Correction Of Hypocalcemia Research Articles

Calcium administration appears not to benefit acute pancreatitis patients with hypocalcemia.

Hypocalcemia occurs commonly among patients with acute pancreatitis (AP) in the intensive care unit (ICU). Calcium therapy could be used to correct hypocalcemia and maintain calcium levels, but its impact on the prognosis has not been demonstrated. Our study aimed to determine whether calcium therapy could benefit the multiple outcomes of AP patients with hypocalcemia. We extracted 807 AP patients with hypocalcemia from the Beth Israel Deaconess Medical Center (MIMIC-IV) database and performed retrospective analyses. The outcomes were in-hospital, 28 days, ICU mortality, and the length of stay (LOS) in the hospital and ICU. We performed propensity matching (PSM) and inverse probability weighting (IPTW) to balance the baseline differences and conducted multivariate regression to investigate the impact of calcium therapy. A total of 620 patients (76.8%) received calcium treatment (calcium group) during hospitalization, while 187 patients (non-calcium group) did not. Patients in the calcium group did not present significant survival differences between groups before and after matching. After including covariates, calcium administration had no association with patients' in-hospital (HR: 1.03, 95% Cl: 0.47-2.27, p = .942), 28 days and ICU mortality and was significantly associated with prolonged length of stay in the hospital (effect estimate: 6.18, 95% Cl: 3.27-9.09, p < .001) and ICU (effect estimate: 1.72, 95% Cl: 0.24-3.20, p < .001). Calcium therapy could not benefit patients in subgroups with exclusive parenteral infusion, early calcium therapy (<48 h), or various degrees of hypocalcemia. AP patients with hypocalcemia could not benefit from calcium administration, which has no association with multiple mortality and is significantly associated with prolonged LOS in the hospital and ICU.

Hypocalcemia in Trauma is Determined by the Number of Units Transfused, Not Whole Blood Versus Component Therapy

IntroductionBlood component resuscitation is associated with hypocalcemia (HC) (iCal <0.9 mmol/L) that contributes to coagulopathy and death in trauma patients. It is unknown whether or not whole blood (WB) resuscitation helps mitigate the risk of HC in trauma patients. We hypothesized that calcium homeostasis is maintained and mortality improved in patients who only receive WB. Materials and methodsThis is a retrospective review of all adult trauma patients who received WB from July 2018 to December 2020. Variables included transfusions, ionized calcium levels, and calcium replacement. Patients were characterized as follows based on blood products received: WB or WB with other blood components. Groups were compared with respect to HC, correction of HC, 24 h, and inpatient mortality. ResultsTwo hundred twenty-three patients received WB and met the inclusion criteria. 107 (48%) received WB only. HC occurred in 13% of patients who received more than one WB unit compared to 29% of WB and other blood component patients (P = 0.02). WB patients received less calcium replacement (median 250 mg versus 2000 mg, P < 0.01). HC and total units transfused within 4 h were associated with mortality in the adjusted model. HC significantly increased after 5 units of blood products were transfused, regardless of product type. WB was not protective against HC. ConclusionsHC and failure to correct HC are significant risk factors for mortality in trauma. Resuscitations with WB only and WB in combination with other blood components are associated with HC especially when more than 5 units of any blood product are transfused. Calcium supplementation should be prioritized in any large volume transfusion, regardless of blood product type.

Admission Hypocalcemia and the Need for Endoscopic and Clinical Interventions among Patients with Upper Gastrointestinal Bleeding

Introduction: Calcium is an essential co-factor in the coagulation cascade, and hypocalcemia is associated with adverse outcomes in bleeding patients, including trauma patients, women with postpartum hemorrhage, and patients with intracranial hemorrhage. In this retrospective, single-center, cohort study, we aimed to determine whether admission-ionized calcium (Ca⁺⁺) is associated with higher rates of therapeutic interventions among patients presenting with acute nonvariceal upper gastrointestinal bleeding (NV-UGIB). Methods: Adult patients admitted due to NV-UGIB between January 2009 and April 2020 were identified. The primary outcome was defined as a need for clinical intervention (two or more packed cell transfusions, need for endoscopic, surgical, or angiographic intervention). Univariate and multivariable logistic regression analyses were performed to determine whether Ca⁺⁺ was an independent predictor of the need for therapeutic interventions. Propensity score matching was performed to adjust the imbalances of covariates between the groups. Results: A total of 434 patients were included, of whom 148 (34.1%) had hypocalcemia (Ca⁺⁺ <1.15 mmol/L). Patients with hypocalcemia were more likely to require therapeutic interventions than those without hypocalcemia (48.0% vs. 18.5%, p < 0.001). Specifically, patients with hypocalcemia were more likely to require endoscopic intervention for control of bleeding (25.0% vs. 15.7%, p = 0.03) and multiple packed cell transfusions (6.8% vs. 0.3%, p < 0.001). Additionally, they had significantly longer hospital stay (5.0 days [IQR 3.0–8.0] vs. 4.0 days [IQR 3.0–6.0], p = 0.01). After adjusting for multiple covariates, Ca⁺⁺ was an independent predictor of the need for therapeutic intervention (aOR 1.62, 95% confidence interval [CI] 1.22–2.14, p < 0.001). The addition of Ca⁺⁺ to the Modified Glasgow Blatchford score improved its accuracy in the prediction of therapeutic intervention from AUC of 0.68 (95% CI 0.63–0.72) to 0.72 (95% CI 0.67–0.76), p = 0.02. After incorporation of the propensity score, the results did not change significantly. Conclusion: These findings suggest that hypocalcemia is common and is associated with an adverse clinical course in patients with NV-UGIB. Measurement of Ca⁺⁺ on admission may facilitate risk stratification in these patients. Trials are needed to assess whether the correction of hypocalcemia will lead to improved outcomes.

