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Autor: Grafiati

Data publikacji: 27 lipca 2024

Data aktualizacji: 28 lipca 2024

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1

Briend, André. Prévention et traitement de la malnutrition: Guide pratique. Paris: Editions de l'ORSTOM, 1985.

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2

Stratton, R. J., C. J. Green i M. Elia, red. Disease-related malnutrition: an evidence-based approach to treatment. Wallingford: CABI, 2003. http://dx.doi.org/10.1079/9780851996486.0000.

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J, Green Ceri, i Elia Marinos, red. Disease-related malnutrition: An evidence-based approach to treatment. Wallingford, UK: CABI Pub., 2003.

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4

A, Ashworth, i World Health Organization, red. Guidelines for the inpatient treatment of severely malnourished children. Geneva, Switzerland: World Health Organization, 2003.

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5

Alihonou, Eusèbe. Réhabilitation nutritionnelle à domicile. Cotonou, République du Bénin: Centre régional pour le développement et la santé, 1992.

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6

Stuart, Gillespie, i United Nations. Administrative Committee on Co-ordination. Sub-committee on Nutrition., red. What works?: A review of the efficacy and effectiveness of nutrition interventions. Geneva: United Nations, Administrative Committee on Coordination, Sub-Committee on Nutrition, 2001.

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7

Organization, World Health, red. Management of severe malnutrition: A manual for physicians and other senior health workers. Geneva: World Health Organization, 1999.

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8

J, Raiten Daniel, i Talbot John M, red. Clinical trials for the treatment of secondary wasting and cachexia: Selection of appropriate endpoints : proceedings of a workshop, May 22-23, 1997. Bethesda, MD: American Society for Nutritional Sciences, 1999.

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9

American Society for Parenteral and Enteral Nutrition. Improve patient outcomes: A.S.P.E.N.'s step-by-step guide to addressing malnutrition. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition, 2015.

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10

Prudhon, Claudine. La malnutrition en situation de crise: Manuel de prise en charge thérapeutique et de planification d'un programme nutritionnel. Paris: Action contre la faim, 2001.

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11

S, Jacobson Marc, red. Adolescent nutritional disorders: Prevention and treatment. New York, N.Y: New York Academy of Sciences, 1997.

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12

Harry, Campbell, Pierce N. F i World Health Organization. Dept. of Child and Adolescent Health and Development., red. Serious childhood problems in countries with limited resources: Background book on management of the child with a serious infection or severe malnutrition. Geneva: Department of Child and Adolescent Health and Development, World Health Organization, 2004.

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13

Doley, Jennifer, i Mary J. Marian. Adult Malnutrition: Diagnosis and Treatment. Taylor & Francis Group, 2022.

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14

Doley, Jennifer, i Mary J. Marian. Adult Malnutrition: Diagnosis and Treatment. Taylor & Francis Group, 2022.

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15

Doley, Jennifer, i Mary Marian. Adult Malnutrition: Diagnosis and Treatment. CRC Press LLC, 2022.

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16

Doley, Jennifer, i Mary J. Marian. Adult Malnutrition: Diagnosis and Treatment. Taylor & Francis Group, 2022.

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17

Adult Malnutrition: Diagnosis and Treatment. CRC Press LLC, 2022.

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18

Dupire, J. Objectif : Malnutrition. Similia, 1999.

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19

Keshav, Satish, i Alexandra Kent. Starvation and malnutrition. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0332.

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Starvation is a state of severe malnutrition due to a reduction in macro- and micronutrient intake. The basis underlying starvation is an imbalance between energy intake and energy expenditure. The commonest cause of starvation is lack of available food, usually due to environmental, social, and economic reasons, although other causes include anorexia nervosa; depression and other psychiatric disorders; coma and disturbance of consciousness; intestinal failure; and mechanical failure of digestion, including poor dentition and intestinal obstruction. Protein energy malnutrition is usually seen in developing countries. This chapter discusses starvation and malnutrition, focusing on their etiology, symptoms, demographics, natural history, complications, diagnosis, treatment, and prognosis.

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20

Riddle of Malnutrition: The Long Arc of Biomedical and Public Health Interventions in Uganda. Ohio University Press, 2017.

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21

Catching up: Report on the Massachusetts Growth and Nutrition Clinics, FY 1985-FY 1989. [Boston, MA] (150 Tremont St., Boston 02111): Commonwealth of Massachusetts, Dept. of Public Health, 1993.

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22

Tappan, Jennifer. The Riddle of Malnutrition: The Long Arc of Biomedical and Public Health Interventions in Uganda. Ohio University Press, 2017.

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23

The Riddle of Malnutrition: The Long Arc of Biomedical and Public Health Interventions in Uganda. Ohio University Press, 2017.

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24

Recuperación de la florifagia tahuaintisuyana para erradicar las enfermedades carenciales. Lima, Perú: Juan Gutemberg Editores-Impresores, 2009.

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25

Beattie, R. Mark, Anil Dhawan i John W.L. Puntis. Nutrition support teams. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0009.

