scholarly journals Silicone Induced Severe Hypercalcemia

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A222-A223
Author(s):  
Dhammi K K Jayathilaka ◽  
Helen Prathiba Gnanapragasam ◽  
Manav Batra
Keyword(s):  
Vitamin D ◽  
Undetectable Viral Load ◽  
Silicone Implants ◽  
Repeat Dose ◽  
Rare Entity ◽  
Severe Hypercalcemia ◽  
Intravenous Hydration ◽  
Granulomatous Diseases ◽  
Disseminated Disease ◽  
Silicone Injections

Abstract Background: Silicone injections are becoming increasingly prevalent for cosmetic enhancement in the transgender population. We report a case of silicone-induced hypercalcemia to highlight the process of extra-renal production of 1,25-hydroxy (OH) vitamin D (calcitriol) and discuss the approaches in managing this rare entity. Clinical Case: A 51-year-old African American transgender female with a past medical history of human immunodeficiency virus (HIV) on antiretroviral therapy with undetectable viral load presented with right flank pain, nausea, and vomiting for one day. On examination, nodules were palpated in both breasts, left lateral hip, and the gluteal area had hyperpigmentation from silicone injections ten years ago. Calcium was elevated at 15.2 mg/dL (8.5–10.5) with albumin 3.8 g/dL (3.5–5), ionized calcium 7.4 mg/dL (4.64–5.28), phosphate 4.5 mg/dL (2.5–4.8) and creatinine of 3.2 mg/dL (0.4–1.4). Imaging revealed right ureteral calculi with hydronephrosis requiring stent placement. PTH was suppressed <5 pg/ml (12–72) and PTHrP were negative. Vitamin D 25 (OH) of 28 ng/mL (30–100) with elevated 1, 25 OH2 D3 144 pg/ml (19–79) and ACE 141 units/L (12–60) were suggestive of a granulomatous process. CT chest and abdomen without contrast did not show any hilar, mediastinal, or abdominal lymphadenopathy to suggest sarcoidosis or lymphoma, but numerous bilateral calcified masses were noted within the breasts consistent with silicone injections. Serum and urine electrophoresis were consistent with monoclonal gammopathy of undetermined significance. Patient deferred further evaluation (PET-CT and skin biopsy for granulomatous changes) as an outpatient. Calcium improved in 4 days to 10.5 mg/dL with intravenous hydration, calcitonin 260 units, IV furosemide 20 mg, and pamidronate of 60 mg. Despite a repeat dose of Pamidronate 60 mg a week later her calcium was rising again to 11.1 mg/dL. Plastic surgery evaluation concluded that due to extensive implants, surgery would be very disfiguring and challenging. She was reluctant to start prednisone as it may affect healing after surgery and the need for antibiotic prophylaxis for HIV, but she later agreed. Prednisone 20 mg daily was started for granulomatous disease and Calcium improved to 10.3 mg/dL. Conclusion/Clinical Lesson: Silicone Induced hypercalcemia is a rare entity with diagnostic and treatment dilemmas. Based on the few reported cases, silicone induced severe hypercalcemia is managed with IV hydration, denosumab, or zoledronic acid. However, glucocorticoids may maintain normocalcemia like in other granulomatous diseases. Removal of silicone implants may improve hypercalcemia, but it is challenging given the extent of implants, disfigurement, and possible disseminated disease and may not be curative. These aspects need to be considered in evaluating and management.

scholarly journals A Curious Case of PTH Independent Hypercalcemia Secondary to Silicone Injections

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A176-A176
Author(s):  
Moises Matos ◽  
Ahsan Farooq ◽  
Heidi Jackeline Peynado De Pena ◽  
Hanford Yau ◽  
Asif Uddin
Keyword(s):  
African American Woman ◽  
Subcutaneous Fat ◽  
American Woman ◽  
Clinical Problem ◽  
Surgical Debridement ◽  
Severe Hypercalcemia ◽  
Granulomatous Tissue ◽  
Granulomatous Diseases ◽  
Silicone Injections

