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ORIGINAL CONTRIBUTION |
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| Year : 2000 | Volume
: 54
| Issue : 10 | Page : 435-441 |
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Clinical significance of lipid profile in cancer patients*
AS Raste, PP Naik
Department of Biochemistry, Tata Memorial Hospital, Dr E Borges Marg, Parel, Mumbai-400 012, India
Correspondence Address: A S Raste Department of Biochemistry, Tata Memorial Hospital, Dr E Borges Marg, Parel, Mumbai-400 012 India

PMID: 11262860
How to cite this article: Raste A S, Naik P P. Clinical significance of lipid profile in cancer patients*. Indian J Med Sci 2000;54:435-41 |
Many Physicians and public health workers have been intrigued in recent years with the possibility that modification of the diet may result in a reduced incidence and mortality from Cancer. Recent reports have focused renewed attention on possible role of dietary and endogenous lipids in the etiology and prognosis of cancer. Cholesterol, which is recognized to be important factor in the etiology of Coronary heart disease, has recently become the focus of attention on the possible role in the etiology of cancer A number of epidemiological studies have been published in recent years showing an increased risk of death from cancer subjects with low plasma cholesterol levels. [1],[2] Although several authors proposed that hypo cholesteremia is a predisposing factor for cancer development, [3],[4],[5] no causative relation has been established so far. However, some authors believe that hypocholesteremia is in fact the result rather than the cause of cancer. [6],[7] Current theories regarding cancer causation have generated interest in variables such as levels of serum cholesterol and triglycerides as potential associations with cancer relating to dietary factors or basic constitutional factors. Curiously enough very few studies exist concerning serum lipid profile inpatients with cancer. [8],[9] Therefore, the present study was undertaken to examine the lipid profile of inpatients with various malignancies in comparison with age matched controls.
| ¤ Materials and Methods | |  |
The material for the study comprised of 60 normal healthy controls and 115 patients having Carcinoma of breast, cervix, oesophagus, colon, stomach and leukemia, attending Tata Memorial Hospital, Mumbai. Before carrying out the estimation it was ascertained in every case from clinical records that the patients had no other diseases (e.g. hypertension, diabetes etc.) except cancer. All cases were histologically or cytologically proven malignant. 10.0 ml blood was collected in a plain test tube and allowed to clot at room temperature. The serum was separated by centrifuging at 2000 rpm for 10 minutes and was then preserved at -20 o C until estimated.
Lipid profile included estimations of serum Cholesterol, HDL-Cholestrol, Triglycerides, Phospholipids, total Lipids and Lipo-protein electrophoresis. Cholesterol, HDLCholesterol, Triglycerides and Phospholipids estimations were assayed on HITACHI 717 autoanalyser. Total Lipids were estimated by colorimetric method based on the Sulphophospho-Vanillin reaction. [10] Cholesterol was estimated by using Boehringer Mannheim's Cholesterol kit which was based on CHOD-PAP method. Triglycerides were assayed by using Human's Triglyceride kit which was based on enzymatic colorimetric method with Lipid clearing factor. Phospholipids were estimated by using Management kit by Menarini which is fully enzymatic method with colorimetric determination at 500 nm. HOL-Cholesterol fraction was determined by using Menagent HDL-Cholesterol reagent which allows the determination of HDLCholesterol fraction after precipiltation of LDL and VLDL fractions with phosphotungstic acid and magnesium chloride. LDL-Cholesterol levels were estimated by calculations using Friedwald et al formula. [11] Lipoprotein electrophoresis was done using agarose gel by the Paragon Lipo kit supplied by WiproBeckman.
| ¤ Results | |  |
The data for the present study were summarised in seven groups Group I: Normal healthy controls (male+female) in the age groups 25-50 years; Group II. Normal healthy female controls in the age group 25-45 years; Group III. Normal healthy children controls in the age group 8-15 years; Group IV. Patients with cancer of breast and cervix in the age group 25-45 years; Group V. Patients with cancer of oesophagus, stomach and colon in the age group 25-50 years; Group VI. Patients with leukemia in the age group 8-15 years; Group VII. Patients with leukemia in the age group 25-50 years.
