Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Energy expenditure and substrate oxidation rate for fat, glucose and protein were evaluated by indirect calorimetry in 20 normal individuals, 35 patients with acute hepatitis and 22 patients with biopsy-proven alcoholic cirrhosis in the postabsorptive state. Measurements were done in the resting state after an overnight fast (10 to 12 hr). Oxygen consumption (ml/min/1.73 m2) in normal subjects, in patients with acute hepatitis and in patients with cirrhosis was 206.5 +/- 4.0 (mean +/- S.E.M.), 216.4 +/- 4.7 and 228.8 +/- 7.1 (p less than 0.05 vs. controls), respectively. When related to body surface area (kcal/min/1.73 m2), resting energy expenditure did not differ between normal subjects (0.98 +/- 0.02), patients with acute hepatitis (1.03 +/- 0.02) and cirrhotic patients (1.06 +/- 0.03). However, when related to 24-hr urinary creatinine excretion as an estimate of lean body mass, energy expenditure was increased in cirrhosis (p less than 0.0001). In cirrhosis an inverse association between the severity of liver disease according to Pugh and oxygen consumption and resting energy expenditure was found. In cirrhotic patients the percentages of total calories derived from fat (86% +/- 5%), carbohydrate (2% +/- 4%) and protein (12% +/- 1%) were different from those of normal controls who metabolized 45% +/- 4%, 38% +/- 4%, 17% +/- 1%, respectively. In acute hepatitis no alterations in metabolism could be found apart from a decreased protein oxidation rate. In conclusion no appreciable changes in energy metabolism exist in acute hepatitis. The pattern of fuel use in cirrhosis resembles that in starvation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Energy metabolism in patients with acute and chronic liver disease. 210 37

Kwashiorkor kills millions of young children in the tropical Third World. It was believed to be a disease of protein starvation. The medical team headed by Professor Ralph Henrickse of the Liverpool School of Tropical Medicine has discovered that aflatoxin, a fungus toxin, may be the triggering factor in this disease which also impairs liver function. In New Zealand, we have a pasture fungus, the spores of which produce a liver toxin that has killed millions of animals this century and impaired the performance of millions more. New Zealand is a pastoral farming country with 70 million sheep and several million cattle. We now protect the animal with zinc medication. This paper describes the similarities between Kwashiorkor and the mycotoxic liver disease in New Zealand livestock, known locally as Facial Eczema. It describes briefly my discovery that pharmacological doses of zinc protected farm animals from pasture contaminated with the spores of the fungus Pithomyces chartarum, which contains the toxin sporidesmin. This paper proposes that Kwashiorkor and Facial Eczema are diseases with similar beginnings and a common end.
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PMID:Kwashiorkor. 649 86

1. Blood alanine was measured in six patients undergoing total hip replacement and in four normal subjects starved for 4 days. Hypoalaninaemia occurred in both groups and persisted in the surgical patients despite an adequate diet. The blood alanine was also low in four insulin-dependent diabetic patients and in four patients with muscular dystrophy; it was normal in four patients with cirrhotic liver disease. 2. The removal of an intravenous L-alanine load (12 g; 133 mmol) was significantly increased after surgery and in the diabetic patients, unaltered by starvation, and decreased in the cirrhotic patients. 3. Increases in blood glucose were observed when alanine infusion was performed 6 h after surgery and after 3 days' starvation. Increases in blood lactate and pyruvate always occurred after alanine infusion but were most marked 6 h after surgery. 4. These results show that the metabolic response to an alanine load and the ability of the body to remove it alter with change in physiological state, and that the hypoalaninaemia after surgery and in diabetes is related to an increased removal of intravenous alanine, whereas that during starvation is not.
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PMID:Relationship between the basal blood alanine concentration and the removal of an alanine load in various clinical states in man. 737 55

Increased energy needs, a reduced synthesis of endogenous substrates and a limited energy yield from exogenous substrates characterize the metabolic dilemma in patients with liver cirrhosis. The metabolic features observed in cirrhosis are highly variable and cannot be considered as clear-cut phenomena. They obviously differ in certain aspects from the metabolic situations known from starvation or type 2 diabetes mellitus. This is not contrary to the idea that cirrhosis may resemble certain aspects of these 'standard' situations. Cirrhosis-induced disturbances in fuel homeostasis cannot be predicted from clinical and biochemical parameters of the disease. Most of the metabolic picture is present at a very early stage of liver disease. Many metabolic features are independent of the clinical course of liver disease, suggesting that they are an early and extra-hepatic manifestation. A better understanding of the variance of cirrhosis-induced alterations in metabolism may come from characterization of the metabolic 'genotype' which adds to disease-related factors in the individual patient.
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PMID:Energy expenditure and substrate metabolism in liver cirrhosis. 812 90

A 46-yr-old multiparous cachetic woman presented with severe hypoalbuminemia in the absence of liver disease, proteinuria, and/or protracted starvation. The clinical presentation and work-up was indicative of protein-losing enteropathy. She developed an acute partial small bowel obstruction, and a presumptive diagnosis of lymphoma of the small intestine was entertained. Surgical resection of the terminal ileum revealed transmural involvement of the bowel by endometriosis. Her postoperative recovery was uneventful, with return of her serum albumin levels to normal.
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PMID:Endometriosis of the small intestine presenting as a protein-losing enteropathy. 842 Feb 54