Abstract Background: Hypercalcemia is a commonly encountered clinical problem with numerous etiologies. Granulomas formed secondary to foreign bodies are a rare but increasingly recognized cause of hypercalcemia. Clinical Case: A 49-year old African American woman, who had received silicone injections for buttock augmentation 15 years ago, was found to have severe hypercalcemia after she presented with complaints of chronic constipation, muscle cramping, polyuria, and mental fog. Her labs on admission showed severe hypercalcemia Ca 17.9mg/dL (normal: 8.4–10.6 mg/dL), with a suppressed PTH 4 pg/mL (normal 14–54 pg/mL). Prior labs from 5 years earlier, had shown an elevated 1,25(OH)2D, therefore differentials including lymphoma and chronic granulomatous diseases, particularly sarcoidosis, were high on the list of possible diagnosis. Additional labs showed a normal PTH-RP 19 pg/mL (normal 14–27 pg/mL), normal ACE levels 64 U/L (normal 9–67 U/L), low 25(OH)D2 1 ng/mL and normal 1,25(OH)2D 62 pg/mL. Her exam was notable for multiple indurated and firm masses palpable over the bilateral gluteal region and lateral thighs. CT abdomen/pelvis showed extensive and markedly confluent infiltration with intervening globules of macroscopic fat throughout the subcutaneous fat layers of the buttocks and lateral hips and speckled linear calcifications consistent with granulomatous reaction. With aggressive fluid hydration and calcitonin, her calcium levels decreased over the following 48 hours, but remained at 12–13 mg/dL. She was started on 30 mg of prednisone daily and her calcium levels dropped to 10.9 mg/dL the following day. She was discharged home on prednisone, her calcium levels remained suppressed, and her prednisone dose was slowly tapered during the following months. She was referred for plastic surgery evaluation and is being evaluated for possible surgical debridement. Conclusion: Hypercalcemia secondary to foreign body granulomas is a rare clinical entity. The diagnosis is usually established through a thorough history and examination. Lab findings may be variable. Treatment of these patients can be challenging, and corticosteroids are the mainstay of treatment in most cases1. Surgical debridement of granulomas has been reported with good results; however, further investigation and longer follow-up is needed2. References: 1.Tachamo, N., Donato, A., Timilsina, B., Nazir, S., Lohani, S., Dhital, R., & Basnet, S. Hypercalcemia associated with cosmetic injections: A systematic review. European Journal of Endocrinology, 2018; 178(4): 425–4302.Edwards, B.J., Saraykar, S., Suna, M., Murphy, W. A., Lin, P., Gagel, R. Resection of granulomatous tissue resolves silicone induced hypercalcemia, Bone Reports, 2016; 5:163–7

scholarly journals Silicone-Induced Granulomatous Reaction Causing Severe Hypercalcemia: Case Report and Literature Review

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Gulshan Man Singh Dangol ◽  
Hilmer Negrete
Keyword(s):  
Vitamin D ◽  
Abdominal Pain ◽  
Incidental Finding ◽  
Disease Entity ◽  
Patient Report ◽  
Severe Dehydration ◽  
Granulomatous Reaction ◽  
Severe Hypercalcemia ◽  
Vitamin D Intoxication ◽  
Granulomatous Diseases

A 67-year-old woman presented to the hospital with complaints of abdominal pain. Physical exam was significant for signs of severe dehydration, mild epigastric tenderness and multiple non-tender hard nodules over her arms and thighs. Incidental finding of severe hypercalcemia led to negative workups for hyperparathyroidism, vitamin D intoxication, and malignancy. However, elevated levels of 1,25-hydroxy vitamin D raised the possibility of granulomatous diseases. Imaging and patient report revealed silicone-induced foreign body granulomatous reaction as the cause of hypercalcemia. Use of silicone for cosmetic enhancement of body contours can result in siliconomas, severe hypercalcemia, and complications. Treatment is unestablished for this condition. Increasing prevalence of cosmetic enhancement should prompt vigilance for this rare disease entity. Providers should counsel and educate individuals undergoing such procedures.

