ASSESSMENT OF THE ALBUMIN, BI-CARBONATE AND CHLORIDE

IN PATIENTS WITH TUBERCULOSIS ATTENDING INFECTIOUS

DISEASE HOSPITAL, KANO

BY

OWOYEMI DAVID TEMITOPE

AHS/16/MDL/00451

A RESEARCH PROJECT SUBMITTED TO THE DEPARTMENT OF

MEDICAL LABORATORY SCIENCE, FACULTY OF ALLIED HEALTH
SCIENCES, COLLEGE OF HEALTH SCIENCES, BAYERO
UNIVERSITY KANO, IN PARTIAL FULFILLMENT OF THE
REQUIREMENT FOR THE AWARD OF BACHELOR OF MEDICAL
LABORATORY SCIENCE (B.MLS) DEGREE

SUPERVISOR: DR MOHAMMAD AHMAD BELLO

MAY, 2024

i
 DECLARATION

I, OWOYEMI DAVID TEMITOPE (AHS/16/MDL/00451) hereby declare that the project

entitled “ASSESSMENT OF THE ALBUMIN, BI-CARBONATE AND CHLORIDE IN

PATIENTS WITH TUBERCULOSIS ATTENDING INFECTIOUS DISEASE HOSPITAL,

KANO” is a bona fide work carried out by me under the guidance of Dr. Mohammad Ahmad

Bello of the Department of Medical Laboratory Sciences, Faculty of Allied Health Sciences,

College of Health Sciences, Bayero University, Kano.

……………………….. ……………………………
OWOYEMI DAVID TEMITOPE Date
(AHS/16/MDL/00451)

ii
 CERTIFICATION

This is to certify that the research work titled “Assessment of the albumin, bi-carbonate and

chloride in patients with tuberculosis attending infectious disease hospital,Kano” conducted

by OWOYEMI DAVID TEMITOPE (AHS/16/MDL/00451) to the Department of Medical

Laboratory Science is a bona fide work carried out by him under my supervision. The project

is new and has not been submitted to any other institution for the award of any degree or

diploma.

……………………………. ...........................................
External Supervisor. Date

………………………….... ..……………………………..
Internal Supervisor Date
Dr. Ahmad Isiyaku Adamu

…………………………… ……………………………
Supervisor Date
Dr. Mohammad Ahmad Bello

……………………………… …………………...........
Head of Department Date
Dr. Lawal Dahiru Rogo

iii
 DEDICATION

This project is dedicated to God almighty, my family and friends for their all-round support,

prayers and words of encouragement.

iv
 ACKNOWLEDGMENT

All the glory and praise be to God. I wish to express my profound gratitude to my ever

supporting supervisor (Dr. Mohammad Ahmad Bello) of the Department of Medical

Laboratory Science, Bayero University, Kano for his timelessly and tirelessly assistance by

ensuring that this project work meets its required top class standard.

My sincere gratitude also goes to the Head of Department Dr. Lawal Dahiru Rogo as well as

all the lecturers and staff of the Department of Medical Laboratory Science, Bayero

University, Kano for their encouragement and constructive corrections and suggestions during

the course of this research project.

Special thanks goes to Chemical Pathology Unit of the Department, and staff of Medical

Laboratory Science Department, Dr. Ahmed Isyaku, Dr. Suleiman Isah, Mal. Halliru Hassan

and Mal. Ado Idris for their word of encouragement and professional guidance towards

completion of this project work.

I wish to acknowledge the effort of Dr. Richard Owoyemi and Professor Azeez Akande and

family whose words of encouragement and professional guidance were a source of motivation

towards completion of this project work. Also, I acknowledge the staff at Aminu Kano

Teaching Hospital and Infectious Disease Hospital (Kano) for all their time and support

towards the success of this project.

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 TABLE OF CONTENTS

TITLE PAGE ……………………………………………………………………………………….... i

DECLARATION........................................................................................................................... ii
CERTIFICATION........................................................................................................................ iii
DEDICATION............................................................................................................................. iv
ACKNOWLEDGMENT................................................................................................................ v
TABLE OF CONTENTS.............................................................................................................. vi
LIST OF TABLES........................................................................................................................ vi
LIST OF APPENDICES........................................................................................................... vii
ABSTRACT.............................................................................................................................. viii
CHAPTER ONE............................................................................................................................1
1.0 INTRODUCTION.................................................................................................................... 1
1.1 Background Study................................................................................................................. 1
1.2 Statement Of The Research Problem.......................................................................................3
1.3 Justification.......................................................................................................................... 3
1.4. Aim And Objectives............................................................................................................. 3
1.4.1. Aim..............................................................................................................................3
1.4.2 Objectives......................................................................................................................4
1.5 Research Questions............................................................................................................... 4
1.6 Significance of The Study......................................................................................................... 4
1.7 Hypothesis............................................................................................................................5
CHAPTER TWO........................................................................................................................... 6
2.0. LITERATURE REVIEW......................................................................................................... 6
2.1 Tuberculosis..........................................................................................................................6
2.1.3 Tuberculosis and HIV..................................................................................................... 9
2.1.4 Host Immune Response.................................................................................................. 9
2.1.5 Signs and Symptoms of Tuberculosis............................................................................. 11
2.1.6 Epidemiology...............................................................................................................12
2.1.7 Tuberculosis Diagnosis................................................................................................. 13
2.2 ALBUMIN..........................................................................................................................15
2.2.1 Diagnostic Importance of Albumin................................................................................ 17
2.2.2 Serum Albumin as Nutritional Marker............................................................................18
2.2.3 Relationship of Albumin and TB....................................................................................19
2.3 ELECTROLYTE.....................................................................................................................20
2.3.1 Chloride........................................................................................................................... 21
2.3.1.1 Chloride Interpretations.............................................................................................. 22

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 2.3.2.2 Electrolyte Imbalance and Clinical Manifestations....................................................... 23
2.4 Bicarbonate......................................................................................................................... 25
2.4.1 Renal Regulation of Acid Base Balance......................................................................... 26
2.3.2 Acid Base Homeostasis................................................................................................. 27
2.3.3 Bicarbonate and Tuberculosis........................................................................................ 28
CHAPTER THREE...................................................................................................................... 29
3.0 MATERIALS AND METHOD.............................................................................................29
3.1 Study Area.......................................................................................................................... 29
3.2 Study Design.......................................................................................................................29
3.3 Study Population................................................................................................................. 29
3.3.1 Inclusion Criteria.............................................................................................................. 29
3.3.2 Exclusion Criteria............................................................................................................. 29
3.4 Ethical Clearance.................................................................................................................30
3.5. Consent..............................................................................................................................30
3.6 Sample Size Determination.................................................................................................. 30
3.9 Sample Collection............................................................................................................... 31
3.10 Sample Storage.................................................................................................................. 31
3.11 Sample Analysis.................................................................................................................31
3.13 Statistical Analysis............................................................................................................. 34
CHAPTER FOUR........................................................................................................................ 35
4.0 RESULTS...............................................................................................................................35
CHAPTER FIVE......................................................................................................................... 41
5.0 DISCUSSIONS, CONCLUSION AND RECOMMENDATIONS........................................... 41
5.1 Discussions......................................................................................................................... 41
5.2 Conclusions........................................................................................................................ 46
5.3 Recommendations............................................................................................................... 47
5.4 Limitations Of The Study..................................................................................................... 47
REFERENCES............................................................................................................................ 48
APPENDIX 1...............................................................................................................................57
consent Form............................................................................................................................57
APPENDIX II..............................................................................................................................58
research Questionnaire.............................................................................................................. 58
APPENDIX III.............................................................................................................................60
Ethical Approval....................................................................................................................... 60

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 LIST OF TABLES

Table 4.1 Characteristics Of The Study Population..………………………………………44

Table 4.2 Comparison Of Albumin, Bicarbonate And Chloride (Mean±Sd) of newly diagnosed,

on anti-TB drug treatment and non -TB control …………………………………………...47

Table 4.3 Correlation Of Severity Of Tuberculosis And Levels Of Biochemical Parameters

Albumin, Bicarbonate And Chloride Among Newly Diagnosed Patients. …………..........49

viii
 LIST OF APPENDICES

Appendix 1 Consent Form…………………………………………………………………67

Appendix II Research Questionnaire………………………………………………………68

Appendix III Ethical Approval……………………………………………………………..69

ix
 ABSTRACT

Tuberculosis is caused by Bacillus Mycobacterium Tuberculosis which can be latent or active

with varying degrees of disease severity. This study investigated the impact of tuberculosis
(TB) on metabolic and physiological functions by analyzing biochemical parameters among
tuberculosis patient who were newly diagnosed, on anti-tuberculosis drug treatment attending
infectious disease hospital Kano. A total of one hundred and twenty six (126) participants
were involved in the study of which forty two (42) were newly diagnosed tuberculosis patient
(33.3%), forty two (42) were patients on anti-tuberculosis treatment (33.3%) and forty two (42)
were non-TB control group (33.3%). Blood samples were collected, centrifuged and plasma
assayed for albumin using bromocresol green method, bicarbonate using van slyke method
and serum chloride using quantitative colorimetric method. The characteristics of the study
population, duration of TB diagnosis and treatment were explored. The data was analyzed
using a statistical package for social sciences package (SPSS). The results revealed significant
differences across the groups with control group exhibiting higher mean and statistically
significant values of serum albumin, bicarbonate, and chloride levels, highlighting the
systemic effects of TB on these biomarkers. The mean albumin level for newly diagnosed
individuals was 38.37±2.0 g/l, Patients under treatment had 42±2.44 g/l and non TB control
was 44.38±3.0 g/l. For bicarbonate, the level for newly diagnosed individuals was 21.3±1.42
mmol/L, patients under treatment was 23±1.53 mmol/L and non TB controls was 24.89±2.19
mmol/L. For chloride, the mean chloride level for newly diagnosed individuals was 96.91±4.9
mmol/L, patients under treatment was 98.7± 2.3mmol/L and non TB control was 102.25 ±2.0
mmol/L. Correlation analysis suggests a positive correlation between TB severity and serum
albumin levels (r-value - 0.471, p-value – 0.024) while negative associations are observed for
bicarbonate and chloride levels (r-value - -0.11, p-value – 0.471) and (r value- -0.024, p-value –
0.885) respectively. These findings emphasized the importance of monitoring these parameters
for early management of TB-related electrolytes derangement. Further research is
recommended to explore their clinical implications in TB diagnosis and treatment. .

