International Journal of Clinical Biochemistry and Research

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Get Permission Muthireddy, Eadala, Vangara, and Mahavadi: A retrospective study of lipid profile during the various phases of timing in renal failure and hypothyroid patients


Introduction

The most important plasma lipids are cholesterol, triglycerides, LDL, HDL and VLDL Cholesterols. Cholesterol is the precursor for the synthesis of steroid hormone, vitamin D and bile acids. It is one of the component in cell and cell membrane. Triglycerides plays a key role as energy source in our body which is synthesized in intestine and liver. They are mostly transported in plasma as lipoproteins. They are classified depending on their size, density, functions, composition and by their mobility in electrophoresis. Triglycerides are transported by chylomicrons and VLDL. Cholesterol by HDL and LDL cholesterol.1

Presently in India there are coming across 2 lakh new cases of renal failure a year.2 Chronic kidney disease is a progressive and gradual impairment of glomerular & tubular function for 3 or more leading to hindrance in its function.3 It is found that many key enzymes and metabolic pathways are disturbed due to CKD leading to the development of disorder in HDL and triglycerides levels. One of reason for the development and progression can be associated with dyslipidemia. Dyslipidemia in CKD patients may actively participate in the progression and deterioration of kidney function.

In world wide population around 10% were affected by CKD which is a common condition in adults and its prevalence is elevating sharply with increasing age. In CKD patients it was found that there is marked elevation in cardiovascular (CV) morbidity and mortality. The most common and modifiable risk factor is dyslipidemia which may be associated with CKD and preferred for treatment in reducing CV disorder.

Prompt and timely detection of patients who are at risk for CKD is needed. Other major risk factors besides dyslipidemia include type I diabetes mellitus, Hypertension, protein barrier, family history of kidney disease, and increasing age may also lead to the progression of CKD. These patients will be having reduction of HDL-C and elevated levels of plasma triglyceride concentrations and also there is a defect in the cholesterol transportation. The factors like reduction in HDL cholesterol levels and declined in the action of reverse cholesterol pathway may contribute to the development of atherosclerotic coronary artery disease in ESRD.4

Hypothyroidism is an endocrine disorder which results from the decreased activity of thyroid hormones leading to weakening of the metabolic processes.5 This is a common disorder found in the general population mostly presenting as increased TSH and reduced T3 and T4. In hypothyroid patients we find decreased synthesis and mobilization of lipids. It mostly affects the cholesterol and LDL cholesterol due to the defect in its receptor.6 Thyroid dysfunction increases with age, especially in women. Hypothyroidism is associated with many biochemical abnormalities.7 Levels of total cholesterol & LDL tend to increase as thyroid function declines. Hypothyroidism is prevalent in developed countries at a rate of 4 to 5 percent.8

It is recommended to measure lipid profile as a part of global risk assessment & the frequency of check-ups is determined by age, sex & risk factors. Generally, fasting lipid profiles are recommended to ensure the most precise lipid assessment, particularly the TGL. Non-fasting lipid profiles determine TC, HDL-C & VLDL-C as well. Recent studies showed virtually no difference in TGL levels during fasting time. Therefore, it is important to consider the non-fasting lipid profile also in analyzing the lipid profile.9

The study was conducted because there were no similar studies done in our region, so we have decided to take part in it to prevent complications and morbidities.

Materials and Methods

This is a retrospective study that is carried over in a tertiary care hospital. We have taken 50 age and sex-matched cases of CKD, Hypothyroid subjects along with normal individuals as controls who are attending the outpatient department. The sample is collected in both fasting and non-fasting period with 2 hours and 4 hours apart after the meal. After centrifuging they were analyzed in an autoanalyzer BS 380, the method for estimation of lipid profile is cholesterol by CHOD-PAP method, TGL by GPO Trinder method, HDL by Direct colorimetric method, VLDL & LDL by Friedwald formula and renal profile which includes creatinine by Jaffe’s method and urea by Berthelot methods. In our study, we included patients who are willing to give consent and a known case of chronic kidney disease and hypothyroidism and patients who are not willing to give consent, patients aged below 20 years and above 60 years, and the patient with other alignments like COPD, known case of cardiovascular/cerebrovascular disorders and hyperthyroid patients were excluded in this study.

