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Rationale: Denosumab, a fully humanized IgG monoclonal antibody, is commonly employed in the management of different types of osteoporosis. Up to now, hypocalcemia linked with denosumab has been predominantly reported in dialysis patients suffering from chronic kidney disease. Interestingly, there have been no reports of hypocalcemia following craniopharyngioma surgery with the use of denosumab., Patient Concerns: A 65-year-old male received a subcutaneous injection of denosumab (60 mg) as a treatment for osteoporosis following the resection of a craniopharyngioma. Remarkably, the patient developed hypocalcemia within 4 days post-injection. However, 6 months subsequent to the initial treatment, the patient underwent another subcutaneous injection of desmuzumab and once again experienced hypocalcemia., Diagnoses: Hypocalcemia., Interventions: The hypocalcemia was successfully managed with intravenous calcium gluconate and oral calcium carbonate D3 tablets, leading to the alleviation of symptoms., Outcomes: Hypocalcemia following the use of denosumab after craniopharyngioma surgery is rare, and its occurrence may be associated with the primary disease and concomitant medications., Lessons: It underscores the necessity for clinicians to perform a thorough evaluation of the patient's overall health status, complete all requisite testing, pay particular attention to those in high-risk categories, and ensure serum calcium levels are monitored, along with conducting other essential tests, prior to and following each administration of denosumab., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

BACKGROUND Calcium gluconate is used to treat neonatal hypocalcemia, severe hyperkalemia, and neonatal convulsions. Calcium gluconate can extravasate into the skin's soft tissues, resulting in redness, skin nodules, and calcification of soft tissue, which can cause tissue necrosis. This report presents 2 cases of neonatal calcinosis cutis following the treatment of hypocalcemia with calcium gluconate. CASE REPORT Case 1. The patient was a 12-day-old male neonate who presented with a mass in the right foot. He was recently discharged from the hospital after evacuation of subdual hematoma triggering his seizures. The swelling was associated with erythema but no discharge. His radiograph showed soft tissue calcification. He had received 2 peripheral intravenous calcium gluconate infusions to manage hypocalcemia during the last hospitalization. Symptomatic treatments were provided, and full resolution of the swelling was reported after 3 weeks. Case 2. The patient was a 1-month-old female infant newly diagnosed with cystic fibrosis who presented with a mass in her left foot. She underwent exploratory laparotomy in another hospital to manage meconium ileus. The mass was not mobile but there was no skin ulceration. Her radiograph showed soft tissue calcification. During her last admission, she had received 3 doses of intravenous calcium gluconate to manage hypocalcemia. The patient was observed and managed symptomatically. After 4 weeks, there was almost complete clinical and radiographic disappearance of the swelling without any skin necrosis. CONCLUSIONS This report has highlighted the importance of monitoring neonates treated with calcium gluconate who may develop skin rashes or nodules due to calcinosis cutis.

Background: Acute hypocalcemia is generally caused by a sudden drop in serum calcium ion and presents with a mild or severe form of tetany. Even though the occurrence of hypocalcemia is well documented with certain drugs such as calcium chelators, bisphosphonates, and cisplatin, it is a very unusual and poorly documented adverse event with cimetidine and nifedipine. Here, we present a case of severe hypocalcemic tetany during simultaneous administration of cimetidine and nifedipine in a hypertensive patient with dyspepsia., Case Presentation: A 46-year-old known human immunodeficiency virus patient from Ethiopia on antiretroviral therapy over the past 14 years presented to the emergency department with acute exacerbation of dyspepsia and hypertensive urgency. She was given intravenous cimetidine (400 mg) and oral nifedipine (30 mg) simultaneously. One hour after the administration of these two drugs, she developed severe hypocalcemic tetany with carpopedal spasm, involuntary plantar flexion, and muscle spasms. She also had severe retrosternal chest pain and shortness of breath. Her blood pressure was 160/110 mmHg during the attack and she had no skin changes, such as urticaria. She was immediately given 1 g of calcium gluconate intravenously over 30 minutes. The carpopedal spasm progressively decreased during calcium gluconate administration. An hour later, she completely regained voluntary movement of her fingers and feet. The chest pain persisted, but resolved over the next 12 hours. The patient was discharged home after 2 days of observation. This is an unusual adverse effect that needs caution during concomitant administration of these drugs., Conclusions: Severe hypocalcemic tetany can occur with concomitant administration of cimetidine and nifedipine. Immediate treatment with calcium gluconate quickly reverses this adverse event. Concomitant administration of these drugs should be done with caution or be avoided if possible., (© 2023. The Author(s).)

