Nutrition care of AIDS patients

Often the complications of the acquired immunodeficiency syndrome (AIDS) have a negative impact on nutritional status. Weight loss and protein depletion are commonly seen among the AIDS population. Though the relationship between disease progression and nutritional status has not been established, maintaining good nutritional status may support response to treatment of opportunistic infections and improve patient strength and comfort. Increased nutrient needs, decreased nutrient intake, and impaired nutrient absorption contribute to malnutrition in AIDS patients. Causes of decreased nutrient intake and absorption may be poor appetite, oral and esophageal pain, mechanical problems with eating, and gastrointestinal complications (diarrhea and malabsorption). Causes of these impediments to maintaining nutritional status are discussed, and suggestions to overcome them are given. Dietitians working with AIDS patients need to understand how the complications of the disease might affect nutritional status so that strategies for nutrition treatment can be developed. Nutrition care of AIDS patients requires that dietitians and their support personnel provide supportive, nonjudgmental care. The patients should be included in decision making regarding their nutrition care. Caring for AIDS patients in the community and through home care agencies represents an area in need of the expertise of a dietetics professional.     

Malnutrition in patients with AIDS

Malnutrition is a frequent problem in persons infected with the human immunodeficiency virus. The origin of malnutrition in patients with AIDS may be multifactorial. The primary mechanisms include disorders of food intake, alterations in intermediary metabolism, and nutrient malabsorption. Attention to the problems of malnutrition in patients with AIDS is of paramount importance because the timing of death in these patients may be more closely related to degree of body cell mass depletion than to any specific underlying infection. Nutritional support can improve nutritional status in selected patients, and repletion of body cell mass may be associated with functional improvement. Early assessment, attention to nutritional requirements, and prompt intervention can minimize wasting and replete body cell mass. This article examines the evidence for malnutrition in patients with AIDS, reviews the studies of nutritional support, and presents an approach to the management of malnutrition in AIDS.     

Nutrition support of the pediatric patient with AIDS

Maintaining optimal nutrition in the pediatric patient with Acquired Immune Deficiency Syndrome (AIDS) is challenging, but it may be one of the most effective therapies. Patients experience numerous complications that compromise nutritional status. Infection, fever, diarrhea, feeding problems, and decreased intake all contribute to malnutrition, which in turn predisposes the patient even more to infection and malabsorption. Nutrition assessment should be done routinely so that new problems may be identified and treated. High-calorie, high-protein feedings, vitamin supplementation, and, when necessary, gavage feedings or parenteral nutrition are recommended to improve nutritional status and prevent further deficits. Maintaining optimal nutrition in the pediatric patient with Acquired Immune Deficiency Syndrome (AIDS) poses a significant challenge to the health care team. Patients may experience numerous complications that compromise nutritional status. The patient is at high risk for opportunistic infections, especially of the lungs, central nervous system, gastrointestinal (GI) tract, and skin. Such infections are common causes of morbidity and mortality. Impaired nutritional status may further impair the patient's immunocompetence. A study by Kotler and Gaety demonstrated severe progressive malnutrition in adult AIDS patients, with the lowest measures of lean body mass occurring in those patients close to death at the time of the study. While no studies of children with AIDS have been done to date, we have subjectively observed feeding problems, weight loss, and malnutrition in most of the patients we have seen.     

D-lactate and metabolic bone disease in patients receiving long-term parenteral nutrition

D-lactate accumulates in some patients with malabsorption who continue oral intake of carbohydrate leading to a clinical syndrome of acidosis and encephalopathy. To assess the possibility that D-lactate contributes to acidosis and/or metabolic bone disease in patients with malabsorption receiving long-term parenteral nutrition yet maintaining oral intake, D-lactate levels in serum and urine were measured in 14 long-term parenteral nutrition subjects (average duration of support 74 months) and 27 control subjects. Significant elevations in both serum and urine D-lactate were found in only two parenteral nutrition subjects. Both subjects with elevated D-lactate levels had bone pain, x-ray evidence of fractures, and biopsy evidence of osteomalacia. These studies suggest that D-lactate accumulation may be a heretofore unappreciated metabolic abnormality associated with metabolic bone disease and acidosis in patients with malabsorption who are supported by long-term parenteral nutrition.     

The effect of age on the caloric requirement of malnourished individuals.

