Presentation Of Hyperparathyroidism Research Articles

The clinical presentation of primary hyperparathyroidism: effects of obesity and vitamin D deficiency

The clinical presentation of primary hyperparathyroidism: effects of obesity and vitamin D deficiency

An uncommon manifestation in the common presentation of primary hyperparathyroidism

An uncommon manifestation in the common presentation of primary hyperparathyroidism

Symptomatic Primary Hyperparathyroidism Presenting as Osteitis Fibrosa Cystica in Young Female

Symptomatic Primary Hyperparathyroidism Presenting as Osteitis Fibrosa Cystica in Young Female

The refractory secondary hyperparathyroidism presenting with retro-orbital brown tumor: a case report

BackgroundTertiary hyperparathyroidism describes the autonomous and excessive secretion of parathyroid hormone (PTH) by the parathyroid glands after longstanding secondary hyperparathyroidism in chronic kidney disease. Brown tumors are a sign of uncontrolled hyperparathyroidism. In this case, we have reported a refractory and destructive hyperparathyroidism storm. Also, it presented with atypical onset and unexpected adenoma location.Case presentationA 37-year-old man was diagnosed with end-stage kidney disease 22 years ago. He has been undergoing dialysis treatment since that time. Recently, he was admitted to the ophthalmology department due to the unilateral anterior bulging of the right eye and drooping of the eyelid. Magnetic resonance imaging exhibited an extraconal mass lesion located in the right orbital posterior superolateral position. Computerized tomography scans considered expansile bone lesion with peripheral calcification and originating from the sphenoid wing. The bone mass lesion was resected via craniotomy due to the compressive effect. The pathological findings were consistent with brown tumors. Plasma intact PTH level was 4557 pg/mL. The patient informed that he underwent parathyroidectomy and two leg fractures operation in a medical query. Parathyroid scintigraphy determined three distinct foci consistent with adenomas and one of them was in mediastenum. Second parathyroidectomy was recommended to the patient but the patient refused surgery. Despite his medication and dialysis regimen being revised, PTH levels were maintained at higher levels in follow-up.ConclusionsWe presented a hyperparathyroidism case that was resistant to all treatments and exhibited all the severe complications in a long-term dialysis patient. Furthermore, this case has revealed the importance and difficulty of secondary hyperparathyroidism management.

Tertiary Hyperparathyroidism and Extra Skeletal Calcification in End Stage Kidney Disease Patients: Case-series and Literature Review

Background:: Tertiary hyperparathyroidism (THPT) is a well-known complication of end-stage kidney disease (ESKD), resulting from a loss of functional renal tissue with subsequent alterations in calcium and phosphate metabolism. Tertiary hyperparathyroidism reflects severe parathyroid hyperplasia with autonomous excessive secretion of parathyroid hormone (PTH) that is no longer responsive to the concentration of plasma calcium and leads to abnormal bone remodelling, soft tissue calcifications, vasculopathy, and other systemic complications. Case Presentation:: The authors, hereby, highlight varied presentations of tertiary hyperparathyroidism (THPT) by presenting 3 interesting cases, describing their clinical course and outcomes. Through sharing these experiences and insights, we hope to contribute to a better understanding of THPT and its optimal management in patients with ESKD. Conclusion:: THPT can have a significant impact on patient health and quality of life. Despite the widespread use of interventions, such as vitamin D analogues, calcimimetics and parathyroidectomy, THPT remains a significant clinical challenge for patients with ESKD.

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.

Tertiary Hyperparathyroidism Presenting as Multifocal Brown Tumors: A Case Report

Brown Tumor (BT) of the bone is a rare manifestation of hyperparathyroidism (HPTH), an unusual reactive bone lesion attributed to disturbed bone remodeling, from long-standing increase in parathyroid hormone level (PTH). Historically, BTs were described with primary HPTH but due to early diagnosis of this entity, and improved survival in patients with end-stage renal disease (ESRD) especially those on renal replacement therapy (RRT), more cases of BT are now described in this population, and less in PHPTH. Thus, it is mostly the consequence of untreated secondary or tertiary HPTH whose major culprits are chronic kidney disease (CKD) and ESRD. The management of brown tumors related to chronic renal failure consists primarily of its prevention through the use of phosphate binders, vitamin D analogues, and calcimimetics with surgical parathyroidectomy reserved as the final resort in refractory cases. Herein, we present the case of a 24-year-old female patient with ESRD on intermittent hemodialysis (IHD) who developed recent onset facial tumefaction. Blood work revealed markedly elevated PTH at more than 5000 pg/ml, upper borderline hypercalcemia, and hyperphosphatemia. Further investigations with chest computed tomography (CT) and Technetium-99m (99mTc)- Sestamibi scan nuclear imaging showed multiple ribs lytic lesions as well as features of extensive BT and parathyroid adenomas. Thereafter, the patient was sent for parathyroidectomy after which the patient developed hungry bone syndrome.

