Abnormal Serum Calcium Research Articles

Features of infratentorial-predominant posterior reversible encephalopathy syndrome

Posterior reversible encephalopathy syndrome (PRES) is a neurotoxic process that typically occurs in the setting of immune dysregulation. In contrast to the characteristic pattern involving parieto-occipital and posterior frontal regions, predominant involvement of the infratentorial brain occurs in a minority of PRES patients. We examined six patients with infratentorial predominant posterior reversible encephalopathy syndrome (IPPRES) relative to those with typical PRES in terms of clinical factors of toxicity and outcomes. We review the current understanding of PRES pathophysiology. An institutional database of PRES patients was created through an IRB-approved search of the electronic record from 2007 to 2012. MR images were reviewed and classified by two neuro radiologists. Clinical data including laboratory data, blood pressure, and discharge outcome were collected through review of existing electronic medical records. Characteristics of the two groups were compared. Six cases among 80 PRES patients displayed an atypical distribution of signal abnormality predominantly involving the infratentorial brain. In IPPRES patients, signal abnormalities within the supratentorial brain, when present, showed a predominantly central distribution rather than the typical peripheral distribution. IPPRES patients showed higher rates of extreme hypertension, renal dysfunction, abnormal serum calcium, and abnormal serum magnesium relative to typical PRES patients. Outcomes were similar between the two groups. In our small series, IPPRES differs from typical PRES patients not only in the distribution of imaging abnormalities but also in rates of extreme hypertension and several laboratory indices. Despite these differences, clinical outcome in the IPPRES group was similar to that of typical PRES.

Abnormal serum calcium levels are associated with clinical response to maximization of heart failure therapy.

Abnormal serum calcium levels are associated with adverse cardiovascular effects. Therapy of heart failure (HF) may result in urinary calcium excretion and calcium apposition to bones, and consequently, in calcemia. The aim of the study was to assess the prevalence of abnormal calcium levels in the blood of patients receiving maximized HF therapy, to explore clinical and laboratory determinants of abnormal serum calcium levels, and to analyze the relation of abnormal calcium levels to prognosis. The study included 722 patients with HF classified as New York Heart Association (NYHA) classes III-IV at baseline (age 53 ±10 years, 13% of women), who underwent HF therapy optimization to maximum tolerated doses. After therapy maximization, the NYHA class improved in 66.7% of the patients, while it did not change in 31.0% and worsened in 2.4%. Hypocalcemia occurred in 166 patients (22.9%) and was more prevalent in patients in whom the NYHA class improved. Hypercalcemia was diagnosed in 63 patients (8.7%) and was more common in patients with no functional improvement or worsening of the NYHA class. This effect was independent of age, sex, etiology of HF, body mass index, kidney function, or the use of thiazides. Hypercalcemia was associated with increased catabolism, hemodynamic compromise, more intensive inflammation, and lower bone mineral density. Lower albumin and higher phosphorus levels, were significant predictors of hypercalcemia, independently of kidney function. Hypocalcemia was associated with reduced catabolism, higher albumin and lower phosphorus levels, use of thiazides, and smoking history. Neither hypocalcemia nor hypercalcemia was associated with poor prognosis. Our study shows that abnormal serum calcium levels are associated with a clinical response to treatment maximization in patients with HF. Mild hypocalcemia after maximization of therapy is not associated with poorer prognosis. Hypercalcemia is associated with lack of response to treatment, and its prognostic value remains unclear.

Serum calcium and phosphorus levels in patients undergoing maintenance hemodialysis: A multicentre study in Korea

