scholarly journals SAT-070 Nutritional Deficiency of Calcium Mimicking P Seudohypoparathyroidism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Yoonji Lee ◽  
Moon Bae Ahn ◽  
Na yeong Lee ◽  
Seonhwa Lee ◽  
Yujung choi ◽  
...  
Keyword(s):  
Vitamin D ◽  
Calcium Carbonate ◽  
Serum Calcium ◽  
Calcium Absorption ◽  
Clinical Manifestations ◽  
Nutritional Deficiency ◽  
Serum Phosphorus ◽  
Vitamin D Metabolism ◽  
Laboratory Findings ◽  
Oral Calcium

Abstract BACKGROUND: Childhood hypocalcemia in general is caused by problems associated with calcium absorption and excretion, parathyroid hormone (PTH) secretion, and vitamin D metabolism. Clinical manifestations can vary from asymptomatic hypocalcemia to life-threatening conditions including convulsions, tetany and laryngeal spasm. As many symptoms are nonspecific, laboratory tests are essential for diagnosis. Nevertheless, the causes of hypocalcemia may not be determined by simple interpretation of baseline calcium, phosphorus, alkaline phosphatase (ALP), PTH and calcidiol (25OHD). Case presentation: We report a case of 11-month-old female with a generalized tonic type seizure with low serum calcium level (5.7 mg/dl), 25OHD (23.2 ng/mL) and calcitriol (1,25OH2D) (12.83 pg/mL). Serum phosphorus (5.9 mg/dL), ALP (209 mg/dL) were above normal range and PTH (484 pg/mL) was markedly elevated. She had a problem with weaning process after age of 5 months and milk powder was her main staple diet. Pseudohypoparathyroidism (PHP) was suspected due to slightly increased serum phosphorus, however Albright’s hereditary osteodystrophy manifestation was absent and no GNAS methylation defect was identified. Serum calcium was normalized by intravenous calcium-gluconate followed by oral calcium carbonate and vitamin D supplement. Two months of oral oral calcium carbonate and vitamin D supplementation alone normalized all laboratory results. Conclusions: Severe nutritional deficiency of calcium could mimic laboratory findings of PHP, therefore clinical judgement should not be made solely on biochemical markers. Keywords: Hypocalcemia, pseudohypoparathyroidism, rickets 제1저자: Yoonji Lee, Moonbae Ahn, Na yeong Lee, Seonhwa Lee, Yujung Choi, Seulki Kim, Shinhee Kim, Wonkyoung Cho, Kyoungsoon Cho, Minho Jung, and Byungkyu Suh* Department of Pediatrics, College of Medicine, Catholic University of Korea

scholarly journals Denosumab Induced Severe Prolonged Hypocalcemia in Metastatic Prostate Cancer

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A190-A190
Author(s):  
Hassan Mehmood ◽  
Farhad Hasan
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Calcium Carbonate ◽  
Serum Calcium ◽  
Calcium Gluconate ◽  
Metastatic Prostate Cancer ◽  
High Dose ◽  
Appendicular Skeleton ◽  
Qtc Interval ◽  
Oral Calcium

Abstract Background: Denosumab is a RANK-l inhibitor that, in addition to the treatment of osteoporosis, is used in patients with advanced cancer and metastatic bone disease to prevent skeletal-related events. Although denosumab is generally safe and effective, it can cause hypocalcemia which in some patients can be severe and life threatening. We present a case of severe prolonged hypocalcemia after a single dose of denosumab in a patient with metastatic prostate cancer. Case: A 78-year-old male with a past medical history of stage 4 prostate cancer on antiandrogen treatment with GnRH antagonist presented with severe hypocalcemia. Physical exam revealed a blood pressure 125/80 mm Hg, pulse 115 per min and weight 135 lb with negative Chvostek’s and Trousseau’s signs. The electrocardiogram showed supraventricular tachycardia with prolonged QTc interval of 503 ms (<430 ms). Labs showed serum calcium 4.9mg/dL (8.5–10.5), albumin 2.5g/dL (3.6–5.1), corrected calcium 5.7 mg/dL, ionized serum calcium 0.64mmol/L (1.05–1.3), creatinine 1.10mg/dL (0.7–1.2), eGFR >60, phosphorus 2.0mg/dL (2.5–4.5), magnesium 1.9 mg/dL (1.6–2.6), 25-OH vitamin D 29.7 ng/mL (30–100), 1,25 dihydroxy vitamin D 174 pg/mL (18–64), iPTH 244.0 pg/mL (11–68) and PSA 1860 ng/mL. Three weeks prior to presentation, the patient received 120 mg of subcutaneous denosumab. Pre-treatment serum calcium was 9.2 mg/dL (8.5–10.5), and Tc-99m bone scan showed multiple osteoblastic osseous metastatic lesions involving both axial and appendicular skeleton. The patient was diagnosed with denosumab-induced severe hypocalcemia and started on intravenous (IV) calcium gluconate infusion, oral phosphate 250 mg twice daily, and ergocalciferol 50,000 IU twice weekly. He required IV calcium gluconate up to 10 g per day in addition to oral calcium carbonate 2 g t.i.d. for 2 weeks to resolve hypocalcemia and normalize QTc interval. Patient was discharged to nursing home on calcium carbonate 2 g q.i.d. with IV calcium gluconate as needed to keep corrected calcium >8.0 mg/dL. After discharge he required up to 4 g of IV calcium and 8 g of oral calcium per day. Unfortunately, he presented again with severe hypocalcemia 5 weeks after discharge. In addition to current regimen of oral and IV calcium boluses, low dose calcitriol was started. We were only able to maintain his serum calcium>8.0 mg/dL by administering high daily dose of oral calcium carbonate 8 g /day and calcitriol 2 mcg daily. Due to poor prognosis, he was transitioned to hospice care and died 2 weeks later. Discussion: There are not many case reports on severe prolonged hypocalcemia secondary to denosumab in cancer patients but normal kidney function. Our patient remained on high dose of calcium even 101 days after denosumab administration. Reference: 1. Milat F et al. Prolonged hypocalcemia following denosumab therapy in metastatic hormone refractory prostate cancer. Bone. 2013 Aug 1;55(2):305–8.

