Abstract: In this study total bilirubin, albumin and electrolytes levels in HIV positive persons were determined followed by anion gap calculation. This is with a view to generating the non-existent baseline data that could aid in monitoring the progression of AIDS in resource limited settings like ours. Results of the various analysis showed that the concentrations of the conjugated, mean total and unconjugated bilirubin in HIV positive persons ranged from 0.50 to 1.3, 1.07 to 2.10 and 0.01 to 1.50 mg/100 mL, respectively while those for the control subjects, (HIV non-infected) were from 0.50 to 1.66, 0.80 to 1.60 and 0.10 to 0.70 mg/100 mL, respectively. Also while the mean total and unconjugated bilirubin concentrations were higher in HIV positive persons than in the non-infected, the reverse was found to be the case for albumin levels. The albumin levels of HIV positive persons ranged from 29 to 37 g L-1 and for the uninfected it was from 34 to 39 g L-1. The results of the electrolyte determination revealed that the mean concentrations of the electrolytes in HIV positive persons were 99.3 mmol L-1 (Cl-), 18.08 mmol L-1 (HCO3-), 132.4. mmol L-1 (Na+) and 3.3 mmol L-1 for K+. For the uninfected the mean values recorded included 100 mmol L-1 (Cl-), 20.3 mmol L-1 (HCO3-), 137.4 mmol L-1 (Na+) and 4.08 mmol L-1 (K+). The results of the electrolytes determination are all within normal range though there were slight decreases in the HIV (+) persons. The anion gap values overlapped between the infected and the non-infected.
INTRODUCTION
The human immunodeficiency virus (HIV), the virus that causes the acquired immune deficiency syndrome (AIDS) was identified in 1983. As at the end of 2003, about 70 million people had been infected and more than 42 million still living with the virus while 15,000 people worldwide are infected each day[1-3]. Sub-Saharan Africa is worst hit as more than 70% of the over 42 million persons infected worldwide live here and AIDS is now the leading cause of death in the region. Nigeria the most populous country in Africa has over 4 million persons living with HIV/AIDS and a national sero prevalence of 5.8% as at the end of 2001[4-6].
Several factors have been identified as fueling the epidemic in Africa. Such factors include ignorance of the disease, lack of access to prevention, low socio-economic status of women, inadequate treatment and care services and stigma and discrimination[5,7-10]. Despite all the progress in HIV and AIDS science since 1981, the epidemic unfortunately continues to progress in the developing world, where over 95% of people infected with HIV live[11]. Though researchers have been making steady progress in the past 11 years, the pace according to Peter Piot the Executive Director of UNAIDS, is not fast enough for all the people who could benefit from it[9,12]. The antiretroviral drugs used in treatment are very expensive and unavailable and cannot reach millions of infected people who need them. As a result, for the uninfected, prevention is still better, but for the infected accurate and timely diagnosis and treatment are needed to prolong life span and improve quality of life as well as reduce the frequency and duration of hospital admission[13].
In countries where resources are plentiful, monitoring of HIV infection includes routine chemical assessment and measurement of CD4+ T lymphocyte counts and plasma HIV load. These indicators are used to determine disease stage and progression, assist in decisions regarding when to start or change ART and assess treatment response. On the other hand, for resource-limited settings Kent et al.[14] asserted that biological and social reasons such as HIV clades, differences in prevalence of co-infections and socio-economic differences make it inappropriate to apply the guidelines developed in wealthy industrialized countries in Sub-Saharan Africa and other poor nations.
From the foregoing, it is imperative that researches are required for the development of simple and rapid diagnostic tests upon which to build the guidelines for treatment that at the moment are exceedingly limited with standard monitoring tests largely inaccessible to many[3].
The present study seeks to measure some biochemical parameters of both HIV/AIDS patients and non HIV patients in Nigeria with a view to generating preliminary data that could be used in identifying the infection early and in monitoring the progression of the disease.
MATERIALS AND METHODS
Ethical approval: Permission was obtained from the Ethical Clearance Committee of the Jos University Teaching Hospital (Ref. JUTH/DCS/ADM/127/VOL-XVI/217).
Sample preparation: Blood samples were taken by venepuncture from 80 HIV positive patients attending Jos University Teaching Hospital and from 80 persons that are HIV negative. Serum was prepared by centrifugation using MSE minor centrifuge model at 1,500 rpm for 5 min. The serum samples were stored at –20°C until needed for analysis.
Determination of bilirubin levels: Bilirubin was determined by the Vanderbergh method[15] based on the diazo reaction. The conjugated, unconjugated and total bilirubin levels were measured in all the samples.
Assay of albumin: The bromo cresol green (BCG) method was employed in the determination of the concentrations of albumin in the serum samples[15].
Analysis of electrolyte concentrations: Chloride concentration was determined using the mercuric nitrate method while bicarbonate was assayed by back titration. Potassium and sodium were analyzed with the flame photometer[15].
Calculation of anion gap: Anion gap was calculated using the following equation:
Anion gap = Na+-(HCO3¯
+ Cl¯) |
RESULTS AND DISCUSSION
The conjugated, mean total and the unconjugated bilirubin levels of HIV patients ranged from 0.50-1.30, 1.07-2.10 and 0.01-1.50 mg/100 mL, respectively. For the non-infected control subjects, values of 0.50-1.66, 0.80-1.60 and 0.10-0.70 mg/100 mL, respectively were obtained for the conjugated, mean total and unconjugated bilirubin levels. The mean total and unconjugated bilirubin concentrations were higher in HIV-infected persons (Table 1). This agrees with Tietz[15] who observed that increase in unconjugated bilirubin may be from increase in formation of bilirubin, or as a result of a defect in its conjugation by the liver or by defective excretion.
| Table 1: | Bilirubin levels in HIV positive and HIV negative persons |
| Table 2: | Albumin concentrations in HIV positive and HIV negative persons |
In addition, liver disease can contribute to this as well.
| Table 3: | Electrolytes concentrations in HIV positive and HIV negative persons |
| Table 4: | Average values of anion gap between HIV infected and Non-infected |
Bilirubin on its own is not transported into the body because it is insoluble in water. In order to be transported into the body, bilirubin becomes attached to serum albumin.
The trend is the reverse in the case of total albumin. The mean total albumin (36.7 g L-1) is higher in the non-HIV infected subjects than in the infected (36.4 g L-1) (Table 2). Since serum protein gets depleted by HIV infection, there will be lower levels of albumin available for transport of bilirubin. Consequently, there will be a high amount of accumulated bilirubin that is untransported. Albumin also gets suppressed as a result of the suppressive effect of HIV and as a result of increased catabolism from cell damage.
The results revealed higher levels of Na+, K+, Cl-and HCO3¯ and these were more in the non-infected subjects than in HIV-positive subjects (Table 3). This is not unexpected since the HIV infected subjects were not down with AIDS yet. However the lower values for the infected suggest some degree of dehydration. Furthermore, the average values for anion gap were very high for both the infected and the uninfected (Table 4). Essentially the values were above the normal range of 10-12 mg L-1. The anion gap is used mainly in diagnosing different causes of metabolic acidosis some disease conditions like diabetes mellitus, lactic acidosis, chronic renal failure. Methanol or ethylene glycol poisoning also lead to increased anion gap. According to Tietz[15], the production or ingestion of organic acid toxins or renal failure cause increased anion gap.
ACKNOWLEDGMENTS
The author is grateful to Ikwuyatum Augustine and Njoku Prisca for enthusiastic assistance.