Background: Calcinosis cutis is a rare condition, characterized by an accumulation of calcium salts in the skin and subcutaneous tissue. There are several types of this condition, including dystrophic, metastatic, idiopathic, calciphylaxis, and iatrogenic calcinosis cutis. The type related to our case is iatrogenic calcinosis cutis, and one its possible causes is calcium intravenous infusion. Physicians should be aware of this condition when giving calcium infusion., Case Presentation: Here we report the case of a 9-month-old Arabic - Saudi baby boy, who presented with abnormal movement for 1 day. Upon further investigation, his abnormal movement was found to be a manifestation of hypocalcemia and vitamin D deficiency. He was treated with intravenous calcium gluconate. Later, he had a treatment-related complication of intravenous calcium at the site of venipuncture causing swelling, which was initially soft but progressed to hard, over the left hand. Eventually, he was diagnosed with a case of iatrogenic calcinosis cutis due to intravenous calcium treatment., Conclusion: There are multiple differential diagnoses of calcinosis cutis, as it resembles many other conditions. Careful history-taking, physical examination, and other investigations, such as radiological investigations, will aid in reaching a more accurate diagnosis and, thus, early treatment and intervention. Frequently checking the intravenous line and diluting the intravenous calcium may help reduce the occurrence of iatrogenic calcinosis cutis., (© 2022. The Author(s).)

Hypoparathyroidism patients present with features of hypocalcemia like carpopedal spasm, numbness and paresthesias but hypocalcemic cardiomyopathy leading to congestive heart failure (CHF) is a rare presentation. We present here a case of 55-year-old Asian man who was a known case of dilated cardiomyopathy for 6 months, presented with the chief complaints of shortness of breath on exertion and decreased urine output. On general physical examination, features suggestive of CHF were seen. Chvostek and Trousseau's sign was positive. The patient had a history of cataract surgery of both eyes 15 years ago. Further investigations revealed hypocalcemia. Echo showed severe global hypokinesia of left ventricle with left ventricle ejection fraction 15%. This CHF was refractory to conventional treatment, though, with calcium supplementation, the patient improved symptomatically. On follow-up after 3 months, an improvement was seen in the echocardiographic parameters with ejection fraction improving to 25%., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

We present a case that illustrates the fluctuations in calcium levels to be expected while managing an infant with maternal gestational diabetes mellitus who also develops subcutaneous fat necrosis (SCFN). There is initial hypocalcaemia due to functional hypoparathyroidism, requiring judicious calcium replacement. But with increased extrarenal production of 1,25-dihydroxyvitamin D due to granulomatous inflammation of subcutaneous adipose tissue, hypercalcaemia ensues. With a self-limiting course, SCFN of the newborn has an excellent prognosis and resolves spontaneously. However, aberrations in serum calcium levels can manifest in life-threatening complications and must hence be closely monitored., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Gitelman syndrome is the most common renal tubulopathy, recently exhibiting a dramatic rise of incidence in Asia.A 50-year-old woman presented with vomiting, fatigue and quadriparesis. Physical examination revealed a positive Trousseau sign , hypotonia and areflexia.Suspecting hypocalcaemia, she was given intravenous 10% calcium gluconate (10 mL administered slowly over 10 min) but her manifestations persisted. An exhaustive laboratory work up revealed the diagnosis of Gitelman syndrome.The peculiarity of this case however, is entailed in its coexistence with hypocalcaemia and hyponatraemia. In addition, the age of primary presentation being 50 years further culminates its atypicality.Multiple electrolyte imbalances were corrected by oral and intravenous supplementation and a high sodium-potassium diet was advocated. Administration of spironolactone imposed a pitfall in the management of our patient due to exacerbation of pre-existing hyponatraemia.On follow-up, her electrolyte profile was stable and corresponding symptoms were alleviated., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Clinically relevant hypocalcemia is a well-documented complication of glucocorticoid administration in people with hypoparathyroidism. The current report describes the phenomenon in a dog. A 7 yr old neutered male Pomeranian was diagnosed with immune-mediated thrombocytopenia, immune-mediated hemolytic anemia, and primary hypoparathyroidism. This dog required long-term parenteral calcium gluconate to prevent clinical hypocalcemia despite appropriate doses of oral calcitriol and calcium carbonate. This is the first description of clinically significant presumptive glucocorticoid induced hypocalcemia in a dog with primary hypoparathyroidism.