Recurrent seizures as manifestation of hypoparathyroidism-related hypocalcemia in a patient with post-subtotal thyroidectomy

Background: Hypocalcemia, a condition where the serum calcium concentration or total serum calcium is below normal, could be associated with various manifestations including severe symptoms requiring immediate hospitalization. The condition can cause by several causes including iatrogenic thyroidectomy. Here, we report a patient of hypocalcemia associated with hypoparathyroidism due to post-thyroidectomy. Case presentation: A 32-year-old woman admitted to the hospital complained of stiffness and tingling in the extremities accompanied by recurrent seizures. The serum calcium level was low and this hypocalcemia condition was associated with low parathyroid hormone levels after subtotal thyroidectomy surgery. Laboratory examination indicated calcium 4.8 mg/dL and parathyroid hormone 2.21 pg/ml. The patient had bradycardia with prolonged QT on electrocardiography (ECG) and developed cataracts in both eyes which could be associated with chronic hypocalcemia. The patient's condition improved after correction of hypocalcemia. After discharge, the patient was given calcium and levothyroxine supplementation due to hypothyroid conditions. Conclusion: The hypocalcemia condition in the patient was associated with low parathyroid hormone level post-subtotal thyroidectomy surgery. This case highlights the impotence of detailed analyses of hormonal, radiological and histological investigations of patients with thyroid gland diseases to diagnose such conditions early and to ensure timely management.

ODP076 A Unique Case of Iatrogenic Hypermagnesemia Induced Symptomatic Hypocalcemia

Abstract Introduction Magnesium plays a role in production, release, and end-organ responsiveness of parathyroid hormone (PTH) and calcium homeostasis. Hypomagnesemia has been well documented to cause hypocalcemia by impaired secretion of PTH or PTH resistance. Iatrogenic hypermagnesemia in pregnant patients receiving intravenous magnesium for suppression of premature labor and pre-eclampsia is an uncommon cause of hypocalcemia. We are reporting a case of symptomatic hypocalcemia caused by iatrogenic hypermagnesemia in post-partum mother, who had high PTH in contrast to previous case reports. CaseA 28-year-old G4P1122 female, postpartum day 16 was admitted for headache, slurred speech, and vomiting. She was found to have elevated blood pressures and was started on IV magnesium for postpartum preeclampsia. On her first day, she received a 4g bolus of magnesium sulfate followed by 2g as maintenance for seizure prophylaxis. The following morning, the patient awoke complaining of numbness/tingling in both arms and twitching in her face and eyelids. Later that day, she had developed bilateral spontaneous carpopedal spasm as well. Labs drawn at that time revealed ionized calcium 0.78mmol/L (1.18-1.32 mmol/L), corrected calcium 7.42mg/dL (8.5-10.1), vitamin D 25-OH 45ng/mL (30-100), PTH 149.1pg/mL (18.5-88), phosphorus 2.9mg/dL (2.3-4.6), GFR116mL/min (&amp;gt;60) and magnesium 3.5mg/dL (1.4-2.2). Patient was started on IV calcium gluconate infusion along with calcium carbonate 1g QID and vitamin D3 5000 units daily. By the evening of the second day, patient's carpopedal spasm and paresthesia completely resolved. Repeat labs demonstrated improved ionized calcium of 1.17mmol/L (1.18-1.32), corrected calcium of 9.78mg/dL (8.5-10.1), and magnesium of 1.5mg/dL (1.4-2.2). Patient was discharged on calcium carbonate 1g TID and Vitamin D3 5000 units daily. Patient self-discontinued calcium and vitamin D supplementation a week after discharge. Repeat labs one week later showed normal corrected calcium, magnesium, and PTH levels. Conclusion Our patient developed transient, symptomatic hypocalcemia with elevated PTH secondary to iatrogenic hypermagnesemia, which improved with intravenous calcium. Hypomagnesemia is a known cause of hypocalcemia, but hypermagnesemia is a significantly less recognized etiology. Hypermagnesemia can cause low PTH due to activation of calcium sensing receptors resulting in inhibition of PTH secretion. Hypermagnesemia can also blunt the peripheral effect of PTH and promote hypercalciuria. Previous studies showed PTH can peak by the end of magnesium infusion but still result in hypocalcemia, although this is an uncommon clinical presentation. Our case highlights this aspect of elevated PTH after the completion of IV Magnesium infusion but still unable to correct hypocalcemia due to PTH resistance from hypermagnesemia. This calls attention to another underrecognized sequalae of hypermagnesemia: blunting of peripheral tissues response to PTH. Clinicians should be aware of development of hypocalcemia with both hypo- and hypermagnesemia as well as the underlying pathophysiology. Presentation: No date and time listed