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xi
 CHAPTER ONE

1.0 INTRODUCTION

1.1 Background Study

Tuberculosis (TB) remains a major public health concern worldwide, with 10.4 million

incident cases and 1.67 million deaths reported in 2016 (Liu et al., 2020). Tuberculosis is

caused by the Bacillus Mycobacterium tuberculosis, which is spread when people who are

sick with TB expel bacteria into the air (e.g. by coughing). About a quarter of the global

population is estimated to have been infected with TB, but most people will not go on to

develop TB disease and some will clear the infection. Of the total number of people who

develop TB each year, about 90% are adults, with more cases among men than women. The

disease typically affects the lungs (pulmonary TB) but can affect other sites as well

(Programme, 2022). Nigeria is ranked sixth nation with the highest number of TB cases

globally. The country, in 2021, contributed 4.4 percent to the total TB cases globally (Uduu,

2023). Mycobacterium tuberculosis, the causative agent of tuberculosis, possesses unique

characteristics that contribute to its virulence and resilience. One of its most distinctive

features is its complex cell wall structure (Daffé and Draper, 1997). Tuberculosis (TB)

infection occurs in several stages, with the progression influenced by the interaction between

Mycobacterium tuberculosis and the immune response of the host (Sterling, 2008).

Tuberculosis (TB) is primarily transmitted through the inhalation of airborne droplets

containing Mycobacterium tuberculosis. The bacteria are released into the air when an

infected person with active TB disease coughs, sneezes, speaks, or even sings. These droplets,

referred to as respiratory aerosols, can contain viable Mycobacterium tuberculosis bacteria

and remain suspended in the air for a period of time. When a susceptible person inhales these
1
contaminated droplets, they can become infected with TB. Additionally, close and prolonged

contact with an infectious individual increases the risk of transmission (Menzies et al.,1995).

Pulmonary Tuberculosis is a major cause of lung disability, surpassing all other lung diseases

combined. PTB can cause lung parenchymal destruction by upregulating several proteases

and dysregulating protease control, eventually resulting in lung remodelling. PTB-associated

lung remodelling provokes pulmonary sequelae characterized by bronchial and parenchymal

structural changes such as bronchovascular distortion, bronchiectasis, emphysematous

changes and fibrotic bands. These changes are irreversible and remain after PTB is cured. It is

therefore important to identify changes in lung function before and after completion of

treatment for PTB (Lee et al., 2015). Identified risk factors for tuberculosis (TB) infection and

progression include Individuals with compromised immune systems, such as those living with

HIV/AIDS, are at a significantly higher risk of developing active TB disease. The weakened

immune response makes it difficult to control latent TB infection, leading to the reactivation

of the bacteria (Uplekar et al., 2015). Malnutrition can weaken the immune system's ability to

respond effectively to TB infection, making individuals more susceptible to developing active

TB disease (Wagnew et al., 2023). Limited access to healthcare services, including diagnostics

and treatment, can delay the identification and management of TB cases, contributing to

disease spread and progression (Oxlade And Murray, 2012).

Notably, serum albumin levels, an important indicator of nutritional status, may be relevant to

TB monitoring, as strong evidence supports the existence of an inverse relationship between

serum albumin level and TB patient mortality. However, in spite of this association, serum

albumin level changes as a potential predictor of clinical anti-TB treatment response has not

yet been reported, prompting this study (Liu et al., 2020). Researches which focused on

electrolyte and acid-base disturbances in pediatric TB patients reveals that chloride levels can
2
be deranged in TB cases, contributing to metabolic acidosis (Krishnan et al., 2021). Other

studies investigated acid-base disorders in critically ill patients with TB. It emphasized the

role of metabolic acidosis and suggested that monitoring bicarbonate levels could be

important for patient management (Smith et al., 2020).

1.2 Statement Of The Research Problem

Tuberculosis (TB) predominantly affects the respiratory system but can have widespread

systemic effects and complications. Current diagnostic and prognostic markers for TB

primarily rely on microbiological and radiological assessments. However, there is a

significant knowledge gap regarding the potential role of serum albumin, bicarbonate, and

chloride levels in the context of TB, despite their critical importance in evaluating nutritional

status, acid-base balance, and electrolyte homeostasis. These serum markers can be influenced

by the systemic inflammation and metabolic changes associated with TB, yet their specific

contributions to TB diagnosis, disease severity assessment, and treatment outcomes remain

poorly understood (Jones and James, 2019; Smith et al., 2020).

1.3 Justification

Despite advancements in TB diagnosis and treatment, there remains a need for reliable and

non-invasive markers that can accurately reflect the disease status and therapeutic efficacy.

1.4. Aim And Objectives

1.4.1. Aim

The aim of the study was to assess the Albumin, Bicarbonate, Chloride level among

Pulmonary Tuberculosis patients in Infectious Disease Hospital (I.D.H) Kano, within Kano

metropolis.

3
1.4.2 Objectives

The objectives of the study are:

1. To determine the serum levels of albumin, bicarbonate, and chloride among TB patients

who are newly diagnosed, on anti-TB drug treatment and non -TB control.

2. To compare the serum level of albumin, bicarbonate and chloride between TB patients

who are newly diagnosed, on anti -TB drug treatment and non TB control.

3. To determine if there is a correlation between the severity of tuberculosis and the serum

levels of albumin, bicarbonate and chloride among newly diagnosed patients.

1.5 Research Questions

1. What are the baseline levels of albumin, bicarbonate, and chloride in newly diagnosed

tuberculosis patients?

Can the levels of albumin, bicarbonate, and chloride be used as potential biomarkers to

monitor the severity of tuberculosis infection?

1.6 Significance of The Study

Assessing serum albumin, bicarbonate, and chloride levels may offer additional insights into

the overall health status and prognosis of TB patients. These markers are routinely measured

in clinical practice, making their integration into TB management cost-effective and feasible.

Understanding their role in TB could contribute to early diagnosis, better risk stratification,

and more effective treatment strategies. This study may provide information on biochemical

markers among tuberculosis patients in our community which may help in the management of

TB patients and preventable measures against the risks.

4
1.7 Hypothesis

Null Hypothesis (H0):

There is no significant difference in the levels of albumin, bicarbonate, and chloride among

patients with tuberculosis compared to a control group without tuberculosis. Any observed

variations are due to random chance or factors unrelated to tuberculosis.

Alternate Hypothesis (H1):

There is a significant difference in the levels of albumin, bicarbonate, and chloride between

patients with tuberculosis and the control group. The observed variations are attributable to

the presence of tuberculosis, indicating potential alterations in these biomarkers in response to

the disease.

5
 CHAPTER TWO

2.0. LITERATURE REVIEW

2.1 Tuberculosis

Tuberculosis (TB), caused by Mycobacterium tuberculosis, remains a persistent global health

challenge, affecting millions of individuals each year. The epidemiology of TB encompasses a

complex interplay of factors, including prevalence, incidence, geographical distribution, and

populations disproportionately burdened by the disease (Dheda et al., 2014). More people

have died from tuberculosis (TB) than from any other pathogen over the previous ten years,

with an average of over 1.65 million deaths annually between 2010 and 2019. Of these deaths,

over 363,000 were caused by HIV/AIDS (Dodd et al. 2023).

HIV infection significantly affects the risk of tuberculosis (TB) in individuals: the chance of

dying from tuberculosis increases sharply with declining CD4 cell counts, as does the risk of

getting TB in those who do not receive treatment (Bruchfeld et al., 2015). When used for

treating persons living with HIV (PLHIV), antiretroviral medication (ART) lowers the

incidence and death from TB (although not to the extent seen in HIV-uninfected individuals)

(Liu et al., 2015). As a result, in environments where there are widespread HIV epidemics,

there have been dynamic TB epidemics, with sharp rises in TB notifications fueled by drops

in the mean CD4 cell counts of persons living with HIV (PLHIV) (Dodd et al., 2023).

2.1.1 Transmission

Tuberculosis is transmitted through aerosol droplets containing Mycobacterium tuberculosis

(M. tb), expelled by active TB patients during activities such as coughing, sneezing, or talking

(Patterson and Wood, 2019). Upon inhalation by a new host, the TB bacteria traverse the

6
respiratory tract and reach the lungs (Bussi and Gutierrez, 2019). The host's innate immune

system responds by involving alveolar macrophages. If the macrophages fail to control the

infection, the bacilli multiply intracellularly, get released, and are phagocytosed by other

macrophages, perpetuating the cycle (Schorey and Schlesinger, 2016). Subsequently,

lymphocytes are recruited to the infection site, initiating a cell-mediated immune response.

Asymptomatic at this stage, the host may eliminate the TB bacteria or enter latency within a

granuloma. In cases of impaired immunity, the disease progresses to active TB with clinical

symptoms (Carabalí-Isajar et al., 2023). These minuscule droplets can remain air airborne

for minutes to hours after expectoration (Gemma, 2011). The number of bacilli in the droplets,

virulence of the bacilli, exposure of the bacilli to UV light degree of ventilation, and

occasions for aerosolization all influence transmission (David et al., 2000.)

