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The effect of coadminstration of nicotinamide and calcium-based phosphate binder on hyperphophatemia in patients undergoing hemodialysis.


Chronic kidney disease (CKD) is a worldwide epidemic and escalating. Approximately 20 million adults in the United States are in various stages of CKD, with more than 400,000 individuals with end-stage kidney disease and over 300,000 individuals requiring maintenance hemodialysis. It has been projected that by 2030, more than 2 million individuals will need dialysis or transplantation for kidney failure as a result of an aging population and the increasing prevalence of type 2 diabetes. The gradual failure of kidney function is accompanied by an increase in cardiovascular disease and a number of metabolic abnormalities, including disordered phosphorus and calcium metabolism. In patients with CKD, these abnormalities cause significant morbidity and directly influence the mortality associated with end-stage kidney disease. Indeed, cardiovascular mortality is 15 times greater in patients undergoing hemodialysis than in the general population [1, 2 3 4].

As glomerular filtration rate (GFR) declines, there is a decrease in phosphate excretion resulting in phosphate retention, while serum calcium decreases and the production of calcitriol (1, 25-dihydroxyvitamin D) is suppressed. These metabolic changes cause the stimulation of parathyroid hormone production as an adaptive response to maintain normal serum phosphate and calcium concentrations [5,6]. Reduced calcitriol levels lead to impaired gastrointestinal calcium absorption, thereby leading to hypocalcaemia. Hyperphosphatemia, hypocalcaemia, and reduced calcitriol synthesis all promote the production of parathyroid hormone and the proliferation of parathyroid cells, resulting in secondary hyperparathyroidism [7].

Hyperphosphatemia is a common complication of end-stage kidney disease, affecting up to 70% of patients on dialysis, despite dietary restrictions and the use of phosphate-binders [8]. The clinical consequences of hyperphosphatemia are well documented and include cardiovascular and metastatic calcifications, secondary hyperparathyroidism, and renal bone disease [9,10,11]. In hemodialysis patients, serum phosphate levels >6.5 mg/dl are associated with significantly increased mortality risk [3,6,12]. Because dietary restriction of phosphorus and conventional dialysis are unable to maintain serum phosphorus within recommended range (2.7-5.5 mg/dl) [13], phosphate binding agents are indicated for treating elevated phosphorus levels in the vast majority of patients undergoing hemodialysis [14].

Oral phosphate binders play the central role in the control of hyperphosphatemia. Effective binders are available; however, aluminum-based binding exerts bone and brain damage in high-dose and long term use, on the other side, calcium (Ca)-containing binders may even contribute to cardiovascular calcification progression when administered in high doses. Non-aluminum-, non-calcium-based binders such as sevelamer hydrochloride (SEV) and lanthanum carbonate (La) seem to offer advantages in this context, but are also closely observed with regard to their gastrointestinal tolerability and to potential hepatic accumulation respectively [15].

Nicotinamide is a water-soluble vitamin of the B complex, which together with nicotinic acid belongs to vitamin B3 or vitamin PP. Nicotinamide and nicotinic acid are also called niacinamide and niacin, respectively. However, the term of niacin in the open literature often refers to both substances. Sources of niacin are among others grains, meat and milk [16]. Despite structural similarities and equivalent nutritional properties, niacinamide and niacin have differing actions and adverse effect profiles. Although niacinamide can cause gastrointestinal discomfort and reportedly lowers platelet counts, it does not cause flushing, which is commonly seen with niacin [17, 18]. In vitro studies have shown that Niacinamide decreases phosphate uptake by inhibiting sodium/phosphorus co-transporters in the renal proximal tubule (Na/Pi2a) and intestine (Na/Pi2b) [19, 20, 21]. An open-label study of Niacinamide in Japanese hemodialysis patients who were not taking phosphorus binders found that dosages up to 1750 mg/d decreased serum phosphorus from 6.9 to 5.4 mg/dl, in addition, HDL cholesterol increased and LDL cholesterol declined during the 12 wk of treatment [22].


To assess the safety and the efficacy of nicotinamide as adjunctive therapy to calcium carbonate (as calcium based phosphate binder).