Vitamin D Deficiency and the Presentation of Primary Hyperparathyroidism: A Mini Review.

The clinical presentation of primary hyperparathyroidism (PHPT) has evolved over the years from a symptomatic disorder to a predominantly asymptomatic condition. Altered vitamin D metabolism seems to play a role in the presentation of PHPT and may exacerbate the severity of disease. The epidemiology of PHPT differs in the developing versus the developed world, where more severe phenotypes occur in regions where vitamin D deficiency is common. Although it has been validated that patients with PHPT should be vitamin D sufficient, the threshold to supplement in relation to the severity of PHPT and the degree of vitamin D deficiency remains controversial. This review will highlight some of the controversy regarding vitamin D deficiency and the different phenotypes of PHPT.

Rare Classic Presentation of Primary Hyperparathyroidism: A Case Report and Literature Review

Rare Classic Presentation of Primary Hyperparathyroidism: A Case Report and Literature Review

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

Clinical Experience of a Long-acting Pegylated Erythropoietin-Stimulating Agent in Pediatric Chronic Kidney Disease.

Management of anemia of chronic kidney disease (CKD) often includes subcutaneous or intravenous administration of erythropoietin-stimulating agents (ESAs). Mircera, a pegylated continuous erythropoietin receptor agonist, has a longer duration of action and requires less frequent administration than other ESAs. Pediatric experience with Mircera is limited. We retrospectively reviewed our long-term experience of Mircera in a national pediatric nephrology center. Patients were identified via an electronic patient record database. Data collected included demographics (sex, age, etiology of CKD, CKD stage, dialysis modality), dosing information, and laboratory data-hemoglobin (Hb), parathormone (PTH), ferritin, hematinics prior to commencing Mircera and all subsequent values associated with dose adjustments. Seventy-seven patients aged 2 to 18 years, with CKD stages 2 to 5T had received at least 1 dose of Mircera, with 75 patients having sufficient data and a total of 1473 doses. No patients discontinued Mircera owing to adverse effects. One patient experienced a potential severe adverse drug reaction. Mircera was effective in improving or maintaining Hb ≥10.0 g/dL in most (58/75, 77.3%) patients. The median dose to achieve Hb ≥10.0 g/dL was 2.1 µg/kg/4 wk. Most doses (1039, 71.5%) were administered 4-weekly. The doses (161, 11.1%) that were administered 6-weekly remained efficacious. Thirty-two patients started Mircera with Hb <10.0 g/dL; 26 (81%) achieved Hb ≥10.0 g/dL within a median time of 4 months. Mircera was less effective if given every 8 weeks, or in the presence of hyperparathyroidism or hyperferritinemia. Mircera appears safe and effective in pediatric patients with CKD.

Brownish limb tumor as a presentation of primary hyperparathyroidism

43-year-old male, with tumor in the anterior region of the right lower limb (figure 1) and biopsy compatible with brown tumor. He presented total serum calcium 12.3 mg/dl and 13 mg/dl (NR: 8.3-10.3), parathormone (PTH) 1057 pg/ml (NR 15-65). With the diagnosis of primary hyperparathyroidism, a 99mTc-MIBI parathyroid scintigraphy with SPECT was requested, which showed hyperfunctioning parathyroid tissue in the projection of the left inferior parathyroid gland. Hand radiographs showed a lytic lesion in punch in the distal phalanx of the first finger of the left hand (figure 2); in the clavicle radiograph: lytic lesion of 10 mm x 8 mm in the right clavicle, no alterations were evidenced in the skull radiograph.

Persistent hyperparathyroidism after preemptive kidney transplantation

BackgroundLong-term dialysis vintage is a predictor of persistent hyperparathyroidism (HPT) after kidney transplantation (KTx). Recently, preemptive kidney transplantation (PKT) has increased. However, the incidence, predictors, and clinical implications of HPT after PKT are unclear. Here, we aimed to elucidate these considerations.MethodsIn this retrospective cohort study, we enrolled patients who underwent PKT between 2000 and 2016. Those who lost their graft within 1 year posttransplant were excluded. HPT was defined as an intact parathyroid hormone (PTH) level exceeding 80 pg/mL or hypercalcemia unexplained by causes other than HPT. Patients were divided into two groups based on the presence of HPT 1 year after PKT. The primary outcome was the predictors of HPT after PKT, and the secondary outcome was graft survival.ResultsAmong the 340 consecutive patients who underwent PKT, 188 did not have HPT (HPT-free group) and 152 had HPT (HPT group). Multivariate logistic regression analysis revealed that pretransplant PTH level (P < 0.001; odds ratio [OR], 5.480; 95% confidence interval [CI], 2.070–14.50) and preoperative donor-estimated glomerular filtration rate (P = 0.033; OR, 0.978; 95% CI, 0.957–0.998) were independent predictors of HPT after PKT. Death-censored graft survival was significantly lower in the HPT group than that in the HPT-free group (90.4% vs. 96.4% at 10 years, P = 0.009).ConclusionsPretransplant PTH levels and donor kidney function were independent predictors of HPT after PKT. In addition, HPT was associated with worse graft outcomes even after PKT.

