Cause Of Hypercalcemia Research Articles

Glucocorticoid-induced adrenal insufficiency: an uncommon cause of hypercalcaemia.

SummaryLong-term use of exogenous glucocorticoids leads to the suppression of the hypothalamic–pituitary–adrenal axis. Therefore, if the glucocorticoid is withdrawn abruptly, patients will develop adrenal insufficiency. Hypercalcaemia is a rare but well-known complication of adrenal insufficiency. However, hypercalcaemia is a rare presentation of glucocorticoid-induced adrenal insufficiency (GI-AI). A 62-year-old patient with a past history of diabetes mellitus, ischaemic heart disease, stroke, hypertension and dyslipidaemia presented with polyuria, loss of appetite, malaise and vomiting for a duration of 2 months. His ionized calcium level was high at 1.47 mmol/L. Intact parathyroid hormone was suppressed (4.3 pg/mL) and vitamin D was in the insufficient range (24.6 ng/mL). Extensive evaluation for solid organ or haematological malignancy including contrast-enhanced CT chest, abdomen, pelvis, multiple myeloma workup and multiple tumour markers were negative. His synacthan-stimulated cortisol was undetectable thus confirming adrenal insufficiency. His adrenocorticotrophic hormone level was 3.82 pg/mL (4.7–48.8) excluding primary adrenal insufficiency. His MRI brain and other pituitary hormones were normal. Further inquiry revealed that the patient had taken over-the-counter dexamethasone on a regular basis for allergic rhinitis for more than 2 years and had stopped 2 weeks prior to the onset of symptoms. Therefore, a diagnosis of GI-AI leading to hypercalcemia was made. The patient was resuscitated with intravenous fluids and replacement doses of oral hydrocortisone were started with a plan of prolonged tailing off to allow the endogenous adrenal function to recover. His calcium normalized and he made a complete recovery.Learning pointsLong-term use of glucocorticoids leads to the suppression of the hypothalamic–pituitary–adrenal axis.If the glucocorticoid is withdrawn abruptly, patients will develop adrenal insufficiency which is known as glucocorticoid-induced adrenal insufficiency.Adrenal insufficiency should be considered in the differential diagnosis of parathyroid hormone-independent hypercalcaemia.A thorough clinical history is of paramount importance in arriving at the correct diagnosis.

Abstract 14: Cause of PTH independent hypercalcemia other than malignancy and granulomatous disorders

Case Report: We report cases of five patients. All females in the age group of 75 to 80 years. They presented to us in altered sensorium. Underlying comorbidities were hypertension and diabetes. After ruling out most probable diagnosis which was stroke, next differential was dyselectrolytemia. We found hypercalcemia in all the patients which was PTH independent with S. Calcium value >12 mg/dl. Prolonged intake of calcium and Vit D supplements was ruled out Keeping age in consideration, the most common differential of PTH independent hypercalcemia malignancy followed by granulomatous disease were ruled out in all the patients by doing PET CT/MR. Activated Vit D and ACE levels were also negative. No evidence of hyperthyroidism or adrenal insufficiency. We managed on the lines of acute hypercalcemia. 4 patients responded well and 1 continued to be in altered sensorium due to superadded sepsis. So excluding other causes, we had made an impression of uncommon cause of hypercalcemia which is immobilization. Although these females had not undergone any trauma. They were mostly bed bound. The pathophysiology of Immobilization related hypercalcemia (IH) is unclear. It is said that muscle activity transmits signal for bone formation through osteocytes and with immobility, mechanical stimulation is reduced, causing unopposed resorption.Conclusion: IH is an unknown complication in immobile patients. If untreated, patients can land up with complications of hypercalcemia.

Differential diagnosis of hypercalcemia in a patient with CKD G5D

Patients with chronic kidney disease are characterized by the development of mineral disorders due to a decrease in the number of functioning nephrons. These changes manifest by the development of secondary hyperparathyroidism (the overproduction of intact parathyroid hormone (PTH) associated with the serum hypocalcemia, hyperphosphatemia), dysfunctional vitamin D metabolism, bone mineralization and also extraosseous calcifications. Decreased serum PTH levels associated with hypercalcemia are suspicious for adynamic bone disease, but at the same time requires an extended differential diagnostic search (e.g. metastatic processes). One of the rare causes of hypercalcemia is a defect in 24-hydroxylase (CYP24A1). We present a case of a patient on hemodialysis with atypical secondary hyperparathyroidism and an established CYP24A1 defect.