Hypervitaminosis D After Prolonged Feeding With a Premature Formula

PEDIATRICS ◽  
1993 ◽  
Vol 92 (6) ◽  
pp. 862-864
Author(s):  
YASUSHI NAKO ◽  
NAOBUMI FUKUSHIMA ◽  
TAKESHI TOMOMASA ◽  
KANJI NAGASHIMA ◽  
TAKAYOSHI KUROUME
Keyword(s):  
Vitamin D ◽  
Premature Infant ◽  
Premature Infants ◽  
Bone Disease ◽  
Calcium Intake ◽  
Metabolic Bone Disease ◽  
Hypervitaminosis D ◽  
Severe Hypercalcemia ◽  
Metabolic Bone ◽  
Prolonged Feeding

Hypervitaminosis D is one of the causes of severe hypercalcemia in children. Most cases of hypervitaminosis D during childhood are due to an excessive supplementation of vitamin D by physicians or parents.1,2 To prevent metabolic bone disease of prematurity (rickets of prematurity), formulas designed for premature infants ("premature formulas"), which contain more calcium and vitamin D than standard formulas, are given to premature infants in addition to human milk.1 In some cases, separate vitamin D products are also given to these infants, although requirements for vitamin D and calcium intake in the premature infant and the formerly premature infant have not been fully estimated.1

scholarly journals Vitamin D and Risk for Vitamin A Intoxication in an 18-Month-Old Boy

2016 ◽  
Vol 2016 ◽  
pp. 1-3
Author(s):  
Valentina Talarico ◽  
Massimo Barreca ◽  
Rossella Galiano ◽  
Maria Concetta Galati ◽  
Giuseppe Raiola
Keyword(s):  
Vitamin D ◽  
Vitamin A ◽  
High Serum ◽  
Renal Ultrasound ◽  
Once Daily ◽  
Hydroxyvitamin D ◽  
Vitamin D Intoxication ◽  
Intravenous Hydration ◽  
25 Hydroxyvitamin D ◽  
Low Levels

An 18-month-old boy presented with abdominal pain, vomiting, diarrhea, and poor appetite for 6 days. He had been given a multivitamin preparation once daily, containing 50.000 IU of vitamin D and 10.000 IU of vitamin A for a wide anterior fontanelle for about three months. He presented with hypercalcemia, low levels of parathyroid hormone (PTH), and very high serum 25-hydroxyvitamin D (25-OHD) levels. Renal ultrasound showed nephrocalcinosis. He did not have sign or symptom of vitamin A intoxication. Patient was successfully treated with intravenous hydration, furosemide, and prednisolone. With treatment, serum calcium returned rapidly to the normal range and serum 25-OHD levels were reduced progressively. In conclusion the diagnosis of vitamin D deficiency rickets without checking 25-OHD levels may cause redundant treatment that leads to vitamin D intoxication (VDI).

scholarly journals Rebound Hypercalcemia After Denosumab Therapy in a Child With Cherubism

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A218-A218
Author(s):  
Melissa Kaori S Litao ◽  
Deepa Badrinath Murthy ◽  
Jason Klein
Keyword(s):  
Vitamin D ◽  
Bone Resorption ◽  
Bone Turnover ◽  
Osteoclast Differentiation ◽  
Distal Tibia ◽  
Drug Discontinuation ◽  
Renal Ultrasound ◽  
Close Monitoring ◽  
Severe Hypercalcemia ◽  
Maxilla And Mandible

