Malnutrition syndrome

The physiological purpose of nausea is to discourage food intake, and vomiting is meant to expel food or other toxic substances present in the upper part of the gastrointestinal tract. Protracted vomiting may not only cause electrolyte imbalance, dehydration, or a malnutrition syndrome, but may also lead to mucosal laceration and upper gastrointestinal hemorrhage (Mallory-Weiss syndrome). 

F4. Fechner, A., Bohme, C., Gromer, S., Funk, M., Schirmer, R., and Becker, K., Antioxidant stams and nitric oxide in the malnutrition syndrome kwashiorkor. Pediatr. Res. 49, 237—243 (2001). F5. Feillet-Coundray, C., Rock, E., Coudray, C., Grzelkowska, K., Azais-Braesco, V., Dardevet, D., and Mazur, A., Lipid peroxidation and antioxidant status in experimental diabetes. Clin. Chim. Acta. 284, 31-43 (1999). 

Iron toxicity can be expected if the amount of free iron released into the plasma exceeds the plasma iron-binding capacity. This is more likely to occur when using iron sorbitol-citric acid complex (iron sorbitex), since the iron is less firmly bound than with iron dextran. Several conditions associated with low iron-binding capacity, such as malnutrition (kwashiorkor, malnutrition syndrome) and previous or simultaneous oral iron therapy appear to predispose to the development of these toxic reactions. In addition, folic acid deficiency has been reported to be a predisposing factor (SED-9, 516), the likely mechanism being altered iron utilization secondary to folic acid deficiency, which results in an increased saturation of ironbinding capacity. 

The effect of a diet free of one of the essential amino acids has been studied in rats. When the animals are simply presented with a diet devoid of one of the amino acids, the rats regulate their food intake accordingly by reducing consumption. If the diet devoid of one of the essential amino acids (except arginine) is force-fed, the rats develop a malnutrition syndrome that has sometimes been compared to that observed in human kwashiorkor. 

Human growth hormone, used as a human pharmaceutical, is approved for only one indication in the United States, treatment of growth failure owing to hGH deficiency, a condition known as pituitary dwarfism. However, clinical trials are under way to test its efficacy in Turner s syndrome, bums, wound healing, cachexia, osteoporosis, constitutional growth delay, aging, malnutrition, and obesity. 

Water-soluble vitamins removed by hemodialysis (HD) contribute to malnutrition and vitamin deficiency syndromes. Patients receiving HD often require replacement of water-soluble vitamins to prevent adverse effects. The vitamins that may require replacement are ascorbic acid, thiamine, biotin, folic acid, riboflavin, and pyridoxine. Patients receiving HD should receive a multivitamin B complex with vitamin C supplement, but should not take supplements that include fat-soluble vitamins, such as vitamins A, E, or K, which can accumulate in patients with renal failure. 

Obtain a thorough history and physical examination that may indicate the possible presence of GH deficiency. Exclude other identifiable causes of growth failure, such as hypothyroidism, chronic illness, malnutrition, genetic syndromes, and skeletal disorders. 

A special form of undemutrition that particularly affects children is known as protein-energy malnutrition (PEM) which is a spectrum of syndromes from marasmus (lack of energy intake) to kwashiorkor (deficient protein intake). 

The answer is D. The most likely diagnosis in this case is CPT-II deficiency, although this is apparently a fairly mild case. The patient s muscle weakness and brown urine (myoglobinuria) are characteristic of this disorder. CPT-I deficiency would most likely manifest as liver dysfunction. A secondary form of carnitine deficiency due to exogenous factors such as malnutrition, infection, or dialysis, is unlikely. MCAD ordinarily manifests within the first 3-5 years of life. The patient s normal stature is inconsistent with Marfan syndrome, which is characterized by tall stature and very long bones in the extremities. 

Vitamin E may be indicated in some rare forms of anemia such as macrocytic, megaloblastic anemia observed in children with severe malnutrition and the hemolytic anemia seen in premature infants on a diet rich in polyunsaturated fatty acids. Also anemia s in malabsorption syndromes have shown to be responsive to vitamin E treatment. Finally, hemolysis in patients with the acanthocytosis syndrome, a rare genetic disorder where there is a lack of plasma jS-lipoprotein and consequently no circulating alpha tocopherol, responds to vitamin E treatment. In neonates requiring oxygen therapy vitamin E has been used for its antioxidant properties to prevent the development retrolental fibroplasia. It should be noted that high dose vitamin E supplements are associated with an increased risk in allcause mortality. 

Physiologically, these plasma changes are included here since they reflect impaired numbers or function of B-lymphocytes. Two broad categories are recognizable. First, such immunodeficiency states may exist on congenital basis and often do so with concurrent defects in the T cells (Fig. 1). Alternatively, severe reductions in immunoglobulin levels often develop in the course of chronic lymphocytic leukaemia and myeloma. Not dissimilar impairment of immune competence is found with nephrotic syndrome, protein-losing enteropathy or even malnutrition, and in these instances is equally profound. 