The effect of age on the response to total parenteral nutrition (TPN) was evaluated in 325 patients by measuring body composition by multiple-isotope dilution at the onset and at 2-wk intervals during the course of TPN. On the basis of their initial body composition, patients were divided into two groups: normally nourished and malnourished. TPN did not alter the body composition of the normally nourished patients. In the malnourished patients, a statistically significant correlation existed between the daily change in the dependent variable body cell mass (BCM) and the independent variables caloric intake, nutritional state, and age. With advancing age, more calories are required to maintain the BCM of malnourished patients. With a similar nutritional intake, a depleted BCM is restored more slowly in older patients. Age is a significant independent variable affecting the response to nutritional support.     

Evaluation of a semi-elemental enteral feed in patients with malabsorption and/or disease-related malnutrition

A semi-elemental energy-dense enteral feed was evaluated to determine its effect on nutritional repletion and tolerance in a diverse group of patients with malabsorption and/or disease-related malnutrition. Forty-nine patients (26 male, 23 female) entered and completed this multicentre study. Mean daily energy requirements were 2107 kcals of which 1704 kcals were prescribed from the enteral feed. Mean daily energy intake from the feed was 1472 kcals and patients consumed the feed for a mean of 13.2 days either as sole source of nutrition or as a supplement. Body weight changes were related to duration of feeding: patients who were fed for more than 14 days experienced a mean increase in body weight of 0.56 kg. Biochemical parameters of nutritional status, i.e. mean total protein and serum albumin, improved during the feeding period. Tolerance of the feed and clinical response to feeding were satisfactory. In patients with malabsorption and/or malnutrition a semi-elemental enteral feed represents a viable and palatable alternative to elemental diets when everyday food and whole protein feeds are not tolerated.     

Cancer cachexia

Cancer cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients bearing disseminated disease, cachexia may be present in the early stages of tumor growth before any signs or symptoms of malignancy. A decline in food intake relative to energy expenditure (which may be increased, normal, or decreased) is the fundamental physiologic derangement leading to cancer-associated weight loss. In addition, abnormalities of host carbohydrate, protein, and fat metabolism lead to continued mobilization and ineffective repletion of host tissue, despite adequate nutritional support. Mediators of cancer anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses. Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Although in one study parenteral nutritional support has improved operative morbidity and mortality in cancer patients, it has not yet improved response to chemotherapy or radiation therapy. Because of metabolic derangements seen in cancer cachexia, effective nutritional treatment regimens will probably require manipulation of host intermediary metabolism in addition to feeding. Insulin therapy or exercise are two such methods which appear to preserve host composition by preferential feeding of the host at the expense of the tumor. Future studies which more clearly define the role of signal molecules in producing cancer cachexia syndrome may lead to new treatment strategies, possibly involving modulation of the effects of such molecules on host metabolism.     

宁波某三甲医院胃结直肠癌I～Ⅲ期患者营养风险、不足、支持情况：前瞻性调查

目的调查宁波某三甲医院外科病房的全部入院患者的营养风险发生率及I～Ⅲ期胃结直肠癌患者的营养风险、营养不足发生率和营养支持应用情况。方法应用定点连续采样的方法,对2012年1至12月胃肠外科、普通外科两个病房能够做营养风险筛查2002的全部住院患者,均收集基础资料录入电子数据收集系统（EDC）。其中277例I～Ⅲ期胃结直肠癌患者按计划调查营养风险、营养不足的发生率;全程记录住院期间是否接受肠外肠内营养支持,调查输入热量、氨基酸、碳水化合物及脂肪的入量和天数,录入EDC,经核查后进行合适的统计分析。结果连续采样的3513例住院患者,总营养风险发生率为17．28％,符合预定诊断的调查对象277例患者,营养风险发生率为45．49％。从营养风险筛查2002中营养缺失部分评分的多指标计算营养不足的发生率为13．36％,按单指标计算（体重指数〈18．5kg/㎡,一般情况差）营养不足的发生率为9．03％,多指标与单指标来源的营养不足发生率差距为4．33％。有营养风险患者的营养支持率为93．65％;无营养风险患者的营养支持率为61．59％;肠外营养与肠内营养的比例为2．67：1,部分肠外营养与肠内营养支持极不规范。结论本院I～Ⅲ期胃结直肠癌患者营养风险发生率较高,营养支持应用不规范,临床医师需继续学习中华医学会“肠内与肠外营养临床诊疗指南”。     

Nine year's survival with short bowel syndrome after occlusion of the superior mesenteric artery in an elderly man: a study of periods of parenteral nutrition

A 70-year-old man with severe short bowel syndrome after acute occlusion of the superior mesenteric artery and massive intestinal gangrene was given total and supplementary parenteral nutrition for six periods of 14 to 28 days; he survived for more than 9 years and died from the effects of nutritional depletion. Studies of the blood chemistry and the urinary excretion of nitrogen and electrolytes during the six periods of intravenous nutrition showed that nutritional repletion of nitrogen and electrolytes was achieved without adverse effects on the liver function. The results suggest that intermittent total and supplementary parenteral nutrition may allow nutritional repletion and thereby prolong the survival time in the elderly patient in whom massive intestinal resection has been performed.     

