Primary Hyperparathyroidism Presenting Research Articles

Symptomatic Primary Hyperparathyroidism Presenting as Osteitis Fibrosa Cystica in Young Female

Symptomatic Primary Hyperparathyroidism Presenting as Osteitis Fibrosa Cystica in Young Female

Primary hyperparathyroidism presenting as slipped capital femoral epiphysis; a case report and literature review

Primary hyperparathyroidism associated with slipped capital femoral epiphysis (SCFE) is rare. We report a case of a 14-year-old girl who presented with limping of gait and was diagnosed to have bilateral SCFE and underwent screw fixation of both hips. She had pain involving multiple joints and tenderness on further evaluation and was found to have biochemical hyperparathyroidism. The patient was initially managed medically, and further investigations revealed a parathyroid lesion in the right superior location. Workup for multiple endocrine neoplasia was negative. She underwent right superior parathyroid adenoma excision, and post-operatively, she was cured of the disease. On follow-up, she is asymptomatic, and her calcium is within normal limits. A literature review showed that SCFE is associated with severe hyperparathyroidism in adolescents.

SAT192 Non-syndromal Primary Hyperparathyroidism Presenting As Asymptomatic Hypercalcemia In A Teenage Patient.

Abstract Disclosure: S. Humayon: None. M. Shah: None. P.N. Kabir: None. C.A. Penaherrera: None. Introduction: Primary hyperparathyroidism is the most common cause of hypercalcemia in the general population, and is often discovered incidentally. The condition rarely presents in patients under age 18, particularly when it is not associated with genetic syndromes such as MEN 1. Case presentation: A previously healthy 17-year-old female was referred to Endocrinology clinic for evaluation of positive thyroid peroxidase antibodies with normal TSH and free T4. Review of laboratory results from 6 months prior, revealed an elevated total calcium level of 12.3 mg/dl. Patient at the time denied any symptoms of hypercalcemia. Repeat testing revealed a calcium level of 13.1 mg/dl, PTH level of 183 pg/ml, alkaline phosphatase 232 IU/L. Her vitamin D level was 28 ng/ml, with elevated calcitriol level of 362 ng/ml. The patient denied a history of kidney stones or other endocrine abnormalities in the past. She did mention a family history of hypercalcemia in her father requiring neck surgery. Patient was admitted to the hospital for management of hypercalcemia with intravenous fluid hydration. Subsequent work-up included a sestamibi parathyroid scan which revealed an asymmetric area of delayed uptake in the left thyroid gland, suggestive of a single parathyroid adenoma. The patient underwent single-gland parathyroidectomy, during which PTH levels decreased from 134 pg/ml to 15 pg/ml. She recovered uneventfully from the procedure and was started on oral calcium supplementation, which was tapered two months after surgery since there was no evidence of post-operative hypoparathyroidism. Conclusion: Primary hyperparathyroidism, when presenting prior to the age of 30, is most commonly associated with genetic syndromes such as MEN1 and typically presents as multi-glandular hyperplasia. Isolated primary hyperparathyroidism, secondary to a single parathyroid adenoma is seen less frequently in this younger subset of patients. This can be found in the absence of other endocrine abnormalities, with or without the presence of a family history. Prompt identification of hypercalcemia followed by evaluation of the same, may prevent delays in diagnosis and subsequent management of primary hyperparathyroidism. This can help prevent morbidity associated with hypercalcemia. Presentation: Saturday, June 17, 2023

Primary hyperparathyroidism presenting as acute hypercalcemic crisis: a case report