Neonatal Rickets, Due to Maternal Vitamin D Deficiency, Complicated by Convulsion and Dilated Cardiomyopathy: Case Report

Deficiency rickets due to maternal hypovitaminosis D cause hypocalcaemia in infants, which may be complicated by dilated cardiomyopathy (DCM) with myocardial dysfunction. Calcium is central in myocardial contraction coupling, and hypocalcemia decreases myocardial contractility. However, dilated cardiomyopathy (DCM) due to hypocalcemia in infants has been rarely reported. Correction of hypocalcemia was associated with resolution of congestive heart failure and the left ventricular (LV) geometry and systolic function.&#x0D; We report the case of an infant who presented deficiency rickets due to maternal hypovitaminosis D, complicated by convulsion and dilated cardiomyopathy, with good improvement under treatment with calcium and vitamin D.

Evaluation of the left ventricular systolic strain in hypocalcemic infants with two-dimensional speckle tracking echocardiography.

Speckle tracking echocardiography (STE) is a new emerging method for evaluation of the cardiac systolic performance. We characterized left ventricular (LV) systolic functions of hypocalcemic infants, and assessed the effects of calcium and vitamin D supplementations on LV systolic functions using two-dimensional STE. A prospective controlled study was conducted in Mansoura University Children's Hospital, Egypt from 2015 to 2018 including 88 hypocalcemic infants (patient group) and 30 healthy controls. We subdivided the patient group into vitamin D deficiency group (n = 32) and normal vitamin D group (n = 56). All infants were investigated for serum phosphorus, alkaline phosphatase and 25-hydroxy vitamin D levels. Both patients and controls were initially evaluated for LV systolic functions using two-dimensional STE. After correction of hypocalcemia and vitamin D deficiency, reevaluation of LV systolic functions was done for the patient group. LV systolic strains were lower in the patient group than controls (p<.001). After recovery of hypocalcemia of the patients, we reported significant improvement of strains and significant reductions of the end-diastolic and end-systolic volumes of the left ventricle (p<.001). Global longitudinal and circumferential strains were lower in patients with vitamin D deficiency than patients with normal vitamin D levels (p<.001). The LV systolic strain improved after correction of vitamin D deficiency and hypocalcemia (p<.001). Two-dimensional STE could detect and follow up early LV systolic dysfunction in infants with hypocalcemia and vitamin D deficiency.

MO796IMPACT OF ACTIVE VITAMIN D AND CALCIUM PREPARATION ON VASCULAR CALCIFICATION MARKERS IN HEMODIALYSIS PATIENTS WITH HYPOCALCEMIA INDUCED BY CALCIMIMETICS

Abstract Background and Aims Recently, we demonstrated the efficacy of etelcalcetide for control of secondary hyperparathyroidism (SHPT) in the DUET trial; a 12-week multicenter, open-label, randomized (1:1:1), parallel-group study treated with etelcalcetide + active vitamin D (Group E+D), etelcalcetide + oral calcium preparation (Group E+Ca), or control groups (Group C) in 124 subjects undergoing maintenance hemodialysis. Moreover, we also showed that active vitamin D was useful in correcting hypocalcemia induced by calcimimetics, but the oral calcium preparation was superior for suppression of hyperphosphatemia. In this post hoc analysis, we evaluated vascular calcification markers, fibroblast growth factor 23 (FGF23) and calciprotein particles (CPPs), in patients using etelcalcetide (n = 77) extracted from the registrants of the DUET trial. Method Serum levels of FGF23 and CPPs were measured at baseline, 6 weeks and 12 weeks after start of the trial. Skewed data (FGF23 and CPPs) were transformed to natural logarithm to achieve normal distribution prior to statistical analysis. The changes in log CPPs and log FGF23 were estimated in a linear mixed model with each treatment group, time point, and interaction of the treatment group and time point as the fixed effects. We compared these changes between treatment the groups using a linear mixed model and also the Tukey-Kramer method to correct for multiplicity. Additionally, we exploratory examined the correlations among changes of FGF23, CPPs and other biomarkers related to bone mineral metabolisms, iPTH, Ca, P, and calcium-phosphate product, tested by Spearman’s rank correlation coefficient. Results The decreases at the 12-week time point after the trial start in log FGF23 were estimated -1.13 pg/mL in Group E+Ca and -0.10 pg/mL in Group E+D in a linear mixed model, respectively. Similarly, the decreases in CPPs were estimated -1.60 AU in Group E+Ca and -0.82 AU in Group E+D, respectively. Changes of both FGF23 (P = 0.017) and CPPs (P &amp;lt; 0.001) in Group E+Ca significantly decreased compared with those in in Group E+D by Tukey-Kramer multiple-comparison test at 12 weeks after the trial start, while both changes in CPPs and FGF23 could not reach the significant differences between two groups at 6 weeks after the trial start (Figure 1). Reductions in FGF23 positively correlated with reductions in calcium (ρ = 0.42, P &amp;lt; 0.01) and phosphate (ρ = 0.48, P &amp;lt; 0.01) at 6 weeks after the trial start, and in calcium (ρ = 0.30, P &amp;lt; 0.01) and phosphate (ρ =0.70, P &amp;lt; 0.01) at 12 weeks after 6 weeks of the trial start), but there was no correlation with reductions in iPTH at any time point. Reductions in CPPs positively correlated with reductions only in phosphate at 6 weeks after the trial start (ρ = 0.47, P &amp;lt; 0.01) and at 12 weeks after 6 weeks of the trial start (ρ = 0.54, P &amp;lt; 0.01). Conclusion In this analysis, vascular calcification markers were significantly decreased in Group E+Ca compared to those in Group E+D. Further studies should be needed, our study suggests that oral calcium preparation may have an advantage against vascular calcification rather than active vitamin D for the correction of hypocalcemia induced by etelcalcetide in hemodialysis patients with SHPT.