Management of a case of parathyroid adenoma- An anaesthetic challenge

Calcium plays a major role in a number of physiological actions. Primary hyperparathyroidism is the most common cause of hypercalcaemia. Many patients with primary hyperparathyroidism are asymptomatic. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism. We present the successful anaesthetic management of a patient with primary hyperparathyroidism and discuss the anaesthetic issues involved.

Dependent and independent causes of hypercalcemia

Previous clinical studies show that the condition is significantly associated with mortality and increased cardiovascular morbidities. Accordingly, it is essential to conduct adequate diagnosis and evaluation to assess these cases properly. Studies show that different etiologies have been associated with hypercalcemia development with variable prevalence rates among different populations. Reduced PTH levels among patients with hypercalcemia indicate the presence of a non-PTH-dependant etiology for hypercalcemia. We have discussed various causes of hypercalcemia, including dependant and non-dependant causes. We found that malignancy-induced hypercalcemia is the commonest non-PTH-dependant etiology of hypercalcemia. Many malignancies were reported in the literature to attribute to the development of hypercalcemia. Vitamin D-mediated hypercalcemia was also reported as another common etiology for the condition. It might occur secondary to overdosing, immobilization, endocrine disorders, and granulomatous diseases. Other familial and congenital causes were also reported in the literature and discussed.

A systematic review of the pharmacotherapy of secondary hyperparathyroidism (SHPT) in grades 3-5 Chronic Kidney Disease (CKD).

The data on the treatment of secondary hyperparathyroidism (SHPT) provided in scientific publications are divergent and contradictory. Therefore, the aim of our systematic review was to evaluate the efficacy of SHPT treatment in (chronic kidney disease) CKD. The Cochrane, PubMed, and Scopus databases were searched independently by two authors. The search strategy included controlled vocabulary and keywords. The effectiveness and side effects of calcifediol, ergocaliferol, calcitriol, paricalcitol, and cinacalcet were compared and analyzed. Extended-release (ER) calcifediol raised the total serum 25-hydroxyvitamin D level over the threshold of 30 ng/mL in 80% of the patients analyzed in the study. It is the level required for intact PTH (iPTH) suppression. ER calcifediol reduced the iPTH level by 30% in about 30% of the patients, whereas only 2.1% of them had hypercalcemia. Calcitriol significantly decreased the iPTH values. It was the cause of hypercalcemia in 1.7% of the patients. The reduction of the iPTH level by more than 30% was observed in 85.7% of the patients in the paracalcitol group after 48-week supplementation. Paricalcitol was the cause of hypercalcemia in 1.9% of the patients. The cinacalcet therapy resulted in the highest percentage of patients with the iPTH level within the limits recommended by the KDOQI (70-110 ng/L for stage 4 CKD and 150-300 ng/L for stage 5 CKD). 92% of the patients met the KDOQI guidelines and the mean decrease in the serum iPTH level was 68%. Calcifediol ER, paricalcitol, and cinacalcet significantly decreased the iPTH level in the patients under study. Paricalcitol increased the serum calcium concentration the most of all the drugs under analysis. It is noteworthy that only cinacalcet does not carry the risk of hypercalcemia.

The Role of Preoperative Ultrasound and Sestamibi Scintigraphy in the Surgical Management of Primary Hyperparathyroidism: A Review of Literature