2.1.2 Pathophysiology

The pathophysiology of pulmonary TB unfolds as M. tb enters the lungs, ingested by

macrophages, leading to the recruitment of immune cells and the formation of

granulomas—the hallmark of TB (Patterson and Wood, 2019). In healthy individuals, latent

infection occurs, but the risk of reactivation persists. Foamy macrophages release lipids upon

necrosis, resulting in caseation (cheese-like structure) (Patterson and Wood, 2019). Caseum

compromises the granuloma's integrity, allowing bacilli to seep into the caseum layer

(Alsayed and Gunosewoyo, 2023). Reactivation leads to M. tb proliferation, causing

granuloma rupture, dissemination of bacteria into airways, and expectoration as contagious

aerosol droplets, restarting the cycle and infecting others (Yang et al., 2023).

The pathophysiology of tuberculosis can be broken down into four distinct phases. The

mycobacteria are inhaled, after which bacteria engage with the resident's macrophages via

cellular receptors and internalize themselves. The contagious droplets spread throughout the
7
respiratory tract after inhalation. Most of the bacilli are lodged in the upper portion of the

airways, where goblet cells that secrete mucus continuously beat the mucus and the particles it

has trapped upward in order to remove them. For the majority of people exposed to

tuberculosis, this mechanism offers the body a first line of defense against infection (friend et

al., 2003). Alveolar macrophages rapidly surround and destroy bacteria in the droplets that

make it past the mucociliary pathway and into the alveoli (John et al., 2018). As the next line

of defence, macrophages are the most prevalent immune effector cells found in alveolar

spaces. They are a component of the innate immune system and give the body the chance to

eliminate invasive mycobacteria and stop infection (Korf et al., 2006).

2.1.2.1 Dissemination Beyond the Lungs:

Hematogenous Spread: In certain cases, M. tuberculosis may disseminate beyond the lungs

through the bloodstream. The bacterium can infect other organs, including the kidneys, bones,

and central nervous system (Moule and Cirillo, 2020).

Risk Factors for Dissemination: Factors such as immunosuppression, co-infection with HIV,

and in adequate treatment contribute to an increased risk of disseminated TB (Moule and

Cirillo, 2020).

2.1.2.2 Challenges in Diagnosis and Treatment:

Extra pulmonary TB Diagnosis: Disseminated TB often presents as extra pulmonary

manifestations, posing challenges in diagnosis. Obtaining specimens for culture and

molecular testing from affected organs may be necessary (Gambhir et al., 2017).

8
Complex Treatment Protocols: Disseminated TB requires more prolonged and comprehensive

treatment regimens. The use of multiple drugs and careful management are essential to

prevent relapse and the emergence of drug-resistant strains (Gambhir et al., 2017).

2.1.3 Tuberculosis and HIV

The relationship between tuberculosis (TB) and human immunodeficiency virus (HIV)

infection is complex. HIV infection impairs the immune system and increases vulnerability to

tuberculosis in the particular patient (Datiko et al., 2008). HIV increases the chance of latent

TB infection reactivation, reinfection, and progression to active illness. It also changes the

clinical presentation of tuberculosis, complicates follow-up, and impairs responsiveness to

anti-TB treatment (Bruchfeld et al., 2015). In the absence of HIV infection, the chance of

having active TB in a population is roughly 10%. It, however multiplies tenfold in

HIV-infected persons. As a result, the number of TB cases has skyrocketed (Datiko et al.,

2008). The proportion of HIV co-infected TB with smear-negative pulmonary TB (PTB) and

extrapulmonary TB (EPTB) is higher (Tiamiyu et al., 2020)

2.1.4 Host Immune Response

Recognition by Innate Immunity

Macrophage Activation: Alveolar macrophages play a pivotal role as the first responders to

Myobacterium tuberculosis. Upon recognition, macrophages attempt to engulf and digest the

bacteria through phagocytosis (Chaplin, 2010).

Cytokine Release: The infected macrophages release pro-inflammatory cytokines, including

interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-α), signaling the activation of the

immune response (Chaplin, 2010).

2.1.4.2 Granuloma Formation

9
Activation of Adaptive Immunity: The host's adaptive immune response is activated,

involving T lymphocytes (CD4+ and CD8+), which migrate to the site of infection (Bold and

Ernst, 2009).

Granuloma Initiation: Granulomas, organized structures comprising immune cells, form

around infected macrophages. These granulomas aim to contain the infection and limit

bacterial dissemination (Bold and Ernst, 2009)

Modulation of Host Immune Responses

Interference with Cytokine Signaling: Mycobacterium tuberculosis can manipulate host

cytokine responses, favoring the production of anti-inflammatory cytokines like interleukin-10

(IL-10) that dampen the immune response (Zhai et al., 2019).

Induction of Immune Tolerance: The bacterium may induce immune tolerance, allowing it to

persist within host cells without eliciting a robust immune reaction (Zhai et al., 2019).

Latency and Reactivation

Establishment of Latency: Mycobacterium tuberculosis can enter a dormant state within

granulomas, leading to latent TB infection. During latency, the bacterium evades immune

detection (Flynn and Chan, 2001).

Reactivation: In individuals with compromised immunity, latent TB can reactivate, leading to

active disease. The interplay involves the bacteria overcoming immune containment

mechanisms (Flynn and Chan, 2001).

10
Role of CD4+ T Cells

Critical Role in Immunity: CD4+ T cells are crucial for coordinating the immune response

against M. tuberculosis. They release interferon-gamma (IFN-γ), activating macrophages to

enhance bacterial killing (Nunes-Alves et al., 2014).

Targeting by the Bacterium M. tuberculosis has developed mechanisms to interfere with

CD4+ T cell function, impairing their ability to control bacterial growth effectively

(Nunes-Alves et al., 2014).

Escape from Granulomas

Intricate Granuloma Dynamics: Mycobacterium tuberculosis can adapt to survive within

granulomas, exploiting the complex dynamics of these structures to persist for extended

periods (Ehlers and Schaible, 2013).

Disruption and Escape: Under certain conditions, M. tuberculosis may disrupt granulomas,

facilitating its escape and dissemination to other tissues (Ehlers and Schaible, 2013).

2.1.5 Signs and Symptoms of Tuberculosis

Depends on where in the body the TB bacteria are growing. TB bacteria usually grow in the

lungs (pulmonary TB). TB disease in the lungs may cause symptoms such as a

1. bad cough that lasts 3 weeks or longer

2. pain in the chest

3. coughing up blood or sputum (phlegm from deep inside the lungs)

Other symptoms of TB disease are:-

1. weakness or fatigue
2. weight loss

11
3. no appetite
4. chills
5. fever
6. Sweating at night
Symptoms of TB disease in other parts of the body depend on the area affected.

People who have latent TB infection

1. Do not feel sick,

2. do not have any symptoms, and Cannot spread TB

The usual symptoms that occur with an active TB infection are:

1. a generalized tiredness or weakness

2. weight loss
3. fever and night sweats.
If the infection in the lung worsens, then further serious symptoms can include:

1. coughing
2. chest pain
3. clothing up of sputum (material from the lungs) and/or blood (hemoptysis), and
4. Shortness of breath.

If the infection spreads beyond the lungs, the symptoms will depend on the infected organ or

region.

2.1.6 Epidemiology

Despite the fact that tuberculosis (TB) is a curable infectious disease, an estimated 1.3 million

individuals died from the disease in 2012. One of the primary causes is that TB continues to

develop antibiotic resistance. Standard treatment based on the two most powerful medications,

isoniazid and rifampicin, leads in good cure rates for individuals with drug-susceptible TB.

Patients infected with isoniazid and rifampicin-resistant strains of tuberculosis, known as

multi drug-resistant (MDR) TB, are nearly incurable with normal first-line treatment (Seung

12
et al., 2015). One of the most pressing and hardest concerns facing global TB control is the

growth of drug-resistant tuberculosis (TB). Patients infected with isoniazid and

rifampicin-resistant strains of tuberculosis, known as multi drug-resistant (MDR) TB, are

nearly incurable with routine first-line treatment (Seung et al., 2015).

MDR-TB caused roughly 450,000 new cases and 170,000 deaths in 2012. Extensively

drug-resistant tuberculosis (XDR) refers to MDR-TB strains that are resistant to

fluoroquinolones and second-line injectable medicines. The main causes of the spread of

resistant tuberculosis include inadequate medical systems, amplification of resistance patterns

through inappropriate treatment, and transmission in communities and facilities. Although

individuals with MDR and XDR strains provide a challenging therapeutic challenge, cure is

usually attainable with early detection of resistance and the adoption of a properly tailored

regimen. Community-based programs can improve treatment outcomes by allowing patients

to be treated in their homes and eliminating socioeconomic barriers to adherence (Seung et al.,

2015).

2.1.7 Tuberculosis Diagnosis

Testing for TB

There are two types of tests for detecting TB infection: the TB skin test and the TB blood test.

The choice of which test to use depends on factors such as the purpose of testing, test

availability, and cost, and should be determined by a person's healthcare provider.

Tuberculin Skin Test (TST)

The Mantoux tuberculin skin test is employed to ascertain if an individual has been exposed

to TB bacteria. The TST outcome is based on the size of the raised, firm area or swelling,

considering the person's risk of TB infection and the potential progression to TB disease.
13
Positive Test:

Indicates prior TB bacterial infection. Further tests are required to ascertain if it's latent TB

infection or TB disease, with subsequent treatment provided by a healthcare professional

(Cole et al., 1998).

Negative Test:

A negative result suggests the person's body did not react to the test, making latent TB

infection or TB disease unlikely.