Association Between Ionized Calcium Level and Neurological Outcome in Endovascularly Treated Patients with Spontaneous Subarachnoid Hemorrhage: A Retrospective Cohort Study.

Spontaneous subarachnoid hemorrhage (SSAH) is associated with significant morbidity and mortality. Pathophysiological processes following initial bleeding are complex and not fully understood. In this study, we aimed to determine whether a low level of ionized calcium (Ca++), an essential cofactor in the coagulation cascade and other cellular processes, is associated with adverse neurological outcome, development of early hydrocephalus, and symptomatic vasospasm among patients with SSAH. This was a retrospective single-center cohort study of all patients admitted for SSAH between January 1, 2009, and April 31, 2020. The primary outcome was an unfavorable neurological status at discharge, defined as a modified Rankin Scale score greater than or equal to 3. Secondary outcomes were the development of early hydrocephalus and symptomatic vasospasm. Multivariable logistic regression was performed to determine whether Ca++ was an independent predictor of these outcomes. A total of 255 patients were included in the final analysis. Hypocalcemia, older age, admission Glasgow Coma Scale (GCS) score, and admission Hunt-Hess classification scale (H&H) grades IV and V were independently associated with unfavorable neurological outcome, with adjusted odds ratios (ORs) of 1.93 (95% confidence interval [CI] 1.1-3.4; p = 0.02) for each 0.1mmolL-1 decrease in the Ca++ level, 1.04 (95% CI 1.01-1.08; p = 0.02) for each year increase, 0.82 (95% CI 0.68-0.99; p = 0.04), and 6.29 (95% CI 1.14-34.6; p = 0.03), respectively. Risk factors for the development of hydrocephalus were hypocalcemia and GCS score, with ORs of 1.85 (95% CI 1.26-2.71; p = 0.002) for each 0.1mmol L-1 decrease in the Ca++ level and 0.83 (95% CI 0.73-0.94; p = 0.005), respectively. Ca++ was not associated with symptomatic vasospasm (OR 1.04 [95% CI 0.76-1.41]; p = 0.81). Among patients with admission H&H grade I-III bleeding, hypocalcemia was independently associated with unfavorable neurological outcome at discharge, with an adjusted OR of 1.99 (95% CI 1.03-3.84; p = 0.04) for each 0.1mmol L-1 decrease in the Ca++ level. Hypocalcemia was also an independent risk factor for the development of early hydrocephalus, with an adjusted OR of 2.95 (95% CI 1.49-5.84; p = 0.002) for each 0.1mmol L-1 decrease in the Ca++ level. Ca++ was not associated with symptomatic vasospasm. No association was found between Ca++ and predefined outcomes among patients with admission H&H grade IV and V bleeding. Our study shows that hypocalcemia is associated with worse neurological outcome at discharge and development of early hydrocephalus in endovascularly treated patients with SSAH. Potential mechanisms include calcium-induced coagulopathy and higher blood pressure. Trials are needed to assess whether correction of hypocalcemia will lead to improved outcomes.

Hypocalcemia is associated with adverse clinical course in patients with upper gastrointestinal bleeding.