BackgroundHyperparathyroid crisis, or “parathyroid storm” is a rare manifestation of primary hyperparathyroidism, characterized by sudden onset of symptomatic, severe hypercalcemia (> 3.5 mmol/L). Hemorrhage into a parathyroid adenoma has rarely been reported as an inciting or associated event. We present a case of hemorrhage into a longstanding adenoma presenting with acute onset of profound hypercalcemia and associated complications.Case presentationA 60-year-old male presented to hospital with sudden onset of confusion, muscle weakness, and ataxia. Initial labs showed serum calcium 4.79 mmol/L, parathyroid hormone 2043 ng/L; creatinine 364 μmol/L. Review of the patient’s medical history indicated a 4-year history of recurrent nephrolithiasis, but no prior documented calcium levels. The hypercalcemia did not respond to 5 days of aggressive medical management with fluid resuscitation, denosumab and calcitonin, and later pamidronate and cinacalcet. He continued to deteriorate, requiring intubation and continuous renal replacement therapy. Imaging demonstrated 4.8 cm cystic right paratracheal mass; Technetium (Tc99m) Sestamibi scintigraphy was non-localizing. Urgent parathyroidectomy was completed, revealing a 5 × 3.3 × 1.8 cm hemorrhagic, atypical hypercellular parathyroid. Unfortunately, the patient died from complications from anticoagulation therapy for treatment of deep vein thrombosis 4 weeks after admission. His renal function had not recovered at the time of his death.ConclusionThis case gives potential insight into the etiology of hyperparathyroid crisis, and the difficulty in achieving control of hypercalcemia with medical means. Surgical intervention is the definitive management in these cases and should be considered urgently.Graphical

Abstract #1324626: Primary Hyperparathyroidism Presenting as Hyperemesis Gravidarum in Pregnancy

Primary hyperparathyroidism is uncommon during pregnancy. Physiologic changes in calcium-regulating hormones make the diagnosis more challenging. Furthermore, nausea and vomiting are common during pregnancy and can lead to hyperemesis gravidarum if severe or intractable. We present the case of a 29-year-old woman who was diagnosed with primary hyperparathyroidism in pregnancy.

LBSAT309 Recurrent Nephrolithiasis As A Presenting Feature Of Primary Hyperparathyroidism

Abstract Introduction Primary hyperparathyroidism entails hyperfunctioning of the parathyroid gland and is characterized by hypercalcemia in the setting of inappropriately normal or elevated PTH. Evidence of nephrolithiasis is an indication for surgical intervention. We present a case of primary hyperparathyroidism presenting as recurrent nephrolithiasis. Case presentation A 57 year old female with past medical history significant for hypertension, pre-diabetes and recurrent nephrolithiasis presented to the ED with subjective fever, chills and dysuria. Of note, she had a long standing history of nephrolithiasis with multiple instances of cystoscopic lithotripsy and stent placement with recurrent UTIs over the past decade. She was noted to be in septic shock secondary to urosepsis. She was managed in the ICU with broad spectrum intravenous antibiotics and pressor support. Her workup revealed hypercalcemia with serum calcium 12 mg/dL (8.6 - 10.3), albumin 3.4 g/dL (3.5 - 5.7) in the setting of inappropriately elevated parathormone PTH at 120.4 pg/ml (12 - 88). Endocrinology was consulted. Extensive chart review revealed that she had a long standing history of hypercalcemia and prior urinary calculi analysis were consistent with calcium oxalate and calcium phosphate stones. She endorsed polyuria, polydipsia, constipation and low mood. Medications were reviewed and she had not been on any agents known to cause hypercalcemia. 25 Hydroxyvitamin D was low at 20 ng/ml (30 -100) and appropriately 24 hour urine calcium was low - suppressed at 157 mg (100 - 300). The Sestamibi scan did not show an adenoma. A parathyroid ultrasound showed a possible hypoechoic area bilaterally in the parathyroid region. She underwent parathyroid exploration with excision of right superior parathyroid adenoma. Pathology report showed hypercellular parathyroid tissue consistent with a parathyroid adenoma. Post operatively, calcium and PTH value normalized. Discussion Primary hyperparathyroidism is associated with nephrolithiasis and nephrocalcinosis. Nephrolithiasis is an indication for surgical intervention. Our patient had the classic signs of primary hyperparathyroidism for at least a decade; however, it was not diagnosed until she presented with urosepsis and ended up in the ICU. Primary hyperparathyroidism is often thought of as a disease commonly seen in the outpatient setting. However, a high radar of suspicion must be maintained in both inpatient and outpatient settings as this disorder, when left untreated can have dangerous consequences. Similarly, in patients presenting with nephrolithiasis, a thorough history and physical examination in addition to a complete review of systems and medication review must be carried out to effectively rule out primary hyperparathyroidism. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Primary hyperparathyroidism presenting as acute pancreatitis: An institutional experience with review of the literature.