The mean values for Cholesterol, HDL Cholesterol, LDL Cholesterol, Triglycerides, Phospholipids and Lipoproteins fractions for all these seven groups are depicted in [Table 1]. Analysis of the data shows that among the various serum lipid parameters all the parameters i.e. Total lipids, Total Cholesterol, HDL Cholesterol, LDL Cholesterol, Phospholipids, alphalipoprotein fractions were significantly lower in patients with various malignancies, when compared with the coo responding mean values of normal healthy control group, whereas the triglycride levels in patients with various malignancies were found to be significantly elevated when compared with the corresponding control group. Elctrophoretic separation of lipoprotein revealed a significant decrease in the mean value of α-lipoprotein inpatients with various malignancies when compared with the corresponding control group. The other fraction beta and pre-beta did not show any change in mean values in patients with cancer as compared to normal corresponding control group.
| ¤ Discussion | |  |
Epidemiologic data that relate serum cholesterol levels and cancer are conflicting. In some studies [5],[9],[12],[14] a negative correlation was found out not in others. In a recent study, a positive association was noted between serum cholesterol levels and the risk for rectal cancer in men. [15],[16] Both positive and negative association were observed at different points in time prior to the diagnosis of cancer. In the present study also patients with cancer had significantly lower mean values for cholesterol and HDL Cholesterol as compared to corresponding normal control group which is in agreement with studies reported by others. However, understanding the nature of the relationship of serum cholesterol to cancer diagnosis. In present study cholesterol levels were studied at the time of diagnosis of cancer. Studies that reported lower levels while those studies that reported the serum cholesterol many years prior to the diagnosis were found normal on high levels. However the studies reported by Winwar et al [17] demonstrated that these apparently conflicting studies are actually consistent because of the trend of decline in the serum cholesterol level gradually during the 10 years preceding the diagnosis of cancer. These are postulated mechanisms regarding the relationship but they do not explain why serum cholesterol is observed to be low in those with cancer. One of the postulated mechanisms is that there His increased membrane premeability to carcinogen induced by transfatty acid. [18] In the present study the mean value of triglycerides in patients with various malignancies were found to be significantly elevated when compared with the corresponding control group. In contrast, C.S. Alexpooulos et al [19] reported no statistically significant difference from the mean of controls.
The mean values of total lipids, phospholipid levels and alpha lipoprotein values were found diminished in malignancy as compared to normal controls in our study. These findings confirm the results of DeAlvares & Goodell [20] who studied lipoproteins in patients with gynecological cancer and Barclay et al [21],[22] who showed decreased lipoprotein levels in breast carcinoma.
The pathogenesis of the decreased lipoprotein values in patients with cancer is not known. The possibilities for decrease lipoprotein and cholesterol levels included decreased synthesis or increased catabolism. The decrease noted with phospholipids may perhaps be caused by decreased levels of lipoprotein known to transport phospholipids and the cholesterol depression may depression may be on the same basis at least in part. [23] Theoretically, synthesis of lipoproteins and cholesterol by the liver could be inhibited by tumour metabolites. The possibility of an increased catabolism accounting for decreased lipoprotein cannot be excluded. Further speculatins concerning the increased lipoprotein and cholesterol loss should also include the observation of Haven et al [24] about the properties of tumours to draw on host for phospholipids. However, Luscher et al [25] have suggested that lipoprotein may have a protective effect against the development of malignant neoplasia. So the decreased lipoprotein may in fact precede the development of cancer. Our study in accordance with Nydegger & Butler [8] confirms the findings that these exist in patients suffering from cancer a decrease in α-lipoprotein phospholipids & cholesterol which seems to be independent of ages, sex, state of nutrition, treatment and organ site of cancer. A decreased level of total lipids, cholesterol, HDL cholesterol and lipoproteins therefore not only reflects the neoplastic state in general, it perhaps may be especially useful in the early detection of cancer. Finally, from our findings from the present study, it can be concluded that serum total lipids, cholesterol, & HDL cholesterol levels are significantly inversely associated with incidence of cancer, whereas triglycerides levels significantly elevated in cancer patients. The inverse association between cancer and serum cholesterol and lipids may reflect a physiological response to early stage of cancer.
| ¤ Summary | |  |
In the present study, we have examined lipid profile in normal healthy age matched control and patients with various malignancies. Analysis of data revealed that total lipids, cholesterol and HDL cholesterol levels are inversely associated with incidence of cancer where as trriglycerides levels were significantly elevated in cancer patients. Electrophoretic separation of lipoproteins revealed a significant decrease in the mean values of alpha fraction in patients with malignancy when compared with the corresponding control group. The other fractions beta and pre-beta did not show any change in the mean values in patients with cancer as compared to the normal corresponding control group.