Study Design

The study was intended to be prospective, interventional, case control randomized trial.

Enrollment and Setting

Patients were recruited at Ain Shams University Specialized Hospital and Al Motamyz hemodialysis center, Cairo, Egypt. A total of sixty hemodialysis patients with a serum inorganic phosphorus level [greater than or equal to] 5.0 mg/dl were enrolled in the trail during the period from August 2010 to December 2010. Patients ranged in age from 30 to 66 years. Each patient received hemodialysis regularly for three to four times per week. All patients gave an informed verbal consent.

Inclusion Criteria

1. Patients on regular hemodialysis for more than three months.

2. Stable dosage of calcium carbonate during the previous two week period.

3. Age above 21 years.

4. Serum inorganic phosphorus level equal to or greater than 5.0 mg/dl on the most recent monthly laboratory data.

Exclusion Criteria

1. Pregnancy

2. History of liver disease

3. Active peptic ulcer disease

4. Treatment with carbamazepine

5. Patients on niacin therapy; and Non compliant patients.

Study Medication and Randomization

Sixty hemodialysis patients with serum phosphorus level [greater than or equal to] 5.0 mg/dl were classified randomly into two groups depending on their medication; group I (control group) in which patients received calcium carbonate tablets in dose of 500 mg to 1000 mg three times daily. And group II (study group) in which patients received calcium carbonate in dose of 500mg to 1000 mg three times daily and nicotinamide tablets in a dose titrated to 1000 mg/day for 8 weeks.


Five ml blood sample was taken twice (before and after study treatment) from each patient upon enrollment into study. Serum calcium, phosphorus and intact parathyroid hormone were measured at week 1 and 9 to assess the efficacy of treatment. Additionally, serum uric acid, liver enzymes (AST and ALT), and complete blood count were obtained at week 1 and 9 to evaluate the safety of using nicotinamide. Lipid panels were drawn at week 1 and 9 to figure out the effect of nicotinamide on lipid profile. All laboratory values were drawn just before dialysis session on the first dialysis treatment of the week.

Dosage Titration

Nicotinamide was administered at a starting dosage of one tablet (500 mg) once daily for one week. Then the dosage was increased to 1000 mg (two tablets) once daily at week two and continued till the end of the study.

Statistical Analysis

IBM SPSS statistics (V. 19.0, IBM Corp., USA, 2010) was used for data analysis. Data were expressed as Mean [+ or -] SD for quantitative parametric measures in addition to Median Percentiles for quantitative non-parametric measures and both number and percentage for categorized data.

The Following Tests Were Done

1. Comparison between two independent mean groups for parametric data using Student t test.

2. Comparison between 2 dependent groups for parametric data using Paired t test.

3. Pearson correlation test to study the possible association between each two variables among each group for parametric data.

For Follow-up Study

The degree of change due to follow-up study (delta change or dC) reflects the actual difference changed through the follow-up study can be calculated for each patient and from which, the mean delta change can be calculated. It is used for follow-up study and for comparison between the subgroups, also for correlation with other variables. It is defined as follow:

Delta change (dC) = (Post-Pre)/Pre

Or the difference between post and pre as regards pre values for each patient.

The probability of error at 0.05 was considered significant while at 0.01 and 0.001 are highly significant.


A total of 75 patients underwent screening, and sixty were randomly assigned into trial. They were categorized into two groups; group I (control) and group II (study or nicotinamide group). Each group included 30 patients. Only 4 patients withdrew the study group and a total 26 patients completed the 8weeks study in group II. All patients in two arms were compliant with medication. Patients characteristics are shown in table 1 and biochemical data are displayed in table 2.

Dosing Characteristics

In accordance with our protocol, the dosage of all medication, prescribed to patients, were not changed for any patients during the study. All control patients completed the study weeks receiving 500 to 1000 mg of calcium carbonate tablets three times daily. However, a total of 26 patients in the study group were successfully completed the trial receiving calcium carbonate tablets in the same dose of control group in addition to 500 mg nicotinamide tablets once daily for the first week. Then dose increased to 1000 mg once daily at week 2 to week 9.