SEVERE IDIOPATHIC HYPERCALCEMIA OF INFANCY

PEDIATRICS ◽  
1957 ◽  
Vol 19 (3) ◽  
pp. 362-371
Author(s):  
George L. Daeschner ◽  
C. William Daeschner
Keyword(s):  
Vitamin D ◽  
Renal Function ◽  
Impaired Renal Function ◽  
Calcium Absorption ◽  
Severe Form ◽  
Additional Case ◽  
Mild Form ◽  
Laboratory Findings ◽  
Pathologic Features ◽  
Motor Retardation

A syndrome occurring in infants and characterized clinically by anorexia, vomiting, constipation, hypotonia, hypertension, characteristic facies, and severe mental-motor retardation, and by the laboratory findings of hypercalcemia, azotemia and impaired renal function has recently been described by British and Swiss workers. The disease apparently occurs in two forms, referred to as mild and severe. The literature concerning the severe form has been reviewed and an additional case reported. Hypersensitivity to vitamin D with excessive calcium absorption has been demonstrated in the mild form of this syndrome and has also been proposed as the metabolic abnormality responsible for the pathologic features of the severe form of the disease.

Renal osteodystrophy

2013 ◽  
pp. 1274-1282
Author(s):  
Thomas Bardin ◽  
Tilman Drüeke
Keyword(s):  
Vitamin D ◽  
Bone Turnover ◽  
Serum Calcium ◽  
Renal Osteodystrophy ◽  
Serum Phosphorus ◽  
Osteitis Fibrosa ◽  
Alkaline Phosphatases ◽  
Calcium Phosphorus ◽  
Turnover Markers ◽  
25 Oh Vitamin D

Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

scholarly journals Afebrile Seizures as Initial Symptom of Hypocalcemia Secondary to Hypoparathyroidism

2016 ◽  
Vol 07 (S 01) ◽  
pp. S117-S119
Author(s):  
Anastasia Gkampeta ◽  
Eftyxia Kouma ◽  
Anastasia Touliopoulou ◽  
Efstathios Aggelopoulos ◽  
Eleni Vourti
Keyword(s):  
Vitamin D ◽  
Calcium Carbonate ◽  
Blood Gases ◽  
Female Child ◽  
Tertiary Hospital ◽  
Initial Symptom ◽  
Serum Electrolyte ◽  
Laboratory Findings ◽  
Normal Thyroid Function ◽  
25 Oh Vitamin D

ABSTRACTHypocalcemia is rare in childhood and caused, among other conditions, by hypoparathyroidism. DiGeorge syndrome is the most common cause of hypoparathyroidism in childhood. Presentation of a rare cause of hypocalcemia in childhood and the necessity of measuring serum electrolyte levels in patients presenting with afebrile seizures. a 7.5-year-old female child presented with afebrile seizures lasting 5 min with postictal drowsiness. A similar episode 1 month ago is described. On admission, a positive Trousseau sign, papilledema, and long QTc on electrocardiography were detected. Laboratory testing revealed hypocalcemia, increased creatine phosphokinase and phosphate levels, decreased levels of parathormone, with normal thyroid function and normal levels of blood gases. considering the diagnosis of hypoparathyroidism possible, we started on calcium gluconate solution 5% intravenously and calcium carbonate per os. 48 h later, the child transferred to tertiary hospital for further evaluation. The laboratory findings revealed 25-OH Vitamin D deficiency with normal cortisol levels and the absence of autoantibodies. Kidney and brain imaging and also the electroencephalogram were normal. Calcium carbonate, magnesium, and Vitamin D were administered per os. The child discharged from hospital with complete resolution of symptoms. Since then, she is in treatment with calcium carbonate and Vitamin D per os. Hypoparathyroidism is rare in childhood. We underline the necessity of measuring serum electrolyte levels in patients presenting with afebrile seizures.

