How to know the increased level of ionized calcium in serum

How to know the increased level of ionized calcium in serum

CBHI, 18, Oct  2017, Canada

How to know the increased level of ionized calcium in serum



Calcium is an essential mineral in the human body. It is stored in not only bones and teeth, but also serum in deferent forms (Ionized calcium, protein calcium, etc.). Ionic calcium that is present in blood plasma and it is significantly involved in physiological activation: Strength of bones and muscular contraction (including heart function), neural transmission, hormone metabolism and blood coagulation. The concentration of ionized calcium is normally almost invariant about 50% in serum. For example, if 500mg of calcium dissolves in blood, the content of ionized calcium estimates about 250mg. A mere 2-3 mg of ionic calcium increase by taking or injection into blood, thyroid immediately reacts and maintains a constant concentration. This is call calcium homeostasis. There are three principal organs for maintaining of the calcium homeostasis: the kidneys, intestines, and bones. Generally, the kidneys have a key role in the control of the calcium balance. Then, how do we know if ionic calcium level increases? What reaction happens in our body? You can check it yourself.

Many studies have shown that temporarily elevated calcium ion excretes through urine for maintaining of calcium homeostasis as quickly as possible. In other words, It depends on personal but healthy people who take SAC calcium (2.5mg ~ 5mg) with water, they must urinate at least once in 30~40 min. After that, they will go washroom several times every 20~30 min. This is the evidence that SAC calcium is absorbed immediately and serum calcium increases. With passive transport method, SAC calcium penetrates mucous membrane directly into the cell-blood vein and enters the cells without a Vitamin D3. Moreover, after enriching a chronic intracellular calcium-ion(Ca2+) deficiency cells, residual SAC calcium releases in their urine.

Therefore, an elevated level of calcium ions from SAC technology strengths the self-healing mechanism of immune cell and provides manifold health effects in fighting against most diseases which is calcium related such as cancer, leukemia, arthritis, osteoporosis etc. without causing hypercalcemia or any other side effects.



 © CBHI, 18, Oct  2017, Canada

SAC and Blood Clotting

SAC and Blood Clotting

When blood vessels are cut or damaged, the loss of blood from the system must be
stopped before shock and possible death occurs. This is accomplished by solidification of
the blood, a process called coagulation or clotting.


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Pharmacology of the calcium sensing receptor – Mini-Review


Calcium sensing receptor (CASR) is a G-protein couple receptor which plays a key role in calcium homeostasis in
vertebrates. Its extracellular domain is sensitive to divalent cations, aminoacids and polyamines. In parathyroid
glands, CASR activation causes parathyroid hormone (PTH) reduction and subsequently a decrease in blood calcium concentration. In PTH-dependent disorders, e.g. primary and secondary hyperparathyroidism (HPT), the need for therapeutic options other than surgery led to the synthesis of various allosteric CASR agonists (calcimimetics), such as cinacalcet. Cinacalcet is the only calcimimetic approved for HPT secondary to chronic kidney disease (CDK), parathyroid carcinoma, and, in some countries, primary HPT. Clinical trials showed that cinacalcet reduced PTH and calcemia both in CDK and primary HPT, lowering the risk of bone fractures, surgery, and cardiovascular complications in the former patients. Long-term safety and pharmacoeconomics have to be fully tested yet. Few both in vitro and in vivo studies showed an association between Arg990Gly-CASR polymorphism and cinacalcet sensitivity, though in patients with severe CASR inactivating mutations the drug substantially retained its positive clinical effects. Recently, a new class of allosteric antagonists of CASR, i.e. calcilytics, has been synthesized. Calcilytics are structurally similar to calcimimetics, but exert their effects acting on a different allosteric site. Infusion of calcilytics was followed by transient rise in PTH and calcium. One of these compounds, ronacaleret, was able to increase femur BMD in post menopausal women, but with induction of mild hyperparathyroidism. In the future, calcilytics may contribute to the osteoporosis treatment choice.

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Cancer Cell Death following Calcium Electroporation

Dose-Dependent ATP Depletion and Cancer Cell Death following Calcium Electroporation, Relative Effect of Calcium Concentration and Electric Field Strength

Emilie Louise Hansen1, Esin Bengisu Sozer2, Stefania Romeo3, Stine Krog Frandsen1, P. Thomas Vernier2, Julie Gehl1*



Electroporation, a method for increasing the permeability of membranes to ions and small molecules, is used in the clinic with chemotherapeutic drugs for cancer treatment (electrochemotherapy). Electroporation with calcium causes ATP (adenosine triphosphate) depletion and cancer cell death and could be a novel cancer treatment. This study aims at understanding the relationship between applied electric field, calcium concentration, ATP depletion and efficacy.


