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Research Article | Volume 10 Issue 2 (July-December, 2024) | Pages 190 - 196
Evaluation Of Patients of Malaria by Clinical, Hematological and By Biochemical Parameters
 ,
 ,
1
MD Medicine, Consultant, Apex Hospital, Bikaner, India
2
Senior Prof, dept of Medicine, SP medical college, Bikaner, India
3
Assistant Professor, dept of Medicine, SP medical college, Bikaner, India
Under a Creative Commons license
Open Access
Received
Nov. 2, 2022
Revised
Nov. 18, 2022
Accepted
Nov. 30, 2022
Published
Dec. 14, 2022
Abstract

Introduction: Malaria remains a major global health issue, causing around 200 million infections and over 500 thousand deaths annually, with the highest mortality in sub-Saharan Africa, while also significantly affecting rural regions in Asia and South America. AIM: To identify and evaluate patients of malaria by clinical, hematological and by biochemical parameters. Methodology: This hospital-based comparative cross-sectional study was conducted over 15 months in the Department of Medicine at S.P. Medical College and P.B.M. Hospital, Bikaner. A total of 54 participants, with 27 cases in each group, were included using a random sampling method. Result: Our study found that malaria affects all age groups, predominantly in rural areas, with clinical findings including hepatosplenomegaly, anaemia, normal or low TLC, thrombocytopenia, mild renal impairment, and elevated liver enzymes, consistent with previous research. Conclusion: In conclusion, malaria affects all age groups, primarily in rural areas, with clinical features of hepatosplenomegaly, anaemia, thrombocytopenia, mild renal impairment, and elevated liver enzymes, highlighting the need for early detection and comprehensive evaluation

Keywords
INTRODUCTION

According to the World Health Organization (WHO), malaria is a significant public health problem in more than 100 countries and causes an estimated 200 million infections each year, with more than 500 thousand deaths annually. Over 90% of these deaths occur in sub-Saharan Africa, where the disease is estimated to kill one child every 30 seconds1. In other areas of the world, malaria causes substantial morbidity, especially in the rural areas of some countries in Asia and South America2,3. In contrast, despite previous elimination in regions like the United States and Western Europe, the phenomenon of “imported malaria” introduced by immigrants and travellers, still contributes with sporadic cases in these regions4

The organism responsible for malaria is the protozoon Plasmodia. In the genus Plasmodium, six species5 have been identified of which five – namely P.falciparum, P.vivax, P.malariae  and two morphologically identical sympatric species of  P.ovale(P.o.curtisi and P.o.wallikeri)are human malaria species that spread by the bite of an infected female Anopheles mosquito. The recently identified sixth species, P. knowlesi, is primarily a parasite of  macaque monkeys and may occasionally spread to humans by zoonotic transmission and cause severe illness. Overall,  P.falciparum and P.vivax continue to be the two most important types of malaria, with P.falciparum being responsible for most complications and deaths due to malaria6.Recently, significant changes have been identified in the epidemiological as well as clinical pattern of malaria. During the last decade of 20th century, cerebral malaria was the predominant manifestation of severe malaria, whereas in recent past the combination of jaundice and renal failure are predominant severe manifestations7.Malaria diagnosis traditionally relies on microscopic examination of thin or thick blood smears, a widely accepted method requiring skilled personnel for accurate interpretation. However, microscopy often struggles with mixed-species infections, sub-microscopic parasitemia, and operates with poor efficiency in many endemic areas. Rapid diagnostic tests (RDTs), which detect parasite antigens like histidine-rich protein II (HRP-II) or lactate dehydrogenase (LDH), are increasingly favored for their sensitivity, low cost, and quick results. Despite these advantages, challenges arise when analyzing frozen blood samples, and RDTs are susceptible to degradation in high humidity and temperatures, limiting shelf life. Variability in test preparation and result interpretation further depends on the technician’s expertise and visual accuracy. While current methods, including microscopy, PCR-based diagnostics, and RDTs, are robust and reliable for symptomatic cases, these limitations highlight the need for innovative approaches to detect low-density parasitemia efficiently and in high-throughput settings.

 

AIM

To identify and evaluate patients of malaria by clinical, hematological and by biochemical parameters.

