova Tuntul , Ismailov Unus 
Published: October 2023

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
SAT222 More Than Skin Deep: A Case Of Psoriasis Associated With Hypoparathyroidism
Authors: Sheth Grishma , Alsayed Mahmoud 
Published: October 2023

Abstract
Disclosure: G. Sheth: None. M. Alsayed: None.
Introduction: Primary hypoparathyroidism is commonly encountered post-surgically, however isolated cases are rarely seen without clear risk factors. Severely low calcium levels have been shown to correlate with flare ups and worsening of psoriasis. Treatment of hypocalcemia has been thought to improve and prevent the progression of this skin rash. This case highlights an interesting presentation of psoriasis in which the severity was likely related to hypocalcemia. Clinical Case: 25 y/o F with no prior past medical history presented to the emergency room with diffusely worsening skin rash and fever. She had bilateral erythematous plaques on her anterior legs for a few months that was progressively worsening. A few days prior, she started noticing erythema and scaling on her upper body and back. Her on arrival labs were remarkable for a calcium level of 4.5 mg/dL (8.8-10.4). Patient declined any symptoms at the time but did state she had noticed tingling in her face and hand/foot cramps occurring on and off over the last 6 months. Her EKG was remarkable for a mildly prolonged QT interval. She was treated with IV calcium gluconate 4 grams without improvement in her calcium. She ultimately was placed on a calcium gluconate drip and oral calcium carbonate 2 grams every 2 hours. Meanwhile, her work up revealed a PTH of &lt;6 pg/mL, phosphate of 7 mg/dL, magnesium of 1.7 mg/dL, and vitamin D of 23 ng/mL. To elucidate the cause of her newly diagnosed primary hypoparathyroidism, iron studies were ordered to rule out hemochromatosis and ceruloplasmin to rule out Wilson’s disease, both of which returned negative. She had no history of radiation therapy or prior blood transfusions. She denied any family history of calcium disorders. Therefore, PTH antibody testing was sent to a send out lab and is currently pending. Patient was ultimately weaned off of the calcium drip with low normal calcium values around 7.5-8.5 mg/dL. She was placed on calcium carbonate 2 grams every 6 hours with plans for close outpatient labs and follow up. She was seen by dermatology in the hospital and was diagnosed with erythrodermic psoriasis. She was given an IL-17 inhibitor, Taltz, with significant improvement in her rash over her 2 day hospital stay. Conclusions: This case brings to light the importance of a thorough investigation of primary hypoparathyroidism and to recognize the rare genetic or autoimmune etiology as a possibility. Additionally, this case identifies the association of psoriasis with hypocalcemia. Studies have recognized a correlation of severity of psoriasis in patients with low calcium as was seen in this patient. Moreover, treatment with calcium supplementation may have a role in improving skin manifestations.
Presentation: Saturday, June 17, 2023
SAT225 An Unexpected Case Of Hypocalcemia
Authors: Nogueira Cordeiro Monica Fabiola , Jason Epstein Eric 
Published: October 2023

Abstract
Disclosure: M. Nogueira Cordeiro: None.