In three human cell lines—H69 (small-cell lung cancer), SW780 (bladder cancer), and U937 (leukaemia), viability was determined after treatment with 1, 3, or 5 mM calcium and eight 99 μs pulses with 0.8, 1.0, 1.2, 1.4 or 1.6 kV/cm. Fitting analysis was applied to quantify the cell-killing efficacy in presence of calcium. Post-treatment intracellular ATP was measured in H69 and SW780 cells. Post-treatment intracellular ATP was observed with fluorescence confocal microscopy of quinacrine-labelled U937 cells.


Both H69 and SW780 cells showed dose-dependent (calcium concentration and electric field) decrease in intracellular ATP (p<0.05) and reduced viability. The 50% effective cell kill was found at 3.71 kV/cm (H69) and 3.28 kV/cm (SW780), reduced to 1.40 and 1.15 kV/cm (respectively) with 1 mM calcium (lower EC50 for higher calcium concentrations). Quinacrine fluorescence intensity of calcium-electroporated U937 cells was one third lower than in controls (p<0.0001).

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Calcium, cancer and killing: The role of calcium in killing cancer cells by cytotoxic T lymphocytes and natural killer cells☆

Eva C. Schwarz, Bin Qu, Markus Hoth ⁎
Department of Biophysics, Saarland University, Homburg, Germany


Killing cancer cells by cytotoxic T lymphocytes (CTL) and by natural killer (NK) cells is of vital importance.
Cancer cell proliferation and apoptosis depend on the intracellular Ca2+ concentration, and the expression
of numerous ion channels with the ability to control intracellular Ca2+ concentrations has been correlated
with cancer. A rise of intracellular Ca2+ concentrations is also required for efficient CTL and NK cell function
and thus for killing their targets, in this case cancer cells. Here, we review the data on Ca2+- dependent killing
of cancer cells by CTL and NK cells. In addition, we discuss emerging ideas and present a model how Ca2+
may be used by CTL and NK cells to optimize their cancer cell killing efficiency. This article is part of a Special
Issue entitled: 12th European Symposium on Calcium.


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Calcium, Magnesium, and Colorectal Cancer

High calcium consumption may confer a reduced risk of colorectal cancer.1,2 Dai and colleagues3 recently reported in a case-control study that intake of calcium may be associated with a decreased risk of colorectal adenoma only when the dietary calcium:magnesium intake ratio is low. This finding provides one possible interpretation for
inconsistencies in previous studies of the association of calcium intake with risk of
colorectal neoplasia.4

Belonging to the same family in the periodic table, calcium (Ca2+) and magnesium (Mg2+) share the same homeostatic control system and have the potential to antagonize each other physiologically.5 A high calcium intake reduces absorption of both magnesium and calcium,6 whereas moderate magnesium deprivation results in negative magnesium balance but increased calcium retention7. Due to the potential competition between magnesium and
calcium, we hypothesized that the dietary calcium:magnesium ratio may modify the effects of calcium supplementation on colorectal carcinogenesis.

We sought to test this hypothesis using data from a randomized clinical trial of calcium supplementation (1200 mg/day) to prevent adenoma recurrence over a 4-year period. The outcome measure in this analysis was the recurrence of adenomas during the pre-specified main risk period (i.e. after a year-1 colonoscopy up to and including a year-4 examination)2. A validated semi-quantitative food frequency questionnaire (FFQ) was given at study entry
to assess usual diet.

Consistent with our hypothesis,3 we found suggestions that the baseline dietary calcium:magnesium intake ratio modified the effect of calcium treatment on adenoma recurrence. Among subjects with the intake ratio above the median, calcium supplementation had no effect on the risk of one or more recurrent adenoma (relative risk [RR]=0.98 [95% confidence interval (CI)=0.75–1.28]) (Table). In contrast, among those with the baseline ratio less than or equal to the median, calcium treatment was associated with reduced risk (RR=0.68 [95%CI=0.52–0.90]; test for interaction, P= 0.075).

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Serum Calcium Levels In Type 2 Diabetes Mellitus

Kanchana. N1, Saikumar. P2 1-Department of physiology / Sree Balaji Medical College, Bharath University, Chennai India / Second year Physiology PG 2- Department of physiology / Sree Balaji Medical College, Bharath University, Chennai India / Professor and HOD


Introduction: Hyperglycemia in Diabetes Mellitus is known to have its effect on almost all body system through alterations in structural and biochemical changes in tissues.From this study, it is hypothesized that alteration in calcium flux may adversely affect the insulin secretion as it is a calcium-dependent process.