Rare Presentation of Primary Hyperparathyroidism in a Young Woman.

Even though primary hyperparathyroidism (PHPT) is a common endocrine disorder, due to better and more regular screening, the usual presentation is only seen in less than 15% of cases of PHPT. The authors present the case of a young female patient with a previous medical history of depression and nephrolithiasis, with one year of bone pain, that had become progressively worse and disabling. In the initial work-up, several lytic bone lesions and moderate hypercalcemia were found, leading to admission of the patient in the Internal Medicine ward for investigation and treatment. The ensuing investigation revealed PHPT due to hyperfunctioning parathyroid adenoma. The patient underwent a parathyroidectomy and at the follow-up assessment two months after discharge, she reported no symptoms and a computer tomography scan showed regression of the lytic lesions. This case is a reminder that severe symptomatic PHPT, a rare form in developed countries nowadays, still exists, and even though it is a medical condition, collaboration with surgical specialties is necessary to ensure the best possible treatment and prognosis.

Widespread presentation of brown tumors mimicking multiple myeloma

Brown tumors or osteitis fibrosa cystica has become a rare presentation of primary hyperparathyroidism in up-to-date clinical practice. Here, we describe a case of longstanding untreated hyperparathyroidism presenting itself with brown tumors in a 65-year-old patient. During the diagnostic work-up of this patient, bone SPECT/CT and 18F-FDG-PET/CT revealed multiple widespread osteolytic lesions. Differentiating from other bone tumors such as multiple myeloma is challenging. In this case, the final diagnosis was made by integrating the medical history, biochemical diagnosis of primary hyperparathyroidism, pathological findings and medical imaging.

Recurrent Acute Pancreatitis as the First Presentation of Primary Hyperparathyroidism

Recurrent Acute Pancreatitis as the First Presentation of Primary Hyperparathyroidism

Late-onset hypocalcemia seizure: An interesting presentation of sporadic maternal primary hyperparathyroidism with hypovitaminosis D

Abstract The cardinal manifestation of primary hyperparathyroidism is secondary to hypercalcemia and high bone turnover disease due to sustained elevation of parathyroid hormone. A high index of suspicion for maternal primary hyperparathyroidism should be kept in the setting of neonatal hypocalcemia. Delayed presentation of hypocalcemic seizure secondary to maternal primary hyperparathyroidism is infrequent. Herein, we report a case of a 2-month-old infant who presented with late-onset (&gt;72 h) hypocalcemic seizure, biochemically mimicking pseudohypoparathyroidism, which eventually led to the diagnosis of maternal hyperparathyroidism with vitamin D deficiency.

Ectopic parathyroid adenoma causing hyperparathyroidism-induced psychosis: A case report

Primary hyperparathyroidism is a disease with multisystemic and heterogeneous manifestations, characterized by underlying high parathormone concentrations. Despite neuropsychiatric involvement being one of the manifestations, psychosis is rare. This is the case of a 68-year-old female with a 10-day clinical course of anorexia, mutism, dysphagia, constipation, and weight loss. The patient had disorganized speech associated with paranoid delusions. Prior to this visit, the patient was recently diagnosed with a mixed anxiety-depressive disorder. For this reason, treatment with antidepressants in combination with atypical antipsychotics was administered without a satisfactory response. Neuroimaging, infectious panel, and toxicology screening showed no abnormal findings. Hypercalcemia secondary to a retropharyngeal ectopic parathyroid adenoma was the causative etiology of her primary hyperparathyroidism, and hypercalcemia treatment resolved the psychotic episode. We highlight the importance of recognizing psychosis as a possible initial presentation of hyperparathyroidism and hypercalcemia. Ruling out organic etiologies prior to diagnosing a primary cause of psychosis is crucial, as their treatment can reverse the psychotic symptoms.

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

PRIMARY HYPERPARATHYROIDISM REVEALED BY ACUTE ALITHIASIC PANCREATITIS: A RARE CASE

Acute pancreatitis is a rare presentation of Primary hyperparathyroidism (PHPT), its prevalence during PHPT is about 1%. The physiopathology of the implication of PHPTs hypercalcemia is not completely elucidated. Several hypotheses plead for the direct or indirect role of hypercalcemia via the activation of pancreatic proteases. Acute alithiasic pancreatitis can be a revealing feature of PHPT wich is a curable disease with the mastery of parathyroid surgery and hypercalcemia treatment. Herein, the authors report a rare case of a patient with PHPT revealed by acute alithiasic pancreatitis with a dreaded complication.