1. First End Point for Evaluating the Efficacy of Nicotinamide

Serum Level of Phosphorus, Calcium, Intact Parathyroid Hormone, and Calcium Phosphorus Product

Among all patients, treatment in group I resulted in an insignificant rise in the mean serum phosphorus from 6.46 to 6.53 mg/dl (p = 0.56). However the treatment with nicotinamide resulted in highly significant fall in the mean serum phosphorus from 6.75 to 5.47 mg/dl (p = 0). Also, there were no significant difference in serum calcium, and calcium-phosphorus product of control group (p = 0.43), (p = 0.76), respectively. Otherwise, a significant decrease in calcium-phosphorus product (from 58.7 to 48.5 mg/dl; p = 0), and a significant increase in serum calcium level (from 8.6 to 8.91 mg/dl; p = 0.005) were reported with nicotinamide group. There were no significant changes in intact parathyroid hormone level in both arms during study period (table 3).

When changes in those variables in nicotinamide vvgroup (group II) compared to those of control group as shown in figure (1&2), a highly significant decrease in serum phosphorus (p = 0.001), with a concurrent significant fall in calcium-phosphorus product (p = 0.008) were reported in nicotinamide group. Serum calcium and intact parathyroid hormone showed no significant difference between two groups (p = 0.43), (p = 0.17), respectively.



A comparison of the degree of changes in ph. Level, ca. level, ph x Ca product, and iPTH in both groups was shown in figure (3). The degree of change reflects the actual difference changed through the study. In this figure there were significant difference in the degree of change of phosphorus level (p =0) in the study group, ph x Ca product (p =0), and iPTH (p = 0.044) whereas the degree of change of ca level was insignificant (p = 0.158).

2. Secondary End Point for Evaluating the Safety of Using Nicotinamide

During 8 weeks of study, the following side effects of nicotinamide were observed.

Gastrointestinal Disturbance, Flushing, Rash, and Blurred Vision

During the study, two patient in nicotinamide group discontinued medication because of flushing and abdominal rash that started with the higher dose of nicotinamide. At day 9, three patients developed gastrointestinal disturbances and diarrhea. Two of them withdrew the study and the one completed the study was advised to take the total daily dose in two divided doses. This patient had spontaneous resolution of his symptoms without a reduction in dosage. Such adverse effects were not reported in control arm.


The Effect of Nicotinamide on the Lipid Profile of Patients

Although nicotinamide lacks the hypolipidmic action of nicotinic acid, a trend toward increasing HDL (from 39.3 to 42.3 mg/dl), and decreasing LDL (from 125.4 to 123.2 mg/dl) and total cholesterol (from 249.5 to 234.5 mg/dl) were reported in this study. The changes observed in those variables were statistically insignificant (p=0.21), (p=0.52), and (p=0.20), respectively.

Hepatotoxicity, Thrombocytopenia, and Uricemia as Side Effect of Nicotinamide

In this study, there were not any significant changes in liver enzymes (AST and ALT), and uric acid at the end of study treatment between control group and nicotinamide group. Platelet count tended to reduced insignificantly upon nicotinamide treatment. Laboratory results at the completion of study of control and nicotinamide are summarized in table 4.


Niacinamide (or nicotinamide) is the corresponding amide form of niacin. Niacinamide is thought to possess less potential for side effects, namely flushing, than niacin. Animal studies have suggested that niacinamide may decrease brush border uptake of phosphate by blocking the sodium phosphate co transporter in the small intestine [19]. In large, multicenter studies, elevated serum phosphorus has been associated with an increase in morbidity and mortality in patients with ESRD [3,23]. Hyperphosphatemia is linked to cardiovascular risk as well as bone disease [24,25], and the hyperphosphatemic milieu may promote vascular calcification through cellular changes in vascular smooth muscle cells [26]. Previous open-label studies by Takahashi et al., Sampathkumar et al. [22,27] and a double-blind trail by Cheng et al. [21] demonstrated that niacinamide lowers serum phosphorus levels in maintenance hemodialysis patients when used in high dosage and the traditional binding agents were withheld. In present study, the efficacy of nicotinamide on phosphorus reduction using lower dose (1000 mg daily) in conjunction with calcium carbonate was assessed on hyperphosphatemic patients undergoing haemodialysis at Ain Shams specialized hospital-based hemodialysis unit and AL Motamayz Hemodialysis center.