To determine risk factors for the development and clinical characteristics of hypoglycemia in patients with sepsis, a case-control study was performed in 52 case-patients who developed spontaneous hypoglycemia (plasma glucose < 50 mg/dl) during episodes of sepsis compared with 49 nondiabetic, control-patients who had sepsis as an immediate cause of death and did not develop hypoglycemia. The presence or absence of potential risk factors for the development of hypoglycemia which consisted of the state of starvation, malnutrition, renal insufficiency, acute or chronic liver disease and malignancy were evaluated in both groups as well as the clinical characteristics of hypoglycemia. The mean of the lowest plasma glucose levels in hypoglycemic patients was 23.4 +/- 14.9 (SD) mg/dl (range 3-47). One-third of patients were found having hypoglycemia since the time of arrival to the hospital. About 90 per cent had septic shock at the time of hypoglycemia. The mortality rate was 90 per cent; 80 per cent died within 48 hours after the first episode of hypoglycemia. Among those risk factors, starvation and liver disease were independently associated with the development of hypoglycemia with odd ratios of 6.38 (95% confidence interval 1.95-20.86; P = 0.002), and 3.59 (95% confidence interval 1.09-11.81; P = 0.035), respectively. In conclusion, hypoglycemia in patients with sepsis was associated with a grave prognosis. The risk of developing hypoglycemia increased significantly in patients who had been fasted for more than 24 hours or had acute or chronic liver disease at the time of sepsis.
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PMID:Hypoglycemia in sepsis: risk factors and clinical characteristics. 947 Mar 28

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

Some viral infections are reported to influence the susceptibility of peripheral blood mononuclear cells (PBMC) to apoptosis, which is related to disease progression. The current study was designed to monitor apoptosis in separated PBMC subsets, CD4+ and CD8+ T lymphocytes, and CD14+ monocytes under apoptotic stimuli in patients with chronic hepatitis C. Apoptosis was induced by serum starvation and by incubation with anti-CD3 antibody and with phorbol 12-myristate 13-acetate. With the escalating severity of liver disease, susceptibility of all PBMC subsets to apoptosis increased under the apoptotic stimulus of serum starvation (P<0.05). Consequently, increased susceptibility to apoptosis was associated with diminished intracellular expression of the antiapoptotic protein Bcl-2 (P<0.05). The current observations demonstrate that the abnormality of PBMC subsets in undergoing apoptosis as a result of the down-regulation of Bcl-2 expression may contribute to viral persistence and progression of liver disease in chronic hepatitis C.
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PMID:Increased susceptibility to apoptosis and attenuated Bcl-2 expression in T lymphocytes and monocytes from patients with advanced chronic hepatitis C. 1210 Dec 62

Hyperemesis gravidarum (HG) is the most severe form of illness within the spectrum of nausea and vomiting of pregnancy. Liver disease, usually consisting of mild serum transaminase elevation, occurs in almost 50% of patients with HG. While multiple risk factors have been proposed, the etiology and underlying mechanism of maternal liver disease associated with HG remains unclear. In this report, we hypothesize that impairment of mitochondrial fatty acid oxidation (FAO) plays a role in the pathogenesis of maternal liver disease associated with HG. We hypothesize that women heterozygous for FAO defects develop HG associated with liver disease while carrying fetuses with FAO defects due to accumulation of fatty acids in placenta and subsequent generation of reactive oxygen species. Alternatively, it is possible that starvation leading to peripheral lipolysis and increased load of fatty acids in maternal-fetal circulation, combined with reduced capacity of the mitochondria to oxidize fatty acids in mothers heterozygous for FAO defects, can also cause HG and liver injury while carrying non-affected fetuses. The rationale for this hypothesis is discussed.
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PMID:Impaired fatty acid oxidation as a cause of liver disease associated with hyperemesis gravidarum. 1604 Feb

Managing infants, children and adolescents, ranging from premature infants to 18-year-old adolescents, on parenteral nutrition (PN) is a challenge. The ability of children to withstand starvation is limited and, unlike adults, children require nutrition for growth. PN in children is often required secondary to a congenital bowel problem rather than because of an acquired condition. Conditions requiring PN include motility disorders, congenital disorders of the intestinal epithelium and short-bowel syndrome (SBS). Intestinal failure may be temporary and children with SBS may be weaned from PN. However, other children require permanent PN. There are no comprehensive guidelines for the nutritional requirements of children and adolescents requiring PN. Practice in individual centres is based on clinical experience rather than clinical trials. Requirements are assessed on an individual basis according to age, nutritional status and clinical condition. These requirements need regular review to ensure that they remain appropriate for the changing age and weight of the child. Assessments of intakes use different methods, e.g. reference tables and predictive equations. Complications of PN include infection, accidental damage to, or removal of, the line and cholestatic liver disease. Home parenteral nutrition (HPN) is associated with fewer line infections and allows continuation of nutritional support in a more normal environment, encouraging normal development and participation in family activities. However, having a child at home on HPN is associated with physical and psychological stresses. A feeling of depression, loneliness and social isolation is common amongst children and their families. Home-care services are essential to supporting children at home and should be tailored to, and sensitive to, the individual needs of each family.
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PMID:Managing children and adolescents on parenteral nutrition: Challenges for the nutritional support team. 1692 5


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