TB Blood Tests

Which is an Interferon Gamma Release Assay (IGRA)

An IGRA is a blood test that can determine if a person has been infected with TB bacteria. An

IGRA measures how strong a person’s immune system reacts to TB bacteria by testing the

person’s blood in a laboratory. Two IGRAs are approved by the U.S. Food and Drug

Administration (FDA) and are available in the United States:

1. QuantiFERON®–TB Gold In-Tube test (QFT–GIT)

2. T–SPOT®.TB test (T–Spot)

Positive IGRA result:

A positive IGRA indicates prior TB bacterial infection. Additional tests are necessary to

determine latent TB infection or TB disease, and subsequent treatment is administered by a

healthcare professional.

14
Negative IGRA:

A negative result means the person's blood did not react to the test, making latent TB infection

or TB disease unlikely.

Diagnosing Latent TB Infection or TB Disease:

If an individual tests positive for TB bacteria, further assessments are conducted to determine

if TB disease is present. Diagnosis involves medical history, physical examination, chest x-ray,

and Microscopic analysis. TB disease is treated with a prescribed regimen of drugs

recommended by a healthcare provider. If TB bacteria are detected, but no active TB disease

is present, the diagnosis is latent TB infection. The decision to treat latent TB infection is

based on the individual's risk of developing TB disease (Vitoria et al., 2009).

2.1.8 Treatment

I. Treatment for latent Tuberculosis, isonaizid which is the most strongly common therapy

for latent TB, Rifampin which are also ATT-drugs

II. Treatment for active TB Ethambutol, isoniazid, Pyrazinamide, Rifampin.

2.2 ALBUMIN

Albumin (ALB), constituting the predominant protein in human plasma at approximately 4.0

g/dL, is produced in the liver as an extensive 585-amino acid peptide with a half-life of

roughly 25 days. Its considerable versatility and wide range of characteristics, including

binding and transport functions, osmotic regulation, as well as antioxidant and buffering

capabilities, have attracted substantial scientific interest throughout the years (Gremese et al.,

2023). Albumin (ALB) has a molecular weight of approximately 66 kDa and a typical

concentration range of 35–45 g/L (around 0.6 mM). Synthesized exclusively in the liver, it
15
emerges as a single polypeptide chain containing 585 amino acid residues, with a total of 35

cysteine (Cys) residues. Out of these, 34 Cys residues partake in the creation of 17

intramolecular disulfide bridges, shaping its distinct heart-shaped tertiary structure. The

remaining single Cys residue at position 34 (Cys34) is free and exhibits redox activity (Tabata

et al., 2021). ALB's primary role in the circulatory system revolves around providing colloidal

osmotic pressure, contributing to approximately 80% of the total colloidal osmotic pressure

due to its abundance and relatively lower molecular weight. Conversely, the synthesis of ALB

in the liver is responsive to colloidal osmotic pressure, regulated by a feedback mechanism,

thus ensuring homeostasis (De León et al., 1982).

Serum ALB plays a pivotal role in maintaining colloidal osmotic pressure homeostasis.

Another significant function of serum ALB is its role as a carrier for a variety of endogenous

and exogenous ligands, encompassing compounds like long-chain fatty acids, bilirubin, metal

ions (zinc, copper, calcium, etc.), and exogenous drug substances such as warfarin and

ibuprofen. With multiple ligand binding pockets and a relatively extended half-life in

circulation (approximately 15 days), serum ALB emerges as an appealing vehicle for

innovative drug delivery systems. Additionally, it actively contributes to redox homeostasis in

circulation (Levitt and Levitt, 2016).

Lastly, serum ALB levels have conventionally served as a biomarker for assessing protein

nutritional status. A level below 35 g/L is defined as hypoalbuminemia. However,

contemporary perspectives regard low serum ALB levels more as a risk factor and predictor

of morbidity and mortality, irrespective of the associated diseases (Keller, 2019).

16
2.2.1 Diagnostic Importance of Albumin

Hypoalbuminemia, defined as a serum albumin concentration below 3.5 g/dl, is prevalent in

hospitalized adult patients, particularly exceeding 70% in the elderly. It emerges as an

important prognostic factor in acute illness, influencing outcomes such as death, length of stay,

and readmission. Patients with albumin levels below 3.5 g/dl exhibit significantly higher

in-hospital mortality (14% vs. 4%) and increased likelihood of prolonged hospitalization and

readmission (Gounden, 2023). Hypoalbuminemia can stem from various clinical conditions,

including impaired hepatic synthesis in liver cirrhosis, increased catabolism in septic patients,

and leakage in malabsorption or nephrotic syndromes. The strong association between serum

albumin and inflammation is evident, where inflammatory processes enhance capillary

permeability, leading to serum albumin leakage (Soeters et al., 2018). Low serum albumin

levels continue to be vital predictors of morbidity and mortality even post-hospital discharge.

Meta-analyses demonstrate that each 10 g/L decrease in serum albumin is associated with

increased odds of mortality (137%), morbidity (89%), and prolonged ICU stay (28%).

Prospective studies link hypoalbuminemia to systemic inflammation and nutritional risk,

independently predicting 30-day mortality (Vincent et al., 2003). Serum albumin levels

significantly impact cardiovascular (CV) pathophysiology, influencing oncotic, antioxidant,

anti-inflammatory, and anticoagulant actions. Hypoalbuminemia prevalence varies across CV

diseases, and it consistently emerges as an independent poor prognostic factor. Lower albumin

levels correlate with increased risks of ischemic heart disease, myocardial infarction, stroke,

and peripheral artery disease (Gounden, 2023).

In patients with CKD, serum albumin serves as a risk-adjusted predictor of progression to

end-stage renal disease (ESRD) and all-cause mortality. Hypoalbuminemia in CKD often

reflects protein-energy wasting, and its assessment can predict atherosclerotic vascular disease

17
beyond traditional risk factors. The protective role of albumin is highlighted in conditions like

IgA nephropathy, where oxidative stress is a key pathogenic factor, emphasizing albumin's

antioxidant capabilities (Gounden, 2023). Despite debates surrounding the clinical efficacy of

albumin supplementation, addressing underlying conditions leading to hypoalbuminemia

remains a priority in managing various diseases. Serum albumin concentration proves to be a

valuable tool for risk stratification and prognosis in emergencies, cardiovascular diseases, and

renal disorders. Its multifaceted roles in maintaining homeostasis, combating inflammation,

and influencing pharmacokinetics underscore its diagnostic importance across diverse clinical

contexts (Soeters et al., 2018).

Routine measurements of prealbumin have been encouraged in various clinical settings, such

as medical intensive care units and surgical patients. The C-reactive protein/prealbumin ratio

proves useful in predicting outcomes in different scenarios. However, prealbumin's sensitivity

to physiological stress, infection, and other factors requires cautious interpretation (Vincent et

al., 2003). Several studies highlight the predictive role of albumin and prealbumin in

prognosis and survival across diverse clinical conditions, including gastric cancer, lung cancer,

and cardiovascular diseases. However, caution is advised in the interpretation, as serum

visceral proteins may not be predictive in specific cases, such as otherwise healthy individuals

severely nutrient-deprived due to reasons like anorexia nervosa (Soeters et al., 2018).

2.2.2 Serum Albumin as Nutritional Marker

Diagnosing malnutrition is challenging due to the lack of a unified definition and standardized

screening methods. Malnutrition often results from a mismatch between nutritional

requirements and intake, exacerbated by disease-related inflammation. This inflammation,

provoking anorexia and altering metabolism, complicates the interplay between nutritional

needs and the actual intake (Cederholm et al., 2019). A review explores laboratory biomarkers'
18
role in diagnosing malnutrition, assessing nutritional risk, and monitoring interventions. A

consensus committee proposed sub-definitions based on energy intake, weight loss, body fat,

muscle mass, fluid accumulation, and grip strength, with caution regarding biomarkers,

particularly serum visceral proteins (Bharadwaj et al., 2016).

Albumin, the most abundant protein in human serum, has been traditionally used as an

indicator of malnutrition in clinically stable conditions. Its concentrations decrease with age

but are not inherently causative of hypoalbuminemia. The relationship between serum

albumin and all-cause mortality is evident in elderly subjects. In patients with hip fractures,

lower albumin levels correlate with post-operative complications and increased mortality.

Despite criticisms related to specificity and a long half-life, albumin remains a valuable

predictor in various clinical conditions (Bharadwaj et al., 2016). Pre albumin, or transthyretin,

is a transport protein synthesized by the liver and catabolized by the kidneys. Its

concentrations less than 10 mg/dl are associated with malnutrition. Unlike albumin,

prealbumin's shorter half-life makes it a favorable marker for acute changes in nutritional

status. It has been suggested as a useful marker during refeeding and in the elderly. An

algorithm incorporating prealbumin helps stratify patients by risk, indicating failure of

nutritional therapy with specific criteria. However, prealbumin levels may be influenced by

factors like renal dysfunction, corticosteroid therapy, or dehydration (Keller, 2019).

2.2.3 Relationship of Albumin and TB

In tuberculosis (TB) patients, serum albumin plays a crucial role in assessing nutritional status.

TB is known to impact nutritional health, leading to weight loss and malnutrition due to

factors such as reduced appetite, metabolic changes, and systemic inflammation. TB often

results in a decline in nutritional status due to decreased food intake, altered metabolism, and

the inflammatory response triggered by the infection (Sari et al., 2019). Serum albumin levels
19
are commonly used to evaluate nutritional status. In TB patients, lower serum albumin levels

may indicate malnutrition and a compromised nutritional state. Inflammatory processes

associated with TB can affect albumin synthesis and lead to decreased levels. Elevated levels

of cytokines, such as IL-6 and TNF-alpha, contribute to the reduction in serum albumin.

Additionally, serum albumin levels have been negatively correlated with C-reactive protein

(CRP) levels, indicating its association with disease severity and inflammation (Niki et al.,

2020).