After 8 weeks of therapy, our patients in nicotinamide arm had highly statistically and clinically significant drop in serum phosphorus (6.75 to 5.47 mg/dl; p=0) with concomitant fall in calcium phosphorus product from 58.7 to 48.55 [mg.sup.2]/[dl.sup.2]; p=0. Also serum calcium increased significantly from 8.68 to 8.91 mg/dl; p=0.005. Despite of using lower dose of nicotinamide in this study, our findings are agreed with previous studies which stated that nicotinamide can effectively reduce serum phosphorus in hemodialysis patients [22,27,21].

Trends toward increasing HDL and decreasing LDL, total cholesterol, triglycerides have been reported in the present study upon nicotinamide treatment. However, the overall changes in those variables were not statistically significant. In fact, nicotinic acid, but not nicotinamide, is known to decrease plasma fatty acids, triglyceride, and LDL by reducing lipase effects in adipose tissue and presumably increase HDL concentration by increasing apoA-1 which is the main lipoprotein of HDL [28, 29]. In some studies, significant or considerable changes in HDL and LDL had been reported.. Takahashi et al., showed that nicotinamide can increase HDL and decrease LDL in hemodialysis patients [22]. And a significant increase in HDL, but no change in LDL and triglyceride has been found in a recent randomized clinical trial [21]. Another recent study showed that nicotinamide can increase HDL, and decrease the values of triglyceride and LDL with clinical significance. No noticeable changes were found in cholesterol levels in that study [30]. At least in our population, nicotinamide was able to cause considerable changes in lipid profile. Although those changes were not statistically significant, the cumulative effect of nicotinamide on lipid metabolism reported in this study may have important benefits on chronic kidney disease and dialysis patients.

Thrombocytopenia has been a concern from previous studies [21]. In our study, a few decrease in platelet count (from 213.46 to 207.2 1000/[mm.sup.3]) was reported in nicotinamide group. This change was statistically insignificant (p = 0.8) when compared to those changes of control group. Nevertheless, no clinical manifestations of thrombocytopenia complicated the administration of study drug in the present study. This finding is in accordance with other authors' findings. In their studies, they stated that there was a trend toward decreasing platelet count in nicotinamide group. Additionally, although nicotinamide was administered in higher dose and for longer duration than used in the current study, that decrease was insignificant [21, 31]. Also there were no episodes of decreasing platelet counts reported in Young's study [32]. Although reduction in platelet counts is non significant in this study, it is still of great clinical importance. And for now, monitoring for thrombocytopenia in dialysis patients on nicotinamide is a must.

Agreed with the most previous studies which mentioned that nicotinamide had no effect on uric acid level [21, 27, 30, 33, 34], our study showed no changes in uric acid level upon nicotinamide therapy.

In the current study, during the 8 wk of study, no hepatotoxicity cases were reported and no significant changes in liver enzymes were noted. This finding is explained by the fact that both nicotinic acid and nicotinamide are relatively safe and cause no liver enzymes abnormalities when used in dosage lower than 3g/day [35].

Most of previous studies concerning the effect of nicotinamide on hyperphosphatemia in HD patients didn't mention the changes in hemoglobin upon the therapy [21,22]. However, a trend toward reduced mean hemoglobin in nicotinamide treated group was demonstrated in Young et al. [32]. In the present study, there are not any significant changes in hemoglobin level of nicotinamide treated group when compared to those of control group.

Nicotinamide lacks the vasodilator action of nicotinic acid [35]. In accordance with this fact, only one case of flushing and another case of abdominal rash were reported in this study at second week with the beginning of higher dose. The two patients withdrew study. Our findings are agreed with those reported in previous studies [21,32]. In Cheng et al., and Young et al. only a case of abdominal rash and another case of pruritic rash were reported respectively. In both studies no one of patients randomized to nicotinamide treatment developed flushing (Cheng, 2008; Young et al., 2009).

