Journal of Current Research in Scientific Medicine

: 2019  |  Volume : 5  |  Issue : 1  |  Page : 39--43

Variation in common serum lipid parameters in patients with malaria: A 1-year cross-sectional study

Prakash Babaliche, Pradeep Gubba 
 Department of General Medicine, KLE's University Jawaharlal Nehru Medical College, Belgaum, Karnataka, India

Correspondence Address:
Prakash Babaliche
Department of General Medicine, KLE's University Jawaharlal Nehru Medical College, Belgaum - 590 010, Karnataka


Background: Variations in serum lipid parameters are commonly and ubiquitously reported in patients with malaria. Different host cell lipid-dependent processes have been observed in the life cycle of the malarial parasite Plasmodium. Aim: The present study was undertaken to assess the serum lipid profile in patients with malaria. Materials and Methods: This 1-year cross-sectional study was conducted from January 2013 to December 2013 at the Department of Medicine. A total of 50 adult patients with positive-smear and quantitative buffy coat test for malaria, as well as with clinical features of malarial infection, were investigated for serum lipid profile changes. Patients on lipid-lowering drugs were excluded from the study. Fasting lipid profile estimation was performed using fully-automated Siemens Dimension Clinical Chemistry System for total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides. Data were analyzed using the independent sample t-test and one-way ANOVA. Results: Majority (86%) of the patients were positive for Plasmodium vivax. Thrombocytopenia was observed in 64% of the patients. Serum lipid profile estimation in these patients revealed that 60% of the patients had low total cholesterol levels (100–150 mg/dL), 56% of patients had low-LDL levels (<50 mg/dL), and 58% of patients had low-HDL levels (<20 mg/dL). However, 92% of the patients had hypertriglyceridemia (>150 mg/dL). Interestingly, patients with low-LDL cholesterol level had low-platelet count (51.25 ± 29.67;P = 0.035). Conclusion: Patients with malaria infections may have lipid parameters alteration in terms of hypocholesterolemia, low-HDL and -LDL levels, and hypertriglyceridemia.

How to cite this article:
Babaliche P, Gubba P. Variation in common serum lipid parameters in patients with malaria: A 1-year cross-sectional study.J Curr Res Sci Med 2019;5:39-43

How to cite this URL:
Babaliche P, Gubba P. Variation in common serum lipid parameters in patients with malaria: A 1-year cross-sectional study. J Curr Res Sci Med [serial online] 2019 [cited 2022 Aug 15 ];5:39-43
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Malarial infection continues to be a significant health problems in tropical and subtropical provinces with high morbidity and mortality. Globally, 250 million malarial cases were reported and around 438,000 people died due to malaria in 2015.[1],[2] Because of the increased transmission risk, migration, and drug-resistant strains the number of malarial cases are intensifying contemporarily making the eradication and elimination of malarial infection a distant prospect.

Multiple infections by different Plasmodium species, nonspecific clinical signs, and apparent misdirecting symptoms contributing to the inappropriate diagnosis.[3]Plasmodium vivax and Plasmodium falciparum contribute to majority of malarial infection in India, and the majority of the global malarial-infection caused by P. vivax are encountered within Ethiopia, India, Indonesia, and Pakistan region.[4],[5]

From the past few decades, studies have confirmed the existence of lipid profile derangement in malaria patients, and lipid profile variation is the characteristics of malaria complication.[6],[7],[8] This discovery established the fact that the malarial parasites utilize the host's lipid profile such as cholesterol and phospholipids which results in the variation of normal serum lipoprotein levels.[6],[7],[8] First-time variation in the high-density lipoprotein (HDL) levels in serum is attributed to the lipid metabolism of the parasite.[8] Lipids are the mandatory requirement for the parasite in both phases of its life cycle. Sporozoites of parasite pass through the bloodstream and invade and eventually modifies the lipid metabolism through their sophisticated mechanisms by altering the hepatocytes of the host.[8],[9] Intracellular pathogens such as Plasmodium have the ability to interfere in the lipid exogenous or endogenous pathways of the host, thereby causing alterations in the lipid profile.[8]

Variation cannot be considered as a definitive manifestation of malarial causality because of the similar phenomenon encountered in various complications such as atherosclerosis. However, low triglycerides, HDL, and Low-density lipoprotein cholesterol levels and elevated very low-density lipoprotein levels are considered as the typical characteristics of malarial infection.[8] The extent of lipid profile variation is related to the severity of the infection.[10] Although the derangement of lipids encountered ubiquitously and partly believed to be host related, definite relation, pathophysiology, and biological mechanism behind the lipid profile variation still remain uncertain. The relation between the human host serum lipid derangement and the pathogenesis of the infection needs to be established. The studies investigating the variation in the host's lipid profile and the extent of derangement need to be known for developing advanced treatment alternatives. Hence, the present study was planned to assess the lipid profile in malaria-infected patients.

