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Because of hyperinflation, the diaphragm of emphysematous patients operates at a disadvantageous position which affects its mechanical arrangement, modifies the configuration of its zone of apposition, increases its radius of curvature, and decreases its muscle fiber length below optimal configuration. The diaphragm in emphysema therefore displays a suboptimal configuration limiting its ability to function properly but shows no inherent structural insufficiency, unless its contractility is impaired by significant arterial blood gas anomalies or severe malnutrition. The demand imposed on the diaphragm in emphysema is increased by both hyperinflation and air-flow obstruction. With altered performance of the diaphragm and increased demand, force reserve is diminished and diaphragmatic fatigue may occur; this imbalance is targeted in some treatment modalities of emphysema such as pulmonary rehabilitation programs and lung volume reduction surgery.
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PMID:The diaphragm in emphysema. 961 11

Malnutrition and weight loss are clinically significant complications of both human immunodeficiency virus (HIV) infection and cancer. Over the last two decades, multiple abnormalities in energy and protein metabolism have been documented in patients with cancer and, more recently, in HIV infection. In HIV infection, studies of the components of energy balance have demonstrated that weight loss results primarily from decreased energy intake, coupled with a failure to consistently reduce resting energy expenditure. Although several studies have shown that resting energy expenditure is elevated in many patients with HIV infection, other studies have shown that not all patients with HIV infection are hypermetabolic. Likewise, protein turnover is increased, decreased, or unchanged in patients with HIV infection and varies with the physiologic state of the patient. In cancer patients, studies of resting energy expenditure have produced similarly varying results, depending in part on tumor type and dietary intake. Protein turnover studies in patients with cancer suggest that support of the tumor may occur at the expense of host skeletal muscle. Abnormalities of glucose and lipid metabolism have been noted as well. Thus, pharmacologic intervention may be needed to restore weight and lean tissue in patients with weight loss associated with either HIV infection or cancer.
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PMID:Energy expenditure and protein metabolism in human immunodeficiency virus infection and cancer cachexia. 962 89

As with many chronic diseases that express themselves late in life, osteoporosis is distinctly multifactorial, both in etiology and pathophysiology. Osteoporotic fractures occur because of a combination of injury and intrinsic bony fragility. Injury comes most often from a combination of falls, falling to the side, poor postural reflexes that fail to protect bony parts from impact, and reduced soft-tissue padding over bony prominences. The bony fragility itself is a composite of geometry, low mass density, severance of microarchitectural connections in trabecular structures, and altered bone material quality. The latter is primarily the result of accumulated fatigue damage, but reduced collagen cross-links and other intrinsic material defects may play a role as well. Reduced bone mass, in turn, is the result of varying combinations of gonadal hormone deficiency, inadequate intakes of calcium and vitamin D, decreased physical activity, comorbidity, and the effects of drugs used to treat various unrelated medical conditions. Finally, the often poor outcome from hip fracture in the elderly is partly due to associated protein-calorie malnutrition. An adequate preventive program for osteoporotic fracture must address as many of these factors as possible and be as multifaceted as the disease is multifactorial.
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PMID:Pathophysiology of osteoporosis. 966 37

There is a high prevalence of protein-energy malnutrition in both nondialyzed patients with advanced chronic renal failure and in those individuals with end-stage renal disease who are receiving maintenance hemodialysis or chronic peritoneal dialysis therapy. Approximately one-third of maintenance dialysis patients have mild to moderate protein-energy malnutrition, and about 6 to 8 percent of these individuals have severe malnutrition. These statistics are of major concern because markers of protein-energy malnutrition are strong predictors of morbidity and mortality. The causes of protein-energy malnutrition in patients with chronic renal failure include: (1) decreased energy or protein intake; (2) concurrent chronic illnesses, and superimposed acute illnesses and possibly increased inflammatory cytokines; (3) the catabolic stimulus of hemodialysis; (4) losses of nutrients into dialysate, particularly amino acids, peptides, protein (with peritoneal dialysis), glucose (when hemodialysis is performed with glucose-free dialysate) and water-soluble vitamins; and (5) diagnostic or therapeutic (e.g., prednisone therapy) procedures that reduce nutrient intake or engender net protein breakdown. Other theoretically possible causes for protein-energy malnutrition include (6) chronic blood loss; (7) endocrine disorders (especially resistance to insulin and insulin-like growth factor-I, hyperglucagonemia, hyperparathyroidism and deficiency of 1,25-dihydroxycholecalciferol); (8) products of metabolism that accumulate in renal failure and may induce wasting, such as organic and inorganic acids; (9) loss of the metabolic actions of the kidney; and (10) the accumulation of toxic compounds that are taken up from the environment (e.g., aluminum).
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PMID:Pathophysiology of protein-energy wasting in chronic renal failure. 991 8