Abstract Background: Cherubism, caused by autosomal dominant mutations in the SH3BP2 gene, is characterized by increased bone resorption with development of bilateral fibro-osseous lesions limited to the maxilla and mandible. The SH3BP2 gene is thought to be involved in osteoclastogenesis. Affected children, while usually asymptomatic at birth, typically present at 2–5 years of age with cheek and jaw swelling with upward tilting of eyes due to expansion of fibrous tissues. Bone resorption and proliferation of lesions continues until puberty after which spontaneous regression occurs. RANKL is a cytokine expressed on the surface of osteoclast precursors and is responsible for inducing osteoclast differentiation. Denosumab is an anti-RANKL monoclonal antibody which prevents osteoclast maturation. However, it has a short half-life, and effects on bone turnover have been found to be rapidly reversible after drug discontinuation. The rebound increased bone turnover can lead to severe hypercalcemia. Clinical Case: A 4 year old boy with cherubism (c.1253C>G pathogenic variant in SH3BP2), after failing a 10-month trial of tacrolimus, was placed on monthly denosumab (2 mg/kg) for a total of 10 doses. During denosumab therapy, he received calcium and vitamin D to prevent hypocalcemia; these were stopped once denosumab was discontinued. He presented to the hospital 4 months after the final denosumab dose with polyuria, polydipsia, fatigue, nausea and abdominal pain. Work-up revealed serum Ca 15.3 mg/dL (N: 8.4–10.2), PTH <3 pg/mL (N: 24–86), 25-OH vitamin D 32 ng/mL (N: >19 ng/mL), 1,25-dihydroxyvitamin D 6.7 pg/mL (N: 19.9–79.3), and urine Ca/Cr 0.48. Renal ultrasound showed normal kidneys with a small amount of layering debris in the bladder. During hospitalization, he received IV fluids, 1 dose of furosemide, 3 doses of calcitonin, 24 hours of hydrocortisone, and a single 0.5 mg/kg dose of pamidronate. He was discharged 48 hours after the bisphosphonate with serum Ca 9.5 mg/dL. He returned with serum Ca 13.5 mg/dL 9 days after the pamidronate and was readmitted. He again received 4 doses of calcitonin and 1 dose of pamidronate (0.5 mg/kg). Calcium levels improved to 9.5 mg/dL at discharge but rose to 11.6 mg/dL a week later. He received a 0.05 mg/kg dose of zoledronate outpatient, with improvement in serum Ca to 10.1 mg/dL. A week later, he twisted his ankle, resulting in transverse impacted buckle fractures of his left distal tibia and fibula; no lytic or sclerotic lesions were noted on x-ray. His leg was immobilized by Orthopedics. Calcium levels remained within range (9.9 mg/dL) 7 months after the zoledronate. Conclusion: Rebound hypercalcemia can occur months after denosumab withdrawal, indicating the need for close monitoring of calcium levels in patients who receive this drug. The hypercalcemia appears to respond best to bisphosphonates, with a more sustained response to zoledrenate compared to pamidronate.

scholarly journals SAT-LB23 Paraneoplastic Hypercalcemia in a PTH Producing Adrenocortical Carcinoma - a Rare and Deadly Condition

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sven Gruber ◽  
Cong Tang ◽  
Mesut Berber ◽  
Stefan Fischli ◽  
David Penton-Ribas ◽  
...  
Keyword(s):  
Vitamin D ◽  
Serum Calcium ◽  
Adrenocortical Carcinoma ◽  
Tumor Resection ◽  
Steroid Synthesis ◽  
Endocrine Differentiation ◽  
Parathyroid Hormone Related Protein ◽  
Severe Hypercalcemia ◽  
H295r Cells ◽  
Paraneoplastic Hypercalcemia