Unlabeled Uses Hyperlipidemia, lung cancer, male contraception, malnutrition, postmenopausal osteoporosis, rheumatoid arthritis, Sjogren s syndrome, trauma/sur-... 

There are several reasons to anticipate that antidepressants might be effective in the treatment of anorexia nervosa. Malnutrition has been shown to produce a syndrome that is virtually indistinguishable from depression, with anhedonia, weight loss, motor retardation, anergia, and decreased ability to think or concentrate. In addition, the high association of co-morbidity between anorexia nervosa and mood disturbances, as well as the preponderance of mood disorders in first-degree relatives of those with anorexia nervosa, have led some clinicians to consider and treat this condition as a depressive variant. 

Treatment of children with short stature should be carried out by specialists experienced in the use of GH. Treatment is begun with 0.025 mg/kg daily and may be increased to a maximum of 0.045 mg/kg daily. Children must be observed closely for slowing of growth velocity, which could indicate a need to increase the dosage or the possibility of epiphyseal fusion or intercurrent problems such as hypothyroidism or malnutrition. Children with Turner syndrome or chronic renal insufficiency require somewhat higher doses. 

CFD is further associated with the following inherited metabolic disorders 5,10-methylen-tetrahydrofolate reductase (MTHFR) deficiency [7], 3-phos-phoglycerate dehydrogenase (PGDH) deficiency [8], dihydropteridine reductase (DHPR) deficiency [9], as well as with Rett syndrome [10], and Aicardi-Gou res Syndrome [11]. Furthermore, folate deficiency may be associated with congenital folate malabsorption, severe malnutrition, and formiminotransferase deficiency. 

The causes of human copper deficiency include (1) low intake - malnutrition, total parenteral nutrition (TPN) (2) high loss - cystic fibrosis, nephrotic syndromes and (3) genetic factors — Menkes disease. Copper deficiency may also be associated with chronic malabsorption, a situation which is made much worse in cases of gastric and bowel resection. Several special diets, including powdered milk, liquid protein and standard hospital diets are a means of inducing copper deficiency. The amount of copper in US food has decreased steadily since 1942, and may be related to the rising incidence of coronary artery disease. A copper deficiency may also occur as the result of the use of chelators for other purposes for example, diethyl dithiocarbamate is an in vivo metabolite of ANTABUSE (disulfiram). 

Davis AJ, Pandher GK, Masson GM, Sheron N. A severe case of ovarian hyperstimulation syndrome with liver dysfunction and malnutrition. Eur J Gastroenterol Hepatol 2002 14(7) 779-82. 

Detoxification refers to the clearing of alcohol from the body and the readjustment of all systems to functioning in the absence of alcohol. The alcohol withdrawal syndrome at the mild end may include only headache and irritability, but about 5% of alcoholic patients have severe withdrawal symptoms manifested by tremulousness, tachycardia, perspiration, and even seizures (rum fits). The presence of malnutrition, electrolyte imbalance, or infection increases the possibility of cardiovascular collapse. 

There are also immunodeficiency states that are primary and can be caused by phagocytic cell defects, deficiencies in the complement system, B- and T-cell deficiency, and other causes. Secondary immunodeficiency disorders can result from malnutrition, cytotoxic drugs, infections with pyrogenic bacteria, and infections with an RNA retrovirus, as in the acquired immunodeficiency syndrome (AIDS). 

Cachexia is loss of weight, muscle atrophy, fatigue, weakness and significant loss of appetite. It is seen in patients with cancer, acquired immunodeficiency syndrome (AIDS), chronic obstructive pulmonary disease and congestive heart failure. Underlying causes are poorly understood, but there is an involvement of inflammatory cytokines, such as TNF-a, IFN-y, IL-6 and tumour-secreted proteolysis-inducing factor. Related syndromes are kwashiorkor and marasmus, although these are most often symptomatic of severe malnutrition. 

Albumin Maintains plasma oncotic pressure. Transports fat-soluble substances, e.g. bilirubin, drugs Reduced levels Low levels cause ascites and increase free plasma concentration of albumin-bound drugs, e.g. oestradiol, phenytoin Albumin is a useful clinical indicator of the liver s synthetic function. The liver produces and exports up to 12 g of albumin per day. Low levels are also seen in malnutrition, hypercatabolism and nephrotic syndrome. Half-life of 20 days, therefore indicator of chronic liver disease... 

When interpreting a patient s albumin level, possible extrahepatic causes for low levels should be considered, for example a reduction in albumin production associated with malnutrition and malignancy, or increased albumin loss seen in inflammatory bowel disease and nephrotic syndrome. 

In most cases the onset of ascites is a sign of decompensated severe chronic liver disease and impaired liver function. However, it can also be present in non-liver conditions such as malnutrition, heart failure and nephrotic syndrome. 

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