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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In summary, little progress has been made in the past several years with respect to the treatment of the baby with BPD. The conduct of convincing clinical research seems to be a casualty of budget cuts and a rush to learn the tools of molecular biology. To date, there are no clinical trials that have convincingly demonstrated that long-term diuretic, bronchodilator, vasodilator, or antioxidant therapy is effective in the treatment of chronic BPD. Short-term corticosteroid therapy hastens extubation, but long-term outcome is unaffected and serious questions remain about its safety. Multicenter clinical trials should be carefully designed and implemented to address the values of these therapies. In the design of these trials, care should be taken to stratify treatment groups for known risk factors for BPD. What are the future directions for the treatment of BPD? It is hoped that new BPD treatment strategies will be based on an improved understanding of mechanisms of lung repair and inflammation. Enzyme, gene, cytokine, antioxidant, and antiprotease therapies are being developed in animal models of lung injury. In addition, the use of lung transplantation has begun to be explored for severe cases of BPD. It is also possible, as has occurred in many chronic idiopathic diseases, that nonspecific treatment may prove beneficial. Perhaps it is only a matter of time before intravenous immunoglobulin, cyclosporine, methotrexate, or "biological response modifiers" will be administered to infants with severe BPD. For example, there is anecdotal evidence that recombinant human growth hormone may improve respiratory muscle function in adults with chronic obstructive pulmonary diseases. In the absence of convincing clinical trials, the clinician should reserve existing therapies for the ventilator-dependent infant or infants whose high oxygen requirement is prohibiting discharge or resulting in complex home care or frequent rehospitalizations. It should be emphasized that continuous oxygen therapy combined with avoidance of environmental inhalant and infectious hazards have the strongest rationale and widest margin of safety for treatment of the infant with BPD. Ironically, oxygen therapy is frequently underutilized and discontinued too rapidly. Early discontinuation of oxygen therapy with alveolar hypoxia results in feeding difficulty, slow growth, nutrient malabsorption, bronchoconstriction, and pulmonary hypertension. Oxygen therapy, although more cumbersome and certainly less glamorous than other pharmacologic agents, remains the essential element of BPD care.
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PMID:Current therapy of bronchopulmonary dysplasia. 152 72

Relationships between nutrition and infection are generally complex, bidirectional, and not perfectly worked out. Healthy people can adapt to simple decreases in intake or increases in expenditure. However, the imposition of infection with associated cytokines may impair such adaptations, resulting in wasting of lean tissue. In human immunodeficiency virus (HIV) infection, nutritional abnormalities are common. Lean body mass depletion is associated temporally with death in a subset of acquired immune deficiency syndrome (AIDS) patients. Weakness, fatigue, and anorexia are important symptomatic complaints affecting quality of life. Pathophysiologic mechanisms remain speculative, although there is reason to suspect four theoretic factors: decreased intake, malabsorption, hypermetabolism, and altered metabolism. More than one disturbance may be necessary for clinical wasting to develop; ie, a primary abnormality plus a failure of homeostatic adaptation. Excess cytokine production also may be involved, but this is uncertain. Therapeutics remain empiric in the absence of known mechanisms. Current options are restricted to diet adjustments or supplements, treatment of underlying diseases (where possible), and rarely, parenteral alimentation. Promising investigational possibilities include an appetite stimulant (megestrol acetate) and therapies to oppose cytokine production or actions, but definitive beneficial effects on nutritional status, subjective performance, disease activity, or survival have not yet been demonstrated. Advances in clinical therapeutics await an improved understanding of pathophysiologic mechanisms and carefully designed clinical trials testing proposed interventions.
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PMID:Current approach to the treatment of human immunodeficiency virus-associated weight loss: pathophysiologic considerations and emerging management strategies. 225 24