Background: Primary hyperparathyroidism (pHPT) is one of the most common endocrine diseases and the most common cause of hypercalcemia. Since routine laboratory testing, the prevalence of the disease has increased from 0.1% to 0.4% worldwide. The only curative treatment is parathyroidectomy. Nowadays, preoperative localization studies have become standard before surgical treatment, and the first stage imaging methods are cervical ultrasonography (US) and/or Sestamibi scintigraphy. Objectives: To describe the accuracy of US and Sestamibi for detection of hyperfunctioning parathyroid adenomas preoperatively in patients with confirmed pHPT from our medical institution. Results: This is a retrospective study from a prospectively kept database that included thirty-one patients with the confirmed diagnosis of pHPT clinically and biochemically. The average age was 57.8 years old. Preoperative US and surgery findings were compared with a sensitivity of 51%. Preoperative Sestamibi and surgery findings were compared resulting in a sensitivity of 71%. Both imaging methods combined, resulted in a sensitivity of 80%. Conclusion: In patients with pHPT, Sestamibi is an effective method for localizing parathyroid pathology preoperatively, but the false negative rate can be high. US tends to have a wider range explained by the operator-dependent factor. The combination of US and Sestamibi reduces the rate of false negatives, as reported in international literature. It is important to mention that these studies cannot be used as a confirmatory test for this disease. It should only be used as an adjunct to help plan the operation.

AACE2021-A-1082: Primary Hyperparathyroidism: A Case Report of Management with Extra Ordinary Low Dose of Cinacalcet in an Elderly Male

Primary Hyperparathyroidism is a common cause of Hypercalcemia and is often seen in endocrine clinics. Majority of patients are found to have solitary parathyroid adenomas which may be associated with other endocrine problems. Common systemic complications are secondary osteoporosis, renal stones, pancreatitis and peptic ulcers. Surgery remains the mainstay of treatment for correction of pathology, however patients who do not meet the criteria or in whom surgery is contraindicated are managed conservatively and with calcimimetic agents such as cinacalcet. Case report and literature review. We are reporting a case of a 73 years old male who was referred to the endocrine clinic for work up of hypercalcemia. His past medical history was significant for well controlled Type 2 Diabetes and Hypertension. During his work up, he was found to have elevated serum calcium of 11.7 mg/dl, elevated serum PTH of 767 ng/L and 24 hours urinary calcium excretion of 446 mg/dl. Renal functions and 25 hydroxy vitamin D levels were within normal limits and the ultrasound and DEXA scan were negative for presence of any renal stone or osteoporosis. His two elder brothers also had a history of parathyroidectomy. He was reluctant for surgery and therefore imaging for the neck was also omitted. He was started on cinacalcet 15 mg/ day with an initial presumption of increase in dose requirement afterwards. However his serum calcium levels showed a remarked improvement and within one month they dropped to 9.9 mg/dl. The second subsequent test showed a serum calcium of 8.9 mg/dl after which the dose was reduced to 15 mg every alternate day. A presumption of tumor necrosis was made but the calcium levels rose higher on stopping cinacalcet and again went back to normal on the extra ordinary low dose of 15 mg every alternate day. His 3 years follow up to our clinic on this maintenance dose has shown steady calcium levels, improvements in serum PTH with fluctuations between 260 – 380 ng/L and no subsequent complication. Primary Hyperparathyrodism is a common cause of hypercalcemia which if left untreated can have serious systemic complications. Surgery remains the mainstay of treatment but in patients not meeting the criteria or in whom surgery is contraindicated, medical therapy is an option which includes dietary measures, bisphosphonates and calcimimetics like cinacalcet. The usual dose of cinacalcet is between 30 – 90 mg/day. Our case represents an unusual story of improvement on a very low dose of calcimimetic. More cases need to be evaluated and tested on low dose and may-be we can have a change in the recommendations in future.