Nicotinamide seems to be well tolerated in general population [36]. In the current study the percentages of GI disturbances and diarrhea are 10% (3 of 30) and 3.3% (1 of 30) of the total study population respectively. And they were 3.6% (1 of 26) and 0% (0 of 26) of study population completed the study. These findings are consistent with Young's study, in which low percentage of patients developed diarrhea [32]. But our results are in a marked contrast to those reported in other studies. The authors in those studies reported that much higher percentage of patients suffered from diarrhea upon nicotinamide therapy [18, 21, 22]. The authors speculated that the higher percentage of diarrhea was a result of co administration of phosphorus binders with high dose of nicotinamide [21].


Icotinamide is effective in controlling serum phosphorus when co-administered with calcium carbonate in hemodialysis patients. Not only reducing serum phosphorus, but also nicotinamide provide beneficial changes in lipid profiles of hemodialysis patients when co administered with calcium carbonate.

All those advantages were reported in this study with less potential side effects noticed.

Dialysis patients in Egypt have poorer phosphorus control and might benefit from the addition of nicotinamide to their binder regimen.


Further studies in larger randomized trials for longer duration and other chronic kidney disease populations are indicated to assess the following:

The efficacy of nicotinamide when used in a dose less than 1000 mg daily.

Whether nicotinamide reduces serum phosphorus level effectively in hemodialysis patients when used alone.

Nicotinamide effects on platelet count, hemoglobin, liver enzymes.

If diarrhea and thrombocytopenia are a dose related side effects of nicotinamide! And if yes, which dose is safe.

The actual effect of nicotinamide on lipid profile of hemodialysis patients using different dosage of nicotinamide for different durations.

DOI: 10.3968/j.ans.1715787020120501.1001


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Shaimaa Allam (1); Manal El-Hamamsy (2), *; Magdy El Sharkawy (3)

(1) B.Sc of Pharmaceutical Science, Misr International University. Cairo, Egypt.

(2) Ph.D., Clinical Pharmacy Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.

(3) MD., Internal medicine and Nephrology Department Faculty of Medicine, Ain Shams University.

* Corresponding author.

Address Ass. Prof. Dr. Manal El-Hamamsy, Ain Shams University, Faculty of Pharmacy, Abassia, Cairo, Egypt.

Received 4 January 2012; accepted 9 March 2012.
Table 1
Patient Characteristics of the Studied Groups I and Group II

Group Number/            Group I              Group II
Parameter               (n = 30)              (n = 26)

* Age (years)      50.2 [+ or -] 9.87    51.63 [+ or -] 8.10
Mean [+ or -] SD

* Dry wt. (kg)     74.18 [+ or -] 6.20   73.81[+ or -] 5.80
Mean [+ or -] SD

* Duration of      4.83 [+ or -] 1.82    5.16 [+ or -] 2.03
dialysis (years)
Mean [+ or -] SD

** Male : Female          22:8                  24:6

Group Number/
Parameter          P-value   Sig

* Age (years)       0.54     NS
Mean [+ or -] SD

* Dry wt. (kg)      0.81     NS
Mean [+ or -] SD

* Duration of       0.51     NS
dialysis (years)
Mean [+ or -] SD

** Male : Female    0.54     NS

SD: standard deviation; n: number of patient; NS: non significant;
*: using one way ANOVA test; **: using chi square test.

Table 2
Biochemical Data of the Studied Groups at Baseline

Parameters                                   Group I (n = 30)

                                            6.46 [+ or -] 0.81
* Ca.level (mg/dl)                          8.87 [+ or -] 1.17
* Ca-Ph product([mg.sup.2]/[dl.sup.2])     57.8 [+ or -] 12.96
* iPTH(pg/ml)                             674.50 [+ or -] 318.2
* Chol.(mg/dl)                             238.2 [+ or -] 133.1
* TRG(mg/dl)                               326.87 [+ or -] 159
* HDL(mg/dl)                                39.07 [+ or -] 7.3
* LDL (mg/dl)                              123.9 [+ or -] 62.67
* Hgb(g /dl)                               11.65 [+ or -] 1.96
* Uric acid(mg/dl)                          7.55 [+ or -] 1.7
* Plt count(1000/[mm.sup.3])                210 [+ or -] 33.20
* SGOT(mg/dl)                              38.23 [+ or -] 15.68
* SGPT(mg/dl)                              28.77 [+ or -] 15.18