Giardiasis is the most common small intestinal protozoal infection and is found worldwide. The mechanisms by which Giardia duodenalis (= G. lamblia) produces chronic diarrhoea and malabsorption have still not been clearly defined. Many infections are associated with mild to moderate mucosal damage which, in animal models of infection, have functional correlates. Possible mechanisms include direct physical injury, release of parasite products such as proteinases or lectin, and mucosal inflammation associated with T cell activation and cytokine release. Other possible mechanisms of malabsorption include associated bacterial overgrowth and bile salt deconjugation, bile salt uptake by the parasite with depletion of intraluminal bile salts, and inhibition of pancreatic hydrolytic enzymes. Thus, there is no single mechanism to explain the diarrhoea and malabsorption caused by Giardia, which currently should be regarded as a multifactorial process.
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PMID:Diarrhoeal disease: current concepts and future challenges. Pathogenesis of giardiasis. 810 43

The HIV wasting syndrome and other HIV-associated weight loss is a major problem in HIV-infected patients. The available data strongly suggest that wasting is associated with decreased survival. It may also further impair immune function. A variety of etiologies probably contribute to this wasting, including hypermetabolism, alterations in metabolism, lessened oral intake, malabsorption, cytokine effects, and endocrine dysfunction. The relative contributions of each of these etiologies to wasting probably varies considerably from patient to patient. Successful treatment calls for identification of possible etiologies of wasting in the individual patient with AIDS. Further treatment may include treating underlying conditions and controlling such symptoms as diarrhea, nausea, or fever. Nutritional support, including both parenteral and enteral nutrition, has shown some promise of efficacy, and a variety of drugs appears to be helpful. Future treatment to reverse wasting may include the use of several of these agents in combination. Currently, there is much that clinicians can do to evaluate and treat the HIV wasting syndrome, with significant potential benefits to their patients.
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PMID:The HIV wasting syndrome: a review. 820 46

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.
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PMID:Anorexia during acute and chronic disease. 905 54

Studies suggest that the development and expression of the regional immune system in the gastrointestinal (GI) tract is relatively independent of systemic immunity. This is reflected in significant differences in functional response of T cells and B cells and affects cytokine patterns and activation pathways when regional immunity is compared to systemic immunity. Nutrients have fundamental and regulatory influences on the immune response of the GI tract and, therefore, on host defense. In addition to the effect of nutrition during development, the local impact of different dietary and antigenic elements on the regional immune system contributes to potential diversion of the two systems throughout life. The route of exposure during antigenic contact is known to affect host immune response, whether it be a normal process, happening in the context of normal environmental encounter with nonpathogenic microbes or planned immunization, or occurring as a result of resolution of a potentially pathologic process i.e., an infectious encounter. Interactions at the local level profoundly influence systemic immune response, in part because of intrinsic differences in these systems, and also because of different requirements for optimal function. Although inflammatory processes are central to host defense in the periphery, the protective blocking action of the secretory immunoglobulin A immune response is crucial to local host defense, and, therefore, to the integrity of GI tract immune function. For these reasons, interaction with normal bacteria of the GI tract may be seen as the model of how the system has evolved and provide clues to the restoration of balance in the immunocompromised host. Reduction of normal commensal bacteria in the context of infection or after antibiotic treatment may interfere with nutrient availability and impair beneficial stimulation of GI immune response. This impairment may be associated with continued colonization with opportunistic microbes and inflammatory immune response that could lead to malabsorption and malnutrition. Study of the impact of nutrient imbalance on the function of the GI tract has profound implications for clinical medicine and may in the future lead to the rational design of preventive approaches to support immune response and host defense.
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PMID:Nutrition and the immune system of the gut. 968 59

Anorexia is a common problem in HIV infection and occurs via several mechanisms, including local pathology in the oral cavity or esophagus, central nervous system disease affecting eating mechanics or the perception of hunger, or secondary anorexia due to systemic infections, malabsorption, or medications, or to nonmedical factors, such as psychosocial problems, poverty, and isolation. The etiologic diagnosis of disorders of food intake is facilitated by using a diagnostic algorithm. The consideration of nutritional management centers around the body's nutritional reserves in addition to caloric intake. The specific management of a patient with poor food intake is based on the precise cause of the problem, and may include food-based and oral supplement therapies, appetite stimulants, or nonvolitional feeding via the enteral or parenteral route. Anabolic agents, cytokine inhibitors, and other therapies, such as resistance exercise, are adjunctive therapies, and do not replace adequate caloric intake.
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PMID:Nutritional management of patients with AIDS-related anorexia. 982 81