Vegetarian and vegan diets are gaining popularity in the United States. Although appropriately planned vegetarian diets, including vegan diets, are healthful and nutritionally adequate and may provide health benefits in the prevention and treatment of certain diseases, not all families are aware of the nutritional supplements that may be required for their children. We describe a case of a 2-year-old previously healthy child consuming a vegan diet who presented to the pediatric emergency department with an acute inability to move her legs. Ionized calcium was found to be 0.89 mmol/L, and symptoms completely resolved within 2 hours of calcium gluconate infusion.

Acute onset of quadriplegia is a rare phenomenon seen with hypocalcemia due to hypoparathyroidism. We describe a 33-year gentleman who presented with weakness of all four limbs and areflexia. ECG showed QT abnormality. Nerve conduction study revealed normal sensory and significantly low motor CMAP amplitudes in both the upper and lower extremities. This nerve conduction study can be seen in acute motor neuropathy of various etiologies, among which GBS is the most worrisome. Our patient found to have low calcium and parathyroid hormone level. His symptoms improved after calcium replacement. Occurrence of quadriplegia in hypoparathyroidism, and its improvement after correction of calcium, suggests crucial role of calcium in neuromuscular transmission. One should suspect electrolyte imbalance, like hypocalcemia in patients presenting with nerve conduction features of AMAN variant of GBS.

A normal serum calcium level is 8 to 10 mg/dL. The diagnosis of hypercalcemia (ie, levels 10.5 mg/dL or greater) should be confirmed with an albumin-adjusted or ionized calcium level. The two most common causes of hypercalcemia are hyperparathyroidism and malignancy. Drugs, notably lithium and thiazide diuretics, also can cause hypercalcemia. Patients with severe or symptomatic hypercalcemia should be treated initially with hydration to decrease calcium levels. The evaluation should include a parathyroid hormone (PTH) level. If the PTH level is low, cancer is a likely cause, particularly multiple myeloma, breast cancer, or lymphoma. If the PTH level is normal or elevated, hyperparathyroidism is the likely cause. Symptomatic patients with hyperparathyroidism and patients with certain clinical markers should be considered for surgery. For patients with mild disease, monitoring is an option. Hypocalcemia often is caused by vitamin D deficiency. Symptomatic patients and patients with calcium levels less than 7.6 mg/dL should be treated with intravenous calcium gluconate; concomitant magnesium deficiency should be addressed. There is no evidence that routine calcium and vitamin D supplementation reduces the risk of fractures, but studies have shown that vitamin D supplementation does decrease the number of falls in older adults at risk., (Written permission from the American Academy of Family Physicians is required for reproduction of this material in whole or in part in any form or medium.)

Hypocalcemia is a serious condition which has a major impact on the transmission of nerve impulses, contraction and relaxation of muscles (including myocardial) and pathological secretion of some hormones. The basic causal treatment is the parenteral administration of calcium, namely calcium gluconate, calcium chloride or calcium gluceptate. Parenteral formulations of these compounds must meet pharmacopoeial requirements, including the aluminum content limit. Each of these molecules has its specific properties that predict their clinical use. In addition to hypocalcemia, they are used to influence a variety of other conditions, such as fluoride or oxalic acid poisoning, decreased myocardial contractility caused by overdose of calcium intake blockers or beta blockers. They are also used as part of parenteral nutrition AIO or as an ancillary treatment for acute allergic conditions, itchy dermatitis, weeping and generalized eczema, continuous renal replacement therapy, seizure convulsion, laryngospasm, bronchospasm and altered mental status. The role of calcium replacement in septic patients remains unclear and requires further study. Although it may appear that calcium chloride infusion solutions provide greater and more highly ionized amounts of calcium, gluconate salts are preferred due to considerably less irritation of the vessel wall and better compatibility with other nutrients in parenteral nutrition.Key words: hypocalcemia calcium gluconate calcium chloride aluminum parenteral nutrition.

Although renal calcium crystal deposits (nephrocalcinosis) may occur in acute phosphate poisoning as well as type 1 renal tubular acidosis (RTA), hyperphosphatemic hypocalcemia is common in the former while normocalcemic hypokalemia is typical in the latter. Here, as a unique coexistence of these two seperated clinical entities, we report a 30-yr-old woman presenting with carpal spasm related to hypocalcemia (ionized calcium of 1.90 mM/L) due to acute phosphate poisoning after oral sodium phosphate bowel preparation, which resolved rapidly after calcium gluconate intravenously. Subsequently, type 1 RTA due to Sjögren's syndrome was unveiled by sustained hypokalemia (3.3 to 3.4 mEq/L), persistent alkaline urine pH (> 6.0) despite metabolic acidosis, and medullary nephrocalcinosis. Through this case report, the differential points of nephrocalcinosis and electrolyte imbalances between them are discussed, and focused more on diagnostic tests and managements of type 1 RTA.