The impact of nutritional support on appetite and food intake

Artificial nutrition (enteral tube feeding and parenteral nutrition) is increasingly being used in hospital and community settings to provide short- and long-term nutritional support to a diverse range of patients with acute and chronic conditions. Despite these methods of feeding being used either in cojunction with diet, or as a sole source of nutrition, the issue of their satiating ability has previously been largely overlooked. The consensus that emerges from this review is that nutrients provided by enteral tube feeding or parenteral nutrition are not as effective as orally ingested nutrients at relieving appetite sensations or suppressing food intake. When artificial nutritional support is used as the sole source of nutrition, distressing appetite sensations may occur, even if full nutrient requirements are met by enteral tube or parenteral feeding. When used as a supplement to ad libitum food intake, enteral tube feeding and parenteral nutrition only partially suppress oral intake, and total energy intake is increased. The mechanisms responsible for the poorer satiating ability of artificial feeding methods, relative to food intake, are not clearly understood, but the bypassing of the upper gastrointestinal tract and associated cephalic phase response by these methods of nutrient delivery may be important.     

Intestinal infection and malnutrition initiate acquired immune deficiency syndrome (AIDS)

AIDS is a complex immunodeficiency syndrome affecting a limited target population, principally male homosexuals. The various immunologic dysfunctions in AIDS, or those persons with the AIDS prodrome, are explained in terms of multiple pathogeninduced alterations in the gastrointestinal tract which result in malabsorption and malnutrition. Malnutrition need not be severe but may be due to failure to transport one or serveral nutrients essential for immune functions. Alteration of gastrointestinal permeability results in an increased uptake of normally excluded microbial products possibly resulting in latent virus activation or enhanced replication of viruses, including the retrovirus HTLV-III. Once this has occurred, transmissible agents are present which may cause or predispose to AIDS in other susceptible populations such as hemophiliacs, persons receiving multiple blood transfusions, drug users sharing needles, populations with repeated close contact, and susceptible populations by virtue of genetic, environmental or disease state. The combination of rigorous parenteral nutrient repletion and antibiotic therapy aimed at abrogating the intestinal infections, and immunologic therapies may be effective in addressing the underlying causes of the immune defects in AIDS. A prevention strategy should be directed toward reducing repeated polymicrobial enteric infections and their attendant malabsorption (e.g., gay bowel syndrome) in addition to reducing exposure to circulating transmissible agents.     

Protein catabolism and requirements in severe illness

Reduced total body protein mass is a marker of protein-energy malnutrition and has been associated with numerous complications. Severe illness is characterized by a loss of total body protein mass, mainly from the skeletal muscle. Studies on protein turnover describe an increased protein breakdown and, to a lesser extent, an increased whole-body protein synthesis, as well as an increased flux of amino acids from the periphery to the liver. Appropriate nutrition could limit protein catabolism. Nutritional support limits but does not stop the loss of total body protein mass occurring in acute severe illness. Its impact on protein kinetics is so far controversial, probably due to the various methodologies and characteristics of nutritional support used in the studies. Maintaining calorie balance alone the days after an insult does not clearly lead to an improved clinical outcome. In contrast, protein intakes between 1.2 and 1.5 g/kg body weight/day with neutral energy balance minimize total body protein mass loss. Glutamine and possibly leucine may improve clinical outcome, but it is unclear whether these benefits occur through an impact on total body protein mass and its turnover, or through other mechanisms. Present recommendations suggest providing 20 - 25 kcal/kg/day over the first 72 - 96 hours and increasing energy intake to target thereafter. Simultaneously, protein intake should be between 1.2 and 1.5 g/kg/day. Enteral immunonutrition enriched with arginine, nucleotides, and omega-3 fatty acids is indicated in patients with trauma, acute respiratory distress syndrome (ARDS), and mild sepsis. Glutamine (0.2 - 0.4 g/kg/day of L-glutamine) should be added to enteral nutrition in burn and trauma patients (ESPEN guidelines 2006) and to parenteral nutrition, in the form of dipeptides, in intensive care unit (ICU) patients in general (ESPEN guidelines 2009).     