Abstract Background: Hypercalcemia is a commonly encountered paraneoplastic manifestation of certain cancers with or without endocrine differentiation. However, the association between adrenocortical carcinoma (ACC) with paraneoplastic hypercalcemia is very rare, and therefore little is known about the cause and its relevance in the disease. Clinical Case: A 40-year-old woman presented in the hospital with a 5-month history of progressive flank pain with unintentional weight loss of 6 kg. MRI revealed a mass of 9x8.1x4.8 cm of the right adrenal gland with inhomogeneous contrast enhancement. Biochemical investigations provided evidence of endogenous hypercortisolism (24-hour urinary cortisol excretion [490 µg, n<236 µg/l], 1mg dexamethasone suppression test [199 nmol/l, n<50 nmol/l], ACTH [28 ng/l, n<61 ng/l]) although the patient did not show any specific clinical sign of overt hypercortisolism. In addition, laboratory testing revealed an exceptionally high plasma level of calcium [max 3.67 mmol/l (albumin-corrected)] and low phosphate [min 0.26 mmol/l] in the setting of low PTH [6.4 ng/l, n>15 ng/l] and PTHrP levels [<0.50 pmol/l]. However, subsequent dilution unmasked a highly elevated PTH concentration of 2171.5 ng/l with persistent low PTHrP levels, indicating false low values due to a hook effect in the initial measurement. Levels of 1,25-dihydroxy vitamin D and 25-hydroxy vitamin D were in the normal range. A PET-CT provided no indications of metabolically active (osseous) metastases. After correction of the serum calcium towards tolerable values, the tumor was removed by open en bloc adrenalectomy. Histologic evaluation confirmed an ACC (TNM pT4 pN1 (2/3), L1, V1, high grade) despite missing immunohistochemically expression of classical adrenal markers (diagnosis of exclusion). Supplemental quantitative RT-PCR studies support the diagnosis of ACC by detecting significant SF-1 and CYP11B2 expression in the tumor cells. Further analyses provided evidence that the mRNA expression of PTH, but not PTHrP, was moderately increased in the ACC sample compared to NCI H295R cells. Upon tumor resection, serum calcium levels swiftly normalized indicating the tumor as the sole source of PTH secretion. Despite initiation of adjuvant mitotane- and salvage chemo-therapy, the patient died 3 months later upon of a massive tumor relapse with a recurrence of severe hypercalcemia. Conclusion: This case demonstrates paraneoplastic hypercalcemia in a PTH producing ACC. PTH may induce hypercalcemia, impair adrenal steroid synthesis and act as an autocrine growth factor in ACC, as described in few individual cases for PTHrp producing ACC [1]. This suggests a poor prognosis for this rare entity. 1. Rizk-Rabin, M., et al., Differential Expression of Parathyroid Hormone-Related Protein in Adrenocortical Tumors: Autocrine/Paracrine Effects on the Growth and Signaling Pathways in H295R Cells. 2008.

scholarly journals SAT-397 Characteristics and Outcomes of Severe Hypercalcemia Related Admissions - a Single Centre 5 Years’ Experience

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jo-Anne Ponce ◽  
Myron Lee ◽  
Amanda Caswell ◽  
Mclaine O Parsons ◽  
Shamasunder Acharya
Keyword(s):  
Vitamin D ◽  
Calcium Level ◽  
Calcium Supplementation ◽  
General Medicine ◽  
Vitamin D Supplementation ◽  
Tertiary Referral Center ◽  
Icu Admission ◽  
Antiresorptive Agent ◽  
Severe Hypercalcemia ◽  
Severe Hypercalcaemia

Abstract Introduction: Severe hypercalcemia (corrected calcium ≥3.5mmol/L) is typically associated with multi-organ dysfunction and increased mortality. We audited 47 consecutive patients who were admitted to a single tertiary referral center over 5 years period (2014-2019) with severe hypercalcemia. Results: The median age 69 years (10-97yrs); 55% females, and median length of stay was 9 days (1-120). Most patients (30%) were admitted under general medicine and 53% received endocrinology consultation. Renal dysfunction (91%) dominated the clinical presentation, but gastrointestinal abnormalities (70%), neuropsychiatric manifestations (53%), and musculoskeletal involvement (45%) were also very common. PTH was measured in 43/47 patients with 37 PTH independent (calcium level 3.82 mmol/L) and 6 PTH dependent (calcium level 3.70mmol/L) hypercalcemia. Recurrence of the condition within five years was recorded for 5 patients (11%), ten (21%) patients died during the admission, and 4 patients (9%) required ICU admission in PTH independent severe hypercalcaemia, majority are due to malignancy; while none of these outcomes were observed in PTH dependent severe hypercalcaemia. The length of hospital stay is longer in PTH independent (15.5 days) as compared to PTH dependent severe hypercalcaemia (12 days). The most common cause of severe hypercalcemia was malignancy (47%) with multiple myeloma as the most common in 32% followed by lung cancer at 27%. The other non-malignancy causes are calcium supplementation, vitamin D toxicity, and hyperparathyroidism implicated in 13% each. Twenty eight patients (65%) were managed by fluid and antiresorptive agent with 26 patients able to decrease calcium level to <3mmol/L (93%). Eight patients (19%) were managed by fluid alone (not effective in 37%), 9% by antiresorptive agent alone (not effective in 25%), and 16% did not receive any fluid nor antiresorptive agent (not effective in 43%). Conclusion: Similar to previous studies, severe hypercalcaemia is commonly seen in patients with malignancy and associated with significant symptoms, recurrence in 5 years, ICU admission and mortality. Calcium and vitamin D supplementation and hyperparathyroidism are also found to commonly cause severe hypercalcemia. The most effective management is combination of fluid resuscitation and antiresorptive agent to decrease the calcium level to <3mmol/L.