 Materials and Methods

The present cross-sectional study was conducted at the Department of Medicine from January 2013 to December 2013, including 50 patients with malaria. Patients >12 years of age with sign and symptoms of malaria and with positive-smear positive and quantitative buffy coat (QBC) test for malaria were included in the study. Patients on lipid-lowering drugs were excluded from the study. Before the commencement of the study, ethical clearance was obtained from the Institutional Ethics Committee. Written informed consent was obtained from the patiens prior to commencement of the study.

Patients were inquired about their demographic data such as age, sex, previous history of similar complaints, and other comorbid conditions. Vital physical examinations, such as pulse rate, temperature, blood pressure, and respiratory rate, were performed and carefully documented. Systemic examinations, such as complete blood count, random blood sugar level, peripheral smear, and QBC test for malaria, were carried out. Fasting lipid profile was estimated using fully-automated Siemens Dimension Clinical Chemistry System for total cholesterol, LDL, HDL, and triglycerides.

Statistical analysis

The categorical data were expressed as rates, ratios, and proportions. The continuous data were expressed as mean ± standard deviation (SD) and compared using the independent sample t-test. More than three mean ± SD were compared using the one-way ANOVA. A value of P ≤ 0.050 at 95% confidence interval was considered as statistically significant.


In the present study, 82% of the patients were men and 18% were women. The male-to-female ratio was 4.55:1, and the mean age was 33.96 ± 12.72 years.

All the patients were suffering from fever with chills and rigors. Generalized body pain (80%), headache (52%), jaundice (26%), and nausea or vomiting (16%) were observed in the patients. The most common clinical signs were pallor (40%) and icterus (28%). Systemic examination findings revealed splenomegaly in 40% of the patients, hepatosplenomegaly in 8%, and hepatomegaly in 6% of the patients [Table 1]. In the current study, 86% of the patients were positive for P. vivax and 8% for P. falciparum; however, 6% of the patients were positive for both P. vivax and P. falciparum [Table 2].{Table 1}{Table 2}

Most of the patients (60%) had cholesterol levels between 100 and 150 mg/dL, and 56% of the patients had LDL levels <50 mg/dL. HDL levels were <20 mg/dL in 58% of the patients. In majority of the patients (92%), triglycerides level was >150 mg/dL [Table 3]. Comparison of mean lipid parameters in men and women showed no statistically significant difference [P > 0.050; [Table 4].{Table 3}{Table 4}

The mean cholesterol level in patients with <30 years of age was 105.46 ± 17.87 mg/dL. Among the patients aged >50 years, the mean cholesterol levels observed were 166.75 ± 42.36 mg/dL [P < 0.001; [Table 5]. Similarly, the mean LDL level in patients aged <30 years was 43.12 ± 18.43 mg/dL, which increased to 94.63 ± 35.99 mg/dL in patients who were aged >50 years (P < 0.001). However, the mean HDL and triglyceride levels were comparable in all the age groups (P > 0.050).{Table 5}

In the present study, 64% of the patients had a platelet count <100,000/mm3. In comparison of mean lipid parameters and platelet count in patients with platelet count <100,000/mm3, LDL levels were significantly low compared to that of the patients with a platelet count of >100,000/mm3 (P = 0.035). However, total cholesterol, HDL, and triglycerides were comparable in both the subsets [P > 0.050; [Table 6].{Table 6}


In the present study, the majority of the patients were males (82%) and 18% were female with a male-to-female ratio of 4.55:1 suggesting male preponderance.

Fever is a distinctive characteristic of malaria infection. Irregular persistence of fever at the beginning and gradual rise in temperature with shivering and chills are the primary symptoms usually encountered in malaria.[11] In the present study, fever with chills and rigors (100%) are the predominant clinical presentation. In a study from north Maharashtra, fever was the most predominant complaint, seen in 97% of the cases. In the same study, 93% of the patients had chills and rigors.[12]

P. falciparum, Plasmodium ovale, Plasmodium malariae, and P. vivax are identified to cause malaria in human beings. In the current study, infection through P. vivax was observed in 86% of the patients and P. falciparum in 8% of the study population. However, 6% of the patients had mixed infection. In contrast to these findings, a recent study reported the infection from P. vivax in 52.54% of patients, followed by P. falciparum (33.75%) and mixed infections (13.69%).[13] According to the WHO, 78% of the cases were discovered in Ethiopia, India, Indonesia, and Pakistan were infected by P. vivax.[4]