Monitoring serum albumin levels in TB patients is clinically significant. It serves as a

valuable marker for healthcare providers to assess the severity of malnutrition, especially

when accompanied by other nutritional assessment tools (Alvarez-Uria et al., 2013). Studies

have shown that nutritional status, as indicated by serum albumin levels, can influence the

response to tuberculosis treatment. Patients with better nutritional status, reflected by higher

serum albumin levels, tend to show more rapid clearance of bacteria and radiographic changes,

in addition to greater weight gain (Gupta et al., 2009). Low serum albumin levels in TB

patients may have predictive value for clinical outcomes, including response to treatment and

overall well-being. It can help identify individuals at higher risk for complications (Gupta et

al., 2009). Recognizing the relationship between serum albumin and nutritional status in TB

patients has implications for their management. Nutritional support and interventions to

address malnutrition become essential components of comprehensive TB care (Samuel et al.,

2016).

2.3 ELECTROLYTE

Electrolytes are essential for basic life functioning, such as maintaining electrical neutrality in

cells, generating and conducting action potentials in the nerves and muscles. Sodium,

20
potassium, and chloride are the significant electrolytes along with magnesium, calcium,

phosphate, and bicarbonates. Electrolytes come from our food and fluids (Shrimanker and

Bhattaria, 2022). These electrolytes can have an imbalance, leading to either high or low levels.

High or low level of electrolytes disrupt normal bodily functions and can lead to even

life-threatening complications (Shrimanker and Bhattaria, 2022). The primary route for ion

excretion is through the kidneys, with smaller quantities expelled through sweat and feces.

Profuse sweating can lead to substantial losses, particularly of sodium and chloride. Intense

vomiting or diarrhea results in the depletion of chloride and bicarbonate ions. The body

maintains ion levels in the extracellular fluid (ECF) by modulating respiratory and renal

functions (Biga, 2019).

2.3.1 Chloride

Chloride stands out as the primary anion within the extracellular space, upholding cellular

integrity by influencing osmotic pressure, water balance, and acid-base equilibrium. The daily

adult requirement for chloride is 80-120 mEq/L as NaCl . Generally, chloride reabsorption

mirrors sodium reabsorption. In the kidney tubules, approximately 140 meq of sodium is

present in 1 liter of filtrate. To maintain electro-neutrality, a similar quantity of anions, mainly

chloride (110 meq), and bicarbonate (24 meq), should be present. Roughly 65-70% of the total

filtered chloride undergoes reabsorption, closely aligning with the fractional reabsorption of

sodium and water (Molnar, 2015). The primary mode of chloride transportation involves

electro-neutral cation-Cl co-transporters, ensuring chloride consistently accompanies cations,

predominantly sodium and potassium, across cellular membranes (Chew et al., 2019). These

co-transporters, categorized as thiazide-sensitive Na-Cl co-transporter, loop diuretic-sensitive

Na-K-2Cl co-transporters, and K-Cl co-transporters, are transmembrane proteins. They play

pivotal roles in various physiological activities, including transepithelial ion absorption and

21
secretion, cell volume regulation, and maintaining intracellular chloride concentration in

relation to its electrochemical potential equilibrium. Furthermore, members of this protein

family significantly contribute to cardiovascular and neuronal pharmacology and

pathophysiology (Yurinskaya and Aa, 2021).

Reference

Normal findings

* Adult/elderly: 98-106 mEq/L or 98-106 mmol/L (SI units)

* Child: 90-110 mEq/L

* Newborn: 96-106 mEq/L

* Premature infant: 95-110 mEq/L (Kamel, G. 2020)

2.3.1.1 Chloride Interpretations

Chloride, as an extracellular fluid anion, plays a pivotal role in preserving a balanced

acid-base equilibrium and, in conjunction with sodium, ensures water balance and serum

osmolality. Predominantly present as sodium chloride or hydrochloric acid, chloride levels are

integral in reflecting variations in sodium, unless encountered in acid-base disorders, where

changes in chloride operate independently of sodium (Chew et al., 2019). Elevated serum

chloride, termed hyperchloremia, manifests in diverse conditions such as renal failure,

nephrotic syndrome, renal tubular acidosis, dehydration, saline overuse, hyperparathyroidism,

diabetes insipidus, metabolic acidosis from diarrhea, respiratory alkalosis,

hyperadrenocorticism, and certain drug usage (Chew et al., 2019). Conversely, reduced serum

chloride, known as hypochloremia, is associated with conditions like vomiting, diarrhea,

gastrointestinal suction, renal failure coupled with salt deprivation, diuretic overuse, chronic
22
respiratory acidosis, diabetic ketoacidosis, excessive sweating, syndrome of inappropriate

antidiuretic hormone excretion (SIADH), salt-losing nephropathy, acute intermittent

porphyria, water intoxication, expansion of extracellular fluid volume, adrenal insufficiency,

hyperaldosteronism, metabolic alkalosis, and specific drug administration (Sharma, 2023).

Serum chloride proves valuable in evaluating normal or high anion gap metabolic acidosis.

Additionally, it aids in distinguishing between hypercalcemia linked to primary

hyperparathyroidism and hypercalcemia related to malignancy, where elevated and low

chloride levels respectively play a crucial role . In clinical assessments, serum chloride is

commonly utilized alongside sodium, potassium, and CO2 to comprehensively evaluate

electrolytes, acid-base balance, and water equilibrium (Lind and Ljunghall, 2009).

2.3.2.2 Electrolyte Imbalance and Clinical Manifestations

Electrolyte Imbalances in TB:

Electrolyte imbalances have been recognized as potential contributors to the clinical

complexity of TB. While sodium and potassium imbalances have been studied extensively,

recent attention has turned to serum chloride levels as a less-explored yet potentially

significant electrolyte in the context of TB. TB, characterized by its systemic involvement,

has the potential to disrupt electrolyte equilibrium, and understanding these disturbances is

vital for a comprehensive understanding of the disease (Lind and Ljunghall, 2009)

Physiological Significance of Chloride:

Chloride, a major extracellular anion, plays a pivotal role in maintaining acid-base balance,

osmotic pressure, and electrical neutrality in bodily fluids. It is actively involved in various

physiological processes, including the regulation of cell volume and the formation of stomach

acid. Given its widespread influence, alterations in serum chloride levels may have cascading

23
effects on multiple organ systems, influencing the clinical presentation of TB (Sharma et al.,

2023).

Association with Clinical Manifestations:

Studies examining the link between serum chloride alterations and the clinical manifestations

of TB have revealed intriguing associations. Chloride imbalances may contribute to the

manifestation of symptoms such as fatigue, weakness, and muscle cramps—common

complaints in TB patients. Moreover, the potential impact on acid-base balance may influence

respiratory symptoms, adding another layer to the complex interplay between electrolyte

disturbances and clinical presentation (Bohn and De Morais, 2017)

Systemic Effects on TB Symptoms:

The systemic effects of electrolyte imbalances on TB symptoms extend beyond mere

correlations. Electrolytes, including chloride, are integral to immune function, and their

disturbances may influence the host response to Mycobacterium tuberculosis. Immune

modulation, oxidative stress, and inflammatory processes—all influenced by

electrolytes—have been implicated in the clinical course of TB. Understanding the systemic

effects provides a more nuanced perspective on the disease's pathophysiology (Luies and Du

Preez, 2020).

Clinical Implications and Diagnostic Considerations:

Recognizing the association between electrolyte imbalances, particularly serum chloride

alterations, and TB symptoms holds clinical implications. These insights may guide clinicians

in considering electrolyte assessments as part of the diagnostic workup for TB, especially in

cases with atypical or severe presentations. Additionally, monitoring electrolyte status during

24
treatment could contribute to a more comprehensive approach, potentially aiding in the

identification of treatment-related complications (Luies and Du Preez, 2020).

Hyperchloremic acidosis

Hyperchloremic metabolic acidosis is a health issue caused by the loss of bicarbonate, not the

production or retention of acid. This bicarbonate loss happens in different ways: through

gastrointestinal (GI) issues like severe diarrhea, pancreatic fistula, suctioning from the

duodenum via a tube, and prolonged use of laxatives. Renal causes involve proximal and

distal renal tubular acidosis, as well as the extended use of carbonic anhydrase inhibitors.

Exogenous factors include consuming acids like ammonium chloride and hydrochloric acid,

along with receiving volume resuscitation using 0.9% saline (Shrimanker, 2023).

2.4 Bicarbonate

The bicarbonate ion (HCO3-) is central to the regulation of acid-base balance in the human

body. Originating primarily from the dissociation of carbonic acid (H2CO3), serum

bicarbonate acts as a critical buffer, helping to neutralize excess hydrogen ions (H+) and

maintain the blood's pH within a narrow, physiologically optimal range. This homeostatic

mechanism is essential for preserving enzymatic function, cellular integrity, and overall

metabolic stability (Hopkins, 2022). Serum bicarbonate levels are routinely assessed in

clinical settings, offering valuable insights into the acid-base status of individuals. Normal

levels typically fall within the range of 22 to 28 milliequivalents per liter (mEq/L). Deviations

from this range can indicate underlying metabolic disorders or systemic disturbances,

prompting further investigation (Raphael et al., 2016). Aberrations in serum bicarbonate levels

are often associated with metabolic acidosis or alkalosis. In metabolic acidosis, decreased

bicarbonate levels are observed, contributing to an imbalance in the acid-base equilibrium.

25
Conversely, metabolic alkalosis is characterized by elevated bicarbonate levels, shifting the

pH towards the alkaline side. Understanding these alterations is crucial in diagnosing and

managing various medical conditions, such as renal dysfunction, diabetic ketoacidosis, or

prolonged vomiting (Burger, 2023).

