Protein energy malnutrition pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
Several studies have shown that a deficiency in the consumption of protein, carbohydrates and fat and in some cases chronic infections particularly those producing diarrhea, but also other diseases such as helminthic infections are mainly responsible for the development of protein energy malnutrition.<ref name="pmid7825621">{{cite journal| author=Cederholm T, Jägrén C, Hellström K| title=Outcome of protein-energy malnutrition in elderly medical patients. | journal=Am J Med | year= 1995 | volume= 98 | issue= 1 | pages= 67-74 | pmid=7825621 | doi=10.1016/S0002-9343(99)80082-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7825621 }} </ref> | Several studies have shown that a deficiency in the consumption of protein, carbohydrates and fat and in some cases chronic infections particularly those producing diarrhea, but also other diseases such as helminthic infections are mainly responsible for the development of protein energy malnutrition.<ref name="pmid7825621">{{cite journal| author=Cederholm T, Jägrén C, Hellström K| title=Outcome of protein-energy malnutrition in elderly medical patients. | journal=Am J Med | year= 1995 | volume= 98 | issue= 1 | pages= 67-74 | pmid=7825621 | doi=10.1016/S0002-9343(99)80082-5 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7825621 }} </ref> The underlying mechanisms include the following: | ||
*Decreased food intake because of anorexia | *Decreased food intake because of anorexia | ||
*Decreased nutrient absorption | *Decreased nutrient absorption | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]
Overview
Protein energy malnutrition is characterized by wasting, edema or both and occurs almost exclusively in children under the age of 5years. The two main diseases under the spectrum of protein energy malnutrition are marasmus and kwashiorkor. Marasmus is defined as severe wasting while kwashiorkor is defined as malnutrition with edema. There is a variant known as marasmic kwashiorkor which is defined as severe wasting in the presence of edema. A unique pathophysiology is responsible for the development of these diseases.
Pathophysiology
Pathogenesis
Several studies have shown that a deficiency in the consumption of protein, carbohydrates and fat and in some cases chronic infections particularly those producing diarrhea, but also other diseases such as helminthic infections are mainly responsible for the development of protein energy malnutrition.[1] The underlying mechanisms include the following:
- Decreased food intake because of anorexia
- Decreased nutrient absorption
- Increased metabolic requirements
- Direct nutrient losses
The pathologic changes involved in protein energy malnutrition include:[2]
- Immunologic deficiency in the humoral and cellular subsystem as a result of protein deficiency.
- Metabolic disturbances cause impaired intercellular degradation of fatty acids as a result of carbohydrate deficiency.
- Poor synthesis of pigments in the hair and skin (e.g., hair colour may change and skin become hyperpigmented) because of a lack of substrate (e.g., tyrosin) and coenzymes.
When subcutaneous fat and muscle are lost because of endogenous mobilization of all available energy and nutrients, marasmus is diagnosed. Kwashiorkor on the other hand usually manifests with edema, changes to hair and skin colour, anemia, hepatomegaly, lethargy, severe immune deficiency and early death. Several theories have been postualted to explain the mechanism of edema seen in children with kwashiorkor. Some of them include: Protein deficiency/hypoalbuminemia : It was initially believed that a deficiency in the consumption of protein was responsible for the development of kwashiorkor in children.
- Albumin concentrations were also noted to increase steadily within two weeks after refeeding.
- Presence of features similar to congenital nephrotic syndrome, in which the primary pathology is renal loss of albumin.[3]
Multiple evidences have now shown that inadequate intake of dietary protein is not the primary trigger for edematous malnutrition.
- Some patients have edematous malnutrition without hypoalbuminemia
- Others develop edematous malnutrition (kwashiorkor) despite adequate proportion of protein in the diet (eg, in exclusively breastfed infants)
- Others recover from edematous malnutrition with supportive care even without enhancing the protein content of the diet.[4][5][6]
2. Oxidant stress : Excessive oxidant stress was also proposed as a mechanism of development of kwashorkor, however, it was discovered that that the administration of antioxidant was not successful in prevention of the development of this malnutrition in a series of trials. Hence the conclusion that antioxidant depletion is a consequence rather than cause of kwashiorkor.[7]
3. Microbiome : Changes in intestinal microbiome has also been suggested as a cause of the development of kwashiorkor. However, these has not been fully supported because evidences show that neither the fecal microbiota transfer nor the local diet alone was sufficient to cause the malnutrition leading to the conclusion that changes in fecal microbiota are only effects rather than causes of kwashiorkor.[8][9][10]
Genetics
Associated conditions
Some of the conditions that are associated with kwashiokor include;
- Vitamin A deficiency
- Vitamin D deficiency
- Thiamine deficiency
- Zinc deficiency
- Dehydration
- Sepsis
- Shigella and Campylobacter infections.
Gross pathology
Post mortem examination of the liver shows the presence of fatty infiltration and necrosis which disappears with adequate treatment.
Microscopic pathology
References
- ↑ Cederholm T, Jägrén C, Hellström K (1995). "Outcome of protein-energy malnutrition in elderly medical patients". Am J Med. 98 (1): 67–74. doi:10.1016/S0002-9343(99)80082-5. PMID 7825621.
- ↑ Lerner AB (1971). "On the etiology of vitiligo and gray hair". Am J Med. 51 (2): 141–7. PMID 5095523.
- ↑ Coulthard MG (2015). "Oedema in kwashiorkor is caused by hypoalbuminaemia". Paediatr Int Child Health. 35 (2): 83–9. doi:10.1179/2046905514Y.0000000154. PMC 4462841. PMID 25223408.
- ↑ Golden MH (1998). "Oedematous malnutrition". Br Med Bull. 54 (2): 433–44. PMID 9830208.
- ↑ Manary MJ, Heikens GT, Golden M (2009). "Kwashiorkor: more hypothesis testing is needed to understand the aetiology of oedema". Malawi Med J. 21 (3): 106–7. PMC 3717490. PMID 20345018.
- ↑ Golden MH (2015). "Nutritional and other types of oedema, albumin, complex carbohydrates and the interstitium - a response to Malcolm Coulthard's hypothesis: Oedema in kwashiorkor is caused by hypo-albuminaemia". Paediatr Int Child Health. 35 (2): 90–109. doi:10.1179/2046905515Y.0000000010. PMID 25844980.
- ↑ Ciliberto H, Ciliberto M, Briend A, Ashorn P, Bier D, Manary M (2005). "Antioxidant supplementation for the prevention of kwashiorkor in Malawian children: randomised, double blind, placebo controlled trial". BMJ. 330 (7500): 1109. doi:10.1136/bmj.38427.404259.8F. PMC 557886. PMID 15851401.
- ↑ Smith MI, Yatsunenko T, Manary MJ, Trehan I, Mkakosya R, Cheng J; et al. (2013). "Gut microbiomes of Malawian twin pairs discordant for kwashiorkor". Science. 339 (6119): 548–54. doi:10.1126/science.1229000. PMC 3667500. PMID 23363771.
- ↑ Prentice AM, Nabwera H, Kwambana B, Antonio M, Moore SE (2013). "Microbes and the malnourished child". Sci Transl Med. 5 (180): 180fs11. doi:10.1126/scitranslmed.3006212. PMID 23576812.
- ↑ Kau AL, Planer JD, Liu J, Rao S, Yatsunenko T, Trehan I; et al. (2015). "Functional characterization of IgA-targeted bacterial taxa from undernourished Malawian children that produce diet-dependent enteropathy". Sci Transl Med. 7 (276): 276ra24. doi:10.1126/scitranslmed.aaa4877. PMC 4423598. PMID 25717097.