BACKGROUNDAcute pancreatitis (AP) presenting as an initial manifestation of primary hyperparathyroidism (PHPT) is uncommon, and its timely diagnosis is crucial in preventing recurrent attacks of pancreatitis.AIMTo determine the clinical, biochemical, and radiological profile of PHPT patients presenting as AP.METHODSThis is a retrospective observational study, 51 consecutive patients admitted with the diagnosis of PHPT during January 2010 and October 2021 at a tertiary care hospital in Puducherry, India was included. The diagnosis of AP was established in the presence of at least two of the three following features: abdominal pain, levels of serum amylase or lipase greater than three times the normal, and characteristic features at abdominal imaging.RESULTSOut of the 51 consecutive patients with PHPT, twelve (23.52%) had pancreatitis [5 (9.80%) AP, seven (13.72%) chronic pancreatitis (CP)]. PHPT with AP (PHPT-AP) was more common among males with the presentation at a younger age (35.20 ± 16.11 vs 49.23 ± 14.80 years, P = 0.05) and lower plasma intact parathyroid hormone (iPTH) levels [125 (80.55-178.65) vs 519.80 (149-1649.55, P = 0.01)] compared to PHPT without pancreatitis (PHPT-NP). The mean serum calcium levels were similar in both PHPT-AP and PHPT-NP groups [(11.66 ± 1.15 mg/dL) vs (12.46 ± 1.71 mg/dL), P = 0.32]. PHPT-AP also presented with more gastrointestinal symptoms like abdominal pain, nausea, and vomiting with lesser skeletal and renal manifestations as compared to patients with PHPT-NP.CONCLUSIONAP can be the only presenting feature of PHPT. Normal or higher serum calcium levels during AP should always draw attention towards endocrine causes like PHPT.

Abstract 112: A case of primary hyperparathyroidism presenting as giant cell tumor

Abstract 112: A case of primary hyperparathyroidism presenting as giant cell tumor

Undiagnosed probable genetic primary hyperparathyroidism presenting with brown tumors and deafness

Undiagnosed probable genetic primary hyperparathyroidism presenting with brown tumors and deafness