Parameters                                  Group II (n = 26)

                                            6.75 [+ or -] 1.02
* Ca.level (mg/dl)                          8.68 [+ or -] 0.72
* Ca-Ph product([mg.sup.2]/[dl.sup.2])     58.70 [+ or -] 10.9
* iPTH(pg/ml)                              585.5 [+ or -] 378.5
* Chol.(mg/dl)                             249.5 [+ or -] 134.5
* TRG(mg/dl)                               332.73 [+ or -] 182
* HDL(mg/dl)                                39.31 [+ or -] 7.2
* LDL (mg/dl)                             125.40 [+ or -] 65.35
* Hgb(g /dl)                               11.24 [+ or -] 1.23
* Uric acid(mg/dl)                          7.56 [+ or -] 1.82
* Plt count(1000/[mm.sup.3])               213.4 [+ or -] 34.43
* SGOT(mg/dl)                              38.58 [+ or -] 16.33
* SGPT(mg/dl)                              29.54 [+ or -] 15.71

Parameters                                P-value    Sig

                                            0.25     NS
* Ca.level (mg/dl)                          0.45     NS
* Ca-Ph product([mg.sup.2]/[dl.sup.2])      0.77     NS
* iPTH(pg/ml)                               0.35     NS
* Chol.(mg/dl)                              0.71     NS
* TRG(mg/dl)                                0.92     NS
* HDL(mg/dl)                                0.93     NS
* LDL (mg/dl)                               0.94     NS
* Hgb(g /dl)                                0.22     NS
* Uric acid(mg/dl)                          0.98     NS
* Plt count(1000/[mm.sup.3])                0.79     NS
* SGOT(mg/dl)                               0.96     NS
* SGPT(mg/dl)                               0.86     NS

Values are expressed as mean  [+ or -] SD n: number of patients; Ph.
Level: inorganic phosphate level; Ca. level: Calcium level; Ph-Ca
product: calcium x phosphorous product product; iPTH level: intact
parathyroid hormone level; Serum Chol.: serum total cholesterol
level; Serum TRG: serum triglyceride level; Serum HDL: serum high
density lipoprotein level; Serum LDL: serum low density lipoprotein
level; Hgb: hemoglobin level; Plt counts: platelet counts; SGOT:
serum glutamate oxaloacetic transaminase; SGPT: serum glutamic
pyruvate transaminase; NS: insignificant.; *: using student t-test

3 Serum Level of ph. Level, ca. Level, phxCa Product, and PTH in the
Studied Groups Before (week 1), and After (week 9) the Study

Group/                                        Group I n = 30

Parameter                                         Week 1

* Serum Ph. (mg/dl) Mean [+ or -] SD        6.46 [+ or -] 0.81

* Serum Ca. (mg/dl) Mean [+ or -] SD        8.87 [+ or -] 1.17

* Serum Ca x Ph product                     57.8 [+ or -] 12.96
([mg.sup.2]/[dl.sup.2]) Mean [+ or -] SD

* Serum iPTH (pg/dl) Mean [+ or -] SD       674 [+ or -] 318.2

Group/                                        Group I n = 30

Parameter                                         Week 9

* Serum Ph. (mg/dl) Mean [+ or -] SD        6.53 [+ or -] 0.81

* Serum Ca. (mg/dl) Mean [+ or -] SD        8.71 [+ or -] 1.02

* Serum Ca x Ph product                     57.3 [+ or -] 12.40
([mg.sup.2]/[dl.sup.2]) Mean [+ or -] SD

* Serum iPTH (pg/dl) Mean [+ or -] SD        697 [+ or -] 302

Group/                                     Group I n = 30

Parameter                                  P-value    Sig.

