Biochemical Markers of Nutrition Among Adult Sickle-Cell Anaemia Patients : Current School News

Assessment of Some Biochemical Markers of Nutritional Status Among Adult Sickle Cell Anaemia Patients in Steady State in Zaria

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Assessment of Some Biochemical Markers of Nutritional Status Among Adult Sickle Cell Anaemia Patients in Steady State in Zaria 

ABSTRACT

Sickle cell anaemia is a chronic haemolytic state which is characterized by hypercatabolism that could predispose to malnutrition. The low socio economic backgroundof our patients may worsen their health status.

The study was aimed atassessing some biochemicalmarkers of nutritional status among adult sickle cell anaemia patients in steady state in Zaria.

It is a crosssectional descriptive study which was conducted in the Departments of Chemical Pathology and Haematology, Ahmadu Bello University Teaching Hospital, Shika, Zaria, Kaduna State.

Some biochemical markers of nutritional status of 60 adult SCA patients in steady state and 60 healthy non SCA controls were assessed.

Mean (±SEM) serum vitamin D concentration was significantly lower in SCA patients 14.55±1.49 ug/L compared with controls 25.87.±4.29 ug/L (p<0.05).

Mean (±SEM) serum calcium concentration was significantly lower in SCA patients 2.20 ±0.06 mmol/L compared with controls2.33±0.04 mmol/L (p<0.05).

Mean (±SEM) serum albumin concentration was significantly lower in SCA patients 33.40±1.66 g/L compared with controls 40.13.±0.85 g/L (p<0.05).

TABLE OF CONTENT

Title page……….………. i
Declaration…………… ii
Certification …………. iii
Acknowledgements…………. iv
Abstract………………v
Table of contents………………vi
List oftables..…………. x
List offigures……….…. xi
Abbreviations/Symbols used………….. xii

1.0 CHAPTER ONE: INTRODUCTION
1.1 Background…………………………………………………..……………………. 1
1.2 Statement of the problem…………………………………………………………. 2
1.3 Justification……………………………………………….………………………. 3
1.4 Aim and objectives…………………………………………………………..…… 3
1.5 Research question/Hypothesis…………………………………………………….. 4

2.0 CHAPTER TWO: LITERATURE REVIEW
2.1 Sickle cell anaemia………………………………………………………………. 5
2.1.1 Historyof Sickle Cell anaemia….……………………………………………………… 5
2.1.2 Epidemiology of Sickle cell disease…………………………………………….. 5
2.1.3 Pathophysiology of Sickle cell anaemia………………………………………… 6
2.1.4 Clinical Features……………………………………………………………..…. 9
2.1.4.1 General Features………………….…………………………………………….. 9
2.1.4.2 Painful Crises…………………………………………………………………… 9
2.1.4.3 Infections…………………………………………………………..…………… 10
2.1.5 Effects on major organ systems…………`……………………………………… 10
2.1.5.1 The Respiratory System……………………………………………………… 10
2.1.5.2 The Cardiovascular system……………………………………………….…. 11
2.1.5.3 The liver and spleen………………………………………………………….. 11
2.1.5.4 The Musculoskeletal System……..………………………………….……… 11
2.1.5.5 The Nervous System…………………………………………………………. 12
1.5.6 The Genito-Urinary system…………………………………………………… 12
2.1.6 Sickle Cell anaemia and Nutrition…………………………………………… 13
2.1.6.1 SCA and Undernutrition…….………………………………………………. 14
2.1.6.2 Effect of Infection on nutrition in SCA………………………………. ..…. 16
2.1.6.3 Implications for growth and maturation abnormality in SCA…………… ……. 16
2.1.6.4 Nutritional intervention in management of SCA……………………..….. 17
2.1.7 Diagnosis of Sickle Cell Disease…………………………………………….. 18
2.1.7.1 Laboratory Diagnosis………………………………………………………… 18
2.1.7.1.1Haemoglobin sickling test……………………………………… ………….… 18
2.1.7.1.2Haemoglobin solubility test………………………………………………… 18
2.1.7.1.3Haemoglobin electrophoresis……………………………………………….. 19
2.1.7.1.4 Isoelectric focusing………………………………………………………..… 19
2.1.7.1.5 High Performance Liquid Chromatography……………………………….. 20
2.1.7.1.6DNA analysis………………………………………………………………… 20
2.1.8 Samples used in antenatal Diagnosis………………………………………… 21
2.1.8.1 Foetal blood sampling…………………………………………………….… 21
2.1.8.2 Chorionic villi or amniotic cell DNA………………………………………. 22
2.1.9 Treatment of sickle cell anaemia…………………………………………… 22
2.1.9.1 Drug treatments…………………………………………………….……… 22
2.1.9.1.1Hydroxyurea……………………………………………………………….. 23
2.1.9.2 Transfusion………………………………………………………………… 23
2.1.9.3 Bone Marrow or Stem Cell Transplantation………………………………… 24
2.2 Methods for assessing nutrition………………………………………………..… 25
2.2.1 Clinical observation and examination………………………………………………………. 25
2.2.2 Anthropometric measurement…………………………………………………. 26
2.2.3 Dietary history…………………………………………………………………… 26
2.2.4 Biochemical methods…………………………………………………………… 26
2.3 Vitamin D………………………………………………………………………. 28
2.3.1 Vitamin D metabolism………………………………………………………… 28
2.3.2 Mechanism of action………………………………………………………….. 29
2.3.3 Functions of vitamin D……………………………………………………….. 30
2.3.4 Vitamin D deficiency…………………………………………………………. 33
2.3.5 Risk factors for vitamin D deficiency………………………………………….. 35
2.3.6 Assessing vitamin D nutritional status in SCA……………………………… 39
2.3.6.1Vitamin D assay…………………………………………………………… 39
2.3.6.2 Extraction and Deproteinization………………………………………. …… 40
2.3.6.3 Column Chromatography……………………………………………………… 43
2.3.6.4Measurement of 25-Hydroxyvitamin D………………………… …………… 43
2.3.6.5Measurement of 1,25-Dihydroxyvitamin D……………………………… …….. 43
2.3.6.6Radioreceptor Assay…………………………….………………………………. 44
2.3.6.7Radioimmunoassay………………………………………….………………….. 44
2.3.6.8 Specimen Requirements……………………………………………………..… 44
2.4Albumin…………………………………………………………………………. 45
2.4.1 Synthesis of albumin…………………………………………………………… 46
2.4.2 Degradation of albumin…………………………………………..……………. 47
2.4.3Role of albumin in maintaining microvascular integrity………………….… 47
2.4.4 The prognostic value of serum albumin………………………………………… 48