Increased cytokine release and increased activity of osteoclasts (reduced osteoclast apoptosis) due to a fall in estrogen is of causal significance in postmenopausal bone loss as well as malfunction of the vitamin D activation and concomitant calcium (Ca) malabsorption. Alfacalcidol prevents rapid postmenopausal bone loss by elimination of Ca malabsorption and by blocking resorbing cytokines. Established osteoporosis in older patients of both sexes is characterized by decoupled bone remodeling induced by sex hormone deficits and by a so-called somatopause (insulin-like growth factor [IGF]-deficit), but also by lack of vitamin D and, very importantly, by reduced synthesis of D-hormone (Calcitriol) in kidneys and bone as well as by a lack of receptors or receptor affinity for D-hormone in the target organs. As a consequence of these facts, a rise in parathormone (PTH) frequently occurs. The lack of D-hormone and IGF-1 evidently causes a reduction in muscle strength as well and reinforces the risk of falling and, thus, the risk of a fracture. Alfacalcidol, a prodrug of D-hormone, is a specific antiosteoporotic therapy. In alfacalcidol therapy, D-hormone is provided to the body in circumvention of its own regulation, by means of which much higher hormone concentrations can be achieved in the target tissues than by administration of plain vitamin D. Chances have been significantly improved of reducing and frequently preventing the real osteoporosis complication for older male and female patients, i. e., bone fractures, by alfacalcidol. A clear distinction should be made between supplementation with low-dosed plain vitamin D and calcium as base supply in elderly housebound subjects or as adjuvant to antiosteoporotic drugs and the specific antiosteoporotic therapy with alfacalcidol in patients with osteoporosis. The expanded understanding of the pathogenesis of corticosteroid-induced osteoporosis with its disturbed Ca homeostasis and the pharmacological effects of alfacalcidol, counteracting such iatrogenic bone loss, explain the particularly good clinical efficacy in this most frequent form of secondary osteoporosis. Normalizing de-coupled bone remodeling due to cytokine modulation and the potential influence on deteriorated bone quality in patients with rheumatoid arthritis and Crohn's disease predestine this form of therapy for prevention and treatment of osteoporosis as a result of chronic inflammatory diseases as well as of transplantation osteoporosis cases in particular.
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PMID:Rationale for treatment of involutional osteoporosis in women and for prevention and treatment of corticosteroid-induced osteoporosis with alfacalcidol. 1048 85