Rare presentations of sarcoidosis

Sarcoidosis affects multiple organs, forming non-caseating granulomas whose cause is unknown and can present with nonspecific features. The diagnosis requires involvement of two or more organs and the demonstration of noncaseating granulomas on biopsy. Non-specific clinical features make delay in diagnosis. It is for this reason that we report herein two cases, one who presented with abdominal pain due to panceratitis- hypercalcemia related and cause of which was sarcoidosis, second patient presented with generalised weakness and shortness of breath. Cases: First case: Thirty-two-year-old man with past history of H. pylori infection, significant weight loss, on and off fever for 1 year, seizures with recurrent bell’s palsy admitted with complaints of pain in abdomen, nausea and vomiting for 3 days. On evaluation his blood calcium level was raised causing pancreatitis which is very rare in sarcoidosis. Diagnosis of sarcoidosis was very challenging in this situation where chest radiograph was perfectly normal and HRCT thorax revealed multiple small nodules, lymphadenopathy and ILD. Lung biopsy revealed chronic granulomatous inflammation. After ruling out infectious and malignancy causes of hypercalcemia, the patient was diagnosed as sarcoidosis, treated with steroids, is still in follow up and is doing fine. Second case: Fifty-six-year-old female with past history of H- pylori infection, raised blood pressure, weight loss and underlying heart condition presented with complaints of itching all over body, generalised weakness and shortness of breath on exertion. Patient was wandering for treatment for past 1 year for her non-specific symptoms and was investigated in line of lymphoma in the past. On investigation she was found to have raised creatinine, calcium, calcitriol and anterior uveitis, probable diagnosis of sarcoidosis was made trial of steroids was given which showed slight improvement but she died due to cardiogenic shock. Conclusion: Sarcoidosis is usually underdiagnosed or misdiagnosed or lately diagnosed leading to loss of life which can be prevented. Pancreatitis in sarcoidosis is very rare and careful history, knowledge and investigation may be helpful in diagnosis of it.

Hypercalcaemia Caused by Sunflower Seeds and Calcium Carbonate Supplements.

Hypercalcaemia is commonly associated with malignancy or endocrinological disorders. However, sometimes it can occur due to increased oral intake of calcium. We present an interesting case of hypercalcaemia due to ingestion of sunflower seeds and calcium carbonate supplements. We present the case of a 53-year-old man with history of T-cell lymphoma and gastroesophageal reflux disease who was brought to the emergency room due to altered mental status, nausea, vomiting and abdominal pain. His calcium level was 3.30 mmol/l (normal value 2.23-2.58 mmol/l). Imaging studies were unremarkable. The patient was hydrated with normal saline and calcium levels improved. Once he was more coherent, he disclosed that he had consumed significant amounts of sunflower seeds and calcium carbonate supplements, which were considered to be the cause of his hypercalcaemia. Hypercalcaemia is common and can lead to critical illness. Although hypercalcaemia is frequently associated with endocrinological disorders, sometimes the presentation is secondary to increased intake. The consumption of sunflower seeds and antacids containing calcium carbonate can cause symptomatic hypercalcaemia. It is important to recognize rare causes of hypercalcaemia in order to treat it in a timely manner and prevent recurrence. Hypercalcaemia can occur due to excessive intake of sunflower seeds and calcium carbonate supplements.Hydration and cessation of oral supplements can result in rapid reversal of hypercalcaemia.It is important to obtain a complete history in order to determine the aetiology of hypercalcaemia.

Hypercalcaemia Caused by Sunflower Seeds and Calcium Carbonate Supplements

Introduction: Hypercalcaemia is commonly associated with malignancy or endocrinological disorders. However, sometimes it can occur due to increased oral intake of calcium. We present an interesting case of hypercalcaemia due to ingestion of sunflower seeds and calcium carbonate supplements. Case Description: We present the case of a 53-year-old man with history of T-cell lymphoma and gastroesophageal reflux disease who was brought to the emergency room due to altered mental status, nausea, vomiting and abdominal pain. His calcium level was 3.30 mmol/l (normal value 2.23–2.58 mmol/l). Imaging studies were unremarkable. The patient was hydrated with normal saline and calcium levels improved. Once he was more coherent, he disclosed that he had consumed significant amounts of sunflower seeds and calcium carbonate supplements, which were considered to be the cause of his hypercalcaemia. Conclusion: Hypercalcaemia is common and can lead to critical illness. Although hypercalcaemia is frequently associated with endocrinological disorders, sometimes the presentation is secondary to increased intake. The consumption of sunflower seeds and antacids containing calcium carbonate can cause symptomatic hypercalcaemia. It is important to recognize rare causes of hypercalcaemia in order to treat it in a timely manner and prevent recurrence.