MATERIALS AND METHODS

This hospital-based comparative cross-sectional study was conducted over 15 months in the Department of Medicine at S.P. Medical College and P.B.M. Hospital, Bikaner. A total of 54 participants, with 27 cases in each group, were included using a random sampling method. The study enrolled participants of either sex aged 18–65 years, who were confirmed to have *Plasmodium vivax* or *Plasmodium falciparum* infection through microscopy and/or rapid diagnostic tests (RDTs). Eligible participants were those who had not received antimalarial treatment prior to sample collection, were willing to provide written informed consent, and complied with the protocol requirements. Patients were excluded if they had significant systemic diseases, such as autoimmune disorders, chronic liver diseases, psychiatric illnesses, or bleeding disorders, as determined by clinical history and physical examination. Those unwilling to consent were also excluded



RESULTS

Table 1:Distribution of cases according to age group in relation to type of malaria

Age Group

Total (n=27)

 
 

No.

%

 

21-30

16

59.3

 

31-40

7

25.9

 

>40

4

14.8

 

Total

27

 

 

t

0.221

 

P

0.827

 

 

The majority of participants (59.3%) were aged 21–30 years, followed by 25.9% aged 31–40 years and 14.8% over 40 years, with no statistically significant difference in age distribution (t = 0.221, p = 0.827).

 

Table 2:Distribution of cases according to residential area in relation to type of malaria

Residential Area

Total (n=27)

 
 

No.

%

 

Rural

24

88.9

 

Urban

3

11.1

 

Total

27

100

 

P

0.869

 

 

Most participants (88.9%) were from rural areas, while 11.1% were from urban areas, with no statistically significant difference in residential distribution (p = 0.869).

 

Table 3:Distribution of cases according to USG findings in relation to type of malaria

USG Findings

Total (n=27)

 
 

No.

%

 

Hepatomegaly

5

18.5

 

Splenomegaly

11

40.7

 

Hepatosplenomegaly

2

7.4

 

Pregnancy

2

7.4

 

NAD

7

25.9

 

Total

27

100

 

 

Ultrasonography findings revealed splenomegaly in 40.7% of participants, hepatomegaly in 18.5%, hepatosplenomegaly and pregnancy each in 7.4%, while 25.9% showed no abnormalities detected (NAD).

 

Table 4:Distribution of cases according to haemoglobin (mg/dl) in relation to type of malaria

Hb (gm/dl)

Total (n=27)

 
 

No.

%

 

<7

4

14.8

 

7.1-9.0

2

7.4

 

9.1-11.0

7

25.9

 

>11.0

14

51.9

 

t

1.230

 

p

0.230

 

 

Among participants, 51.9% had hemoglobin levels >11.0 g/dL, 25.9% had 9.1–11.0 g/dL, 7.4% had 7.1–9.0 g/dL, and 14.8% had <7.0 g/dL, with no statistically significant difference observed (t = 1.230, p = 0.230).

 

Table 5:Distribution of cases according to TLC(X103/mm3) in relation to type of malaria

TLC (Th)

Total (n=27)

 
 

No.

%

 

<4

8

29.6

 

4-11

19

70.4

 

>11

0

-

 

T

0.368

 

P

0.716

 

Total leukocyte count (TLC) was within the normal range (4–11 × 10³/µL) in 70.4% of participants, while 29.6% had TLC <4 × 10³/µL, with no cases exceeding 11 × 10³/µL and no statistically significant difference (t = 0.368, p = 0.716).

 

 

 

 

 

 

 

Table 6:Distribution of cases according to platelet count(105/mm3) in relation to type of malaria

Platelet Count (lacs)

Total (n=27)

 
 

No.

%

 

<1.5

24

88.9

 

1.51-3.50

3

11.1

 

>3.50

0

-

 

t

0.298

 

p

                                                            0.768

 

Platelet counts were <1.5 lacs in 88.9% of participants and between 1.51–3.50 lacs in 11.1%, with no cases exceeding 3.50 lacs and no statistically significant difference observed (t = 0.298, p = 0.768).

 

Table 7:Distribution of cases according to serum creatinine and  serum bilirubin(mg/dl) total parameters in relation to type of malaria

Serum Creatinine

Total

Serum Bilirubin (Total)

Total

No.

%

No.

%

No.

%

No.