Calcitriol and oral calcium supplementation remains the standard of care in the management of hypoparathyroidism. The targeted serum calcium level for this condition is quite narrow, typically at the lower end of the reference range to avoid hypercalciuria, but above the calcium level from which a patient may develop symptoms. Pharmacokinetic and pharmacodynamic properties vary among different over-the-counter (OTC) calcium salt preparations, therefore it is important for the provider and patient to understand the differences in calcium formulations to meet therapy goals. We present a case of symptomatic hypocalcemia related to a patient unknowingly switching from calcium carbonate to tricalcium phosphate supplementation. A 71 year-old woman with a history of thyroid cancer status post total thyroidectomy complicated by permanent hypoparathyroidism, CKD stage III, nephrolithiasis and hypercalciuria presented for a follow up visit complaining of perioral numbness for approximately one month. Laboratory evaluation revealed hypocalcemia, hyperphosphatemia, hypomagnesemia and a normal 25-OH-vitamin D level: Ca 7.3 mg/dL (8.5-10.5 mg/dL), Phos 5.6 mg/dL (2.5-4.5 mg/dL), Mg 1.1 mg/dL (1.7-2.8 mg/dL), 25-OH-vit D 45 ng/mL (30-60 ng/mL). Prior to this, her serum calcium had been well controlled, avoiding symptomatic hypocalcemia and hypercalciuria, for years. She had remained on her usual dose of calcitriol, but had changed her calcium supplement to 500 mg of tricalcium phosphate three times per day from calcium carbonate 650 mg three times a day. Rather than adjust her calcitriol, she was recommended to stop tricalcium phosphate and restart the previous regimen of calcium carbonate; serum calcium and phosphorus improved within 72 hours (Ca 7.7 mg/dL, Phos 3.8 mg/dL) and two weeks later her calcium level was back at goal (8.2 mg/dL), phosphate level had normalized (4.5 mg/dL) and she was no longer symptomatic. Tricalcium phosphate is not generally recommended for patients with hypoparathyroidism given they are less available and not as well tested. Previous studies have shown conflicting outcomes for serum calcium elevation after an oral load of tricalcium phosphate when compared with calcium carbonate. Elderly individuals might also experience an elevation in phosphate levels after a tricalcium phosphate load. Additionally, the elemental calcium in OTC tricalcium formulations is often less than what is available in similar appearing calcium carbonate or citrate supplements. Although calcium carbonate and citrate are the most commonly prescribed calcium supplements, other preparations are available OTC and it is difficult to tell these apart. Given the narrow goal of serum calcium for patients with hypoparathyroidism, providers should confirm the calcium formulation at each visit and counsel the patient to notify them if any changes are made in their oral calcium supplementation.
Presentation: Saturday, June 17, 2023
SAT227 A 17-year old Teenager With Recurrent Syncopes In The Setting of Hypocalcemia
Authors: Chartoumpekis Dionysios V , Bountouris Panagiotis , Dimitropoulos Konstantinos , Habeos Ioannis G 
Published: October 2023

Abstract
Disclosure: D.V. Chartoumpekis: None. P. Bountouris: None. K. Dimitropoulos: None. I.G. Habeos: None.
Background: One of the main reasons of syncope is the long QT syndrome. The exercise-induced hypocalcemia in a background of primary hypoparathyroidism is sometimes overlooked in the differential diagnosis. Clinical Case: A 17-year old female was transferred to the emergency room of the University Hospital of Patras after having experienced a syncope while swimming. She described in the past 6 months similar episodes during exercise (running, cycling). A basic investigation with full blood count, sodium, potassium, cortisol and TSH levels along with a brain MRI and an ECG were performed at her primary care physician. Due to a discovered long QT she was addressed to a cardiology private office for further investigation. However, before the planned appointment she had this episode while swimming and she was admitted to the cardiology department. During her hospitalization a serum calcium of 4.7 mg/dl and a serum P of 9.4 mg/dl were discovered with a non-detectable PTH. The endocrinology division was called for further evaluation. Chvostek and Trousseau’s signs were positive. The patient was administered a calcium gluconate drip and in parallel a treatment with calcium carbonate and alphacalcidol was initiated. The possibility of an autoimmune polyendocrine syndrome was excluded as the patient did not present candidiasis, adrenal insufficiency, autoimmune thyroid disease or diabetes. After her exit from the hospital she was followed up at the outpatient endocrinology clinic and her daily doses of calcium carbonate and alphacalcidol was modified several times as the [CaxP] was always higher than 55 mg2/dl2 and when the dose of calcium carbonate was lowered she developed symptomatic hypocalcemia. During the first month of her follow-up a cataract in the right eye was discovered and a brain MRI unveiled basal ganglia calcifications. No signs of renal stones or nephrocalcinosis were seen in the ultrasound. As the calcium and phosphate levels, after almost 9 months of changes in the treatment schemes, were not optimal, a treatment with recombinant PTH was initiated. This treatment aided the patient to reach low normal levels of calcium and [CaxP] lower than 55 mg2/dl2. The patient is followed up every six months in the endocrinology outpatient clinic. Conclusion: This is an interesting case of primary hypoparathyroidism possibly of autoimmune origin. The presence of syncopes during exercise could be due to a further drop of calcium levels due to transient respiratory alkalosis. This case can be useful in the teaching of differential diagnosis of long QT syndrome, the management and evaluation of an hypocalcemia and the rule out of autoimmune polyendocrine syndromes in the context of a primary hypoparathyroidism.