Epilepsia partialis continua (EPC) is a syndrome clinically defined as continuous spontaneous jerking confined to one part of the body, sometimes aggravated by action or sensory stimuli, occurring over hours, days or even years. In adults the more frequent recognized cause of EPC is an acute cerebrovascular disease. Acute severe hypocalcemia is a highly epileptogenic ionic disturbance, abnormally increasing neuronal excitability. In this short communication we describe the first probable case of acute hypocalcemia-related EPC. Eight months after a left parietal lobe cardioembolic stroke, a 74-year-old woman experienced a generalized tonic-clonic seizure for the first time in her life, at the beginning of a Clostridium difficile enterocolitis. Four days later, while the abdominal symptoms were clinically improving, continuous semi-rhythmic jerks of right face, shoulder and arm began suddenly. Despite several appropriated antiepileptic treatments those involuntary movements did not cease. On routine biochemical examination we noted a total calcium serum level of 1.2 mmol/L (normal range 2.1-2.8 mmol/L), not previously known. After intravenous calcium gluconate supplementation, the jerks started to fade, disappearing completely as a total calcium serum level of 1.9 mmol/L was reached. Two separated CT brain scans did not reveal new cerebral lesions. Neurophysiological studies did not show any cortical activity related to jerks. Taken together, the treatment refractoriness and the clinical improvement after ionic imbalance correction point towards a highly possible role of hypocalcemia in sustaining the activity of a previously silent epileptogenic focus., (Copyright © 2011 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.)

Objective: Hypocalcaemia is a frequently arising complication following total thyroidectomy. Routine postoperative prophylactic administration of vitamin D or metabolites and calcium reduce the incidence of symptomatic hypocalcaemia; this article reports evaluating its cost-effectiveness in Colombia., Methods: Meta-analysis was used for comparing the administration of vitamin D or metabolites to oral calcium or no treatment at all in patients following total thyroidectomy and a cost-effectiveness analysis was designed based on a decision-tree model with local costs., Results: The OR value for the comparison between calcitriol and calcium compared to no treatment and to exclusive calcium treatment groups was 0.32 (0.13-0.79 95 %CI) and 0.31 (0.14-0.70 95 %CI), respectively. The most cost-effective strategy was vitamin D or metabolites and calcium administration, having a US $0.05 incremental cost-effectiveness ratio., Conclusion: Prophylactic treatment of hypocalcaemia with vitamin D or metabolites + calcium or calcium alone is a cost-effective strategy.

Background: Hypothyroidism and hypocalcemia are common after thyroid and parathyroid surgery. In this article, the authors provide clinically-oriented recommendations to help surgeons, general practitioners, internists, and endocrinologists give their affected patients adequate hormone replacement therapy., Methods: Selective evaluation of original articles and reviews that were retrieved by a PubMed search over the years 1980 to 2010, as well as of the recommendations of medical societies including the Endocrine Society (USA), the German Society for Endocrinology (Deutsche Gesellschaft für Endokrinologie), and the American and European Thyroid Associations., Results: Important issues in L-thyroxine replacement therapy include: the selection of the hormone preparation (T4 or T4/T3), combination with iodine (yes/no), the definition of therapeutic TSH ranges (particularly after surgery for thyroid cancer), the extent of remaining thyroid tissue after goiter surgery and its significance, underlying diseases, and drug interactions. The major issues in the treatment of postoperative hypoparathyroidism are: the selection of suitable calcium and vitamin D preparations, the definition of therapeutic goals, the treatment of hypercalciuria and hyperphosphatemia, and the option of recombinant parathormone therapy., Conclusion: Effective treatment requires an appropriate choice of medication and an understanding of its pharmacokinetics as well as of the possible effects of the patient's underlying disease, comorbidities, and other medications on its absorption and metabolism.

Hypoparathyroidism is associated with chronic hypocalcaemia which can have a variety of manifestations including cardiovascular changes. We describe here a case of primary hypoparathyroidism associated with systolic dysfunction of left ventricle presenting as a dilated cardiomyopathy in addition to other manifestations.