In the present study, nearly two-third of the study population (60%) had cholesterol levels between 100 and 150 mg/dL. The mean and median cholesterol levels were 126 ± 41.07 and 113 mg/dL, respectively (range 65–246 mg/dL) suggesting hypocholesterolemia. The mean cholesterol levels in patients aged <30 years and >50 years were 105.46 ± 17.87 and 166.75 ± 42.36 mg/dL, respectively, suggesting that as age advances the cholesterol levels also increases (P < 0.001). However, the mean cholesterol levels were comparable in men and women (P = 0.554). Previous studies conducted by Orimadegun andOrimadegun,[14] Dias et al.,[9] Chukwuocha and Eke,[15] and Kittl et al.[16] had reported a similar relation between severe malaria and serum cholesterol. Contrastingly, in a meta-analysis[8] among 36 studies, 30 studies reported hypocholesterolemia manifested by the presence of reduced cholesterol level in malarial complications. A study by Krishna et al.[17] also reported raised cholesterol levels (199.4 ± 27.2 mg/dL) compared to the control group (130 ± 28.6 mg/dL). It concludes that significant fluctuations in the total serum cholesterol levels encountered during the course of malarial infection, which is in accordance with the findings of the current study.

Lipids are the main structural elements of every biological membrane. Parasites show special prominence to lipids and manipulate the host's lipid metabolism through their sophisticated mechanisms to enhance the availability of lipids. Lipids are also one of the pathogenic factors that help pathogens to avoid the host's immunity and cause diseases.[18] Protozoal parasites cause an oxidative modification in the host's lipoprotein mechanisms possibly due to acute-phase responses. This modification results in the enhancement of cytoadherence of infected erythrocytes; this signifies the prominence of lipoprotein oxidation in the pathogenicity of malarial infection.[19]

In this study, more than half of the study population (56%) had LDL levels <50 mg/dL. The mean LDL levels were 60.90 ± 38.14 mg/dL. No statistically significant difference was noted in men and women P = 0.270. However, the mean LDL levels in patients aged <30 years were significantly low (43.12 ± 18.43 mg/dL) compared to those who were aged >50 years (94.63 ± 35.99 mg/dL). Further, an increasing trend in LDL level was observed with advancing age (P < 0.001). These findings suggest that LDL level in patients with malaria is low and dependent on the age of the patient. A systematic review,[8] including 16 studies assessed LDL in patients with malaria. It was found that 81% of studies (13 out of 16 studies) reported lower LDL levels in patients with malaria concluding that LDL levels are significantly depressed in infected individuals.

In the present study, 96% of patients had HDL level below the normal range of 40 mg/dL in which HDL level was <20 mg/dL in most of the patients (58%). Approximately, one-third of the study population had HDL levels between 20 and 30 mg/dL (36%). These findings suggest that patients with malaria possess very low-HDL level. However, no statistically significant difference was observed in men and women as well as in different age-groups (P > 0.050). It has been postulated that acute infection and inflammation produce a moderate fluctuation in plasma lipoprotein pattern in man, with a typical decline in HDL cholesterol. Faucher et al.[7] reported that malaria infection produces moderate changes in plasma lipid profile in man, with typical decline in HDL concentration. Another study by Ogbodo et al.[19] proposed that oxidative modification of HDL and reduced serum levels of this class of lipoprotein was associated with the pathophysiology of malaria.

Studies observed increased levels of triglycerides in malaria patients, especially in severe patients. The mechanism behind it still remains uncertain but it is speculated that parasite-related constituents might be responsible. Reports suggest that association exists between hypertriglyceridemia and malaria, especially in severity.[20] In the current study, the majority of the patients (92%) had triglyceride levels of >150 mg/dL. The mean and median triglyceride levels were also suggestive of hypertriglyceridemia, that is, mean triglycerides level was 274.38 ± 141.57 mg/dL, and the median level was 228 mg/dL ranging between 53 and 710 mg/dL. A study conducted by Parola et al.[20] showed a similar result. These findings conclude that triglycerides were higher in patients with malaria.

In the current study, 64% of the patients had a platelet count of <100,000/mm3 suggesting thrombocytopenia. Among them, LDL levels were significantly low compared to that of the patients having a platelet count of >100,000/mm3 (51.25 ± 29.67 vs. 78.06 ± 45.83/mm3; P = 0.035); however, total cholesterol, HDL, and triglycerides levels were comparable in both the subsets. The present study showed that patients with malaria are prone to lipid derangement with hypocholesterolemia, lower LDL and HDL cholesterol, and hypertriglyceridemia.