POST TRAUMATIC CAROTID CAVERNOUS FISTULA PRESENTING AS PARATHYROID CRISIS

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: This is a case of two rare entities causing non-specific symptoms. Carotid-cavernous sinus fistula (CCF) arises from miscommunication of carotid arterial flow and the cavernous sinus. Post traumatic CCF presents bilaterally are uncommon, only 1-2% of patients. While already a rare diagnosis, our patient presented in an acute parathyroid crisis defined by symptomatology caused by markedly elevated calcium and parathyroid hormone, which may have masked our diagnosis of CCF. CASE PRESENTATION: A 57-year-old Colombian female presented with dizziness, anorexia, nausea, and vomiting. She also endorsed intermittent diplopia in the left eye. Physical exam revealed left sided ptosis. She reports a remote history of head trauma a month prior. Serum calcium on presentation was 13.6 mg/dL, ionized calcium of 6.8 mg/dL, and parathyroid hormone (PTH) was 219.8 pg/mL. Subsequently, a Technetium 99m sestamibi scan showed increased radioisotope along the right lower pole of the thyroid gland confirming primary hyperparathyroidism. She was resuscitated with normal saline fluid and started on Cinacalcet for hypercalcemia. Attempts to lower serum calcium can be achieved using bisphosphonates and may be effective within the first 24 hours. In our patient, Cinacalcet did not achieve sufficient calcium lowering thus, Zoledronic acid was used due to its potency with small doses. Nausea, vomiting, and positional dizziness resolved. Despite resolution of symptoms, she continued with ptosis; thus prompting further work up. Magnetic resonance angiography and venography revealed extensive time of flight enhancement throughout the bilateral cavernous sinuses. A cervical and cerebral angiography revealed bilateral carotid cavernous fistulas with ophthalmic vein arterialization. The next day, she underwent left cavernous sinus embolization with coiling. Parathyroidectomy was delayed due to recurrence of ptosis and need for a second embolization for persistent diplopia that resulted in resolution of symptoms. DISCUSSION: Each of these diagnoses are rare and both require timely evaluation and treatment. The patient's symptoms are classically seen in a parathyroid crisis, with nausea, vomiting, and anorexia being the most common symptoms in up to 48% of parathyroid crises. Like the aforementioned, CCF symptomatology also includes non-specific symptoms; however, may pose more of a challenge during diagnosis as symptoms wax and wane depending on the hemodynamic flow within the fistula. CONCLUSIONS: This case highlights the necessity of a thorough physical exam and further as a reminder that a clinician must be vigilant in ruling out alternative pathologies supported by the objective findings no matter how rare or unlikely. REFERENCE #1: Churojana A, Chawalaparit O, Chiewwit P, Suthipongchai S. Spontaneous occlusion of a bilateral post traumatic carotid cavernous fistula. Interv Neuroradiol. 2001;7(3):245-252. doi:10.1177/159101990100700311 REFERENCE #2: Singh DN, Gupta SK, Kumari N, et al. Primary hyperparathyroidism presenting as hypercalcemic crisis: Twenty-year experience. Indian J Endocrinol Metab. 2015;19(1):100-105. doi:10.4103/2230-8210.131763 REFERENCE #3: Lowell AJ, Bushman NM, Wang X, et al. Assessing the risk of hypercalcemic crisis in patients with primary hyperparathyroidism. J Surg Res. 2017;217:252-257. doi:10.1016/j.jss.2017.06.041 DISCLOSURES: No relevant relationships by Roman Bernstein, source=Web Response No relevant relationships by Ariol Labrada, source=Web Response No relevant relationships by Tram Nguyen, source=Web Response No relevant relationships by Elena Tellez, source=Web Response No relevant relationships by Yaswanraj Yuvaraj, source=Web Response

A case report of Primary hyperparathyroidism presenting as a brown tumor in the mandible

A case report of Primary hyperparathyroidism presenting as a brown tumor in the mandible

A case report of Primary hyperparathyroidism presenting as a brown tumor in the mandible

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

A case report of Primary hyperparathyroidism presenting as a brown tumor in the mandible

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Primary Hyperparathyroidism Presenting With Atrial Fibrillation and Calcified Pericardial Effusion