BackgroundIn many countries, nephrologists follow clinical practice guidelines for mineral bone disorders to control secondary hyperparathyroidism (SHPT) associated with abnormal serum calcium (Ca) and phosphorus (P) levels in patients undergoing maintenance hemodialysis (MHD). The Kidney Disease Outcomes Quality Initiative (KDOQI) Guidelines have long been used in Korea, and this study was undertaken to investigate the current status of serum Ca and P control in MHD patients. MethodsData were collected from a total of 1,018 patients undergoing MHD without intercurrent illness, in 17 hemodialysis centers throughout the country. Serum levels of Ca, P, and intact parathyroid hormone (iPTH) were measured over 1 year, and the average values were retrospectively analyzed. ResultsSerum levels of Ca, P, and the Ca×P product were 9.1±0.7mg/dL, 5.3±1.4mg/dL, and 48.0±13.6mg2/dL2, respectively. However, the percentages of patients with Ca, P, and Ca × P product levels within the KDOQI guideline ranges were 58.7%, 51.0%, and 70.7%, respectively. Of the 1,018 patients, 270 (26.5%) had iPTH >300pg/mL (uncontrolled SHPT), whereas 435 patients (42.7%) showed iPTH <150pg/mL. Patients with uncontrolled SHPT had significantly higher values of serum Ca, P, and Ca×P product than those with iPTH ≤300pg/mL. ConclusionDespite the current clinical practice guidelines, SHPT seems to be inadequately controlled in many MHD patients. Uncontrolled SHPT was associated with higher levels of serum Ca, P, and Ca × P product, suggestive of the importance of SHPT management.

Characteristics, management and outcome of primary hyperparathyroidism in South Africa: a single-centre experience

IntroductionPrimary hyperparathyroidism (PHPT) is a common endocrine disorder characterised by hypercalcaemia and elevated parathyroid hormone (PTH) levels. However, it remains a relatively underdiagnosed disease in the developing world primarily due...

Assessment of serum calcium in relation to dietary calcium intake in a rural population in Cameroon

The serum calcium levels of patients were assessed as they attended a district hospital in a rural population for a period of one month. A majority of the patients were between the age group of 38-77 years. 55 cases were studied. The ratio of males to females was 3:8. The results show an increase in abnormal serum calcium level with age. The abnormality in serum calcium was higher in females than in males. The demonstration of poor nutritional intake and lack of other calcium supplements was a predisposing factor to the abnormal calcium levels. It was concluded that the abnormal levels of calcium were as a result of lack of calcium diet.

Current Recommendations for Laboratory Testing and Use of Bone Turnover Markers in Management of Osteoporosis

Osteoporosis is a major health problem worldwide, and is projected to increase exponentially due to the aging of the population. The absolute fracture risk in individual subjects is calculated by the use of algorithms which include bone mineral density (BMD), age, gender, history of prior fracture and other risk factors. This review describes the laboratory investigations into osteoporosis which include serum calcium, phosphate, creatinine, alkaline phosphatase and 25-hydroxyvitamin D and, additionally in men, testosterone. Parathyroid hormone (PTH) is measured in patients with abnormal serum calcium to determine its cause. Other laboratory investigations such as thyroid function testing, screening for multiple myeloma, and screening for Cushing's syndrome, are performed if indicated. Measurement of bone turnover markers (BTMs) is currently not included in algorithms for fracture risk calculations due to the lack of data. However, BTMs may be useful for monitoring osteoporosis treatment. Further studies of the reference BTMs serum carboxy terminal telopeptide of collagen type I (s-CTX) and serum procollagen type I N-terminal propeptide (s-PINP) in fracture risk prediction and in monitoring various treatments for osteoporosis may help expedite their inclusion in routine clinical practice.

A Calculation Model for Serum Ionized Calcium Based on an Equilibrium Equation for Complexation

Measurement of ionized calcium is more important than measurement of total calcium in serum samples. In the present study, equations were derived from complexation and acid dissociation equilibrium equations, and were used to determine the concentration of ionized calcium from the observed serum concentrations of total calcium, albumin, total protein, and inorganic phosphate. The ionized calcium concentration was calculated in 67 serum samples from healthy subjects and 34 outpatients previously identified as having abnormal serum calcium levels. The correlation coefficient between our method (y) and the calcium-ion-selective electrode method (x) was 0.953 and the linear regression equation was y = 0.97x at pH 7.4 with a factor of α = 0.21, which was based on the differences between the concentrations of calcium phosphorus compounds obtained by the electrode method and by calculation. The developed calculation is as useful and accurate as the electrode method, and therefore extremely useful for clinical diagnoses.