The findings of present study extends the observation of earlier studies by reinforcing the findings of lipid profile disturbance in patients with malaria. This significant variation in lipid profile may serve as a tool for the proper management and diagnosis of the infection. The current study clearly demonstrates that the malarial infection produces a unique discrepancy in the plasma lipoprotein metabolism and this variation is manifested in the host's lipoprotein profile.


Findings of the current study shows that, malarial patients have altered lipid parameters in terms of hypocholesterolemia, low-HDL and -LDL levels, and hypertriglyceridemia.


All the authors have contributed equally to the development of this manuscript.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1World Health Organization. Fact Sheet: World Malaria Day 2016: World Health Organization; 2016. Available from:[Last accessed on 2017 Jan 01].
2World Health Organization. Geneva. Switzerland: World Health Organization; 2016.
3Lalloo DG, Shingadia D, Bell DJ, Beeching NJ, Whitty CJM, Chiodini PL, et al. UK malaria treatment guidelines 2016. J Infect 2016;72:635-49.
4World Health Organization World Malaria Report 2016. Geneva: WHO Embargoed Until; 2016.
5Anvikar AR, Shah N, Dhariwal AC, Sonal GS, Pradhan MM, Ghosh SK, et al. Epidemiology of Plasmodium vivax malaria in India. Am J Trop Med Hyg 2016;95:108-20.
6Seshadri C, Shetty BR, Gowri N, Venkataraghavan S, Chari MV. Serum cholesterol and total lipids in Plasmodium vivax malaria – A preliminary study. Indian J Med Res 1981;74:513-6.
7Faucher JF, Ngou-Milama E, Missinou MA, Ngomo R, Kombila M, Kremsner PG. The impact of malaria on common lipid parameters. Parasitol Res 2002;88:1040-3.
8Visser BJ, Wieten RW, Nagel IM, Grobusch MP. Serum lipids and lipoproteins in malaria – A systematic review and meta-analysis. Malar J 2013;12:442.
9Dias RM, Vieira JL, Cabral BD, da Silva IR, Brasil LM, Araújo ED, et al. Lipid profile of children with malaria by Plasmodium vivax. J Trop Med 2016;2016:9052612.
10Sengupta A, Ghosh S, Das BK, Panda A, Tripathy R, Pied S, et al. Host metabolic responses to Plasmodium falciparum infections evaluated by 1H NMR metabolomics. Mol Biosyst 2016;12:3324-32.
11Bartoloni A, Zammarchi L. Clinical aspects of uncomplicated and severe malaria. Mediterr J Hematol Infect Dis 2012;4:e2012026.
12Mehta. Clinical pattern of malaria epidemics in Rajasthan. J Physicians India 2001;48:211-5.
13Muddaiah M, Prakash PS. A study of clinical profile of malaria in a tertiary referral centre in South Canara. J Vector Borne Dis 2006;43:29-33.
14Orimadegun AE, Orimadegun BE. Serum apolipoprotein-A1 and cholesterol levels in nigerian children with Plasmodium falciparum infection. Med Princ Pract 2015;24:318-24.
15Chukwuocha UM, Eke KN. Malaria parasite status and cholesterol level of malaria patients in parts of the IMO river basin of Nigeria. Asian Pac J Trop Med 2011;4:993-6.
16Kittl EM, Diridl G, Lenhart V, Neuwald C, Tomasits J, Pichler H, et al. HDL cholesterol as a sensitive diagnostic parameter in malaria. Wien Klin Wochenschr 1992;104:21-4.
17Krishna AP, Chandrika, Kumar S, Acharya M, Patil SL. Variation in common lipid parameters in malaria infected patients. Indian J Physiol Pharmacol 2009;53:271-4.
18Ramakrishnan S, Serricchio M, Striepen B, Bütikofer P. Lipid synthesis in protozoan parasites: A comparison between kinetoplastids and apicomplexans. Prog Lipid Res 2013;52:488-512.
19Ogbodo SO, Ogah O, Obu HA, Shu EN, Afiukwa C. Lipid and lipoprotein levels in children with malaria parasitaemia. Curr Pediatr Res 2008;12:12-7.
20Parola P, Gazin P, Patella F, Badiaga S, Delmont J, Brouqui P. Hypertriglyceridemia as an indicator of the severity of falciparum malaria in returned travelers: A clinical retrospective study. Parasitol Res 2004;92:464-6.