| ¤ References | |  |
| 1. | Committee of principal investigators. A co-operative trial in the primary prevention of ischemic heart disease using clofibrate, Br Heart J 1978;40:1069-1118. |
| 2. | Feinleib M. Review of the epidemiological evidence for a possible relationship between hypocholesterolemia and cancer, Cancer Res 1983: 43:2503-2507. |
| 3. | Rose G, Blackburn H, Keys A, Taylor HL, Kanel WB, Paul O. et al. Colon cancer and blood cholesterol, Lancet 1974;1:181-183. |
| 4. | Beaglehole R, Foulkes MA, Prior IAM. Cholesterol and mortality in New Zealand Maories, BMJ. 1980; 1:285-287. |
| 5. | Kark JD, Smith AH, Hames CG. The relationship of serum cholesterol to the incidence of cancer in Evans Country, Georgia. J Chronic Dis 1980;33:311-322. [PUBMED] |
| 6. | Cambien F, Ducimitiene A, Richard J. Total serum cholesterol and mortality in a middle aged male population, Am J Epidemiol 19801;112:388-394. |
| 7. | Rose G, Shipley MS. Colon cancer and blood cholesterol, Lancet. 1980; 1:523-526. |
| 8. | Nydegger UE Butler RE. Serum lipoprotein levels in patients with cancer, Can Res. 1972;32:1756-1760. |
| 9. | Miller SR, Tartter PI, Papatetsas AE, Slater G, Aufses J. Serum Cholesterol and Human colon cancer, J Natt Can Inst. 1981;67:297-300. |
| 10. | Christopher S Frings, Ralph T Dunn. A colorimetric method for determination of Total Serum Lipids based on the sulfo-phosphovanillin reaction, Am J Clin Path 1970;53:89-90. |
| 11. | Friedwald WT, Levy RI Friedrickson DS. Estimation of the concentration of LDL cholesterol in plasma without the use of the preparative ultracentrifuge, Clin Chem 1972;18:499-502. |
| 12. | McNamara PM, Kannel W, B Kannel Dawber TR.. Cancer incidence by levels of cohlesterol, JAMA 1981;245:247-252. |
| 13. | Rose G, Blackburn H, Keys A et al. Colon cancer and blood cholesterol, Lancet. 1974;1:181-183. |
| 14. | Stemmerman GN, Nomura AMY, Heilbrun KL, Pollack ES, Kagan A. Serum cholesterol and colon cancer incidence in Hawarian Japanese men, JNCI 1981;67:1179-1182. |
| 15. | Dyer AR, Stamler J, Paul O et al. J Chronic Dis 1981;34:249-260. |
| 16. | Mabee TM, Meyer P, Denbesten L, Mason EE. The mechanism of increased gallstone formation in obese human subjectj, Surgery. 1976;79:460-468. [PUBMED] |
| 17. | SdE Wainaweu, BJ Flehinger, J Buchalter, E Herbert, M Shike. Declining serum Cholesterol levels prior to Diagnosis of Colon cancer, JAMA. 1990;263:2083-2085. |
| 18. | Enig M0, Munn RJ, Keeney M. Dietary fat and Cancer trends a critique, Fed Proc 1978;37:2215-2220. |
| 19. | Alexopoulos CG, Blatsios B, Avgerinos A. Serum lipids and lipoproteins disorders in cancer patients, Cancer 1987;60:3065-3070. |
| 20. | De Alvarez RR, Goodell BW. Serum lipid partitions and fatty acid composition in gynecological cancer, Am J OBST Gynec 1964;88:1039-1062. |
| 21. | Barclay M, Cogin GE, Escher CG, Kaufman RJ, Kidder F,, Petermann MI. Human plasma Lipoproteins, I. in Normal women and in women advanced carcinoma of the Breast Cancer 1955 April 8:253-260. |
| 22. | Barclay M. Escher CG, Kaufman RJ. Terebus - Kekish O, Greene Elbl, Skipski VP. Clin Chem Acta 1964;10:39-47. |
| 23. | Fredickson 135, Levy RI, Lees RS. Fat transport, N E J Med 1967;276: 34-44. |
| 24. | Haven FL, Bloor W, Randall C. Nature of fatty acids of rats growing Walker carcinoma, Cancer Res 1951;11:619-623. |
| 25. | Luscher EF, Kaser Glanzmann R, Bretschmann M. The University of Chicago press, Chicago. 1967 pp 161-167. |
[Table 1]
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