BACKGROUND: In an elderly population of surgical patients, poor mobility, poor diet and chronic disease contribute to a significant risk of malnutrition. Malnutrition is associated with muscle weakness, fatigue, poor wound healing and immunological dysfunction. The aim of the study was to establish the prevalence of malnutrition in vascular surgical patients and to compare postoperative infection rates in well nourished and malnourished patients. METHODS: A nutritional assessment was performed on 71 patients (49 men; median age 65 (range 26-85) years) attending preassessment for vascular surgical procedures. Nutritional status was measured using validated indicators of malnutrition: estimated weight changes over 3 months; body mass index; mid-arm muscle circumference (MAMC) calculated using triceps skin fold thickness (TSF) and mid-arm circumference (MAC) (MAMC = MAC - (3.14 x TSF)); and serum albumin concentration. Fifty-nine patients were followed after vascular surgery. The incidence of postoperative infections was related to preoperative nutritional status. RESULTS: Nineteen patients (27 per cent) had normal values for all nutritional indicators examined. The remaining 52 patients (73 per cent) had one (37), two (12), three (two) or four (one) nutritional indicators within the range for malnutrition. Among the 59 patients who underwent surgery there were five chest infections, seven wound infections, one urinary tract infection and one infected central line in 13 patients following six femorodistal bypasses, four abdominal aortic aneurysm repairs and three miscellaneous arterial procedures. The incidence of septic complications was zero in 14 patients with normal nutritional indicators and 41 per cent (13 of 32) in patients with indicators of malnutrition (P < 0.05, Fisher's exact test). CONCLUSION: Malnutrition is prevalent among vascular patients and may contribute to postoperative morbidity. Malnourished patients should be identified and referred to the dietician at the earliest opportunity to minimize the morbid effects of undernutrition.
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PMID:Vascular surgical society of great britain and ireland: contribution of malnutrition to postoperative morbidity in vascular surgical patients 1036 Dec 8

Circulating leptin, insulin, insulin-like growth factor-I (IGF-I), cortisol, and albumin concentrations and the growth hormone (GH) response to provocation were measured in 30 children with severe protein-energy malnutrition (PEM), 20 with marasmus and 10 with kwashiorkor, as well as 10 age-matched normal children (body mass index [BMI] >50th and <90th percentile for age and sex) and 10 prepubertal obese children (BMI >95th percentile for age and sex). Patients with PEM had a significantly lower BMI, midarm circumference (MAC), and skinfold thickness (SFT) compared with the age-matched control group. Basal cortisol and GH concentrations were significantly higher in the malnourished groups versus controls. Leptin and IGF-I were significantly lower in the marasmic and kwashiorkor groups versus normal children. Fasting insulin levels were significantly decreased in the kwashiorkor group compared with marasmic and normal children. The BMI correlated significantly with leptin (r = .77, P < .001), basal insulin (r = .61, P < .001), and IGF-I (r = .77, P < .001) and negatively with basal GH (r = -.52, P < .001). These findings suggest that during prolonged nutritional deprivation, the decreased energy intake, diminished subcutaneous fat mass, and declining insulin (and possibly IGF-I) concentration suppress leptin production. In support of this view, serum leptin levels were positively correlated with triceps, scapular, and abdominal SFT (r = .763, .75, and .744, respectively, P < .0001) in all of the children. Moreover, basal insulin and circulating IGF-I were correlated significantly with leptin concentrations (r = .47 and .62, respectively, P < .001). Basal levels of cortisol and GH were significantly elevated in the 2 groups with severe PEM. It is suggested that low leptin levels can stimulate the hypothalamic-pituitary-adrenal (HPA) axis and possibly the hypothalamic-pituitary-GH axis to maintain the high cortisol and GH levels necessary for effective lipolysis to ensure a fuel (fatty acids) supply for the metabolism of brain and peripheral tissue during nutritional deprivation. In summary, during prolonged PEM, the decreased synthesis of IGF-I and the low level of insulin and/or its diminished effect due to an insulin-resistant status in the presence of high circulating GH and cortisol levels ensure substrate diversion away from growth toward metabolic homeostasis. Leptin appears to be an important signal in the process of metabolic/endocrine adaptation to prolonged nutritional deprivation.
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PMID:Serum leptin concentrations during severe protein-energy malnutrition: correlation with growth parameters and endocrine function. 1090 89