2.4.1 Renal Regulation of Acid Base Balance

The regulation of the body's acid-base balance by the kidneys primarily focuses on the

metabolic aspect of the buffering system. While the respiratory system, along with breathing

centers in the brain, manages blood levels of carbonic acid by controlling CO2 exhalation, the

renal system oversees blood bicarbonate levels (Quade et al., 2021). A reduction in blood

bicarbonate can occur due to carbonic anhydrase inhibition by specific diuretics or excessive

bicarbonate loss through diarrhea. Individuals with Addison’s disease, characterized by

chronic adrenal insufficiency, and those with renal damage like chronic nephritis typically

exhibit lower blood bicarbonate levels due to reduced aldosterone or kidney function.

Additionally, individuals with unmanaged diabetes mellitus may experience low bicarbonate

levels, as elevated ketone levels in the filtrate bind to bicarbonate, hindering its conservation

(Biga, 2019).

Almost all physiological systems in the body rely on proper acid-base balance to function

normally. The intracellular and interstitial pH values are greatly influenced by arterial blood

pH, which ranges between 7.35 and 7.45 under normal physiological conditions. When pH

falls outside of its usual range, pH-dependent enzymes and membrane transport proteins may

not function properly, and metabolic pathways may be harmed (Adeva-Andany et al., 2014).

Acidemia, defined as an arterial pH less than 7.35, can induce a number of problems,

including arterial vasodilation, insulin resistance, impaired immunological function, and

26
decreased neuronal excitability. Alkalemia, defined as an arterial pH more than 7.45, can

potentially induce a variety of problems, including decreased myocardial blood flow and

seizures. Thus, it is imperative that the value of blood pH is tightly controlled (Quade et al.,

2021).

2.3.2 Acid Base Homeostasis

The preservation of blood pH despite a daily acid load of approximately 40–70 mEq H+ from

diet and metabolism, known as net endogenous acid production (NEAP), requires robust

homeostatic mechanisms (Adeva-Andany et al., 2014). The regulation of blood pH, and

consequently the entire extracellular fluid compartment, relies on the dynamic interplay

between two systems: (i) the urinary system, which governs the blood bicarbonate

concentration ([HCO3 −]), and (ii) the neuro-respiratory systems, which oversee the partial

pressure of CO2 (pCO2). The kidneys play a crucial role in generating, releasing, and

recycling HCO3 − into circulation, while the lungs expel CO2, regulated by chemosensitive

neural circuitry (Brinkman, 2023). The extracellular fluid compartment is fortified against pH

changes by various buffer systems, with the CO2/HCO3 − buffer system being the most

potent. Its effectiveness is attributed to the body acting as an open system for CO2, allowing

its escape. A notable feature of the CO2/HCO3 − buffer system is the initial slow reaction in

the interconversion between CO2 and HCO3 − (CO2 + H2O ⇌ H2CO3 ⇌ HCO3 −+ H+),

which requires catalysis by a carbonic anhydrase (CA) enzyme for efficient buffering

(Adeva-Andany et al., 2014).

Achieving stability in whole-body acid-base homeostasis relies on the body functioning as an

open CO2/HCO3− buffer system. The regulation of blood/extracellular pH within a precise

physiological range is contingent upon the dual and independent functions of both the kidneys

and the lungs. The kidneys influence blood [HCO3−] through the adjustment of urine acid
27
secretion, while the lungs impact blood pCO2 by regulating ventilation (Adeva-Andany et al.,

2014).

2.3.3 Bicarbonate and Tuberculosis

Tuberculosis, marked by a complex interplay of inflammatory responses and immune evasion

strategies by the pathogen, may impact the acid-base balance in the host. Disruptions in this

tightly regulated equilibrium can manifest as metabolic acidosis, and bicarbonate levels may

serve as a dynamic marker reflecting these alterations. Monitoring bicarbonate alongside

traditional clinical parameters could enhance the diagnostic accuracy and depth of

understanding in tuberculosis cases (De Martino et al., 2019).

Studies investigating bicarbonate levels in tuberculosis patients have revealed potential

correlations with disease severity. The interplay between the host immune response and

Mycobacterium tuberculosis may influence the acid-base equilibrium, leading to alterations in

bicarbonate levels. Early evidence suggests that deviations from normal bicarbonate levels

could be indicative of the severity of TB, providing clinicians with an additional tool for risk

stratification (Chandra et al., 2022).

Beyond its potential as a severity marker, bicarbonate levels may offer insights into the

presence of TB-related complications. Tuberculosis can give rise to diverse complications,

such as pleural effusion, miliary TB, and extrapulmonary manifestations. Investigating how

bicarbonate levels correlate with these complications could aid clinicians in identifying and

addressing them promptly, contributing to a more holistic management approach (Barman et

al., 2017).

28
 CHAPTER THREE

3.0 MATERIALS AND METHOD

3.1 Study Area

The study was carried at Infectious Disease Hospital Kano (I.D.H) Kano, within Kano

metropolis. Kano state lies between latitude 11º30´N and longitude 8º30´E. Kano state borders

Katsina to the north-west, Jigawa state to the north-east, Bauchi state to the south-east and

Kaduna to the south-west. The total land area of Kano state is 20,760 square kilometers with a

population of 9,383,682 based on the official 2006 National Population and Housing Census

(Ado et al., 2009).

3.2 Study Design

This study was an analytical cross sectional study design, convenient sampling was employed

for the recruitments of patients, control and collection of socio demographic data was done

using questionnaire

3.3 Study Population

Tuberculosis patients who attended TB clinic within our study area and consented to take part

in the study

3.3.1 Inclusion Criteria

• Subjects who consented to participate in the study among newly diagnosed TB patients and

TB patients on anti-TB drug treatment and non- TB control group above the age of 18years .

3.3.2 Exclusion Criteria

• Subjects with kidney disease, liver disease, diabetes, asthma and pregnant were excluded

from this study.

29
3.4 Ethical Clearance

Ethical clearance to conduct the research was obtained from the ethics committee of Kano

State Ministry Of Health (KSMH) before the commencement of the research study.

3.5. Consent

Consent was obtained from all participants before commencement of the study

using approved protocols.

3.6 Sample Size Determination

Sample size was determined using the formula for the calculation of minimum

sample size used in study involving human subjects and sample size was determined using the

formula for the calculation of minimum size

n = z2 pq (Cochran 1977)
d2
Where

n- minimum sample size

z- confidence interval on normal distribution curve and is given as 90% = 1..64

p- estimated previous prevalence = 4% (Abiodun et al., 2007).

d-degree of precision given as 5% = (0.05)

n = z2 pq (Cochran 1977)

d2

n = 1.64² ×0.04 (1−0.04) /0.05²

n=1.64² ×0.04 (0.96)/0.05²

n=0.10222/0.0025

n= 42

Test - 84

30
Control - 42

Total Sample = 42 + 42 + 42= 126

3.9 Sample Collection

Two (2) ml of venous blood sample was collected from the subject into lithium heparin

container, centrifuged at 3500rpm for five (5) minutes to obtain plasma and transferred in to

a labeled plain sample container as serum was needed throughout the study.

3.10 Sample Storage

The serum sample was stored at (-20 °C) until when ready for assay.

3.11 Sample Analysis

3.11.1 Estimation of Serum Albumin Using Bromocresol Green (BCG) (Reitman and Frankel,

1957)

Principle

Albumin binds to the indicator dye bromocresol green (BCG) in pH 4.1 to form a blue- green

colored complex. The intensity of the blue-green color is directly proportional to the

concentration of albumin in the sample. It was determined by measuring

spectrophotometrically at 625nm.

Procedure

Tubes were labeled 'test 'for each sample and then one tube each as 'standard' and 'blank'. To

each of the tubes, 1ml of Reagent (R) was dispensed. To the standard, 0.01ml of standard

solution was added, to the test, 0.01ml of sample was added and then 0.01ml of distilled water

to the blank. This was then mixed and incubated at 25°C for 5 minutes and the reading was

taken at 623nm against reagent blank.

31
Calculations

Albumin conc (mmol/L) = Absorbance of test x Concentration Of the standard

Absorbance of standard.

3.11.2. Estimation of Serum Bicarbonate Using Van Slyke Method (1919)

Principle

When 1ml of 0.01N HCL is mixed with serum sample (0.2ml), part of the acid will

be neutralized by the serum. The excess acid is titrated against 0.01N NaOH. The resultant

volume remaining is proportional to the amount of bicarbonate neutralized by HCL

2HCL + HCO3¯→ H2O + CO2 + HCL (excess)

HCL (excess) + NaOH → H2O + NaCL

Protocols

Two (2.0)ml of distilled water was pipetted into a conical flask. 1ml of 0.01N HCL was added.

0.2ml of plasma/serum was added and shaked well to liberate CO2. Add 1-2 drops of neutral

red indicator. The mix was titrated against 0.01N NaOH

Calculations

Volume of HCL utilized by HCO3¯ = (1-y) ml

Concentration = (1-y) x 50 where y = titre

32
3.11.3 Estimation of Chloride Using Quantitative Colorimetric Method (Teco Diagnostic

Reagent) (Chen., 1988)

Principle

Chloride ions form a soluble, non-ionized compound, with mercuric ions and will displace

thiocyanate ions from non-ionized mercuric thiocyanate. The released thiocyanate ions react

with ferric ions to form a color complex that absorbs light at 480 nm. The intensity of the

color produced is directly proportional to the chloride concentration.