Written consent was taken from the study subjects after clearly explaining in their local language. And the patient can withdraw from the study at any point of time without giving any reasons. I have also taken ethical clearance from our institutional ethical committee.

Data was collected in excel sheet and were analyzed statistically by Graph pad version 9. The results will be explained by using simple T test comparing the mean ± standard deviation for quantitative variables p<0.05 shall be considered as significant changes with an intended power of study as 95%.

Results

A total of 150 patients were screened and 50 patients were having thyroid disorder, 50 patients were having CKD and 50 as controls. Patients of various age groups were selected. Serum triglyceride (TG) and VLDL were also found to be significantly raised in both CKD and hypothyroid individuals (P = 0.038, P = 0.040 and P=0.028, P=0.036 respectively).

Table 1

Comparing the lipid profile mean±SD between fasting and postprandial samples

Hypothyroidism

CKD

Controls

TC

Fasting

254.2±42.41

153.6±53.97

191.2±43.7

Postprandial

267.5±44.6

162.8±58.19

194.5±38.4

P

0.129

0.414

0.689

TG

Fasting

172.3±82.77

151.4±46.79

162.35±74.51

Postprandial

212.3±106.6

177±66.63

203.2±107.73

P

0.038*

0.028*

0.030*

HDLc

Fasting

42.2±2.80

42.1±1.86

40.5±2.09

Postprandial

41.3±2.87

41.9±2.15

39.9±2.61

P

0.115

0.62

0.207

LDLc

Fasting

124.4±34.83

82.2±47.57

118.2±42.75

Postprandial

132.3±34.99

83.4±52.51

113.9±34.15

P

0.260

0.904

0.579

VLDL

Fasting

34.45±16.55

30.28±9.35

32.51±14.90

Postprandial

42.39±21.31

35.63±15.2

40.6±21.54

P

0.040*

0.036*

0.031*

Table 2

Comparing the lipid profile mean±SD between fasting and random samples

Hypothyroidism

CKD

Controls

TC

Fasting

254.2±42.41

153.6±53.97

191.2±43.7

Random

271.5±48.24

177.47±50.42

210.1±41.31

P

0.059

0.02*

0.028*

TG

Fasting

172.3±82.77

151.4±46.79

162.35±74.51

Random

224.8±107.7

200.53±69.50

203.65±106.65

P

0.007*

0.001*

0.027*

HDLc

Fasting

42.2±2.80

42.1±1.86

40.5±2.09

Random

40.9±2.96

41.3±2.61

40.2±2.04

P

0.026*

0.080*

0.469

LDLc

Fasting

124.4±34.83

82.2±47.57

118.2±42.75

Random

147.5±39.43

95.9±51.31

126.9±40.57

P

0.044*

0.169

0.299

VLDL

Fasting

34.45±16.55

30.28±9.35

32.51±14.90

Random

44.95±21.54

37.09±19.46

43.1±19.74

P

0.007*

0.028*

0.003*

Table 3

Comparing the lipid profile mean±SD between postprandial and random samples

Hypothyroidism

CKD

Controls

TC

Postprandial

267.5±44.6

162.8±58.19

194.5±38.4

Random

271.5±48.24

177.47±50.42

210.1±41.31

P

0.667

0.18

0.05*

TG

Postprandial

212.3±106.6

177±66.63

203.2±107.73

Random

224.8±107.7

200.53±69.50

203.65±106.65

P

0.408

0.087

0.981

HDLc

Postprandial

41.3±2.87

41.9±2.15

39.9±2.61

Random

40.9±2.96

41.3±2.61

40.2±2.04

P

0.494

0.212

0.523

LDLc

Postprandial

132.3±34.99

83.4±52.51

113.9±34.15

Random

147.5±39.43

95.9±51.31

126.9±40.57

P

0.002**

0.231

0.546

VLDL

Postprandial

42.39±21.31

35.63±15.2

40.6±21.54

Random

44.95±21.54

37.09±19.46

43.1±19.74

P

0.408

0.676

0.086

Figure 1

Comparing the lipid profile of fasting, postprandial and random samples in hypothyroid patients

https://typeset-prod-media-server.s3.amazonaws.com/article_uploads/8a14707b-72e6-491e-a953-5db5ba62bb46/image/7e240a27-39d6-4e5e-a08f-9519ae13e965-uimage.png