* Serum Ph. (mg/dl) Mean [+ or -] SD         0.56      NS

* Serum Ca. (mg/dl) Mean [+ or -] SD         0.43      NS

* Serum Ca x Ph product                      0.76      NS
([mg.sup.2]/[dl.sup.2]) Mean [+ or -] SD

* Serum iPTH (pg/dl) Mean [+ or -] SD        0.09      NS

Group/                                        Group II n = 26

Parameter                                         Week 1

* Serum Ph. (mg/dl) Mean [+ or -] SD        6.75 [+ or -] 1.02

* Serum Ca. (mg/dl) Mean [+ or -] SD        8.68 [+ or -] 0.72

* Serum Ca x Ph product                     58.70 [+ or -] 10.9
([mg.sup.2]/[dl.sup.2]) Mean [+ or -] SD

* Serum iPTH (pg/dl) Mean [+ or -] SD       585.5 [+ or -] 378

Group/                                        Group II n = 26

Parameter                                         Week 9

* Serum Ph. (mg/dl) Mean [+ or -] SD        5.47 [+ or -] 1.28

* Serum Ca. (mg/dl) Mean [+ or -] SD        8.91 [+ or -] 0.87

* Serum Ca x Ph product                    48.55 [+ or -] 11.53
([mg.sup.2]/[dl.sup.2]) Mean [+ or -] SD

* Serum iPTH (pg/dl) Mean [+ or -] SD       547.6 [+ or -] 477

Group/                                     Group II n = 26

Parameter                                  P-value    Sig.

* Serum Ph. (mg/dl) Mean [+ or -] SD        0.001      HS

* Serum Ca. (mg/dl) Mean [+ or -] SD        0.005      S

* Serum Ca x Ph product                     0.001      HS
([mg.sup.2]/[dl.sup.2]) Mean [+ or -] SD

* Serum iPTH (pg/dl) Mean [+ or -] SD        0.46      NS

n: number of patients; Ph. Level: inorganic phosphate level; Ca.
level: Calcium level; Ca-Ph product: calcium x phosphorous product;
iPTH level: intact parathyroid hormone level; NS: statistically non
significant values; HS: highly statistically significant value; S:
statistically significant value; * comparison carried using paired

Table 4
Laboratory Results of the Studied Groups at the End of the Study

Parameters                      Group I (n = 30)

Chol.(mg/dl)                  235.30 [+ or -] 123
TRG(mg/dl)                   281.60 [+ or -] 165.16
HDL(mg/dl)                    42.27 [+ or -] 8.06
LDL (mg/dl)                   118.2 [+ or -] 52.26
Hgb(g /dl)                    12.43 [+ or -] 2.44
Uric acid(mg/dl)               7.02 [+ or -] 1.57
Plt count(1000/[mm.sup.3])    220.5 [+ or -] 29.60
SGOT(mg/dl)                   38.23 [+ or -] 15.80
SGPT(mg/dl)                   28.90 [+ or -] 14.93

Parameters                     Group II (n = 26)      P-value    Sig

Chol.(mg/dl)                 234.5 [+ or -] 130.15      0.99     NS
TRG(mg/dl)                   272.60 [+ or -] 162.55     0.84     NS
HDL(mg/dl)                    42.38 [+ or -] 8.21       0.98     NS
LDL (mg/dl)                  120.22 [+ or -] 53.76      0.90     NS
Hgb(g /dl)                    12.31 [+ or -] 0.87       0.81     NS
Uric acid(mg/dl)               7.09 [+ or -] 1.57       0.90     NS
Plt count(1000/[mm.sup.3])   207.26 [+ or -] 34.66     0.061     NS
SGOT(mg/dl)                   38.65 [+ or -] 16.52      0.94     NS
SGPT(mg/dl)                   29.62 [+ or -] 15.42      0.89     NS

n: number of patients; Serum Chol.: serum total cholesterol level;
Serum TRG: serum triglyceride level; Serum HDL: serum high density
lipoprotein level; Serum LDL: serum low density lipoprotein level;
Hgb: hemoglobin level; Plt counts: platelet counts; SGOT: serum
glutamate oxaloacetic transaminase; SGPT: serum glutamic pyruvate
transaminase; NS: insignificant. * using student t-test
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Author:Allam, Shaimaa; El-Hamamsy, Manal; El Sharkawy, Magdy
Publication:Advances in Natural Science
Article Type:Report
Geographic Code:7EGYP
Date:Mar 31, 2012
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