Acute non-variceal upper gastrointestinal bleeding (NV-UGIB) is associated with significant morbidity and mortality. Early and efficient risk stratification can facilitate management and improve outcomes. We aimed to determine whether the level of ionized calcium (Ca++), an essential co-factor in the coagulation cascade, is associated with the severity of bleeding and the need for advanced interventions among these patients. This was a retrospective single-center cohort study of all patients admitted due to NV-UGIB. The primary outcome was transfusion of ≥ 2 packed red blood cells, arterial embolization, or emergency surgery. Secondary outcomes included (1) transfusion of ≥ 2 packed red blood cells, (2) arterial embolization, or emergency surgery, and (3) all-cause in-hospital mortality. Multivariable logistic regression was performed to determine whether Ca++ was an independent predictor of these adverse outcomes. 1345 patients were included. Hypocalcemia was recorded in 604 (44.9%) patients. The rates of primary adverse outcome were significantly higher in the hypocalcemic group, 14.4% vs. 5.1%, p < 0.001. Secondary outcomes-multiple transfusions, need for angiography or surgery, and mortality were also increased (9.9% vs. 2.3%, p < 0.001, 5.3% vs. 2.8%, p = 0.03, and 33.3% vs. 24.7%, p < 0.001, respectively). Hypocalcemia was an independent predictor of primary and all the secondary outcomes, except mortality. Hypocalcemia in high-risk hospitalized patients with NV-UGIB is common and independently associated with adverse outcomes. Ca++ monitoring in this population may facilitate the rapid identification of high-risk patients. Trials are needed to assess whether correction of hypocalcemia will lead to improved outcomes.

Vitamin D Deficiency and Low Serum Calcium as Predictors of Poor Prognosis in Patients with Severe COVID-19

BackgroundThe severity of Coronavirus Disease 2019 (COVID-19) is a multifactorial condition. An increasing body of evidence argues for a direct implication of vitamin D deficiency, low serum calcium on poor outcomes in COVID-19 patients. This study was designed to investigate the relationship between these two factors and COVID-19 in-hospital mortality.MaterialsThis is a prospective study, including 120 severe cases of COVID-19, admitted at the department of Reanimation-Anesthesia. Vitamin D was assessed by an immuno-fluoroassay method. Total serum calcium by a colorimetric method, then, corrected for serum albumin levels. The association with in-hospital mortality was assessed using the Kaplan-Meier survival curve, proportional Cox regression analyses and the receiver operating characteristic curve.ResultsHypovitaminosis D and hypocalcemia were very common, occurring in 75% and 35.8% of patients. When analyzing survival, both were significantly associated with in-hospital mortality in a dose-effect manner (pLog-Rank = 0.009 and 0.001 respectively). A cutoff value of 39 nmol/l for vitamin D and 2.05 mmol/l for corrected calcemia could predict poor prognosis with a sensitivity of 76% and 84%, and a specificity of 69% and 60% respectively. Hazard ratios were (HR = 6.9, 95% CI [2.0–24.1], p = 0.002 and HR = 6.2, 95% CI [2.1–18.3], p = 0.001) respectively.ConclusionThis study demonstrates the high frequency of hypocalcemia and hypovitaminosis D in severe COVID-19 patients and provides further evidence of their potential link to poor short-term prognosis. It is, therefore, possible that the correction of hypocalcemia, as well as supplementation with vitamin D, may improve the vital prognosis.

Refractory hypercapnic respiratory failure in an elderly female

The most common cause of hypercapnic respiratory failure is acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Many other factors can contribute to hypercapnia and may lead to refractory hypercapnia in AECOPD. One of the important causes is electrolyte imbalance. We report a case of refractory hypercapnic respiratory failure in an elderly female due to postthyroidectomy hypocalcemia. The patient responded well after the correction of hypocalcemia.

Hidden Hypocalcemia as a Risk Factor for Cardiovascular Events and All-Cause Mortality among Patients Undergoing Incident Hemodialysis

Lower corrected calcium (cCa) levels are associated with a better prognosis among incident dialysis patients. However, cCa frequently overestimates ionized calcium (iCa) levels. The prognostic importance of the true calcium status defined by iCa remains to be revealed. We conducted a retrospective cohort study of incident hemodialysis patients. We collected data of iCa levels immediately before the first dialysis. We divided patients into three categories: apparent hypocalcemia (low iCa; <1.15 mmol/L and low cCa; <8.4 mg/dL), hidden hypocalcemia (low iCa despite normal or high cCa), and normocalcemia (normal iCa). The primary outcome was the composite of all-cause death and cardiovascular diseases after hospital discharge. Among the enrolled 332 patients, 75% of the patients showed true hypocalcemia, defined as iCa <1.15 mmol/L, 61% of whom showed hidden hypocalcemia. In multivariate Cox models including other potential risk factors, true hypocalcemia was a significant risk factor (hazard ratio [HR], 2.34; 95% confidence interval [CI], 1.03–5.34), whereas hypocalcemia defined as corrected calcium <8.4 mg/dL was not. Furthermore, hidden hypocalcemia was significantly associated with an increased risk of the outcome compared with normocalcemia (HR, 2.56; 95% CI, 1.11–5.94), while apparent hypocalcemia was not. Patients with hidden hypocalcemia were less likely to receive interventions to correct hypocalcemia, such as increased doses of active vitamin D or administration of calcium carbonate, than patients with apparent hypocalcemia (odds ratio, 0.45; 95% CI, 0.23–0.89). Hidden hypocalcemia was a strong predictor of death and cardiovascular events, suggesting the importance of measuring iCa.