Aim And Objectives: This study was done to estimate the serum calcium levels in type 2 Diabetes mellitus.


  1. Estimation of blood glucose levels in all subjects.
  2. Estimation of serum calcium levels in diabetes and non-diabetes.
  3. Compare the serum calcium levels in diabetes and non-diabetes.

Materials and methods:

Case control study.

Study Design: Diabetes subjects (cases) n=50 Age and sex matched

Diabetes subjects (cases) n=50 Age and sex matched

Age and sex matched non diabetes (controls) n=50

Plasma glucose levels was estimated by GOD-POD method.Serum calcium level was estimated by calcium Arsenazo method for all subjects at central lab of SBMCH,Chennai.

Results And Conclusion: Results were analyzed using anova single factor.f statistical was greater than f critical value.

A negative correlation was observed between serum calcium levels and plasma blood glucose levels. Also the p value was found to be less than 0.05 which confirmed that correlation was statistically significant.

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Vitamin D, calcium, and retinol intake, and pancreatic cancer in a population-based case–control study in the San Francisco Bay area

Lydia B. Zablotska • Zhihong Gong • Furong Wang • Elizabeth A. Holly • Paige M. Bracci



Objective The aim of this study was to evaluate a complex association among intake of dietary vitamin D, calcium,
and retinol, and pancreatic cancer risk. Methods Pancreatic cancer cases (n = 532) diagnosed in 1995–1999 were identified using rapid case ascertainment methods and were frequency matched to population-based controls (n = 1,701) in the San Francisco Bay Area. Detailed dietary data were collected during in-person interviews using a validated semi-quantitative food frequency questionnaire. Adjusted unconditional logistic regression was used to estimate odds ratios (ORs) and confidence intervals.

Results In men, increased pancreatic cancer risk was associated with currently recommended dietary vitamin D intake levels (highest (C450 IU/day) vs. lowest (\150 IU/ day) intake, OR = 2.6, trend-p = 0.009) and total vitamin D intake from diet and supplements (for \800 IU/day). ORs for dietary vitamin D intake remained increased after adjustment for intake of retinol and calcium, although confidence intervals included unity. Stratified analyses showed that ORs were higher among men with a lower intake of retinol and lower physical activity but there was no evidence of statistical interaction. No associations with vitamin D intake were observed among women, although ORs typically were elevated. ORs increased with increased dietary calcium intake among men (trend-p = 0.008) and not women.

Conclusions Our results among men showing an increased risk of pancreatic cancer associated with dietary
intake of vitamin D and of calcium require confirmation in further studies. Continued investigation is needed to clarify the complex role of vitamin D and calcium in pancreatic cancer risk and to determine their optimal intake level and preventive effects for pancreatic cancer.


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Dairy products, calcium, and prostate cancer risk in the Physicians’ Health Study

Dairy products, calcium, and prostate cancer risk in the Physicians’ Health Study

June M Chan, Meir J Stampfer, Jing Ma, Peter H Gann, J Michael Gaziano, and Edward L Giovannucci


Background: A high calcium intake, mainly from dairy products, may increase prostate cancer risk by lowering concentrations of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], a hormone thought to protect against prostate cancer. The results of epidemiologic studies of this hypothesis are inconclusive.

Objective: We investigated the association between dairy product and calcium intakes and prostate cancer risk in the
Physicians’ Health Study, a cohort of male US physicians.


At baseline, the men answered abbreviated dietary questionnaires. During 11 y of follow-up, we documented 1012 incident cases of prostate cancer among 20 885 men. We estimated dairy calcium intake on the basis of consumption of 5 major dairy products and used logistic regression to estimate relative risk.


At baseline, men who consumed >600 mg Ca/d from skim milk had lower plasma 1,25(OH)2D3 concentrations than did those consuming ≤150 mg Ca/d [71 compared with 85 pmol/L (30.06 compared with 35.64 pg/mL); P = 0.005]. Compared with men consuming ≤0.5 daily servings of dairy products, those consuming > 2.5 servings had a multivariate relative risk of prostate cancer of 1.34 (95% CI: 1.04, 1.71) after adjustment for baseline
age, body mass index, smoking, exercise, and randomized treatment assignment in the original placebo-controlled trial. Compared with men consuming ≤150 mg Ca/d from dairy products, men consuming > 600 mg/d had a 32% higher risk of prostate cancer (95% CI: 1.08, 1.63).


These results support the hypothesis that dairy products and calcium are associated with a greater risk of prostate cancer.

Am J Clin Nutr 2001;74:549–54.

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