The citrate based anticoagulant ACD is commonly used in apheresis procedures. Due to its ability to decrease ionized calcium, citrate may cause unpleasant symptoms, such as paresthesias and muscle cramps, in patients undergoing therapeutic and donor apheresis. We noticed that patients with multiple myeloma (MM) undergoing autologous stem cell leukapheresis appeared to have more citrate reactions when compared to other patients undergoing the same procedure. A retrospective chart review was performed to evaluate 139 (of 151) consecutive patients with MM, amyloidosis, hematological and solid malignancies who had autologous peripheral blood stem cell collection between January 2007 and February 2008. Citrate reactions, ranging from mild (e.g., perioral tingling and parasthesias) to severe (e.g., nausea/vomiting and muscle cramps) were noted for 35 patients. Twenty-three of 63 patients with MM had documented citrate reactions, which was significantly higher than those with other hematological and solid malignancies (37% vs. 20%; P < 0.05, Relative Risk (RR) = 1.9). The severities of citrate reactions were the same in both groups; approximately 50% of patients in each group received i.v. calcium gluconate for treatment of hypocalcemia. No correlation between bisphosphonate therapy and citrate reactions were noted in our study group. Examination of available laboratory values related to calcium homeostasis, liver, and renal function failed to reveal a mechanism for the increase in citrate reactions observed. In summary, this single institution retrospective study indicates that patients with MM are more sensitive to citrate-induced hypocalcemia during leukapheresis when compared to patients with other hematological and solid malignancies. Strategies for decreasing citrate reactions (e.g., supplemental calcium and slowing return rates) should be considered for patient safety and comfort, especially in the MM population, on a prophylactic rather than reactive basis.

Unlabelled: Chromosome 10p terminal deletion accounts for a rare subset among patients presenting with DiGeorge syndrome, and is designated as DiGeorge 2 syndrome. We report a neonate with DiGeorge-like phenotype having a deletion of distal 10p (p13-pter) and a duplication of terminal 3q (q29-qter) derived from paternal balanced translocation between 3q29 and 10p13. She had facial dysmorphism, atrial and ventricular septal defect, impaired T-cell function, hypoparathyroidism, sensorineural hearing loss, renal abnormalities and developmental delay. Her phenotype corresponded well with the typical characteristics of partial monosomy 10p and the small duplication of terminal 3q did not involve the critical region of 3q duplication syndrome. Clinically, hypoparathyroidism-related hypocalcemia lasted for three weeks and resulted in repeated episodes of heart failure. It was not until the calcium level was normalized that her heart failure improved markedly., Conclusion: Cytogenetic analysis can help to recognize patients early on who have terminal 10p deletion when microdeletion of 22q11.2 is not the cause of DiGeorge syndrome. Hypoparathyroidism-related hypocalcemia impacts heart failure control in partial monosomy 10p and should be managed aggressively on critical care.

Though hypocalcemic stridor is a well-recognized pediatric emergency, it has rarely been reported in the elderly, and hypocalcemia of nutritional origin presenting with stridor in this group has not previously been reported. We report an elderly patient who presented with stridor and intermittent sudden airway obstruction resulting from laryngospasm secondary to hypocalcemia of nutritional origin and we present a brief review of this life-threatening complication of hypocalcemia.

Dermal exposure to hydrofluoric acid could potentially result in severe serum calcium and magnesium depletion induced by binding with fluoride anion. This report describes the case of a 48-year-old man who developed hypocalcemia and hypomagnesemia accompanied by hypokalemia-an interesting finding-following a chemical injury with exposure to 70% hydrofluoric acid. Successful treatment included administration of calcium gluconate and magnesium both intravenously and topically.

Background: Our recent data indicate that 21% of critically ill, adult, multiple-trauma patients receiving specialized nutrition support experience hypocalcemia. However, evidence-based methods for the treatment of moderate to severe acute hypocalcemia (ionized calcium concentration [iCa] <1 mmol/L) are lacking., Methods: The efficacy of an infusion of 4 g of calcium gluconate was evaluated in 20 critically ill, adult, multiple-trauma patients with moderate to severe hypocalcemia (iCa <1 mmol/L). The calcium gluconate was infused at a rate of 1 g/h in a small volume admixture. A serum iCa determination was obtained on the following day., Results: Calcium gluconate infusion significantly increased serum iCa from 0.90 +/- 0.08 mmol/L to 1.16 +/- 0.11 mmol/L (p < .001) on the following day. This dosage regimen was successful for achieving a serum iCa >1 mmol/L for 19 of 20 (95%) hypocalcemic patients and achieved a concentration >1.12 mmol/L in 14 (70%) of the patients. Two patients developed mild hypercalcemia (iCa of 1.34 mmol/L and 1.38 mmol/L) postinfusion., Conclusions: A short-term infusion of 4 g of intravenous (IV) calcium gluconate for the treatment of moderate to severe hypocalcemia appears to be a promising regimen for critically ill, adult, multiple-trauma patients.