HYPERCALCEMIA UNMASKING UNDERLYING MYCOBACTERIUM AVIUM-INTRACELLULARE INFECTION

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: Common causes of hypercalcemia include malignancy and granulomatous disease; however nontuberculous mycobacteria (NTM) infections are also rarely associated with hypercalcemia. We present a case of hypercalcemia secondary to underlying Mycobacterium avium-intracellulare (MAI) infection in a patient with acquired immunodeficiency syndrome (AIDS). CASE PRESENTATION: A 36-year-old male with recently diagnosed AIDS (CD4 count 17 cell/uL, viral load 52,400 copies/mL at diagnosis) on anti-retroviral therapy (ART) presented with three days of generalized weakness, nausea, vomiting, and poor appetite associated with night sweats, 20-pound weight loss, dyspnea, and non-productive cough. Vital signs were unremarkable, physical exam revealed moderate lower abdominal tenderness with hepatosplenomegaly, and bloodwork was notable for a corrected calcium of 13.1 mg/dL, undetectable parathyroid hormone (PTH) of <1 pg/mL, elevated 1,25-dihydroxyvitamin D to 112 pg/mL, and decreased PTH-related protein of 7 pg/mL. Hypercalcemia was treated with intravenous fluid hydration and pamidronate. Computed Tomography of Chest/Abdomen/Pelvis revealed bulky retroperitoneal and mesenteric adenopathy and splenomegaly, concerning for lymphoma versus paradoxical worsening of existing opportunistic infection secondary to immune reconstitution with the initiation of ART (CD4 70 cell/uL, viral load 42 copies/mL). He underwent diagnostic laparoscopy with mesenteric lymph node biopsy for definitive diagnosis, with both biopsy and acid-fast bacillus (AFB) culture positive for MAI, clinical picture consistent with disseminated infection. He was started on Ethambutol and Azithromycin and discharged with close infectious disease follow-up. DISCUSSION: Many etiologies exist for hypercalcemia, the most notable being malignancy and granulomatous diseases. In patients with AIDS, NTM infection should also be considered in the differential. To date, there have only been eight reported cases of MAI-associated hypercalcemia, making this the ninth case, and the fourth one with hypercalcemia as the presenting symptom [1]. Though the mechanism is not well understood, one theory postulates the involvement of immune reconstitution inflammatory syndrome (IRIS). In newly diagnosed AIDS patients, the restoration of the immune system due to ART to fight off latent infection causes rebound production of interferon-gamma, which enhances granuloma formation to facilitate the eradication of infection. In turn, granulomas produce 1-alpha hydroxylase, leading to increased 1,25-vitamin D and calcium production [2]. CONCLUSIONS: Non-PTH-mediated hypercalcemia is often attributed to malignancy. However further investigation is warranted to rule out opportunistic infections, especially in newly diagnosed cases of AIDS. REFERENCE #1: Ayoubieh H, Alkhalili E. Mycobacterium avium-intracellulare and the unpredictable course of hypercalcemia in an AIDS patient. Braz J Infect Dis. 2017;21(1):116-118. doi:10.1016/j.bjid.2016.08.002 REFERENCE #2: Tsao YT, Wu CC, Chu P. Immune reconstitution syndrome-induced hypercalcemic crisis. Am J Emerg Med. 2011;29(2):244.e3-244.e244006. doi:10.1016/j.ajem.2010.03.013 DISCLOSURES: No relevant relationships by Sudheer Konduru, source=Web Response No relevant relationships by SANA MULLA, source=Web Response No relevant relationships by Mrunal Sharma, source=Web Response No relevant relationships by Vihitha Thota, source=Web Response No relevant relationships by Manaswitha Thota, source=Web Response

Concomitant familial hypocalciuric hypercalcemia and single parathyroid adenoma: a case report

