Serum Albumin Level in Sudanese Children with Edematous and Non-Edematous Malnutrition

نویسندگان

  • Sami F Abdullah
  • Mohamed F Lutfi
چکیده

Introduction Edema formation in malnourished children is multifactorial and not necessarily caused by hypoalbuminemia. In Sudan, studies that evaluate serum albumin level in malnourished children are scarce, if any. The aim of this study is to assess serum albumin concentrations in Sudanese children with edematous and non-edematous malnutrition. Material and Methods The study involved 23 males matched for age and weight with 17 females. The ages of studied subjects ranged between 6 – 36 months. Weight and serum albumin levels were measured according to the standards. Patients were classified according to the presence of edema, Wellcome and Gomez classifications. In addition, patients were classified according to their levels of albumin into normal (3.5 4.8 g/dl), mild (2.8 3.4 g/dl), moderate (2.1 2.7 g/dl) and severe (< 2.1 g/dl) hypoalbuminemia. Results Serum albumin levels were significantly lower in malnourished subjects with edema (M±SD = 2.4±0.8 g/dl) compared to those with malnutrition but no edema ((M±SD = 3.1±0.8 g/dl, P = 0.026) However, classifying studied malnourished children according to their albumin levels revealed no significant differences in the mean of albumin when albumin levels of edematous patients were compared with non-edematous subjects in each class (P> 0.05). There was no significant correlation between weight and serum albumin level (correlation coefficient (CC) = 0.156, P = 0.337). Conclusion The current study demonstrates the tendency of edematous malnourished children to have hypoalbuminemia; nevertheless, some children with significantly low albumin are still not suffering from edema. These paradoxical results display the possible variations in the pathophysiological response to food deprivation. Cite this article as: Sami F Abdullah, Fathel rahman E Ahmed, Mohamed F Lutfi. Serum Albumin Level in Sudanese Children with Edematous and Non-Edematous Malnutrition. Asian Journal of Biomedical and Pharmaceutical Sciences; 04 (38); 2014, 47-49. Sami F Abdullah et al: Asian Journal of Biomedical and Pharmaceutical Sciences; 4(38) 2014, 47-49. © Asian Journal of Biomedical and Pharmaceutical Sciences, all rights reserved. Volume 4, Issue 37, 2014. 47 NTRODUCTION World health organization (WHO) defines severe acute malnutrition as a very low weight for height (below 3Z scores of the median WHO growth standards), by visible severe wasting, or by the presence of nutritional edema[1].There are many classifications for malnutrition. In Gomez classification, the child's weight is compared to that of a normal child (50th percentile) of the same age. Accordingly three categories can be distinguished: mild (75%-90% weight for age); moderate (60%-74% weight for age) and severe (<60%weight for age) malnutrition[2]. Alternatively, Wellcome classification considers both weight and presence edema as follows: kwashikor (weight for age 60-80% with edema), undernutrition (weight for age 60-80% without edema), marasmickwashiorkor (weight for age < 60% with edema) and marasmus (weight for age < 60% without edema) [3]. The major clinical syndromes of severe childhood malnutrition (SCM) are marasmus (non-edematous SCM), kwashiorkor and marasmic-kwashiorkor (edematous SCM). Edema formation in edematous malnutrition is multifactorial. Hypoproteinemia and electrolytes disturbance are claimed to be among the major contributing factors [4]. These facts were supported by the work of Gopalan and others [5, 6] who demonstrated clinical and biochemical cure of Kwashiorkor patients with diet rich in protein. However, a study conducted by Golden et al showed no difference in the concentration of plasma albumin before and after the loss of edema when patients were put on restricted diet [7]. Furthermore Golden demonstrated improvement of edema in these children treated with high energy diets and not with protein rich meals [8], it was reported that Indian children on poor diet can develop either kwashiorkor or marasmus regardless of the quantitative or qualitative differences in their diet [9]. Chronic food deprivation children with non-edematous malnutrition can maintain body protein breakdown at the same rate as when they are well nourished but children with edematous malnutrition cannot [10]. Nutritional edema is associated with increased secretion of an antidiuretic substance that prevent normal execratory response to water intake[11].The functional and structural hepatic changes associated with malnutrition may lead to in activation of antidiuretic (ADH) and aldosterone hormones and hence water retention[12]. Other factors that may contribute to nutritional edema include antioxidant depletion[1315], low hepatic transaminases[16], excessive lipid peroxidation[17], free circulating iron[18 ] and ferritin[19]. In Sudan, studies that evaluate serum albumin level in malnourished children are scarce, if any. The aim of this study is to assess serum