C-terminal telopeptide of type I collagen, osteocalcin, alkaline phosphatase, and parathyroid hormone in healthy and hospitalized foals

Hypocalcemia is a common finding in critically ill equine patients. Parathyroid hormone (PTH) helps to maintain calcium homeostasis in hypocalcemic patients by promoting renal calcium reabsorption and bone resorption. Increased serum PTH concentrations have been reported in critically ill people and animals, including horses and foals. It is unknown whether increased secretion of PTH is associated with markers of bone turnover in hospitalized foals. The goals of this study were to measure markers of bone resorption (C-terminal telopeptide of type I collagen [CTX-I]) and bone formation (osteocalcin [OCN]; alkaline phosphatase [ALP]) and to determine their association with PTH concentrations, disease severity, and mortality in hospitalized foals. This prospective, multicenter, cross-sectional study was conducted on 75 newborn foals ≤3 d old divided into hospitalized (n = 65; 41 septic; 24 sick nonseptic) and healthy (n = 10) groups. Blood samples were collected on admission to measure serum CTX-I, OCN, and PTH concentrations and ALP activity. Data were analyzed by nonparametric methods and univariate logistic regression. Serum CTX-I and PTH concentrations were significantly higher, whereas OCN concentrations were lower, in septic compared with healthy foals (P < 0.05). Serum ALP activity was not different between groups; however, it was lower in hospitalized and septic foals with low OCN concentrations (P < 0.05). In hospitalized foals, PTH concentrations were positively correlated with CTX-I concentrations and inversely associated with ALP activity (P < 0.05). High CTX-I and low OCN concentrations were associated with disease severity (P < 0.05). Hospitalized nonsurviving foals had significantly lower OCN concentrations compared with survivors (P < 0.05), but CTX-I concentrations were not associated with survival. Hospitalized foals with PTH concentrations >12.4 pmol/L were more likely to die (OR = 1.5; 95% CI = 1.1–4.16; P < 0.05). Elevated PTH and CTX-I together with reduced OCN concentrations and ALP activity in sick foals indicates that bone resorption is increased during critical illness, which may be a compensatory mechanism to correct hypocalcemia or reflect a response to systemic inflammation and metabolic imbalances. Bone resorption could negatively impact skeletal development in the growing foal. Low OCN and high PTH concentrations were predictors of nonsurvival in hospitalized foals.

Early Discharge and Selective Calcium Supplementation after Thyroidectomy Based on Post-Operative Day 1 Parathormone and Calcium Level: A Prospective Study.

Aim:This study aimed to evaluate a protocol using post thyroidectomy parathyroid hormone (PTH) levels on the day after surgery to facilitate early discharge of patients.Methods:This prospective observational study was done in Christian Medical College, India over 1 year with 125 consecutive patients who had serum PTH and calcium values measured in the morning following thyroidectomy/first postoperative day (D1). Patients with no symptoms and signs of hypocalcemia and with serum calcium ≥8 mg/dL and PTH ≥6 pg/ml according to the protocol were discharged without supplements on D1. Patients were followed up and tested for a week after surgery in the outpatient clinic to assess hypocalcemia and readmission rates.Results:Seventy five patients (60%) could be discharged early on D1without calcium supplementation; only one patient had mild hypocalcemia symptoms managed with oral calcium supplements during outpatient follow-up within 1 week and none who followed the protocol required readmission. Temporary biochemical hypocalcemia was encountered in 36 patients (28.8%) including symptomatic hypocalcemia in 13 patients (10.4%). Among the 36 patients with hypocalcemia, 26 patients (72.2%) had a PTH level <6 pg/ml. Three patients required intravenous calcium infusion to correct hypocalcemia. Sensitivity, specificity and positive predictive value, and ROC of PTH 6 pg/ml in predicting hypocalcemia were 70.5%, 94.5% and 83.3%, 0.86, respectively. The low PTH could also guide early supplementation of calcium and all the severe hypocalcemia patients had PTH lower than the cut off of 6 pg/ml.Conclusion:A PTH and calcium-based protocol can be effectively used for early discharge of thyroidectomy patients the day after surgery without calcium supplementation. The compliance of the patient for early discharge was good.

Controversies in the Management of Secondary Hyperparathyroidism in Chronic Kidney Disease.