Presentation: Saturday, June 17, 2023
SAT229 Symptomatic Hypocalcemia In The Setting Of Crohn’s Disease With Severe Hypomagnesemia
Authors: Cuan Katherine , Reisman Tamar 
Published: October 2023

Abstract
Disclosure: K. Cuan: None. T. Reisman: None.
Introduction: People with Crohn’s Disease (CD) are at risk for various nutritional deficiencies due to decreased oral intake, malabsorption, and increased intestinal losses. CD often causes a negative calcium balance, which does not usually cause hypocalcemia because the bones serve as a reservoir for calcium. However, symptomatic hypocalcemia may occur if a concurrent severe hypomagnesemic state is present. The factors resulting in hypocalcemia in patients with magnesium deficiency are impaired PTH secretion, PTH resistance, and vitamin D deficiency. Clinical Case: A 33-year-old man with CD and rheumatoid arthritis presented following a seizure with additional symptoms of hand cramping and facial twitching. He had previously undergone three small bowel resections and had a history of hypocalcemia due to malabsorption. Although this patient had previously been admitted due to a hypocalcemic seizure, he did not start oral calcium supplements at that time. No issues with magnesium were identified previously. On this encounter, he was found to have a corrected calcium (cCa) of 5.3 mg/dL, undetectably low magnesium at &lt;0.7 mg/dL, normal phosphorus, 25-hydroxyvitamin D at 3.5 ng/mL, and an elevated intact PTH (iPTH) at 169 pg/mL. Aggressive intravenous calcium and magnesium repletion improved cCa to 7.4 mg/dL and magnesium to 2 mg/dL with no further seizure activity. He was discharged on calcium carbonate, calcitriol, and ergocalciferol. A month later, he presented to our endocrinology clinic asymptomatic but with a cCa of 6 mg/dL and magnesium at &lt;0.7 mg/dL. Further biochemical workup revealed normal phosphorus, 25-hydroxyvitamin D at 7.9 ng/mL, and an inappropriately normal iPTH at 49 pg/mL. He was readmitted to the hospital where intravenous repletion improved cCa to 8.1 mg/dL and magnesium to 1.9 mg/dL. His recurrent hypomagnesemia was attributed to malabsorption. An increased dose of calcitriol and oral magnesium were added to his discharge medication regimen, in addition to his ergocalciferol and calcium carbonate. Three days later, he had a cCa level of 7.1 mg/dL as an outpatient. Conclusion: Patients with CD often have nutrient deficiencies, especially if they have had surgical resection within the intestinal tract. Our patient initially developed hypocalcemia from malabsorption, which was then exacerbated by the severely hypomagnesemic state. During his initial hospital encounter, the elevated iPTH level indicated PTH resistance. On his second encounter, the normal iPTH level suggested hypoparathyroidism. Given the relationship between magnesium and calcium homeostasis, addressing the hypomagnesemia eventually aided in achieving stabilization of serum calcium levels. Thus, in patients who are at risk for malabsorption and have recurrent symptomatic hypocalcemia, it is prudent to check magnesium levels as it can affect long term management of hypocalcemia.
Presentation: Saturday, June 17, 2023
SAT234 Variations In Clinical Practice Patterns For Hypoparathyroidism
Authors: Deering Kathleen L , Harshaw Qing , Mitchell Deborah M , Larsen Niccole J , Weiss Blandine , Loustau Patrick , Allas Soraya 
Published: October 2023

Abstract
Disclosure: K.L. Deering: None. Q. Harshaw: None. D.M. Mitchell: None. N.J. Larsen: None. B. Weiss: None. P. Loustau: None. S. Allas: None.