scholarly journals Hypercalcemia: A Metabolic Complication of an AIDS-Defining Illness

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A198-A199
Author(s):  
Dorothy E Bennett ◽  
Ruba Riachy ◽  
Lucas S Blanton ◽  
L Maria Belalcazar
Keyword(s):  
Vitamin D ◽  
Immune Reconstitution ◽  
Kidney Injury ◽  
Thyroid Stimulating Hormone ◽  
High Serum ◽  
Hiv Viral Load ◽  
Dihydroxyvitamin D ◽  
Metabolic Complication ◽  
Granulomatous Diseases ◽  
Hiv 1

Abstract Background: Hypercalcemia may result from the activation of macrophages in granulomatous diseases with increased production of 1,25 dihydroxyvitamin D/calcitriol. Its occurrence in patients with human immunodeficiency virus-1 (HIV-1) infection may be atypical and signal major changes in immune status. We report on a patient with acquired immunodeficiency syndrome (AIDS) presenting with new-onset hypercalcemia after months of treatment for mycobacterium avium complex (MAC) infection and normal calcitriol levels. Clinical Case: A 37-year-old man on treatment for HIV-1 and disseminated MAC infection presented to the hospital 6 months after initial diagnosis with worsening headache, cough, and abdominal pain. On arrival he was afebrile and without palpable lymphadenopathy. He was found to have a high serum calcium (13.4 mg/dL, n 8.6–10.6 mg/dL) and acute kidney injury (AKI) (creatinine 4 mg/dL, n 0.6–1.25 mg/dL). His CD4 count had increased from 24 at time of diagnosis to 162 cells/μL (n 410–1,590 cells/μL); his HIV viral load was undetectable. Workup for hypercalcemia revealed an elevated phosphorus (5.2 mg/dL, n 2.5–5.0 mg/dL), low 25-OH vitamin D level (<13 ng/mL, n 25–80 ng/dL), low PTH (4.8 pg/mL, n 12–88 pg/mL), and calcitriol level of 31.4 pg/mL, n 19.9–73.3 pg/mL). Additional tests, including serum electrophoresis, thyroid stimulating hormone, and parathyroid hormone-related peptide levels, were unremarkable. The patient was diagnosed with hypercalcemia secondary to dysregulated calcitriol production in the setting of disseminated MAC and possible immune reconstitution. Hypercalcemia resolved with hydration and prednisone 20 mg daily. Patient was discharged with an 8-day prednisone taper, but readmitted to the hospital 3 weeks later with recurrent hypercalcemia (13.8 mg/dL) and AKI. Urine calcium was found to be elevated (484 mg/24 hours, n100-300 mg/24 hours) and repeat calcitriol was 53.6 pg/ml. Patient was restarted on prednisone 40 mg daily with normalization of calcium within 5 days (calcium 10.3 mg/dL). Conclusion: Hypercalcemia due to increased calcitriol production in the setting of MAC infection, an AIDS-defining illness, may occur months after initiation of effective antibiotic and antiviral therapy and could represent a manifestation of immune reconstitution. The deleterious effects of excess calcitriol may be present even in patients with chronic vitamin D deficiency and a calcitriol level that inappropriately remains within the normal range.

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