%

0-1.5 (Normal)

24

88.9

0-1 (Normal)

10

37.0

1.51-3.0 (Increased)

3

11.1

1.1-3.0

17

63.0

>3.0 (Severe malaria)

0

-

>3.0

0

-

t

1.334

 

0.081

p

0.194

 

0.936

 

Serum creatinine levels were normal (0–1.5 mg/dL) in 88.9% of participants and mildly elevated (1.51–3.0 mg/dL) in 11.1%, while serum bilirubin was normal (0–1 mg/dL) in 37.0% and mildly elevated (1.1–3.0 mg/dL) in 63.0%, with no cases of severe elevations and no statistically significant differences (serum creatinine: t = 1.334, p = 0.194; serum bilirubin: t = 0.936, p = 0.081).

 

Table 8:Distribution of cases according to SGOT (U/L) and  SGPT (U/L) in relation to type of malaria

SGOT

Total

SGPT

Total

No.

%

No.

%

No.

%

No.

%

<40

7

25.9

<56

9

33.3

41 to 5xUNL

20

74.1

57 to 5x UNL

18

66.7

>5xUNL

0

-

>5x UNL

0

-

t

1.746

 

0.067

P

0.093

 

0.947

 

SGOT levels were elevated (41 to 5×UNL) in 74.1% of participants, with 25.9% within normal limits (<40 U/L), while SGPT levels were elevated (57 to 5×UNL) in 66.7% and normal (<56 U/L) in 33.3%, with no cases exceeding 5×UNL and no statistically significant differences observed (SGOT: t = 1.746, p = 0.093; SGPT: t = 0.067, p = 0.947)



DISCUSSION

Malaria is protozoal disease transmitted by the bite of an infected female anopheles mosquito. Six species of malaria namely P. falciparum, P. vivax, P. malariae and two morphologically identical sympatric species of P. ovale (Curtisi and Wallikeri), P. knowlesi are responsible for malaria in humans8

 

Our study showed that malaria affected individuals across all age groups, with the highest prevalence (59.3%) in those aged 21–30 years, followed by 25.9% in the 31–40 group, and 14.8% over 40 years. Statistical analysis showed no significant age-related differences (t = 0.221, p = 0.827). These findings highlight the importance of age-targeted public health interventions and preventive measures in endemic areas.

 

In our study, higher percentage of cases belonged to rural area (88.9%) as compared to urban area (1.1%).The results were supported by Gardiner et al9 study which showed low parasite rate (1.6%) in urban areas while parasite rate in rural area was 22%.

 

In present study, we found that hepatometaly was present in 5 cases, splenomegaly was present in 11 cases and out of them 1 case PF positive, hepatosplenomegaly was present in 2 case and 1 was PF positive. These results were in accordance to Zha et al10 found and splenomegaly is associated with the most of the cases of malaria.

In the present study, 4 cases had severe and 2 cases and moderate anaemia.Maximum 14 cases (51.9%) had normal haemoglobin.  Previous studies have presented with a wide range of anaemia (<11 g/dL) from 30%11 to 86.0%12. Anaemia is a frequent finding in malaria cases, particularly in developing nations. The pathogenesis of anaemia is multifactorial and includes hemolysis of infected RBCs, accelerated destruction of parasitized and non parasitized RBCs, bone marrow dyserythropoiesis, splenic pooling. This often occurs on a background of chronic anaemia in the developed nations where intestinal parasites and malnutrition prevail particularly in women.

 

In present study, majority of the cases (70.4%) had their TLC within normal range (4×103/mm3- 11×103/mm3). 29.6% cases had low TLC (<4×103/mm3) while no case had their TLC >11×103.  The results were in accordance to the study by Surve et al13 who observed that majority of the malaria patients had normal total WBC count (72%).

 

The mechanism of thrombocytopenia in malaria is uncertain. Immune- mediated lysis, sequestration in the spleen and a dyspoetic process in the marrow with diminished platelet production have all been postulated. Abnormalities in platelet structure and function have been described as a consequence of malaria and in rare instances platelets can be invaded by malarial parasites themselves14.

 

In our study, 3 cases had increased serum creatinine. No case had serum creatinine value which met the criteria of severe malaria.Acute renal failure in malaria is usually oliguric or anuric but urine output may be normal or increased, making daily measurement of serum creatinine to be the most important investigation15.