Procedure

1. Test tube were labeled “Test” "blank," "calibrator," etc.

2. Chloride reagent (1.5ml) was pipetted into each tube.

3. Calibrator and sample 0.01ml (10µl) was pipetted to respective tubes and mixed.

4. The mixture was Incubated at room temperature for five (5) minutes.

5. The spectrophotometer was set to 480nm and zero with reagent blank.

6. The absorbance of all tubes were read and recorded.

Calculations

Conc. of chloride (mEq/L) = Absorbance of unknown x Concentration of calibrator

Absorbance of calibrator

Concentration of calibrator = 100mEq/L

33
3.12 Classification of Severity Using Gene Xpert Mtb/Rif Assay

Gene Xpert MTB/RIF assay is a diagnostic molecular test that works by detecting the

presence of Mycobacterium tuberculosis (MTB) DNA in sputum samples. It utilizes real-time

polymerase chain reaction (PCR) technology to amplify and detect specific regions of the

MTB genome, PCR involves multiple cycles of heating and cooling to amplify a target DNA

sequence, making it easier to detect even small amounts of DNA. Additionally, it can

simultaneously detect rifampicin resistance-associated mutations, providing information about

drug resistance. Severity analyzed by Gene Xpert is presented on a scale ranging from "Trace"

“ Low ” “ Medium ” and "High," reflecting varying degrees of TB disease severity and

rifampicin resistance.

3.13 STATISTICAL ANALYSIS

The data collected was analyzed using a statistical package for the social sciences (SPSS) for

Windows version 22 and the mean and standard deviation were computed and results was

expressed as a mean ± SD . Analysis of variance (ANOVA) was used to compare the

differences between means and correlation was performed using Pearson’s Correlation

Coefficient and Statistical Significance was set at p<0.05.

34
 CHAPTER FOUR

4.0 RESULTS

4.1 Characteristics of The Study Population

Table 4.1 shows the characteristic of the study population, a total of one hundred and twenty

six (126) participants were recruited in the study of which forty two (42) were newly

diagnosed tuberculosis patient (33.3%), forty two (42) were patients on anti-tuberculosis

treatment (33.3%) and forty two (42) were non-TB control group (33.3%).

The distribution by gender varied across the groups. Among the newly diagnosed TB patients,

there were (61.90%) females and (38.10%) males while patients on anti-TB treatment had

(47.6%) males and (53.38%) females. non-TB control group had males (71.43%) and (28.57%)

females.

The majority of newly diagnosed TB patients fell within the age range of 46-55 years (28.57%),

then 15-25 years (23.81%), while patients on anti-TB treatment fell within the age range of

26-35 years (42.86%). non-TB control individuals were distributed across the age groups of

15-25 years (42.86%) and 26-35 years (45.24%).

The majority of newly diagnosed TB patients (88.10%) have been diagnosed within 0 to 4

weeks prior to the study and patients on anti-TB treatment showed varied distribution with

significant proportions undergoing treatment for four (4) weeks to two (2) months (42.86%)

and 2 month to 4 months (30.95%), while a smaller percentage of patients fell into other

categories of treatment duration, ranging from 2 months to 6 months and above.

35
Table 4.1 Characteristics of The Study Population

Variables ND-TB TBP-T NTB

n( %) n( %) n( %)

Gender

Females 26 (61.90%) 22 (53.38%) 12 (28.57%)

Males 16 (38.10%) 20 (47.6%) 30 (71.43%)

Total 42(100%) 42(100%) 42(100%)

Age (years)

15-25 10 (23.81%) 8 (19.05%) 18 (42.86%)

26-35 6 (14.29%) 9 (21.43%) 19 (45.24%)

36-45 7 (16.67%) 7 (16.67%) 3 (7.14%)

46-55 12 (28.57%) 6 (14.29%) 2 (4.76%)

55 - Above 7 (16.67%) 12 (28.57%) 0

Total 42 (100%) 42 (100%) 42 (100%)

DOTB

≤1 month 37 (88.10%) 13 (30.95%)

1 mth - 3mths 5 (11.90%) 20 (47.62%)

4 mths -6 mths - 5 (11.90%)

Above 6 mths - 4 (9.52%)

DOTBT

≤1 month 5 (11.90%)

1mths - 2mths 18 (42.86%)

2mths - 4mths 13 (30.95%)

4mths - 6mths 3 (7.14%)

≥ 6mths 3 (7.14%)

Key: ND-TB- newly diagnosed TB patients, TBP-T - TB patients on drugs treatment, NTB - Non Tuberculosis, DOTB -
Duration of tuberculosis, DOTBT - Duration of TB treatment, mths - months

36
4.2 Comparison of Albumin, Bicarbonate And Chloride (Mean±Sd) Between Newly

Diagnosed Tuberculosis Patients, Tuberculosis Patient On Treatment And Non

Tuberculosis Control

Table 4.2 Shows the comparison of the Biochemical parameters between the groups. One way

Analysis between newly diagnosed tuberculosis patient, tuberculosis patients on treatment

and control group was conducted to explore the differences between parameters.

The mean albumin level for newly diagnosed individuals was 38.37±2.0 g/l, Patients under

treatment had 42±2.44 g/l, while for controls, the level was 44.38±3.0 g/l. For bicarbonate, the

level for newly diagnosed individuals was 21.3±1.42 mmol/L, for patients under treatment was

23±1.53 mmol/L, while the mean bicarbonate level for controls was 24.89±2.19 mmol/L. For

chloride the mean chloride level for newly diagnosed individuals was 96.91±4.9 mmol/L,

patients under treatment was 98.7± 2.3mmol/L while the chloride levels for controls was

102.25 ±2.0 mmol/L.

37
Table 4.2 Comparison of Albumin, Bicarbonate And Chloride (Mean±Sd) Between
Newly Diagnosed Tuberculosis Patients, Tuberculosis Patient On Treatment And Non
Tuberculosis Control.
GROUP N ALB(g/l) BC(mmol/L) CL̩¯(mmol/L)

ND-TB 42 38.7± 2.0 21.3 ±1.42 97 ±4.90

TBP-T 42 42 ± 2.44 23 ±1.53 98.7± 2.30

NTB 42 44.8 ±3.0 25± 2.19 102.3± 2.0

P value 0.001 0.001 0.001

Key: alb– albumin, bc: bicarbonate, cl: chloride, ND-TB- newly diagnosed TB patients, TBP-T - TB patients on drugs
treatment, NTB - Non Tuberculosis, - mean , SD – standard deviation. (p ≤ 0.05) is statistically considered significant.
ANOVA test

38
4.3 Correlation Of Severity Of Tuberculosis To Level Of Biochemical Parameters
Albumin, Bicarbonate And Chloride Among Newly Diagnosed Patients
The correlation between serum albumin and severity of TB is shown in Table 4.3 was r = 0.471

and p= 0.024. The correlation between bi-carbonate and severity of TB was observed to be r =

-0.117 and p= 0.471, while the correlation of serum chloride to severity of TB was obtained as

r = -0.024 and p = 0.885. where r = coefficient of Pearson correlation, p = p value, p value

≤0.05 is statistically considered significant.

39
Table 4.3 Correlation of Severity Of Tuberculosis to Level Of Biochemical Parameters
Albumin, Bicarbonate And Chloride Among Newly Diagnosed Patients
Parameters r value p value

ALB (g/l) vs Severity 0.471 0.024

BC (mmol/l) vs severity -0.117 0.471

CL ̄ (mmol/l) vs severity -0.024 0.885

Key : alb - albumin, bc - bi-carbonate, cl - chloride, r = coefficient of Pearson correlation, p = p value, p value ≤0.05 is
statistically considered significant

40
 CHAPTER FIVE

5.0 DISCUSSIONS, CONCLUSION AND RECOMMENDATIONS

5.1 Discussions

The research study assessed the levels of albumin, bicarbonate, and chloride among patients

with tuberculosis (TB) across three groups: newly diagnosed patients, patients on

anti-tuberculosis treatment and a control group.

The mean albumin level for newly diagnosed individuals and patients on anti-tuberculosis

treatment was low when compared to non-TB control group. Previous studies reported that

increase in serum albumin levels among patients with favorable treatment outcomes suggests

a positive response to anti-TB treatment (Liu et al., 2020).

Previous studies also suggest that increase in serum albumin as a marker of nutritional status

and inflammation, and its increase may indicate improved nutritional intake and resolution of

inflammation during treatment. Also, the lack of significant changes in serum albumin levels

among patients with poor outcomes may reflect ongoing inflammation and disease

progression despite treatment efforts (Liu et al., 2020).

The mean bicarbonate level for newly diagnosed individuals and patients on anti-tuberculosis

treatment group was lower when compared to non-TB control group. Previous study

suggested that this decrease of chloride may be a compensatory mechanism to the balance

positively and negatively charged ions (cations and anions) in the body's fluids and tissues to

maintain electrochemical neutrality due to imbalance in chloride levels (electrolyte levels)

(Ganiger et al., 2018).

The mean chloride level for newly diagnosed individuals and patients on anti-tuberculosis

treatment group was lower compared to non-TB control group. A previous studies suggest the
41
difference may be attributed to vomiting and dehydration which are common symptoms of TB,

leading to electrolyte imbalances. These findings align with previous studies (Ganiger et al.,

2018).

Previous studies suggested that the significant differences observed in the levels of albumin,

bicarbonate, and chloride among the groups indicated potential alterations in metabolic and

electrolyte balance associated with TB infection and its treatment. The lower levels of these

biochemical markers observed in newly diagnosed TB patients and patients on

anti-tuberculosis treatment group compared to the control group may indicate nutritional

deficiencies and metabolic disturbances commonly seen in TB patients (Afriani et al., 2023).

The lower levels of serum chloride in newly diagnosed TB patients and patients on

anti-tuberculosis treatment group compared to non-TB control group could also be indicative

of electrolyte imbalances associated with TB infection or its treatment (Patil and Mrudula,

2019).

The statistical significant of findings in this study highlights the importance of assessing these

parameters in TB patients to monitor their nutritional and metabolic status and guide clinical

management. A study conducted by (Liu et al., 2020) revealed patients with lower baseline

serum albumin levels (<35 g/L) experienced significant increases in albumin levels during

treatment, particularly at 1 month, 2 months, and treatment completion. This suggests that

patients with lower baseline albumin levels may benefit more from anti-TB treatment in terms

of improving nutritional status and resolving inflammation.