Abstract Background: Primary hyperparathyroidism is the most common cause of hypercalcemia and is frequently associated with skeletal and renal complications. It affects the older population and female gender more commonly. Cardiovascular complications due to altered calcium homeostasis are not well recognised or studied but recently cases of calcification of the pericardium, myocardium, valves and dysrhythmias have been reported. Case: A 47-year old female presented to her GP with atrial fibrillation. Initial blood tests revealed an incidental hypercalcaemia; an adjusted calcium of 2.77 (normal 2.20-2.60mmol/L), raised PTH level of 14.0 (normal 1.6–6.9pmol/L), normal phosphate level and thyroid profile. 25-OH vitamin D level was low 39 (normal 50-120nmol/L). Autoantibody screens and CRP was normal. She was initiated on edoxaban, bisoprolol, and cholecalciferol and treated with a short course doxycycline for a presumed chest infection. There was no history of previous pericarditis but she had long standing hypertension and was obese with BMI of 37kg/m2. Retrospectively patient had sustained a recent wrist fracture and reported classic symptoms of hypercalcemia including fatigue, polydipsia, nocturia, constipation, depression in the endocrinology clinic. Further blood tests found a high C-terminal telopeptide (CTX) level of 0.68 (0.10-0.50ug/L) indicative of high bone turnover.24 urinary calcium/creatinine clearance ratio was 0.0189mmol/mmol (R>0.01 for exclusion of FHH). She was prepped for DC cardioversion and Echocardiogram demonstrated Moderate sized pericardial effusion with some organisation but good biventricular function and dilated LA. Subsequent localisation studies with SPECT CT neck revealed a 9mm parathyroid adenoma along with calcified persistent moderate pericardial effusion putting the patient at risk of pericardial constriction. Patient was referred to the parathyroid surgeon for consideration of urgent parathyroidectomy and will be followed up by the cardiologist to see the impact of normalisation of hypercalcemia on the cardiac complication. It is thought that already established calcification of pericardial effusion is unlikely to resolve but achieving normocalcemia could slow the progression of pericardial calcification and improve bone turnover makers by switching off the excess parathyroid hormone. Patient will be followed up with repeat Echocardiogram post parathyroidectomy to elucidate the effects. Conclusion:Cardiac complications of primary hyperparathyroidism are increasingly becoming more evident with the advent and use of SPECT-CT for localising parathyroid adenomas. Simple screening tests like electrocardiogram may potentially point towards a cardiovascular complication and should be considered routinely in hypercalcaemic patients. Further studies to understand the mechanism of developing cardiac complication in such patients are needed.

Primary Hyperparathyroidism with Multiple Fractures and Brown Tumors in a 14-year-old Girl: Case Report & Review of Literature

Primary hyperparathyroidism (PHPT) presenting as pathological fractures with brown tumors is very rare in children. The rarity and variable presentation of PHPT can make its diagnosis a challenge – especially in the developing countries where malnutrition may mask hypercalcemia. We report a case of a 14–year-old girl who presented with muscle pain, multiple fractures and bone pain. Laboratory tests revealed normocalcemia with vitamin D insufficiency. Subsequent biochemical, radiographic and scintigraphic findings were consistent with primary hyperparathyroidism due to a parathyroid adenoma. Tumor resection was done in a local hospital and histopathology confirmed parathyroid adenoma. Following parathyroidectomy, fractures were treated conservatively with supplementation of calcium and vitamin D. We found her quite capable of self-care and walking in good health at 1 year follow up. Though rare, PHPT-causing brown tumors related skeletal fractures is an important differential diagnosis in the evaluation of patients presenting with multiple foci of radiotracer uptake in bone scintigraphy.
 Bangladesh J. Nuclear Med. 22(2): 130-136, Jul 2019

Primary hyperparathyroidism presenting as recurrent acute pancreatitis: A case report

The association between pancreatitis and primary hyperparathyroidism (PHPT) is controversial. We report a 22-year-old female who presented with three episodes of acute pancreatitis. Primary hyperparathyroidism was diagnosed after the third episode of pancreatitis. He had no additional risk factors for pancreatitis. After successful parathyroid surgery, there has been no recurrence of abdominal pain and his serum calcium is within the normal range.

Primary Hyperparathyroidism Presenting as Posterior Reversible Encephalopathy Syndrome: A Report of Two Cases

Primary Hyperparathyroidism Presenting as Posterior Reversible Encephalopathy Syndrome: A Report of Two Cases

A case of primary hyperparathyroidism presenting with acute pancreatitis

A case of primary hyperparathyroidism presenting with acute pancreatitis

Primary Hyperparathyroidism Presenting as Recurrent Pancreatitis Due to Parathyroid Adenoma

AbstractRecurrent attacks of acute pancreatitis as initial manifestation of primary hyperparathyroidism is rare. We report two cases of young women presenting with recurrent attacks of pancreatitis due to parathyroid adenoma. After surgical excision of the parathyroid adenoma, symptoms of pancreatitis resolved, and serum parathormone and calcium levels returned to normal.

Primary Hyperparathyroidism Presenting With Mandibular Brown Tumor As First Clinical Manifestation

Primary Hyperparathyroidism Presenting With Mandibular Brown Tumor As First Clinical Manifestation