Objective: The purpose of this investigation was to evaluate the dose-dependent characteristics of intravenous calcium gluconate therapy for hypocalcemic critically ill patients., Methods: The dose-dependent characteristics of 2 g versus 4 g of intravenous calcium gluconate therapy were evaluated in 25 critically ill, adult multiple trauma patients with hypocalcemia. The calcium gluconate was infused at a rate of 1 g/h for both groups. Patients weighed within 90% to 120% of ideal body weight, had normal renal function, did not receive diuretic therapy, and did not have anasarca., Results: Fifteen patients with mild hypocalcemia (serum ionized calcium concentration [iCa] 1-1.12 mmol/L) were given 2 g of calcium gluconate. Ten patients with moderate to severe hypocalcemia (iCa <1 mmol/L) were given 4 g. Each dosage group had a significant (P < or = 0.001) increase in iCa (from 1.07 +/- 0.05 to 1.17 +/- 0.05 mmol/L and from 0.92 +/- 0.08 to 1.16 +/- 0.11 mmol/L, respectively). Each dosage group retained about half of the dose in the exchangeable calcium space (P = NS between groups), but the higher dosage group retained significantly more elemental calcium overall (81 +/- 38 versus 201 +/- 50 mg, respectively, P < or = 001). Serum ionized calcium concentrations achieved a plateau without a further decline in iCa by 10 h after completion of the infusion for each dosage., Conclusion: About half of the administered elemental calcium dose was retained for each dosage group, with the higher dose (4 g) resulting in significantly more elemental calcium retention in the exchangeable calcium space. An iCa determination performed about > or =10 h after the completion of the calcium gluconate infusion should be sufficient time to ensure equilibration of iCa to assess the efficacy of the therapy. This mode of calcium therapy serves as an effective means for providing calcium to the acutely hypocalcemic, critically ill, multiple trauma patient.

Malignant infantile osteopetrosis is a rare autosomal recessive disorder characterized by presentation in the first few months of life with manifestations relating to an underlying defect in osteoclastic bone resorption. This report describes a 10 day-old boy in whom neonatal hypocalcemia was present and whose brother had died with the diagnosis of osteopetrosis.

Hungry bone syndrome is a common clinical entity which is accompanying of hypocalcemia, hypomagnesemia, and hipophosphatemia, results from an increase in bone formation. It is related to a pathological scenario which causes an imbalance between osteoclast-mediated bone resorption and osteoblast-mediates bone formation, favouring the latter. Its classic presentation occurs after parathyroidectomy in hyperparathyroydism's patients. Its clinical features are largely due to plasmatic calcium levels reduction. Hungry bone syndrome is frequent in hyperparathyroid's patients who have development bone disease before surgery. Even less frequent, it has also been described after thyroydectomy in patients with hyperthyroidism. We hereby report a case of hungry bone syndrome in one patient who suffers a Graves' disease. Then, we will provide a brief review of pathogenesis and therapeutic features.

The case reports a neonate (twin 2 of a twin girl pregnancy) presenting with seizures due to hypocalcaemia. The presumptive cause of the hypocalcaemia was maternal hyperparathyroidism with concurrent vitamin D deficiency. The first twin remained free of hypocalcaemia and was vitamin D replete, despite similar exposure in the pregnancy and similar postnatal care.

Background: Recent data indicate that critically ill, adult multiple trauma patients receiving specialized nutrition support commonly experience hypocalcemia (ionized serum calcium [iCa] < or =1.12 mmol/L). However, validated methods for the treatment of acute hypocalcemia are lacking., Methods: The efficacy of a single dose of calcium gluconate using an empiric IV calcium gluconate graduated dosing regimen was evaluated in 37 patients. Patients with an iCa of 1-1.12 mmol/L (mild hypocalcemia) were provided 1-2 g of IV calcium gluconate. Patients with an iCa of <1 mmol/L (moderate to severe hypocalcemia) were given 2-4 g. The calcium gluconate was infused at a rate of 1 g/h in a small-volume admixture. Serum iCa determination was repeated on the following day., Results: One to 2 g of IV calcium gluconate was effective in normalizing iCa for 23 out of 29 patients (79%) with mild hypocalcemia and 2-4 g was effective for 3 of 8 patients (38%) with moderate to severe hypocalcemia. The individual response to calcium therapy (g/d) or when normalized to body weight (mg/kg/d) was highly variable., Conclusions: One to 2 g of IV calcium gluconate were effective for most patients with mild hypocalcemia; however, treatment of moderate to severe hypocalcemia with 2-4 g of IV calcium gluconate was often unsuccessful. Further study with frequent serial ionized serum calcium and phosphorus determinations and electrocardiographic monitoring appears to be indicated for patients with moderate to severe hypocalcemia.