Comparison of biochemical parameters showed the non-TB control group exhibited

significantly higher mean albumin levels when compared to both newly diagnosed individuals

and patients on anti-tuberculosis treatment. Previous studies suggests a potential depletion of

42
albumin in TB patients, possibly due to the inflammatory response and nutritional deficiencies

associated with the disease (Gerardo Alvarez et al., 2013). Similarly, the control group showed

significantly higher mean bicarbonate levels compared to newly diagnosed individuals and

those on treatment. Previous studies conducted suggests this may indicate alterations in

acid-base balance and metabolic processes in TB patients, which may result from disease

pathology or treatment-related factors. The non-TB control group also demonstrated

significantly higher mean chloride levels compared to newly diagnosed individuals and those

on anti-tuberculosis treatment. These findings align with previous findings which suggests

electrolyte disturbances in TB patients, possibly reflecting the impact of the disease on renal

function or fluid balance (Olalekan et al., 2015).

The lower levels of these biochemical markers in newly diagnosed TB patients compared to

the non-TB control group indicate potential metabolic abnormalities and physiological

dysregulation associated with TB infection. These findings may reflect the systemic effects of

TB on various organ systems, including the liver, kidneys, and gastrointestinal tract, leading

to alterations in protein metabolism, acid-base balance, and electrolyte homeostasis (Olalekan

et al., 2015; Liu et al., 2020).

Hypoalbuminemia is linked to an increased risk of treatment failure among TB patients. This

finding is consistent with previous studies that highlighted the prognostic significance of low

serum albumin levels in predicting adverse outcomes in TB patients. Low serum albumin

levels reflect poor nutritional status, which may compromise immune function and host

defense mechanisms against Mycobacterium tuberculosis (MTB). Animal experiments

suggest that hypoalbuminemia can impair host immunity and contribute to TB progression

(Liu et al., 2020). Conversely, successful treatment outcomes are associated with increased

serum albumin levels. Effective anti-TB regimens lead to a reduction in bacterial load,
43
resulting in decreased inflammation and improved nutritional status, as reflected by rising

albumin levels (Liu et al., 2020).

The significant differences observed in these biochemical parameters highlight the importance

of comprehensive clinical assessment and management of TB patients to address potential

nutritional deficiencies, metabolic disturbances, and electrolyte imbalances (Ganiger et al.,

2018; Afriani et al., 2023). Monitoring albumin, bicarbonate, and chloride levels in TB patients

may serve as valuable biomarkers for assessing disease severity, nutritional status, and

metabolic health. The identification of abnormalities in these biochemical parameters can

guide clinicians in tailoring treatment strategies and implementing supportive interventions to

optimize patient outcomes and reduce the risk of complications associated with TB infection

(Olalekan et al., 2015).

The assessment of albumin, bicarbonate, and chloride levels among newly diagnosed

tuberculosis (TB) patients, in conjunction with correlation of these biochemical parameters

with the severity of TB determined by GeneXpert MTB/RIF assay, offers valuable insights

into the relationship between TB severity and metabolic markers. Severity analyzed by

GeneXpert is presented on a scale ranging from "Trace" “Low” “Medium” and "High,"

reflecting varying degrees of TB disease severity and rifampicin resistance (Gerardo

Alvarez-Uria et al., 2013). The correlation analysis revealed findings regarding the

relationship between TB severity and these biochemical parameters.

Albumin and high severity showed a positive correlation (r = 0.471) between TB severity and

serum albumin levels, with a statistically significant p-value of 0.024. A positive correlation

was observed between TB severity and serum albumin levels. As TB severity increased from

"Trace" to "High," serum albumin levels tended to decrease. This suggests that lower albumin

44
levels may be indicative of more severe TB disease burden, possibly reflecting heightened

systemic inflammation and nutritional depletion commonly observed in advanced stages of

TB.

Bicarbonate and high Severity showed a negative correlation (r = -0.117) is observed between

TB severity and serum bicarbonate levels, although this correlation is not statistically

significant (p = 0.471). Although a weak negative correlation was noted between TB severity

and serum bicarbonate levels, this correlation was not statistically significant. The levels of

bicarbonate did not exhibit a consistent trend with increasing TB severity categories. This

implies that bicarbonate levels may be minimal or not be strongly associated with TB severity

in newly diagnosed TB patients as determined by GeneXpert MTB/RIF assay.

Chloride and high Severity showed a negative correlation (r = -0.024) between TB severity

and serum chloride levels, and this correlation is not statistically significant (p = 0.885). Thus,

TB severity does not appear to have a significant relationship with chloride levels in newly

diagnosed TB patients. The levels of chloride did not demonstrate a clear pattern across

different TB severity categories. Therefore, chloride level may not serve as reliable indicators

of TB severity based on GeneXpert results.

The positive correlation between TB high severity and serum albumin levels suggests that

albumin may serve as a useful biomarker for assessing disease severity and nutritional status

in TB patients. Decreased albumin level may reflect the severity of systemic inflammation

and metabolic dysregulation associated with advanced TB disease. The lack of significant

correlations between TB severity and serum bicarbonate and chloride levels indicates that

these parameters may not be reliable indicators of disease severity in newly diagnosed TB

45
patients. Other factors, such as renal function and fluid balance, may contribute to bicarbonate

and chloride levels independently of TB severity (Gerardo Alvarez-Uria et al., 2013).

Thus, monitoring serum albumin levels may aid in assessing TB severity and guiding clinical

management decisions, such as nutritional support and therapeutic interventions. While

bicarbonate and chloride levels may not be directly associated with TB severity, they remain

important markers of metabolic and electrolyte balance in TB patients and should be

monitored as part of routine clinical care.

5.2 Conclusions

The level of serum albumin, bicarbonate and chloride was determined and analysis shows

lower level of albumin, bicarbonate, and chloride among newly diagnosed patients and

patients on anti-tuberculosis treatment compared to non-TB control which highlights the

systemic effects of tuberculosis on these vital biomarkers. The correlation between

tuberculosis severity and biochemical parameters among newly diagnosed patients offers

further understanding of disease progression and potential biomarkers for monitoring. While

serum albumin levels showed a significant positive correlation with high disease severity,

bicarbonate and chloride levels exhibited non significant negative associations. These findings

emphasize the need for continued research to clarify the role of these biochemical parameters

in tuberculosis pathogenesis and their clinical utility. Overall, the study highlights the

importance of monitoring biochemical parameters for early detection and management of

tuberculosis-related abnormalities.

46
5.3 RECOMMENDATIONS

1. Further investigations is recommended to validate these findings and explore their

clinical implications in tuberculosis biochemical diagnosis.

2. Longitudinal studies are suggested to assess the long-term impact of serum albumin

levels on TB treatment outcomes and patient prognosis.

5.4 LIMITATIONS OF THE STUDY

1. The cross-sectional design of the study limits the ability to establish causal relationships

between tuberculosis and biochemical parameters, emphasizing the need for longitudinal

studies.

2. Potential confounding factors such as medication use, and dietary factors were not

accounted for in the analysis, which could influence some of the observed outcomes of

tuberculosis.

47
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 APPENDIX 1

CONSENT FORM

My name is OWOYEMI DAVID TEMITOPE, a final year student from the Department of
Medical Laboratory Science, Faculty of Allied Health Sciences, Bayero University, Kano.
I am carrying out a research on "ASSESSMENT OF THE ALBUMIN, BICARBONATE
AND CHLORIDE IN PATIENTS WITH TUBERCULOSIS ATTENDING INFECTIOUS
DISEASE HOSPITAL KANO .”
Your participation in this study is voluntary and your full consent to participate will be needed.
Please feel free to ask any question about the study and your sincere response is very vital to
the success of the study. Your response will be kept strictly confidential and will be used for
research purpose only.
Also, venous blood will be taken if permissible by you. You may feel a slight pain or a sting
when the needle pricks your skin during the blood collection. Apart from these, having your
blood drawn involves minimal discomfort.
CONSENT: Now, that the study has been explained to me and I am also fully aware of it, I am
willing to take part.
…………………. ……….……………………………

Respondent’s name Signature and date

………………….. ………………………………………….

Researcher’s name Signature and date

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 APPENDIX II

RESEARCH QUESTIONNAIRE

DEPARTMENT OF MEDICAL LABORATORY SCIENCE

FACULTY OF ALLIED HEALTH SCIENCES
BAYERO UNIVERSITY KANO

Please tick appropriately /fill

Patient ID No: _______________________
Section A: Socio demographic data
1. Gender: Male ( ) Female ( )
2. Nationality: Nigerian ( ) Non-Nigerian ( )
3. Age Group: (a) 0-10yrs (b) 11-20yrs (c) 21-30yrs (d) 31-40yrs (e) 41-60yrs (f)
61- above
4. Location: Urban ( ) Semi Urban ( ) Rural ( )
Section B: Clinical Data
1. How long have you been diagnosed with tuberculosis
(a) 0-3months (b) 4- 6months (c) Above 6 months
2. Have you been on Tuberculosis treatment? Yes ( ) No ( )
If yes, when? (a) 0-3 months (b) 4-6 months (d) Above 6 months
3 .Do you experience any of these symptoms:
(a) Fever/Chills (b) Fatigue/Weakness (c) Nasal discharge (d) Sore throat (e)Breathing
difficulty/Rapid breathing (f) Lack of appetite (g) nausea
4. Do you have any of the following conditions/diseases?
(a) Diabetes ( ) (b) kidney Disease ( ) (c) Liver Disease ( )
(d) Pregnant ( ) (e) asthma ( )
SECTION C: Laboratory Investigations
1- Serum Albumin ………..………………………………………………g/L
2- Serum Bi-carbonate……………. …………………….……..………mmol/L
3- Serum Chloride………………..……………………………………..mmol/L

58
 APPENDIX III

ETHICAL APPROVAL

59