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Malnutrition 68Suggested core composition of the NST 69Roles of the NST 69There has been a considerable increase in the use of intensive nutritional support (both parenteral and enteral) in the management of children with chronic disorders. In addition, awareness of overt or potential malnutrition among hospital inpatients has increased. The identification of those with (or at risk from) malnutrition, and provision of effective nutritional intervention requires a multidisciplinary team approach since the skills required to deal with the details of assessment, prescription, administration, and monitoring of treatment frequently fall outside the remit of a single practitioner....

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26

Spector, Jonathan M., i Timothy E. Gibson, red. Atlas of Pediatrics in the Tropics and Resource-Limited Settings. American Academy of Pediatrics, 2005. http://dx.doi.org/10.1542/9781581104271.

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All-new convenient take-along guide to the full spectrum of more than 80 pediatric tropical diseases and conditions. A full-color comprehensive resource for treatment of pediatric tropical disease. Includes dosing information for all diseases discussed, at-a-glance endemicity maps, and weight/height tables for use in assessing nutritional status. Includes a bonus free tool for field screening for malnutrition.

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27

O’Riordan, Stephen MP, i Antoinette Moran. Cystic fibrosis-related diabetes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0008.

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This chapter on CFRD reviews the ever-evolving topic and provides up-to-date information on how to diagnose and manage cystic fibrosis-related diabetes CFRD in the acute and chronic setting. The treatments necessary to treat and prolong life in CF, including their unique dietary requirements, must always be followed as a first priority, with diabetes care adjusted accordingly. Early intervention with insulin has been shown to reverse clinical deterioration, even in those with mild diabetes. Newly emerging treatments for CF which have the potential to restore defective chloride channels may have implications for the development and treatment of CFRD. Whilst CFRD shares features of both type 1 and type 2 diabetes, there are important differences which necessitate a unique approach to diagnosis and management. Factors specific to CF that variably affect glucose metabolism include chronic respiratory infection and inflammation, increased energy expenditure, malnutrition, glucagon deficiency, and gastrointestinal abnormalities.

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28

(Editor), Marc S. Jacobson, Neville H. Golden (Editor), Charles E. Irwin (Editor) i Jane M. Rees (Editor), red. Adolescent Nutritional Disorders: Prevention and Treatment (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1997.

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29

(Editor), Marc S. Jacobson, Jane M. Rees (Editor), Neville H. Golden (Editor) i Charles E. Irwin (Editor), red. Adolescent Nutritional Disorders: Prevention and Treatment (Annals of the New York Academy of Sciences, Vol. 817). New York Academy of Sciences, 1997.

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30

Machado, Pedro M. Inclusion body myositis. Redaktorzy Hector Chinoy i Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.

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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.

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31

Kliger, Alan S., i Rita Suri. Frequent haemodialysis. Redaktor Jonathan Himmelfarb. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0262_update_001.

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Haemodialysis is a renal replacement treatment, an ‘artificial kidney’ that performs some of the functions of the normal kidney. It is an inelegant device, providing only a fraction of native kidney’s ability to filter toxins from the blood, but with none of the responsiveness to volume, fine feedback control to regulate solute concentrations, or endocrine functions of the healthy organ. Conventional haemodialysis performed three times a week for 4 hours per treatment filters the blood for only 12 of 168 hours each week, and removes less than 10 per cent of small solutes like urea than does the normal kidney. It is therefore not surprising that haemodialysis patients suffer high morbidity and mortality. A dialysis patient’s expected remaining lifetime is substantially shorter than a comparable person with normal kidney function. For example, a woman aged 40–44 years old in the general population can expect on average 40 more years of life, but if she is on dialysis her life expectancy is only 8.1 years. She is also more likely to have co-morbid disease, including hypertension, cardiovascular disease, metabolic bone disease, anaemia, sepsis, depression, malnutrition and inflammation, and physical and cognitive impairment.

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32

World Health Organization (WHO). Serious Childhood Problems in Countries with Limited Resources. World Health Organization, 2004.

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33

Gladman, Matthew, i Lorne Zinman. Symptomatic Management in Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0024.

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Although ALS remains an incurable disease, there are specific treatments that can significantly improve quality of life and some that can modify survival. Patients are best followed in multidisciplinary ALS clinics where a number of medical experts can address a wide range of symptoms. Additional studies are needed to develop evidenced-based best practice guidelines to further improve care for patients with ALS. Bulbar dysfunction eventually affects the vast majority of ALS patients, and progressive dysphagia results from weakness and spasticity of the muscles involved in swallowing. Dysphagia is associated with increased risk of aspiration and choking, as well as with long-term risk of malnutrition, weight loss, and dehydration. Appropriate measures to enhance caloric intake contribute to a greater sense of well-being. Augmentative communication devices and ventilator support can also be used to reduce suffering.

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34

Voinescu, Alexandra, Nadia Wasi Iqbal i Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Redaktor David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.

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In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.

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