Objectives: Emerging evidence regarding optimal treatment for patients with chronic hypoparathyroidism (cHP) has led to the development of updated evaluation and management guidelines. The goal of this study was to determine how current practice patterns for individuals with cHP compare with these guidelines. Methods: We extracted data from a large US claims database (130 million patients) from Oct 2014 to Dec 2019. cHP was defined as an HP diagnosis claim ≥6 months following neck surgery or ≥2 claims ≥6 months apart. Patient data were extracted from 1 year prior to surgery (if applicable) and up to 2 years following their qualifying HP claim. Additionally, a panel comprised of 103 endocrinologists and nephrologists (US=40, UK=21, France=21, Germany=21) was assembled and conducted chart reviews with each participant contributing data for 5 patients with cHP in their practice. Results: 5,302 patients met criteria for cHP from the claims database, while the physician panel chart review included 515 cHP patients. In the claims database, 33.0% saw an endocrinologist and 9.4% or less saw a nephrologist during the 1-year follow-up. Panel physicians reported being the decision maker for 93% of their cHP patients and 90% of the patients were seen at least twice per year. Guidelines recommend all new and established cHP patients be monitored for key laboratory values every 3-12 months. Overall, while neither study found monitoring practices consistent with guidelines, there was less laboratory monitoring in the database study than in the physician panel: serum magnesium (36.6%; 57%), serum phosphorous (36.8%; 90%), urine calcium (10.0%; 57%), and renal imaging (20.9%; 34%). Additionally, patients were monitored for bone health in the database study and physician panel (bone mineral density: 10.7%; 44%; bone markers: 5.2%; 25%). Conclusion: Real-world practice patterns vary from guideline recommendations; however, the practice patterns from the physician panel study align more closely with recommendations than the claims database study. This discrepancy may be due to patients less frequently utilizing physicians specialized in cHP in the database study. Our data underscore challenges with optimizing care for patients with this rare disorder. In addition, they suggest that ongoing efforts to educate both patients and physicians about management guidelines may improve care and ultimately enhance health and quality of life in cHP.
Presentation: Saturday, June 17, 2023
THU596 Heteromerization Of The Angiotensin II Type 1 Receptor And The Bradykinin Type 2 Receptor
Authors: Johnstone Elizabeth K M , Pfleger Kevin D G 
Published: October 2023

Abstract
Disclosure: E.K. Johnstone: Grant Recipient; Self; Australian Research Council. K.D. Pfleger: Grant Recipient; Self; Australian Research Council. Stock Owner; Self; Dimerix Bioscience Pty Ltd.
Background: Receptor heteromerization is the phenomenon whereby two different receptors form a functional complex that attains unique pharmacological properties. Consequently, receptor heteromers can be considered novel drug targets, with the potential to achieve greater therapeutic selectivity and specificity. In a landmark study, the first receptor heteromer to be associated with a disease was the heteromer that forms between the angiotensin II type 1 (AT1) receptor and the bradykinin type 2 (B2) receptor (1). The AT1-B2 heteromer reportedly led to increased angiotensin II signalling, which was implicated in the angiotensin II hypersensitivity involved in pre-eclampsia. However, the validity of this study was questioned by a collaboration of several groups who were unable to find any evidence for a physical or a function interaction between the two receptors (2). As a consequence of these conflicting studies, the existence of the AT1-B2 receptor heteromer has remained controversial. Aim: Investigation of evidence for heteromerization of the AT1 receptor and the B2 receptor. Methods: AT1 receptor and B2 receptor pharmacology and potential heteromerization was investigated in HEK293FT cells using various bioluminescence resonance energy transfer (BRET)-proximity based assays, as well as Dimerix’s Receptor-Heteromer Investigation Technology (Receptor-HIT) (3). Receptor-HIT enables the investigation of receptor heteromers through their specific ligand-induced proximity to interacting proteins. BRET assays, including in the Receptor-HIT configuration, allow real time, live cell monitoring of proximity between biomolecules of interest. Results: Using the Receptor-HIT assay, we confirmed the existence of the AT1-B2 receptor heteromer in HEK293FT cells. We found that the heteromer was able to recruit various GPCR interacting proteins, such as G proteins and arrestin in a bradykinin-dependent manner. Additionally, the heteromer also internalised and trafficked through the cell upon treatment with bradykinin. The close proximity of the two receptors was confirmed using a variation of the Receptor-HIT assay, which monitors receptor-ligand binding rather than protein-protein interactions. Discussion: Our study supports the existence of the AT1-B2 receptor heteromer and identifies various pharmacological properties of the complex. Further studies are required to relate these molecular properties to physiological consequences of heteromerization. (1)AbdAlla et al. Nat Med2001, 7 (9), 1003 1009.(2)Hansen et al. J Biol Chem2009;284(3):1831 1839.(3)Johnstone et al. Biochem Soc T. 2021;49:1555–65.