Biomarkers of Kidney Disease

This is the 1st edition of Continuous Renal Replacement Therapy (CRRT), a new pocketsized handbook on acute renal failure or, as it is now known, acute kidney injury (AKI). It is aimed not just at renal professionals but at anyone dealing with AKI. Most intensive care units deal with patients requiring renal replacement therapy of some form or another. While renal nurses are aware of the differences between the various methods and their particular uses, those outside the specialty are less aware. This book helps the readers understand the needs of their patient who has AKI and describes the benefits of the different methods of CRRT. The chapter on choosing renal replacement therapy in AKI lists the various methods and their particular pros and cons. For example, peritoneal dialysis is much gentler than haemodialysis but will take longer to correct biochemical disturbances and requires abdominal catheter access. It is suitable for the patient in acute heart failure with mild biochemical abnormality but less than ideal for those with dangerously high potassium levels. Another very useful chapter that looks at CRRT in children clearly highlights the particular issues when considering RRT in children. This book is the ideal companion to those dealing with AKI. It condenses a lot of the more practical information found in larger text books into a smaller more manageable size. I strongly recommend this to those who deal with CRRT regularly. Those of us who have been involved in renal disease for more than about 15 years will likely remember terrible cases of calciphylaxis. This is when the tissue outside the bone takes on the characteristics of bone due to abnormal serum calcium and phosphate levels. It can lead to tissue necrosis and significant morbidity and mortality for the patient. While these cases have been largely confined to history with better understanding of the importance of calcium/phosphate balance and improved dialysis and pharmaceutical therapies, other potentially significant problems related to these biochemical disturbances are still eperienced by the patients. Ongoing research has implicated the imbalance of calcium and phosphate in a whole host of renal related disorders, not the least of which is renal cardiovascular disease. In 2006, the term chronic kidney disease–mineral and bone disorder (CKD– MBD) was coined by the kidney disease fraternity to help highlight the importance it played in the patients outcome. This book draws together the leading world experts in the field of CKD–MBD. It is a follow-up and 2nd edition to The Spectrum of Renal Osteodystrophy published in 2000. The field has moved on significantly since that time and this 2nd edition includes hot topics such as the ‘bone-vascular-kidney’ axis. This book is highly recommended for all who deal with renal disease. It brings the latest research on CKD–MBD together in one volume and is a must as a reference tool. The Spectrum of Mineral and Bone Disorders in Chronic Kidney Disease

The Spectrum of Mineral and Bone Disorders in Chronic Kidney Disease

Journal of Renal NursingVol. 3, No. 3 Book ReviewsThe Spectrum of Mineral and Bone Disorders in Chronic Kidney DiseaseChris JonesChris JonesSearch for more papers by this authorChris JonesPublished Online:29 Sep 2013https://doi.org/10.12968/jorn.2011.3.3.152bAboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article FiguresReferencesRelatedDetails 1 May 2011Volume 3Issue 3ISSN (print): 2041-1448ISSN (online): 2052-2894 Metrics History Published online 29 September 2013 Published in print 1 May 2011 Information© MA Healthcare LimitedPDF download

Incidental Parathyroid Disease during Thyroid Surgery: Should We Remove Them?

Aim. Despite an incidence of parathyroid “incidentalomas” of 0.2%–4.5%, only approximately 135 cases have been reported in the literature. We present eight patients in whom an incidental abnormal parathyroid gland was found during routine thyroid surgery. We have reviewed the literature and postulate whether these glands could represent further evidence of a preclinical stage of primary hyperparathyroidism. Methods. A retrospective analysis of all 236 thyroid operations performed by a single surgeon was performed to identify patients in whom abnormal parathyroid tissue was removed at surgery. Results. 8/236 patients (3.39%) had a single macroscopically abnormal parathyroid gland removed and sent for analysis. Seven patients were found to have histological evidence of a parathyroid adenoma or hyperplasia. None of the patients had abnormal serum calcium detected preoperatively. Postoperatively, four patients had normal calcium, three had temporary hypocalcaemia and one refused followup. No patients had recurrent laryngeal nerve impairment. Conclusions. Despite the risk of removing a histologically normal gland, we believe that when parathyroid “incidentalomas” are found during surgery they should be excised and sent for histological analysis. We have found this to be a safe procedure with minimal morbidity to the patient. As the natural history of primary hyperparathyroidism is better understood, these glands found in normocalcaemic patients may in fact represent the early or preclinical phase of the disease. By removing them at the original operation, the patient is saved redo neck surgery with its high complication rate as or when clinically apparent primary hyperparthryoidism develops in the future.