Nutritional support in acute pancreatitis.

This paper reviews the current practice of nutritional support in acute pancreatitis. Appropriate interventions depend on the severity and duration of the pancreatitis and its complications. Current trends are away from restriction of oral or enteral intake, instead preferring this route to parenteral administration if possible. The role of the gut mucosal barrier in the pathogensis of the systemic response in pancreatitis has led to attempts to use enteral nutritional support to prevent complications, in addition to meeting nutritional needs in patients with long-term severe illness. Many clinicians believe that the management of acute pancreatitis should start from the concept of "pancreatic rest." Based on a simple understanding of pancreatic physiology and a belief that further stimulation of the pancreas during an attack of pancreatitis would exacerbate the inflammatory process by releasing more enzymes, traditional teaching has been that it is necessary to avoid all oral intake to prevent any inappropriate stimulation of pancreatic enzyme production. Accordingly, patients with acute pancreatitis are often deprived of enteral nutrition, and may be given intravenous parenteral nutritional support. Such an approach to nutritional support needs to be revised, since evidence emerging from many recent studies consistently indicates that an enteral route of nutrition is far superior.     

Nutritional support in HIV infection and AIDS

Weight loss and wasting are common features of HIV infection and AIDS.Patterns of weight loss can be acute or chronic which appear to be related primarily to systemic infections and gastrointestinal pathology, respectively. However, weight loss is not inevitable. and periods of weight stability and weight gain have been documented. Reduced food intake appears to be a major cause of weight loss in HIV infection. Since time of death has been associated with degree of wasting, it seems reasonable to suggest that nutritional support may contribute to enhancing survival and quality of life. All patients should have early access to a qualified dietitian such that assessment of individual situations can be made and appropriate dietary advice given, within a multi-disciplinary approach. Choice of nutritional therapy should be made based on an assessment of the causes of weight loss and an assessment of gut function. Treating infections and alleviating symptoms is vital for ensuring effective nutritional support. Enhancing the energy and protein density of foods and use of oral supplements should be considered if a normal diet alone cannot meet nutritional requirements. Unnecessary dietary restrictions should be avoided. Enteral feeding is indicated for patients unable to meet their needs via the oral route, and in cases of inadequate gut function, parenteral nutrition may be necessary. There is currently insufficient clinical evidence to justify the need for special enteral formulae specifically for patients with HIV infection.     

Changes in nutritional assessment variables caused by total parenteral nutrition in anorexia nervosa

Nutritional assessment variables were measured weekly in 10 young women with severe anorexia nervosa during treatment with total parenteral nutrition (TPN) for a 5 week period. Before the start of treatment the patients had lost 25-53% of their habitual weight, triceps skin fold (TSF) and arm muscle circumference (AMC) measurements were below the 5th percentile and all were anergic in the delayed hypersensitivity (DH) response. Plasma protein levels were normal except in fibronectin and prealbumin where levels below the reference interval was found in five patients. During TPN the body weight increased most likely due to rehydration and increase in lean body mass. Significant increases were seen in body weight weekly, but in TSF and AMC only after 4 and 3 weeks respectively. TSF and AMC were still below or at the 5th percentile after 5 weeks of TPN. DH response as well as fibronectin and prealbumin levels normalised in all patients. Despite only partial recovery in body cell mass the clinical picture had changed markedly so that the patients now were amenable to psychotherapy and had an adequate intake of food orally, enabling further nutritional therapy to be completed without parenteral support.     

贵州省中小医院住院患者营养风险筛查及营养支持应用现状

目的调查贵州省中小医院住院患者营养风险、营养不足、超重和肥胖发生率及营养支持的应用现状。方法采用定点连续抽样,选择2008年2月至2009年3月贵州省4家中小医院普通外科、胸外科、神经内科、消化内科、呼吸内科、。肾内科住院患者进行营养风险筛查2002（NRS2002）,于患者入院次日早晨实施,并调查患者2周内（或至出院时）的营养支持状况,分析营养风险和营养支持的关系。NRS2002i〉3分为有营养风险,体重指数〈18．5kg／m。并结合患者临床情况判定为营养不足。结果共1668例患者人选并全部完成NRS2002筛查,营养不足和营养风险的发生率分别为12．2％和30．2％,504例有营养风险的患者中54例（11．7％）接受营养支持,所有营养支持均为肠外营养。结论NRS2002适用于住院患者的营养筛查;营养支持在贵州省中小医院应用不足,应用方式单一,需进一步规范基于循证医学证据的营养支持应用。     