Presentation: Thursday, June 15, 2023
THU598 Pseudohypoaldosteronism Type 2: A New Variant Of A Rare Disease
Authors: Gray Cater Taylor Lauren , Borges Espinosa Luis 
Published: October 2023

Abstract
Disclosure: T.L. Cater: None. L. Borges Espinosa: None.
Introduction: Familial hyperkalemia and hypertension syndrome or pseudohypoaldosteronism type 2 (PH2) is a rare monogenic hypertension resulting from WNK1, WNK4, KLHL3, or CUL3 gene mutation. Subsequent interference at the Na-Cl co-symporter, epithelial Na, or ROMK channel results in metabolic acidosis, hyperkalemia, and hypertension responsive to thiazide treatment. This case demonstrates PH2 resulting from a KLHL3 gene variant not previously described. Mutations to KLHL3 decrease Na-Cl cotransporter expression in the distal convoluted tubule leading to increased sodium and chloride reabsorption, volume expansion, hypertension, and, therefore, less sodium available for potassium exchange in the collecting duct. Case Description: A 30-year-old female G1P0 with twin gestation was admitted at 33 weeks for preeclampsia with severe features. PMH was unremarkable. She underwent C-section and was discharged home with healthy twin daughters. BMP during admission showed hyperkalemia with peak potassium 5.2 mmol/L which improved to 4.6 mmol/L by discharge. Essential hypertension was diagnosed 3 months later (BP 130/90, 78 bpm, RR 16, BMI 30.0 kg/m2). Labetalol 50 mg BID was initiated. BMP obtained showed hyperkalemia as high as 6.4 mmol/L. Further workup showed undetectable renin with normal aldosterone, hyperchloremic metabolic acidosis with chloride 111 mmol/L and bicarbonate 20 mmol/L, and normal EKG. She was managed in the ED where her potassium improved to 5.1 mmol/L with persistent hyperchloremic metabolic acidosis. A diagnosis of pseudohyperkalemia was presumed initially. Labetalol was discontinued in favor of hydrochlorothiazide 12.5 mg daily. Lost to follow-up, she presented 10 years later to Endocrinology at age 41 for chronic hyperkalemia and hyperchloremic metabolic acidosis. Labs showed potassium 6.5 mmol/L, chloride 108 mmol/L, and bicarbonate 23 mmol/L. Exam showed BP 133/98, BMI 26.63 kg/m2. She recounted several ER visits over the past decade for hyperkalemia with highest reported potassium of 7.8. She had stopped her thiazide due to dizziness, palpitations, and fatigue. Family history was now notable for hyperkalemia in her father, two brothers, and fraternal niece but no genetic testing was available. We resumed hydrochlorothiazide 12.5 mg every other day; follow-up labs showed improved potassium 5.2 mmol/L. Genetic testing revealed heterozygosity in the KLHL3 gene for the c.1064T &gt G sequence, a variant that has not been reported in the literature or large population database. Conclusion: Hypertension in PH2, distinct in its presentation with hyperkalemia and metabolic acidosis, requires a detailed family history and hormonal evaluation to make the diagnosis. Genetic testing in our case patient revealed a variant at the KLHL3 gene not previously described, underscoring the utility of genetic testing in understanding this rare condition.
Presentation: Thursday, June 15, 2023