Giant J-wave (Osborn wave) unrelated to hypothermia

A 30-year-old male was admitted for gastroenteritis with abnormal serum calcium [ionized Ca2+ (ICa) of 4.1 mg/dL] which was corrected …

Urine Calcium: Laboratory Measurement and Clinical Utility

Urine calcium measurement is a commonly ordered test in clinical laboratories. Unlike other urine markers, the utility of urine calcium is less clear to many laboratorians and physicians. Urine calcium can be used to assess parathyroid disease and familial hypocalciuric hypercalcemia (FHH). Although not predictive of stone formation, urine calcium is frequently elevated in patients with lithiasis. The primary clinical value of urine calcium measurement is to aid in the differential diagnoses of patients and direct optimal treatment options for patients with abnormal serum calcium.

The expression of molecular mediators in the idiopathic cutaneous calcification and ossification

Idiopathic cutaneous calcification and ossification occur in the absence of an abnormal serum calcium level or pre-existing tissue abnormality. The pathogenesis has not been fully elucidated. The aim of this study was to investigate the expression of several molecular mediators in the idiopathic cutaneous calcification and ossification. Immunohistochemical study was used to evaluate the expression of molecular mediators, bone morphogenetic protein 4 (BMP-4), beta-catenin, osteopontin, osteonectin and osteocalcin, and cell markers, smooth muscle actin, CD29 and CD44. And confocal laser scanning microscopy was used to evaluate the colocalization of BMP-4 and BMP receptor type IA. BMP-4, beta-catenin, osteopontin, osteonectin and osteocalcin were expressed on the calcified and ossified tissue. Especially, BMP-4 was expressed on the surrounding mesenchymal cells. Smooth muscle actin positive mesenchymal cells were on around the immature ossified tissue. Mesenchymal stem cell markers, CD29 and CD44 were not expressed. Our data suggest that BMP-4, beta-catenin, osteopontin, osteonectin and osteocalcin may be involved in the idiopathic cutaneous calcification and ossification. And smooth muscle actin positive mesenchymal cells may be involved in the cutaneous ossification. This study suggests that the idiopathic cutaneous calcification and ossification is highly complicated and regulated active process like ectopic calcification of other tissues.

Causes of Hypocitraturia in Recurrent Calcium Stone Formers: Focusing on Urinary Potassium Excretion

Multiple factors associated with hypocitraturia have been identified. However, limited studies addressing the causal relationship to hypocitraturia are available. We therefore conducted this study to determine factors associated with hypocitraturia and show their causal relationship in recurrent calcium stone formers. Dietary review and 24-hour urine samples were obtained from all recurrent calcium stone formers referred for metabolic workup in the stone clinic. One month of oral potassium chloride supplementation was prescribed to stone formers to determine the causal relationship between urinary potassium and citrate levels. Eighty-three subjects, 44 men and 39 women, were recruited to participate in this study. Hypocitraturia (citrate < 300 mg/d [<1.43 mmol/d]) was found in 50.6% of subjects. Four independent urinary variables associated with hypocitraturia were identified, including potassium level, net gastrointestinal alkaline absorption, calcium level, and titratable acid. Urinary potassium level was the strongest predictor of urinary citrate level. Hypocitraturic subjects also had lower fruit intake compared with subjects with high urinary citrate levels. Potassium chloride supplementation to a subgroup of this population (n = 58) resulted in a significant increase in urinary citrate excretion (350.73 +/- 27.25 versus 304.15 +/- 30.00 mg/d [1.67 +/- 0.13 versus 1.45 +/- 0.14 mmol/d]; P < 0.02), but no alteration in fractional excretion of citrate (19.7% +/- 2.7% versus 23.1% +/- 2.4%; P > 0.05). Hypocitraturia was found to be a common risk factor associated with recurrent calcium stone formation and low urinary potassium level, low alkaline absorption, low urinary calcium level, and high titratable acid excretion. Hypocitraturia is predominantly of dietary origin. Estimation of fruit intake should be included in the metabolic evaluation for recurrent calcium stone formation.