Secondary hyperparathyroidism is a frequent complication of chronic kidney disease that begins early in the course of renal insufficiency as an adaptive response to maintain mineral homeostasis. This complex disorder affects the bone, leading to an increase in fracture risk and is associated with increased risks of vascular calcification and mortality. PURPOSE OF REVIEW: In this review, we examine the different strategies available to manage secondary hyperparathyroidism. Particularly, we focus on the adequate control of serum phosphorus by restricting intake and the use of phosphate binders, correction of hypocalcemia while minimizing calcium burden, and reduction in PTH levels through the use of vitamin D sterols and calcimimetics. RECENT FINDINGS: It was observed that although numerous agents directed at the correction of these abnormalities have demonstrated effectiveness on biochemical markers, there is still a relative scarcity of studies demonstrating treatment effectiveness as measured by hard clinical outcomes. In addition, most agents have side effects that may limit their use, even in patients in which the treatment has demonstrated efficacy in controlling these parameters. There is still controversy as to what therapeutic regimens to choose for a particular patient and what parameter should be used to follow their effects, including outcomes, side effects, pill burden, and costs, among others. In the present article, we analyze controversial aspects of the different therapeutic agents available. Although many tools and regimens are available, no one by itself is enough for an adequate management of the patient. But rather, combined therapy and individualization of approaches are recommended for better results. We suggest that new studies analyzing the effectiveness of therapeutic approaches to the management of secondary hyperparathyroidism should be directed not only to controlling parathyroid hormone levels but also to the evaluation of long-term outcomes, based on modification of morbidity, mortality, and end organ impact, while reducing side effects and controlling costs, among others.

Concomitant Fahr\u2019s syndrome and thoracic ossification of the posterior longitudinal ligament caused by idiopathic hypoparathyroidism \u2013 case report

BackgroundFahr’s syndrome presenting multiple and symmetric calcification of basal ganglia and cerebral cortex is rare, and idiopathic hypoparatyroidism is known as one of the causes. The relationship between ossification of posterior longitudinal ligament (OPLL) and idiopathic hypoparatyroidism is also reported in a few cases. Here, we report a patient presenting concomitant Fahr’s syndrome and thoracic OPLL developed by idiopathic hypoparatyroidism.Case presentation53-year-old female patient presented myelopathic sign including gait disturbance and both leg weakness (Grade 3) for 4 months after slip down, and has the history of anti-epileptic medication for several years. Magnetic resonance imaging revealed cord compression by the mixed-type OPLL from T5 to T9, and decompressive surgery was planned. Sudden onset generalized tonic-clonic seizure attack developed before the surgery. Hypocalcemia (3.7 mg/dL) with QT prolongation on electrocardiogram, hypomagnesemia (1.4 mg/dL), hyperphosphatemia (7.7 mg/dL), hypoparathyroidism, and normal range of vitamin D was noted. Brain study showed Fahr’s syndrome with multiple and symmetric calcification of basal ganglia, cerebral cortex, and cerebellum. Decompressive laminectomy was performed after transient correction of hypocalcemia. The myelopathic symptoms improved to normal walking by the 14-month follow-up. The cause of hypoparathyroidism was concluded to be idiopathic.ConclusionConcomitant expression of Fahr’s syndrome and OPLL related with idiopathic hypoparatyroidism is very rare. However, we recommend considering the possibility of hypoparathyroidism and Fahr’s syndrome when we evaluate the patients with OPLL to avoid the risks of sudden onset seizure and cardiac arrhythmia due to cerebral lesions and hypocalcemia.

SUN-516 Fahr's Syndrome: A Rare Sequela of Hypoparathyroidism

Fahr’s syndrome (FS) is rare, progressive neurodegenerative disorder characterized by bilateral symmetric calcifications in the basal ganglia and cerebral cortex. Etiology of FS includes endocrine disorder, mitochondrial disease, dermatological or infectious disease. The prevalence of FS due to hypoparathyroidism (HP) is unknown. The presentation varies from movement disorders, pyramidal signs, neuropsychiatric manifestations to cognitive impairment. Case: We present a 46-year-old female with history of Grave’s disease s/p subtotal thyroidectomy, postsurgical HP and hypothyroidism for over two decades. She had history of chronic nonadherence with medications and clinic visits. Serum calcium levels were consistently below 7 mg/dl. She was found unresponsive and required intubation. Vital signs were within normal range. Physical examination except for neurological exam was unremarkable. Laboratory data: serum calcium- 6.2 mg/dl (8.4-10.2 mg/dl), ionized calcium- 0.77 mmol/L (1.13-1.32 mmol/L), phosphate - 6.4 mg/dl (2.7-4.5 mg/dl), 25 vitamin D- 21 ng/ml ( 30-100 ng/ml ), PTH- 7 pg/ml (15-65 pg/ml ), magnesium- 1.5 mg/dl (1.6-2.6 mg/dl ), creatinine - 5.16 mg/dl ( 0.4-1.1 mg/dl), WBC- 19.6 x 103/ uL (4-10 x 103/uL), TSH- 35 IU/ml (0.27-4.2 IU/ml), Free T4 – 0.96 ng/dl (0.9-1.7 ng/dl), lactate – 1.4 mmol/L (0.5 – 2.2 mmol/L). Urine toxicology was negative. EKG revealed prolonged QTc of 524 msec. Head CT showed no acute pathology however, revealed extensive bilateral calcifications of the dentate nuclei, basal ganglia, thalami and white matter, leading to consideration of FS. Calcium rose above 8 mg/dl with treatment (calcium gluconate infusion; oral calcium acetate and calcitriol via nasogastric tube). However, her mentation improved only after serum calcium remained above 8 mg/dl for the next five days. She regained consciousness and was oriented but mentation did not return to baseline. Conclusion: Although FS with extensive intracranial calcifications is a rare sequela of HP, HP is the most common cause of FS. The pathogenesis of these brain calcifications is not clear. Our patient had long standing HP and chronic non-adherence to medications. Her age at the time of diagnosis of FS rules out mitochondrial disorders. Her clinical presentation, extensive intracranial calcification with characteristic distribution and the absence of infection, dermatological lesions, traumatic or toxic causes or family history favor the diagnosis of FS. The progression of FS is thought to be associated with the calcium/phosphorus ratio, severity and duration of hypocalcemia. This emphasizes the importance of early stabilization of serum calcium level in HP to prevent development of complications. In most patients, clinical improvement and reversal of neuropsychiatric symptoms is notable after the correction of hypocalcemia. Hence, early recognition of HP as an etiology of FS is critical.