3.0 CHAPTER THREE: MATERIALS AND METHODS
3.1 Study area…………………………………………………………………….. 50
3.2 Study population and Design…………………………………………….. 50
3.2.1 Inclusion criteria……………………………………………………………. 51
3.2.2 Exclusion criteria……………………………………………………………. 51
3.2.3 Informed Consent…………………………………………………………. 51
3.2.4 Ethical consideration………………………………………………………… 51
3.2.5 Sample size determination..……………………………………….…………. 52
3.3 Sampling technique…………………………………………..………….…… 53
3.4 Blood collection and processing……………………………..……….……… 54
3.5 Chemicals……………………………………………………………….……. 54
3.6 Equipment…………………………………………………………………… 54
3.7 Quality control………………………………………………………..……… 54
3.8 Analytical methods………………………………………………………… 55
3.8.1 Measurement of serum Vitamin D………………………………………… 55
3.8.2 Measurement of serum calcium…………………………………………… 56
3.8.3 Measurement of serum phosphate………………………………………….. 57
3.8.4 Measurement of serum albumin………………………………………….. 58
3.9 Statistical analysis……………………………………………………………. 59

4.0 CHAPTERFOUR: RESULTS……………………………………………………60

5.0 CHAPTER FIVE: DISCUSSION……………………………………………… 66

6.0 CHAPTER SIX: CONCLUSION AND RECOMMENDATION…………… 69
6.1 CONCLUSION………………………………………………………………..… 69
6.2 RECOMMENDATIONS……………………………………………………….. 69
REFERENCES………………………………….…………………………………… 70
APPENDICES………………………………………………………………………… 92

INTRODUCTION  

Sickle cell anemia (SCA) is a genetic disease that results from the substitution of valine for glutamic acid in the β-globin chain of the hemoglobin molecule (Pauling and Itano, 1949).

The consequence of this amino acid substitution is the formation of hemoglobin S (HbS). Under low oxygen tension and/or conditions of acidosis. 

HbS precipitates and forms polymerized crystals called tactoids (hemoglobin polymers), which distort the red blood cells (Nelson and Cox, 2005; Ganong, 2003).

The resulting sickle-shaped red cells lose their pliability and cannot navigate the small capillaries, become sticky, and adhere to the small veins, small arteries, and other blood vessels causing vaso-occlusion (Aster, 2005; Bunn and Forget, 1977).

In addition, red blood cells homozygous for HbS (HbSS) are susceptible to premature destruction, with a red blood cell life span of 8–25 days as compared to 100–120 days for normal red blood cells (Solankiet al, 1988).

 

REFERENCES

Akinyanju, O. O. (1989). A profile of sickle cell disease in Nigeria. Annals of the New York
Academy of Sciences, 565(1), 126-136.

Akohoue, S. A., Shankar, S., Milne, G. L., Morrow, J., Chen, K. Y., Ajayi, W. U., and Buchowski,
M. S. (2007). Energy expenditure ,inflammation, and oxidative stress in steady-state
adolescents with sickle cell anemia. Pediatric research, 61(2), 233-238.

Akuyam, S. A., P. O. Anaja, O. G. Ogunrinde, A. Abubakar, N. Lawal, S. M. Ya’uba, A. Musa et
al. (2014): “Liver function test profile of Nigerian children with sickle cell anaemia in
steady state.” Nigerian Journal of Basic and Clinical Sciences 11, no. 1 13.

Allain, T. J., and Dhesi, J. (2003). Hypovitaminosis D in older adults.Gerontology, 49(5), 273-
278.

Allon, M. (1990).Renal abnormalities in sickle cell disease. Archives of internal medicine, 150(3),
501-504.

Al-Saqladi, A. W., Cipolotti, R., Fijnvandraat, K., and Brabin, B. J. (2008).Growth and nutritional
status of children with homozygous sickle cell disease. Annals of Tropical Paediatrics:
International Child Health, 28(3), 165-189.

 

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