Two Cases of Dystrophic Calcinosis Cutis in Burn Scars

Dystrophic calcinosis cutis is defined as the abnormal deposition of insoluble calcium salts in dead or degenerated cutaneous tissues in the absence of abnormal serum calcium or phosphate concentrations. Although dystrophic calcification can occur in various diseases, its occurrence on a burn scar has rarely been reported in the dermatologic literature. Herein we describe two patients who presented with a solitary non-healing ulcer in a postburn scar, with histopathologic evidence of calcium deposition in the dermis.

Hypercalcemia of Malignancy: Part I

Oncology nurses are responsible for the ongoing assessment of hypercalcemia, including reviewing laboratory findings as well as evaluating patient symptomatology. Abnormal serum creatinine, calcium, electrolytes, magnesium, and phosphate levels and symptoms such as constipation, lethargy, and weakness may alert clinicians to problems with this oncologic emergency. Resolution of hypercalcemia is highly successful when appropriately monitored and treated and leads to a better quality of life and improved patient outcomes.

Localized squamous cell carcinoma of the bladder causing hypercalcemia and inhibition of PTH secretion

We report a case of symptomatic hypercalcemia in a patient with muscle-invasive, resectable squamous cell carcinoma of the bladder. Serum parathyroid hormone was consistent with secretion of parathyroid hormone-related protein. After radical cystoprostatectomy, calcium levels returned to normal. Patients with squamous cell carcinoma and an abnormal serum calcium level may have localized disease and should not be denied definitive local therapy.

Hyperparathyroidism in the hemodialysis population: A survey of 612 patients

There are no epidemiologic studies documenting the prevalence of hyperparathyroidism in the US hemodialysis population. We looked at a random sample of 612 hemodialysis patients enrolled in 10 outpatient dialysis units in Mississippi. Fifty percent of the patients surveyed had an intact serum parathyroid hormone (PTH) level more than three times normal (mean, 622 pg/mL). Another 25% had a less than normal PTH level (mean, 33 pg/mL), suggesting adynamic bone disease. Abnormal serum calcium was also common. Seventeen percent of patients were hypocalcemic and 14% were hypercalcemic. These high point prevalences occurred despite widespread use of calcium supplements and/or vitamin D (used in 90% of the patients surveyed). Black patients tended to have a lower serum calcium and higher PTH level than white patients. We also found that diabetic patients are less likely to have an elevated PTH level than nondiabetic patients. Elevated serum phosphorus was the most important factor correlating with the development of secondary hyperparathyroidism. Causes of inadequate control of hyperparathyroidism in this population require further study.

P53 tumour suppressor gene expression in hyperparathyroidism.

Mutations of the p53 tumour suppressor gene lead to the loss of control of normal cellular proliferation and differentiation and have been shown to be associated with the development of malignancy. Archival paraffin resection specimens from 86 cases of hyperparathyroidism treated surgically using the rabbit polyclonal CMI antibody were investigated to detect p53 immunoreactivity in these sections. Eighteen of the 86 sections examined (21%) showed nuclear immunoreactivity. No correlation was detected between tumour histology and p53 immunoreactivity (P = 0.45), nor was there any correlation between tumour clonality and immunoreactivity (P = 0.54). Multiple endocrine neoplasia type 1 (MEN 1) status did not correlate with p53 immunoreactivity. A significant correlation between p53 immunoreactivity and preparathyroidectomy calcium levels of > 1.5 mmol/L was detected (P < 0.005) although no correlation was noted between p53 immunoreactivity and higher levels of preparathyroidectomy intact parathyroid hormone (PTH) levels. A relationship is postulated between abnormal serum calcium regulation and p53 mutation in hypercalcaemic states associated with hyperparathyroidism.

Polymorphous ventricular tachycardia associated with acute myocardial infarction.

During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.