The cachexia-anorexia syndrome occurs in chronic pathophysiologic processes including cancer, infection with human immunodeficiency virus, bacterial and parasitic diseases, inflammatory bowel disease, liver disease, obstructive pulmonary disease, cardiovascular disease, and rheumatoid arthritis. Cachexia makes an organism susceptible to secondary pathologies and can result in death. Cachexia-anorexia may result from pain, depression or anxiety, hypogeusia and hyposmia, taste and food aversions, chronic nausea, vomiting, early satiety, malfunction of the gastrointestinal system (delayed digestion, malabsorption, gastric stasis and associated delayed emptying, and/or atrophic changes of the mucosa), metabolic shifts, cytokine action, production of substances by tumor cells, and/or iatrogenic causes such as chemotherapy and radiotherapy. The cachexia-anorexia syndrome also involves metabolic and immune changes (mediated by either the pathophysiologic process, i.e., tumor, or host-derived chemical factors, e.g., peptides, neurotransmitters, cytokines, and lipid-mobilizing factors) and is associated with hypertriacylglycerolemia, lipolysis, and acceleration of protein turnover. These changes result in the loss of fat mass and body protein. Increased resting energy expenditure in weight-losing cachectic patients can occur despite the reduced dietary intake, indicating a systemic dysregulation of host metabolism. During cachexia, the organism is maintained in a constant negative energy balance. This can rarely be explained by the actual energy and substrate demands by tumors in patients with cancer. Overall, the cachectic profile is significantly different than that observed during starvation. Cachexia may result not only from anorexia and a decreased caloric intake but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions). In any case, the major deficit of a cachectic organism is a negative energy balance. Cytokines are proposed to participate in the development and/or progression of cachexia-anorexia; interleukin-1, interleukin-6 (and its subfamily members such as ciliary neurotrophic factor and leukemia inhibitory factor), interferon-gamma, tumor necrosis factor-alpha, and brain-derived neurotrophic factor have been associated with various cachectic conditions. Controversy has focused on the requirement of increased cytokine concentrations in the circulation or other body fluids (e.g., cerebrospinal fluid) to demonstrate cytokine involvement in cachexia-anorexia. Cytokines, however, also act in paracrine, autocrine, and intracrine manners, activities that cannot be detected in the circulation. In fact, paracrine interactions represent a predominant cytokine mode of action within organs, including the brain. Data show that cytokines may be involved in cachectic-anorectic processes by being produced and by acting locally in specific brain regions. Brain synthesis of cytokines has been shown in peripheral models of cancer, peripheral inflammation, and during peripheral cytokine administration; these data support a role for brain cytokines as mediators of neurologic and neuropsychiatric manifestations of disease and in the brain-to-peripheral communication (e.g., through the autonomic nervous system). Brain mechanisms that merit significant attention in the cachexia-anorexia syndrome are those that result from interactions among cytokines, peptides/neuropeptides, and neurotransmitters. These interactions could result in additive, synergistic, or antagonistic activities and can involve modifications of transducing molecules and intracellular mediators. Thus, the data show that the cachexia-anorexia syndrome is multifactorial, and understanding the interactions between peripheral and brain mechanisms is pivotal to characterizing the underlying integrative pathophysiology of this disorder.
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PMID:Central nervous system mechanisms contributing to the cachexia-anorexia syndrome. 1105 8

Epidemiological studies have demonstrated a marked negative relationship between diarrhoea and physical growth and development of a child. Each day of illness due to diarrhoea produces a weight deficit of 20-40 gms. Poor nutrition is associated with more serious prolonged diarrhoea. 'Catch-up growth' often does not occur in malnourished children. Malnutrition, particularly wasting, is a strong predictor of diarrhoeal duration and the prolonged illness could exacerbate nutritional faltering, thereby increasing the subsequent risk of death. Poor appetite, vomiting, deliberate withholding of food resulting in poor intake; malabsorption of macro and micronutrients; hastening of intestinal transit time; disturbance of metabolic and endocrine functions; and direct loss of protein and other nutrients in gastrointestinal tract are some of the known mechanisms which have an impact on the nutrition during an episode of diarrhea. In addition diarrhoea of infectious origin causes cytokine induced malnutrition which results from the actions of proinflammatory cytokines like tumour necrosis factor and interleukin 1, 6 and 8. Preexisting malnutrition is associated with decreased turnover of epithelial cells resulting in delayed recovery which may prolong an episode of infectious diarrhoea by itself as well as by promoting tissue invasion by other enteropathogens. Malnutrition may also alter protective host factors and thereby favour intestinal colonization by the pathogenic microbes. Mucosal damage varying from moderately severe changes to flat lesions indistinguishable from those of celiac disease may occur in kwashiorkar. Diarrhoea malnutrition interaction represents a dangerous web which can be distangled by prevention of disease transmission by promoting exclusive breast feeding, hygienic weaning practices, safe drinking water and handwashing, improved host defences by breast feeding, improved nutrition, measles vaccine and other vaccines against enteropathogens in the offing; and promotion of standard case management with special emphasis on nutritional support and rehabilitation.
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PMID:Diarrhoea and malnutrition interaction. 1113 59


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