Objectives: In this study, we presented 2 cases and evaluated the evidence for symptomatic hypocalcemia after treatment with magnesium sulfate alone or combined with use of nifedipine., Study Design: Case reports, such as the one that follows, and literature review were used. A 25-year-old gravida presented at 33 weeks' gestation with advanced preterm labor. She received magnesium sulfate followed by nifedipine and experienced bilateral hand contractures 12 hours after discontinuation of magnesium sulfate. Total serum calcium was 5.4 mg/dL. A 35-year-old gravida presented at 26 weeks' gestation with ruptured membranes and received magnesium sulfate until it was discontinued prematurely because of pulmonary edema. Twenty hours later she experienced bilateral hand contractures; total serum calcium was 5.9 m/dL. Symptoms for both patients resolved with calcium gluconate therapy., Results: Hypocalcemia is a well-recognized complication of magnesium sulfate infusion. These are the fifth and sixth symptomatic case reports, as identified by Medline Search. Our first case is the only report in which the subsequent use of nifedipine may have been a factor. Little has been reported on the possible toxicity associated with the combined or sequential use of magnesium sulfate and nifedipine., Conclusion: Marked hypocalcemia is clearly associated with magnesium sulfate infusion, is likely dose related, and may appear after discontinuation of magnesium sulfate therapy. Moreover, while the evidence for synergistic toxicity of magnesium sulfate and nifedipine is sparse, caution is advised when these agents are used together.

Background: Citrate-related side effects are common adverse reactions during PBPC apheresis. To reduce the incidence of citrate-related reactions, the effect of a continuous calcium-gluconate infusion on the appearance of hypocalcemic symptoms and on the subjective tolerance toward large-volume leukapheresis (LVL) was tested., Study Design and Methods: A double-blinded, placebo-controlled trial was carried out in 50 patients undergoing standardized LVL at a median ACD-A ratio of 1.99 mg per kg and minute. Patients were randomly assigned to receive a continuous IV infusion of either saline or calcium-gluconate at a dose of 1.8 mmol calcium per hour. Subjective tolerance toward LVL was determined by standardized rating systems. Further, hormonal and electrolyte changes were monitored to assess the effect of continuous calcium infusion on calcium homeostasis., Results: Continuous IV administration of calcium-gluconate throughout LVL reduced the incidence of citrate-related effects by 65 percent. In patients who developed signs of hypocalcemia, the symptoms were weaker, and less medical intervention was needed to resolve clinical symptoms. The subjective tolerance toward LVL was superior in patients receiving calcium support compared to control patients. Continuous calcium infusion attenuated changes in serum phosphorus compared to patients receiving saline. No differences were observed in the variation of serum potassium and serum magnesium between the control group and the treatment group. The administration of calcium was not associated with technical problems related to the apheresis procedure, neither was any effect of calcium support on the total number of CD34+ cells collected observed., Conclusion: These results indicate that continuous support of calcium-gluconate during LVL is an effective means of reducing the incidence of citrate-related symptoms and improving subjective tolerance toward LVL, without affecting the technical performance or the number of CD34+ cells collected.

The occurrence of hypocalcemia in a term infant after the first few days of life is known to result from excessive dietary phosphate, hypomagnesemia, neonatal hypoparathyroidism, hypovitaminosis D, and maternal hyperparathyroidism. Less well recognized is the possibility that maternal ingestion of antacids may cause late neonatal hypocalcemia. Our observations suggest that taking large doses of calcium carbonate during pregnancy may be a potential cause of neonatal hypocalcemia.