BackgroundPrimary hyperparathyroidism (PHPT) is a common endocrine disorder and the most frequent benign cause of hypercalcemia. PHPT is characterized by autonomous hypersecretion of parathyroid hormone (PTH), regardless of serum calcium levels. Familial hypocalciuric hypercalcemia (FHH) is a rare, benign syndrome only affecting the regulation of calcium metabolism. FHH is an autosomal-dominant genetic disease with high penetrance, caused by an inactivating variant in the CASR gene encoding the calcium-sensing receptor (CaSR). We present a unique case of concomitant PHPT and FHH without clinically actionable variants in MEN1.Case presentationA 47-year-old Caucasian man with severe hypercalcemia, genetic FHH, and initially normal parathyroid scintigraphy was referred for endocrine evaluation due to nonspecific symptoms. Biochemical evaluation showed elevated serum ionized calcium and PTH. The calcium–creatinine clearance ratio was low. All other biochemical measures were normal, including kidney function. Genetic evaluation was redone and confirmed FHH. A new parathyroid scintigraphy showed a significant single adenoma corresponding to the lower left gland. The patient underwent parathyroidectomy, and a parathyroid adenoma was removed. A reduced level of hypercalcemia persisted due to FHH.ConclusionsThe correct diagnosis of the underlying cause of hypercalcemia is important to ensure the right treatment. Patients with FHH should avoid operative treatment, and PHPT should be differentiated from MEN1 to determine whether surgery should include parathyroidectomy with removal of one adenoma or 3.5 hyperplastic parathyroid glands.

Primary Hyperparathyroidism - Case Report of a Female Patient with Hypercalcemic Crisis

Primary hyperparathyroidism is a result of increased and uncontrolled function of the parathyroid hormone caused by hyperfunction of one or more parathyroid glands. The cause of hyperfunction of the parathyroid glands could be adenoma, hyperplasia, and carcinoma. Primary Hyper parathyroidism is the most common cause of Hypercalcemia in outpatient population. The paper presents the case report of a 60years old female treated in our Hospital in March 2013. She presented in outpatient department with complaints of joints pain, Hypertension and renal failure for last 8years. After clinical, laboratory and radiological examination she was diagnosed as a case of PHPT due to a Giant Parathyroid Adenoma. After supportive, symptomatic and surgical treatment, the patient was back to normal daily activities without any signs of disease.

An unusual case of neck hematoma and hypercalcemia

One of the most frequent cause of hypercalcemia is primary hyperparathyroidism, which can lead to systemic involvement and life-threatening conditions. We described a rare case of a parathyroid adenoma rupture with consequent bleeding and respiratory airway compression. An 84-year-old man presented to the emergency department complaining neck swelling and related dysphagia. A computer tomography of the neck revealed an extensive left lateral hematoma, and a neck ultrasonography evidenced a hemorrhagic parathyroid adenoma, later confirmed by a 99 mTc-MIBI scintigraphy. To date only 40 cases of ruptured parathyroid adenomas have been described in literature, however due to the possibility of massive bleeding and compression of the airways this diagnosis should always be ruled out. The rupture of a parathyroid adenoma is a rare, but possibly life-threatening event due to airways compression and hemodynamic instability. Testing for hypercalcemia and hyperparathyroidism is mandatory to obtain a correct diagnosis.

Primary Hyperparathyroidism Superimposed on a Pre-existing Familial Hypocalciuric Hypercalcemia Diagnosis

Familial hypocalciuric hypercalcemia is a rare clinical condition of persistently elevated serum calcium and reduced urinary calcium levels with an autosomal dominance inheritance pattern to the three out of four large types of this condition known. This rare condition goes largely undiagnosed as patients are largely asymptomatic and where symptoms are present, other causes of hypercalcemia are considered first. Hyperparathyroidism, super-imposing on FHH, is an even rarer occurrence. We present the case of an adult male with an initial provisional assessment of FHH, which was later confirmed with a genetic study. He went on to develop hyperparathyroidism (with evident enlarged parathyroid glands on Sestamibi parathyroid scan done, and an eventual histologic diagnosis of parathyroid adenoma after surgery). It remains to be established if this is an incidental occurrence or if there is a causal relationship between FHH and an onward development of parathyroid hypertrophy or adenoma(ta).