albumin concentrations in Sudanese children with edematous and non-edematous malnutrition. MATERIAL AND METHODS The study involved 40 malnourished children; 23 males matched for age and weight with 17 females. The volunteers were recruited mainly from Albuluk and Ibraheem Malik teaching hospitals – Khartoum –Sudan. The ages of studied subjects ranged between 6 – 36 months. Weight scale (Health O-Meter USA) was used for measuring weight. Venous blood samples were obtained from the femoral vein. Spectrophotometer BTS 310 (Bio System Company Germany) was used to measure serum albumin using bromcresol (SPINREACT). Patients were classified according to the presence of edema, Wellcome and Gomez classifications. In addition, patients were classified according to their level of albumin into normal (3.5 4.8 g/dl), mild (2.8 3.4 g/dl), moderate (2.1 2.7 g/dl) and severe (< 2.1 g/dl) hypoalbuminemia. Statistical evaluation was performed using SPSS (SPSS for windows 19.0). Normal distribution of studied variables was examined using Kolmogorov-Smirnova and Shapiro-Wilk tests. Unpaired T-test and MannWhitney U test were used to assess significant difference in the means of albumin levels in the different groups. Screening for significant correlations between albumin levels and weight were performed using bivariate correlations. P < 0.05 was considered significant. RESULTS The study involved 17 (42.5%) females and 23 (57.5%) males. The females age (M±SD = 13.1±4.8 months) and weight (M±SD = 5.6±1.2 Kg) were not significantly different when compared to the males (M±SD = 16.8±8.0 months and 6.1±1.1 Kg respectively, P > 0.05). Serum albumin level was significantly lower in malnourished subjects with edema (M±SD = 2.4±0.8 g/dl) compared to those with malnutrition but no edema ((M±SD = 3.1±0.8 g/dl, P = 0.026) (figure 1 and 2). However, classifying studied malnourished children according to their albumin levels revealed no significant differences in the mean of albumin concentration when albumin levels of edematous patients were compared with non-edematous subjects in each class (figure 3). Moreover, there was no significant correlation between children weights and serum albumin levels (correlation coefficient (CC) = 0.156, P = 0.337) (figure 4). I Sami F Abdullah et al: Asian Journal of Biomedical and Pharmaceutical Sciences; 4(38) 2014, 47-49. © Asian Journal of Biomedical and Pharmaceutical Sciences, all rights reserved. Volume 4, Issue 37, 2014. 48 Figure-1: Distribution of serum albumin level in malnourished subjects grouped according to the presence of edema Figure-2: Distribution of serum albumin level in malnourished subjects grouped according to Wellcome classification Figure-3: Comparison of malnourished patients with and without edema when grouped accordingto serum albumin levels Figure-4: Distribution of serum albumin level in malnourished subjects when grouped according to Gomez classification DISCUSSION It is evident from the current results that serum albumin concentrations tend to be lower in edematous malnourished children, however, classifying studied children according to their albumin levels revealed no significant differences in the mean when albumin levels of edematous patients were compared with nonedematous subjects in each group. These two findings are not necessarily contradictory; in contrast they demonstrate the variations of the pathophysiological response of malnourished children to food deprivation [20. 21]. In addition the current study weaken the general believe that edema of malnutrition is solely an outcome of the decreased oncotic pressure caused by associated hypoalbuminemia[22 ]. The explanation for decreased serum albumin concentrations in edematous malnourished children is not simply attributable to poor food intake. There are several studies that confirmed the variations in the rate of protein metabolism in patients with edematous malnutrition compared to non-edematous conditions. By the end of the last century, Manary et al reported that kwashiorkor patients had slower rates of wholebody protein breakdown than did patients with marasmus [21 ]. Six years later, Jahoor and his group were able to prove that these differences in the rate of protein catabolism were because of inherent differences in protein turnover among corresponding patients and not due to dissimilar physiological adaptation to low food intake[2 0]. Therefore, Serum albumin may not be a useful marker for malnutrition especially in patients with chronic illnesses[23]. Pediatricians should pay more attention to the clinical manifestations of malnutrition and anthropometric measurements while evaluating malnourished children. In general, edema of malnutrition is easy to explain by starling principle [2 4] which declares that capillary filtration rate across the capillaries is proportional to difference between hydrostatic and colloidal osmotic pressure. Low plasma albumin associated with malnutrition is expected to decrease plasma colloidal osmotic pressure and induce generalized edema [25]. However, previous reports showed that the edema secondary to hypoalbuminemia would not appear unless plasma albumin decreased to as low as 2-2.5 g/dl [26]. In addition, the extend edema might not correlate well with plasma protein concentration[27]. These reports preclude from drawing a conclusion that edema of malnutrition is mainly due to the decreased oncotic pressure caused by associated hypoalbuminemia. In conclusion, the current study demonstrates the tendency of edematous malnourished children to have hypoalbuminemia; nevertheless, some children with Sami F Abdullah et al: Asian Journal of Biomedical and Pharmaceutical Sciences; 4(38) 2014, 47-49. © Asian Journal of Biomedical and Pharmaceutical Sciences, all rights reserved. Volume 4, Issue 37, 2014. 49 significantly low albumin are still not suffering from edema and some with normal serum albumin were stilledematous. These paradoxical results display thepossible variations in the pathophysiological responseto food deprivation in those suffering frommalnutrition. In addition the current study attenuate the general believe that edema of malnutrition is solelyan outcome of the decreased oncotic pressure causedby associated hypoalbuminemia.REFERENCES1.Physical status: The use and interpretation of anthropometry.Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:161–2.2.Gomez F, Galvan RR, Cravioto J, Frenk S. Malnutrition in infancyand childhood, with special reference to kwashiorkor. AdvPediatr.1955;7:131–169.3.Waterlow JC. Classification and definition of protein-caloriemalnutrition. Br Med J. 1972 Sep 2;3(5826):566-9.4.Allyne GAO. The effect of severe calorie malnutrition on the renalfunction of Jamicanchildren. Pediatrics 1967;39:400-125. GopalanC,SrikantiaSG. Clinical trials with vegetable protein foodin kwashiorkor.Indian J Med Res 1960;48:637-446.GopalanC.VenkataachalanPS,SrikanitaSG,MehtaG.Treatment ofnutritional edema syndrome(kwashiorkor)with vegetable protein diet.Am J Clin Nut 1962;11:127-337.Golden MH,GoldenBE,JacksonAA.Albumin and nutritionaledema.Lancet 1980:i:114-68.Golden MHN.Proteindeficiency,energy deficiency and the edemaof malnutrition.Lancet 1982:i:1261-59.Gopalan C. Kwashiorkor and marasmus: evolution anddistinguishing features. 1968. Natl Med J India. 1992;5(3):145-51.10.Jahoor F, Badaloo A, Reid M, Forrester T. Protein kineticdifferences between children with edematous and nonedematoussevere childhood undernutrition in the fed and postabsorptivestates. Am J ClinNutr. 2005 Oct;82(4):792-800.11.GopalanC.VenkatachalamPS.The pathogenesis of nutritionaledema.Indian J Med sci 1952; 6:713 12.SrikantiaG. Feeritin in nutritional edema. Lancet 1958; i: 667-813.Jackson AA. Blood glutathione in severe malnutrition inchildhood. Trans R Soc Trop Med Hyg. 1986;80(6):911-314.Sive AA, Subotzky EF, Malan H, Dempster WS, Heese HD. Redblood cell antioxidant enzyme concentrations in kwashiorkor andmarasmus. Ann Trop Paediatr. 1993;13(1):33-815.Becker K, Bötticher D, LeichsenringM.Antioxidant vitamins inmalnourished Nigerian children. Int J Vitam Nutr Res. 1994;64(4):306-10.16. Mclean EM. Hepatic failure in malnutriotion. LANCET 1962; 2:1292 – 4.17. Lenhartz H, Ndasi R, Anninos A, Bötticher D, Mayatepek E, Tetanye E, Leichsenring M. The clinical manifestation of thekwashiorkor syndrome is related to increased lipid peroxidation. JPediatr. 1998 May;132(5):879-81.18. Sive AA, Dempster WS, Malan H, Rosseau S, Heese HD. Plasmafree iron: a possible cause of oedema in kwashiorkor.-Arch DisChild. 1997 Jan;76(1):54-6.19. Ramdath DD, Golden MH.Non-haematological aspects of ironnutrition. Nutr Res Rev. 1989 Jan;2(1):29-49.20.Jahoor F, Badaloo A, Reid M, Forrester T. Protein kineticdifferences between children with edematous and nonedematoussevere childhood undernutrition in the fed and postabsorptivestates. Am J ClinNutr. 2005 Oct;82(4):792-800.21. Manary MJ, Broadhead RL, Yarasheski KE. Whole-body protein kinetics in marasmus and kwashiorkor during acute infection. Am JClinNutr. 1998 Jun;67(6):1205-9.22. Mobarhan S. The role of albumin in nutritional support. J AmCollNutr. 1988 Dec;7(6):445-52.23.Baron M, Hudson M, Steele R; Canadian Scleroderma Research Group (CSRG). Is serum albumin a marker of malnutrition inchronic disease? The scleroderma paradigm. J Am CollNutr. 2010Apr;29(2):144-51.24. Starling Eh. On the absorption of fluids from the connectivetissue spaces. J Physiol 1896; 19: 312-326.25. Michel CC. Fluid exchange in the microcirculation. J Physiol.2004 June 15; 557(Pt 3): 701–702.26. Coward WA, FiorottoM.The pathogenesis of oedema inkwashiorkor--the role of plasma proteins. ProcNutr Soc. 1979 May1;38(1):51-9.27. Coward WA. Serum colloidal osmotic pressure in thedevelopment of kwashiorkor and in recovery: its relationship to albumin and globulin concentrations and oedema. Br J Nutr. 1975Nov;34(3):459-67.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Evaluating the level of adherence to Ministry of Health guidelines in the management of Severe Acute Malnutrition at Garissa Provincial General hospital, Garissa, Kenya