Background: ACD-A solution containing sodium citrate and citric acid is used as an anticoagulant agent during peripheral blood progenitor cell (PBPC) harvesting, and in rare cases can cause fatal citrate intoxication. The aim of this study was to establish effective methods for stabilizing ionized calcium (ICa) levels during PBPC harvesting., Study Design and Methods: ICa was measured during 46 apheresis procedures conducted in 26 patients. Four patients in four procedures were infused with calcium gluconate solution before PBPC harvesting; three patients in six procedures were infused with calcium gluconate when symptoms of citrate intoxication appeared; and four patients in five procedures received a continuous infusion. Five patients in five procedures took an isotonic sports drink containing calcium when hypocalcemic symptoms appeared. The ICa level, blood pressure, and pulse rate were measured., Results: ICa declined rapidly from the preapheresis level of 1.081(+/-0.092) mM to 0.937(+/-0.081) mM (13.3%, p < 0.0001) 10 minutes after the start of apheresis and continued to decline until the completion of the procedure. When patients received a continuous infusion of calcium during apheresis, ICa was relatively stabilized. ICa significantly rose (6.1 +/- 3.6%, p < 0.02) within 2 to 5 minutes after oral intake of an isotonic sports drink containing calcium and was maintained within normal range for 31 to 55 minutes., Conclusion: An isotonic sports drink containing calcium has a quick stabilizing and a longer maintenance effect on ICa. Thus, we recommend the intake of an isotonic sports drink containing calcium as the easiest and best method for preventing hypocalcemia during apheresis.

Seizures during the neonatal period have a broad differential diagnosis, many with a specific treatment and prognosis. In the case reported, a combination of dietary and endocrinologic abnormalities resulted in hypocalcemic seizures, which continued despite aggressive correction of serum ionized calcium levels. Serial electroencephalograms (EEG) performed during the hospitalization were markedly abnormal, and treatment with anticonvulsant drugs was considered given the persistence of seizures despite normalization of serum calcium levels. After 4 days of intravenous calcium administration, the seizure activity resolved, and the patient returned to his normal baseline level of functioning. This case highlights the clinical course of neonatal hypocalcemic seizures, EEG findings in several cases, and possible mechanisms for both hypocalcemic precipitation of seizures and anticonvulsant ineffectiveness.

A case of functional second degree atrioventricular block is reported in a preterm infant secondary to early onset hypocalcaemia. An infusion of 10% calcium gluconate rapidly corrected the arrhythmia.

Healthy term babies undergo a physiological nadir in serum calcium levels by 24-48 hours of age. This nadir may be related to the delayed response of parathyroid and calcitonin hormones in a newborn. This nadir may drop to hypocalcemic levels in high-risk neonates including infants of diabetic mothers, preterm infants and infants with perinatal asphyxia. This early onset hypocalcemia which presents within 72 hours, requires treatment with calcium supplementation for at least 72 hours. In contrast late onset hypocalcemia usually presents after 7 days and requires long term therapy. Ionized calcium is crucial for many biochemical processes and total serum calcium is a poor substitute for the diagnosis of hypocalcemia.

Hydrofluoric acid readily penetrates the skin and mucous membranes, causing deep tissue layer destruction. Dermal exposure can produce hypocalcaemia, hypomagnesaemia, hyperkalaemia, cardiac dysrhythmias and death. We report the case of a 52-year-old man who presented hypocalcaemia and hypomagnesaemia due to occupational dermal contact with hydrofluoric acid. Hypocalcaemia and hypomagnesaemia were corrected by i.v. administration of calcium gluconate and magnesium sulphate.

Background: Prediction of the extent of calcium supplement will facilitate safe and efficient management of hypocalcemia in the early postoperative stage of total parathyroidectomy with autotransplantation (PTXa) in patients with renal osteodystrophy., Methods: The correlation between the extent of calcium deficiency, estimated by the amount of calcium supplement over 48 h after PTXa and using various parameters such as carboxy terminal parathyroid hormone (c-PTH), intact PTH (i-PTH), alkaline phosphatase (ALP), serum calcium, serum phosphorus, duration of hemodialysis, total weight of resected parathyroid glands and degree of subperiosteal resorption of the middle phalanx was examined in 49 patients who underwent PTX with subcutaneous autotransplantation. Bone mineral density (BMD) was also determined before, 3 months and 1 year after PTXa with dual energy X-ray absorptiometry (DEXA) in 13 patients., Results: There was a positive correlation between pre-operative i-PTH level (r=0.56, P<0.0005) or ALP level (r=0.50, P<0.0005) and the amount of calcium supplement over 48 h after PTXa in these patients. Furthermore, the degree of subperiosteal resorption, determined by Jensen's classification, was significantly correlated with the amount of calcium supplement after PTX (P<0.05). Bone mineral density 3 months after (P<0.0005) and 1 year after PTXa (P<0.001) significantly increased compared with BMD before PTXa in all patients examined., Conclusion: These findings suggest that the pre-operative determination of i-PTH, ALP levels and degree of subperiosteal resorption allow the management of hypocalcemia safely and efficiently in renal osteodystrophy patients after PTXa.