Clenbuterol treatment increases muscle mass and protein content of tumor-bearing rats maintained on total parenteral nutrition

Treatment of tumor-bearing (TB) and control rats with the anabolic beta-2 agonist drug clenbuterol (CLE) for 14 days reduced food intake for 4 days initially. Feeding was increased in anorectic TB rats, however, during the last 7 days of drug administration. Since minimal muscle savings were observed in chow-fed TB rats treated with CLE, the anabolic effects of this drug were investigated in a second experiment on TB rats maintained on total parenteral nutrition (TPN). Sixteen days after the subcutaneous transplantation of methylcholanthrene-induced sarcomas rats was begun on a 2-week schedule of TPN. One group of these rats was treated daily for 14 days with CLE, while the remaining rats received injections of saline. Additional groups of TB and nonTB rats were maintained on rat chow for this period and treated with saline. Although TB rats maintained on rat chow or TPN and treated with saline exhibited significantly decreased gastrocnemius muscle weight and protein content, treatment of TB-TPN rats with clenbuterol normalized muscle mass and increased muscle protein content significantly and increased plasma concentrations of branched-chain amino acids. These results indicate that although nutritional support of TB organisms does not result in protein repletion, the addition of an anabolic drug renders the nutritional support highly efficacious.     

Weight gain and nutritional efficacy in anorexia nervosa

To evaluate the usefulness of interval weight change in assessing nutritional support efficacy, we studied four anorexia nervosa patients (52% ideal body weight) requiring long-term total parenteral nutrition (TPN) for 63 +/- 18 days. Fluid and electrolyte deficits were corrected before the initiation of nutritional support. Resting energy expenditure was measured before the initiation of TPN and weekly thereafter, using indirect calorimetry. Daily caloric expenditure was estimated at 1.1 X resting energy expenditure, based on previous studies of continuous heart rate monitoring in this patient population. Daily excess calories were calculated as caloric intake minus caloric expenditure. Each patient was weighed daily and linear regression analysis (excess calories versus weight change) was performed for individual patients and the group over intervals of varying length. There was no individual or group correlation between excess calories and weight gain on a daily or weekly interval basis. Cumulative weight changes over the long-term course of TPN correlated significantly with cumulative excess calories for each patient and the whole group (r = +0.82, p less than 0.01). The excess calories required to gain a kilogram body weight ranged from 5569 to 15619 kcal/kg with a mean of 9768. Cumulative long-term weight changes during nutritional repletion in anorexia nervosa are meaningful indicators of caloric balance, but short interval weight changes (daily, weekly) are not. The caloric cost of weight gain is variable in this population.     

Successful management of chronic intestinal pseudo-obstruction with home parenteral nutrition

Chronic intestinal pseudo-obstruction is a disorder of gut motility resulting in severe abdominal pain, bloating, nausea, and vomiting after eating. The avoidance of food in order to minimize symptoms causes malnutrition. To date, no medical or surgical treatment has been shown to be of lasting benefit. We treated 10 patients disabled by chronic intestinal pseudo-obstruction using home parenteral nutrition. All were rendered minimally symptomatic as long as they refrained from significant oral intake. Nine of the 10 patients were malnourished prior to the institution of treatment. Home parenteral nutrition increased mean total body weight from 74.7 +/- 2.9 to 93.5 +/- 3.7% (p less than 0.001), mean lean body mass from 78.4 +/- 6.5 to a mean of 92.7 +/- 2.6 (p less than 0.02), and mean body fat from 57.1 +/- 8.8 to 83.8 +/- 8.2% of expected values (p less than 0.05). Mean total body potassium increased from 68.8 +/- 13.1 to 80.5 +/- 10.7 g (p less than 0.05). We conclude that in chronic intestinal pseudo-obstruction, home parenteral nutrition coupled with minimal oral intake effectively relieves symptoms and significantly improves the nutritional depletion.     

Nutrition in pediatric patients before liver transplantation

Malnutrition leading to growth failure is one of the main problems in maintainig children with chronic liver diseases. The pathogenesis of malnutrition is complex and includes reduced calorie intake, fat malabsorption, impaired protein metabolism and increased energy expenditure. The nutritional status is an important risk factor for survival post liver transplantation. Aggressive nutritional support with careful monitoring is essential, particularly where liver transplantation is considered. When the oral nutrition is inadequate, the enteral feeding with nocturnal intragastric tube should be started. In case of gastrointestinal intolerance, severe malnutrition and gastrointestinal bleeding, parenteral nutrition should be considered.