INTRODUCTION Half of Kenya's high infant and under five mortality rates is due to malnutrition. Proper implementation of World Health Organization's (WHO) Evidence Based Guidelines (EBG) in management of severe acute malnutrition can reduce mortality rates to less than 5%. The objectives were to establish the level of adherence to WHO guideline and the proportion of children appropriately manag...

متن کامل

In vivo rates of erythrocyte glutathione synthesis in children with severe protein-energy malnutrition.

Although the compromised GSH status of children with edematous protein-energy malnutrition (PEM) has been documented, the in vivo kinetic mechanism(s) responsible for this is not known. To determine if decreased synthesis contributes to the alteration of GSH homeostasis, the fractional and absolute rates of synthesis of erythrocyte GSH were determined shortly after admission (study 1), approxim...

متن کامل

Omitting edema measurement: how much acute malnutrition are we missing?

BACKGROUND Acute malnutrition is a major public health issue in low-income countries. It includes both wasting and edematous malnutrition, but the terms wasting and acute malnutrition are often used interchangeably. Little is known about the burden of edematous malnutrition, and few large-scale surveys measure it. OBJECTIVE Most acute malnutrition might be captured by the measurement of wasti...

متن کامل

Cranial Magnetic Resonance Imaging (MRI) Changes in Severely Malnourished Children before and after Treatment

Protein energy malnutrition is an important problem in developing countries. Neurological changes is associated with sever malnutrition. Aim of Work: Our study seeks to document the morphological changes in the brain of infants suffering from severe malnutrition of both edematous and non-edematous types and to follow up these changes and its outcome after nutritional rehabilitation according to...

متن کامل

Sulfur amino acid metabolism in children with severe childhood undernutrition: methionine kinetics.

BACKGROUND Children with edematous but not nonedematous severe childhood undernutrition (SCU) have lower plasma and erythrocyte-free concentrations of cysteine and methionine, which suggests a decreased availability of methionine for cysteine synthesis. We propose that methionine production and metabolism will be slower in children with edematous SCU than in those with nonedematous SCU. OBJEC...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2015