Figure 2

Comparing the lipid profile of fasting, postprandial and random samples in CKD patients

https://typeset-prod-media-server.s3.amazonaws.com/article_uploads/8a14707b-72e6-491e-a953-5db5ba62bb46/image/334a774a-88da-440a-ad13-a22a2fe76d99-uimage.png

Figure 3

Comparing the lipid profile of fasting, postprandial and random samples in controls

https://typeset-prod-media-server.s3.amazonaws.com/article_uploads/8a14707b-72e6-491e-a953-5db5ba62bb46/image/58ea31a4-ab35-4066-9f5f-efe3602f26e4-uimage.png

Discussion

The present study is done on lipid profiles in hypothyroid and renal disorders, in patients attending to the tertiary care center on an outpatient basis from our surrounding areas. Some derangement in lipid metabolism is observed in both disorders.

Any decline in renal function may alter the lipid metabolism, as the elevation of LDL cholesterol and degree of hypertriglyceridemia which is proportional to its severity of impairment and it is the commonest feature in patients with renal failure. It occurs with elevation of VLDL, chylomicron and their remanants.10, 11, 12 Triglycerides are produced more liver and prolonged catabolism of triglycerides in the peripheral tissues.13, 14, 15 Elevated production of VLDL in liver leads to increased triglycerides in kidney disease. Our study is correlating with the present study where the patient having dyslipidemia showed hypercholesterolemia, hypertriglyceride-mia, and elevation of VLDL cholesterol in different phases.16 There are many studies which are showing similarities.17

This study is more coinciding with the study of Dhaka by Khan et al.,5 which is showing an increase in cholesterol, triglycerides, and LDL cholesterol with a decrease in HDL cholesterol. One of the studies showed that there is an elevation of HDL cholesterol in hypothyroidism by Olukoga.18 The decrease of LDL receptors leads to the elevation of LDL levels by reducing its degradation.19 Triglycerides levels are increased due to decreased activity of lipoprotein lipase in hypothyroid patients which ultimately leads to reduced degradation of triglycerides.20 Cholesterol ester transport protein and hepatic lipase will be causing reduces HDL levels in hypothyroid patients.

Samples are collected randomly, there are several arguments in collecting samples for lipid profile in different timings.21 We have noticed that there is a slight change in collecting the sample at different times. Evidence is not complete for proving that fasting sample is most suitable than non fasting sample. For reducing variability in estimation of lipid profile especially triglycerides, fasting sample is preferable. There are several studies stating that their will be a increase triglycerides after meal.22 Our study is coinciding with the above studies. There was study in China stating that after meal triglyceride levels were higher than fasting and also other lipid parameters their was no significant change from fasting sample.23 Variation in random samples of lipid profile is due to changes in hormone and enzyme levels which was stated in another similar study.24 Any how by seeing all the studies we may conclude that there will be a very minor changes in lipid profile and major changes in triglyceride levels. But elevation of triglycerides in non fasting state shows a change in the ratio of TG - total cholesterol ratio which may violates the Friedwald method which leads to overestimation of LDL cholesterol, so we can measure LDL cholesterol directly.25 In clinical point of treatment goal, collection for triglycerides to be considered when TG is >450 mg/dl.23

It is intended to conduct the study on a larger sample size so that it can be used in the future.

Conclusion

Derailment of lipid profile is frequently encountered in hypothyroidism and CKD patients. And also the time of collecting sample for analyzing lipid profile plays a key role in diagnosing and treatment. As there is no much significance in random and postprandial sample, so we will recommend random sample is most preferable and comfortable for analyzing the sample. This study suggests to check the lipid profile at the time of diagnosing both diseases in order to prevent mortality and morbidity occurring in this which may be due to cardiovascular/cerebrovascular diseases. Early screening and change of life style modification can help in prevention of co-morbidities.

Source of Funding

None.

Conflict of Interest

None.

References

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Article type

Original Article


Article page

129-133


Authors Details

Latha Rani Muthireddy, Suresh Eadala*, Durga Prasad Vangara, Srihita Mahavadi


Article History

Received : 25-05-2023

Accepted : 20-06-2023


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