 

In the present study, it was observed that the liver enzyme levels were elevated in malaria patients. 63% cases had serum bilirubin levels between 1.1- 3.0, 74.1% cases had AST between 41- 5×UNL and 66.7% cases had ALT between 57- 5×UNL. None of the cases had values of liver enzyme in the range of severe malaria. The finding of the present study correlated with finding of previous studies of  Oluwole et al16 and ELbadawi et al17 who reported that most of the malaria patients show elevation in liver enzymes indicating liver damage.The elevation of serum bilirubin levels in malaria patients indicate increased red blood cell haemolysis. It has also been associated with hepatocellular damage and biliary tract obstruction. The observed increase in ALT could be due to leakage from hepatic cells that were injured by the auto immune process or by abnormal cell activation induced by parasite.

CONCLUSION

In conclusion, our study highlights that malaria affects individuals across all age groups, with a higher prevalence in younger adults and predominantly in rural areas. Clinical findings, such as hepatomegaly, splenomegaly, and anaemia, align with previous studies and emphasize the importance of early detection and intervention. Most patients exhibited normal TLC levels, consistent with Surve et al.'s findings, while thrombocytopenia mechanisms remain multifactorial, involving immune-mediated and splenic processes. Serum creatinine elevations were observed in a few cases but did not meet severe malaria criteria. Elevated liver enzyme levels in malaria patients, correlating with previous research, indicate red blood cell haemolysis and hepatic cell damage, underscoring the need for comprehensive clinical and laboratory evaluations.

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    2. Center for Disease Control and Prevention (CDC). Malaria Parasites; Publisher: City, Country, 2010. Available online: http://www.cdc.gov/malaria/about/biology/parasites.html (accessed on 18 October 2011).
    3. Snow RW, Guerra CA, Noor AM, Myint HY, Hay SI. The global distribution of clinical episodes of Plasmodium falciparum malaria. Nature 2005; 434: 214–7.
    4. Price RN, Tjitra E, Guerra CA, Yeung S, White NJ, et al. Vivax malaria: neglected and not benign. Am J Trop Med Hyg 2007; 77 (6 Suppl). 79–87.
    5. Olszewski KL, Morrisey JM, Wilinski D, Burns JM, Vaidya AB, et al. Host-parasite interactions revealed by Plasmodium falciparum metabolomics. Cell Host Microbe 2009; 5:191–9.
    6. Mishra SK, Newton CR. Diagnosis and management of the neurological complications of falciparum malaria. Nat Rev Neurol 2009; 5:189–98.
    7. Francischetti IM. Does activation of the blood coagulation cascade have a role in malaria pathogenesis? Trends Parasitol 2008; 24:258–63.
    8. Nicholas WH, Joel BG. Harrison’s Principles of Internal Medicine 19th edi McGrawHill Education 2015; 1368-77.
    9. Gardiner C, Biggar RJ, Collins WE, Nkrumah FK. Malaria in urban and rural areas of southern Ghana: a survey of parasitaemia, antibodies and antimalarial practices. Bull World Health Organ. 1984; 62(4): 607-613
    10. Zha Y, Zhou M, Hari A, Jacobsen B, Mitragotri N, Rivs Bet al. Ultrasound diagnosis of malaria: examination of the spleen, liver, and optic nerve sheath diameter. Wrold J Emerg Med 2015; 6(1):10-15.
    11. Naha K, Dasari S, Prabhu M. Spectrum of complications associated with plasmodium vivax infection in a tertiary hospital in South Western India. Asian Pac J Trop Med 2012; 5:79-82.
    12. Kochar DK, Kochar SK, Agrawal R, Kumawat BL. Incidence of anemia in malaria. Southeast Asian J Trop Med Pub Hlth 1997; 28:2.
    13. Ketaki Motram Surve, Anjali S. Kulkarni, Santosh G. Rathod*, Rajan S. Bindu. Study of haematological parameters in malaria. Int J Res Med Sci 2017; 5(6):2552-7.
    14. Lacerda MV, Mourao MP, Coelho HC, Santos JB. Thrombodytopenia in malaria. Who cares? Mem Inst Oswaldo Cruz 2011; 106:52-63.
    15. Prakash J, Singh AK, Kumar NS, Saxena RK. Acute renal failure in P. vivax malaria. JAPI 2003; 51:265-7.
    16. Oluwole O, Sia S, Mohmmed M. Plasmodium falciparum-induced kidney and liver dysfunction in malaria patient sin free town, sherlene. J of Biochemical Research 2010; 2(1): 70-74.
    17. ELbadawi NEE, Mohamed MJ, ELZaki N, Mohamed AA, Ounsa GE, et al. The effect of malaria on biochemical liver function parameters in sudanese pregnant women. J Physiobiochem Metab 2012; 1:2.
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