scholarly journals Vitamin D metabolism and its possible role in the developing chick embryo

1981 ◽  
Vol 194 (1) ◽  
pp. 103-109 ◽  
Author(s):  
M Kubota ◽  
E Abe ◽  
T Shinki ◽  
T Suda
Keyword(s):  
Vitamin D ◽  
Chick Embryo ◽  
Bone Formation ◽  
Calcium Binding ◽  
Calcium Absorption ◽  
Chorioallantoic Membrane ◽  
Calcium Content ◽  
Binding Activity ◽  
Vitamin D Metabolism ◽  
Osteoblastic Activity

The relationship between bone formation and vitamin D metabolism was investigated in the developing chick embryo. Fertilized White Leghorn eggs were incubated at 38 degrees C in an incubator for 21 days. The fresh weight and calcium content of embryonic tibiae began to increase at day 12 and attained maximal values at day 19. Bone alkaline phosphatase and citrate decarboxylation activities, both of which represent osteoblastic activity, also began to increase at days 10-12, reached maximal values at day 19 and sharply declined thereafter. Both bone enzyme activities were highly correlated with CA2+-binding activity in the chorioallantoic membrane measured by the Chelex 100 assay. When mesonephric and metanephric homogenates were incubated with 25-hydroxy[3H]cholecalciferol, a marked and concomitant increase occurred in the metanephric 1 alpha- and 24-hydroxylase activity after day 14. The production of 1 alpha, 25-dihydroxycholecalciferol attained a maximal value at day 19 and decreased thereafter, whereas that of 24,25-dihydroxycholecalciferol continued to increase until hatching. The production rate of 1 alpha, 25-dihydroxycholecalciferol by the metanephros coincided with the changes in Ca2+-binding activity in the chorioallantoic membrane and osteoblastic activity. Since both intestinal calcium absorption and bone mineral mobilization do not occur in embryonic life, these results support the idea that 1 alpha, 25-dihydroxycholecalciferol may be involved directly in bone formation or induction of a calcium-binding protein in the chorioallantoic membrane.

Role of prolactin in vitamin D metabolism and calcium absorption during lactation in the rat

1982 ◽  
Vol 94 (3) ◽  
pp. 443-453 ◽  
Author(s):  
C. J. Robinson ◽  
E. Spanos ◽  
M. F. James ◽  
J. W. Pike ◽  
M. R. Haussler ◽  
...  
Keyword(s):  
Vitamin D ◽  
Alkaline Phosphatase ◽  
Parathyroid Hormone ◽  
Alkaline Phosphatase Activity ◽  
Plasma Levels ◽  
Calcium Absorption ◽  
High Plasma ◽  
Intestinal Calcium Absorption ◽  
Vitamin D Metabolism

Intestinal calcium absorption and plasma levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) were measured in lactating and non-lactating rats and the effects of bromocriptine and exogenous prolactin treatment were evaluated. In lactating rats calcium absorption and plasma levels of parathyroid hormone, 1,25(OH)2D3 and alkaline phosphatase activity were significantly increased. Bromocriptine treatment significantly reduced the enhanced calcium absorption and levels of plasma 1,25(OH)2D3 and alkaline phosphatase but had no significant effect on plasma levels of parathyroid hormone. Prolactin administered with bromocriptine to lactating animals prevented all the changes observed with bromocriptine treatment alone. It was concluded that the increased plasma levels of prolactin during lactation lead to high plasma levels of 1,25(OH)2D3 which are responsible for the enhanced intestinal calcium absorption.

Effects of Dietary Calcium and Phosphorus on Vitamin D Metabolism and Calcium Absorption in Hamster

1996 ◽  
Vol 211 (3) ◽  
pp. 281-286 ◽  
Author(s):  
H. P. Schedl ◽  
T. Conway ◽  
R. L. Horst ◽  
D. L. Miller ◽  
C. K. Brown
Keyword(s):  
Vitamin D ◽  
Calcium Absorption ◽  
Dietary Calcium ◽  
Vitamin D Metabolism ◽  
Calcium And Phosphorus
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