This paper examines three aspects of hunger disease: the effect of initial fat stores on macronutrient fuel selection during total starvation (no energy) and how it influences survival; the effects of different rates of weight loss on tissue and body function; and the importance of appetite sensations, including hunger, during malnutrition and during enteral and parenteral nutritional support. Long-term starvation studies in humans reveal major differences in fat carbohydrate and protein metabolism between lean and obese subjects, including a 2-4-fold lower contribution of protein oxidation to energy expenditure in obese subjects, which ensures that more of the excess body fat is oxidized. The rate of weight loss, determined by recent dietary intake, can have major effects on tissue and body function, including wound healing, the acute phase protein response, muscle fatigue and psychological/behavioural function in both clinical and non-clinical settings. In depleted states uncomplicated by disease, changes in appetite sensations can result in energy intakes as high as 6000 to 10,000 kcal/day ( 25-42 MJ/day). Long-term enteral tube feeding and parenteral nutrition are associated with frequent disturbances in appetite sensations, and in those able to eat normally they tend to add rather than replace oral intake to an extent that appears to depend on the regimen. It is concluded that 1) differences between lean and obese subjects in macronutrient fuel selection during starvation are adaptive because they optimize survival in both groups of subjects; 2) the rate of weight loss in health and disease has a major effect on certain tissue and body functions, independently of the magnitude of weight loss; and 3) clinically relevant disturbances in appetite sensations are common subjects receiving long-term enteral and parenteral nutrition. The clinical modulation of all these variables would be aided by greater knowledge of the mechanisms involved.
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PMID:Hunger disease. 1110 87

Malnutrition is a common clinical problem in dialysis patients, which is multifactorial in origin. It is most often found in a patient of chronic renal failure (CRF) during the period when the glomerular filtration rate (GFR) falls below 10 ml/min, but dialysis is yet to be started. The loss of proteins, aminoacids and other essential nutrients during the procedure of dialysis may further aggravate the malnutrition. Poor nutrition in dialysis patients is associated with increased morbidity and mortality in the form of delayed wound healing, malaise, fatigue, increased susceptibility to infection and poor rehabilitation. In view of the above consequences, all patients on dialysis must undergo nutritional assessment. It is very vital to maintain good nutritional status in-patients on dialysis by adequate protein and calories intake, appropriate supplementation of iron, calcium, minerals and water-soluble vitamins and, of course, the supplementation should be individualised. Nutritional needs are enhanced in presence of stresses like infection or surgery to limit excessive tissue catabolism and therefore, these are the situations, which demand intensive nutrition therapy. Total parenteral nutrition (TPN) may be required for patients on dialysis in intensive care unit, using a central venous catheter. However, enteral route is always preferred to parenteral ones, whenever possible. Even after adequate dialysis has been given, dietary counselling is often required for both hemodialysis and peritoneal dialysis patients to ensure that they ingest the recommended amount of protein, calories and essential micronutrients.
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PMID:Nutrition in dialysis patients. 1127 10

The diagnosis of cancer has traditionally been associated with malnutrition and wasting. Oncology patients are at risk for nutrition-related problems because of the cancer itself, as well as the treatment prescribed. Clinical manifestations of cachexia include anorexia, weight loss, muscle wasting, and fatigue, resulting in poor performance status. Control of symptoms, such as anorexia, nausea and vomiting, and mucositis is imperative in the management of cancer cachexia. Current pharmacologic therapies, as well as complementary and alternative methods, are presented. The nurse plays a key role in ensuring that the nutritional needs of oncology patients are met.
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PMID:Management of cancer cachexia. 1128 21

Lisa Capaldini, a physician who treats patients with HIV-related fatigue, discusses symptoms, diagnosis techniques, and treatments of depression, anemia, and various other roots of fatigue in HIV-positive patients. Biochemical depression, caused by abnormal levels of serotonin and norepinephrine in the brain, is easily misdiagnosed or overlooked. Physical and emotional symptoms of depression mirror common effects of HIV such as exhaustion, anger, and irritability. Knowing the history of depression prior to HIV infection, including previous drug abuse and family history of depression, will help to diagnose fatigue. Dr. Capaldini recommends antidepressants provided the condition is properly diagnosed and the side effects are not harmful to the patient. Selective serotonin reuptake inhibitors (SSRI), the most frequently prescribed antidepressants, can cause short term sexual dysfunction. Bupropion and Wellbutrin can be prescribed to avoid this side effect. Psychotherapy can be effective if therapists are familiar with HIV disease and can distinguish between symptoms brought on by behavior, addictive habits, or pre-existing depression. Consideration also must be given to drug interactions, particularly with the antiretrovirals ritonavir and delavirdine, which can cause seizures or disturb cardiac rhythm. Anemia is most noticeable after physical exertion, and symptoms are more evident based on the increased rate that red blood cells move out of the normal range. To determine the course of treatment, physicians need to clarify the cause of anemia. Anemia can be caused by drugs, vitamin deficiencies, or other nutritional problems. Adrenal insufficiency, methemoglobinemia, and malnutrition are also causes of fatigue. Diagnosing fatigue due to hepatitis B or C, rather than HIV, can be achieved by measuring hepatitis levels and observing T cell counts and viral load. Dr. Capaldini suggests that proper diet and exercise prevent fatigue from getting worse.
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PMID:Fatigue and HIV: interview with Lisa Capaldini, M.D. Part II. Interview by John S. James. 1136 84


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