SAT-499 Denosumab for Treatment of Hypercalcemia in Myelofibrosis

Introduction Hypercalcemia is a rare complication of myeloproliferative neoplasms. As a result, the underlying mechanisms and optimal treatment options remain under investigation. We present a case of hypercalcemia in post-essential thrombocythemia (ET) related myelofibrosis that was responsive to treatment with denosumab 60mg. Clinical Case A 65-year-old woman with ET for 10 years and recent progression to myelofibrosis (confirmed by bone marrow biopsy) was admitted for failure to thrive. Significant labs include: Ca 11.5 mg/dL (n: 8.5-10.5 mg/dL), corrected Ca 13.2 mg/dL, phosphorous 3.7 mg/dL (n: 2.4-4.7 mg/dL), PTH 5 pg/mL (n: 16-87 pg/mL), 25-OH Vitamin D 20.2 ng/mL (n: 30-100 ng/mL), 1,25 Vitamin D: 6.5 pg/mL (n: 19.9-79.3 pg/mL), PTHrP <2 pmol/L (n: <2 pmol/L), Vitamin A 9.4 ug/dL (n: 36.4-108.0 ug/dL), bone specific alkaline phosphatase 58 ug/L (n: 8.1-31.6 ug/L), TSH 0.16 uIU/mL (n: 0.34-5.60 uIU/mL), pancytopenia on CBC with 3% blasts on differential, LDH 3157 U/L (n: 100-200 U/L), and uric acid 7.4 mg/dL (n: 2.7-7.3 mg/dL). There were no lytic lesions on CT head/chest/abdomen/pelvis. Corrected Ca levels improved to 11 mg/dL after i.v. fluids and calcitonin. Denosumab 60 mg was administered on day 9 of hospitalization when corrected Ca reached 14.5 mg/dL. Cholecalciferol 1000 IU daily was started. Ca levels normalized three days after denosumab. However, clinical course then rapidly deteriorated with transformation into acute leukemia with hemophagocytic lymphohistiocytosis (HLH), tumor lysis syndrome, septic shock, and acute renal failure. Venous ionized Ca levels dropped to 0.80 mmol/L (n: 1.14-1.29 mmol/L) six days after denosumab dose. She required i.v. calcium gluconate, oral Ca, and adjusted Ca bath in dialysis to correct hypocalcemia. The patient died on day 19 of hospitalization. Conclusion While hypercalcemia is uncommon in myelofibrosis, it needs to be recognized as a potential complication. Although the underlying pathogenesis remains unknown, suggested mechanisms include: ectopic 1,25 Vitamin D production, osteolytic metastases, immobilization, and RANKL activation. Our patient did not have known bone metastases, prolonged periods of immobility or elevated 1,25 Vitamin D levels. However, our patient’s response to denosumab supports a RANKL mediated process. It is likely that there is an extensive release of cytokines in myelofibrosis even in the absence of osteolytic lesions. This would shift the RANKL/OPG balance towards osteoclast differentiation and subsequent hypercalcemia. Our case illustrates effective treatment of hypercalcemia in myelofibrosis with denosumab 60 mg. Low dose denosumab can be considered for treatment in myelofibrosis patients with a high risk of acute clinical decompensation. However, more research to elucidate the underlying mechanism and optimal treatment of hypercalcemia in myeloproliferative disorders is necessary.

Liver transplantation for acute liver failure due to hepatitis E in a pregnant patient.

Liver transplantation for acute liver failure due to hepatitis E in a pregnant patient.