Parathyroid hormone-independent hypercalcemia and hypercalciuria of a patient with nephrolithiasis and nephrocalcinosis and impaired vitamin D metabolism due to a defect in the &lt;i&gt;CYP24A1&lt;/i&gt; gene

Hypercalcemia associated with impaired vitamin D metabolism is a rare autosomal recessive disorder. The mechanism of this pathology is the impairment of inactivation of active metabolites of vitamin D because of mutations in the CYP24A1 gene, which leads to an increase of calcium absorption and the development of hypercalcemia, hypercalciuria, nephrocalcinosis and nephrolithiasis. The phenotype of the disease ranges from severe forms which are diagnosed in early infancy (severe hypercalcemia associated with dehydration, vomiting, nephrocalcinosis, and sometimes death) to milder forms, that often are diagnosed in adulthood and manifested with recurrent nephrolithiasis and nephrocalcinosis. Differential diagnosis is carried out with the most common causes of hypercalcemia: primary hyperparathyroidism and malignant neoplasms. To diagnose, the determination of vitamin D metabolites and genetic research are used. As a treatment for mild forms, it is recommended to limit dairy products, to keep a drinking regimen, to refuse taking vitamin D and calcium preparations, and use of sunscreens. The article presents a clinical case of parathyroid hormone-independent hypercalcemia due to mutation of the CYP24A1 gene of a 20-year-old patient suffering from nephrolithiasis and nephrocalcinosis since the age of 16 with a confirmed violation of vitamin D metabolism.

Systems-Level Opportunities in the Management of Primary Hyperparathyroidism: An Informatics-based Assessment.

Primary hyperparathyroidism (PHPT), a leading cause of hypercalcemia and secondary osteoporosis, is underdiagnosed. This work aims to establish a foundation for an electronic medical record-based intervention that would prompt serum parathyroid hormone (PTH) assessment in patients with persistent hypercalcemia and identify care gaps in their management. A retrospective cohort study was conducted in a tertiary academic health system of outpatients with persistent hypercalcemia, who were categorized as having classic or normohormonal PHPT. Main outcome measures included the frequencies of serum PTH measurement in patients with persistent hypercalcemia, and their subsequent workup with bone mineral density (BMD) assessment, and ultimately, medical therapy or parathyroidectomy. Among 3151 patients with persistent hypercalcemia, 1526 (48%) had PTH measured, of whom 1377 (90%) were confirmed to have classic (49%) or normohormonal (41%) PHPT. PTH was measured in 65% of hypercalcemic patients with osteopenia or osteoporosis (P < .001). At median 2-year follow-up, bone density was assessed in 275 (20%) patients with either variant of PHPT (P = .003). Of women aged 50 years or older with classic PHPT, 95 (19%) underwent BMD assessment. Of patients with classic or normohormonal PHPT, 919 patients (67%) met consensus criteria for surgical intervention, though only 143 (15%) underwent parathyroidectomy. Within a large academic health system, more than half of patients with confirmed hypercalcemia were not assessed for PHPT, including many patients with preexisting bone disease. Care gaps in BMD assessment and medical or surgical therapy represent missed opportunities to avoid skeletal and other complications of PHPT.

Unusual Etiology of Hypercalcemia in an Adolescent With Acute Gastroenteritis

We present the report of an adolescent female who presented with acute gastroenteritis, weight loss, and hypercalcemia. Further evaluation revealed hyperthyroidism to be the cause of hypercalcemia. Treatment of hyperthyroidism successfully corrected the hypercalcemia in our index case.

Rare Causes of Hypercalcemia: 2021 Update.

Primary hyperparathyroidism and malignancy are the etiologies in 90% of cases of hypercalcemia. When these entities are not the etiology of hypercalcemia, uncommon conditions need to be considered. In 2005, Jacobs and Bilezikian published a clinical review of rare causes of hypercalcemia, focusing on mechanisms and pathophysiology. This review is an updated synopsis of rare causes of hypercalcemia, extending the observations of the original article. Articles reporting rare associations between hypercalcemia and unusual conditions were identified through a comprehensive extensive PubMed-based search using the search terms "hypercalcemia" and "etiology," as well as examining the references in the identified case reports. We categorized the reports by adults vs pediatric and further categorized the adult reports based on etiology. Some included reports lacked definitive assessment of etiology and are reported as unknown mechanism with discussion of likely etiology. There is a growing understanding of the breadth of unusual causes of hypercalcemia. When the cause of hypercalcemia is elusive, a focus on mechanism and review of prior reported cases is key to successful determination of the etiology. The ever-expanding reports of patients with rare and even unknown mechanisms of hypercalcemia illustrate the need for continued investigation into the complexities of human calcium metabolism.