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A potent superoxide dismutase mimic: Manganese octabromo-meso-tetrakis-(N-methylpyridinium-4-yl) porphyrin chronic superficial gastritis definition discount misoprostol on line. Photo-oxidative killing of human colonic cancer cells using indocyanine green and infrared light gastritis diet soy sauce order cheap misoprostol line. Neuroprotection against oxidative stress by estrogens: Structure-activity relationship gastritis translation best misoprostol 100mcg. Resveratrol inhibits metal ion-dependent and independent peroxidation of porcine low-density lipoproteins gastritis quizlet purchase misoprostol uk. Temperature dependence of carotenoids on C18 no xplode gastritis misoprostol 200 mcg discount, C30 chronic gastritis h pylori cheap misoprostol 200 mcg, and C34 bonded stationary phases. Formation and reduction of glutathione-protein mixed disulfides during oxidative stress. Lipid peroxidation: A review of causes, consequences, measurement and dietary influences. Tissue concentrations of coenzyme Q in liver of rats intoxicated by carbon tetrachloride. The determination of 5-hydroxytryptamine, related indolealkylamines and 5-hydroxyindoleacetic acid in the bovine eye by gas chromatography-negative ion chemical ionization mass spectrometry. Inhibition by coenzyme Q of ethanol and carbon tetrachloride-stimulated lipid peroxidation in vivo and catalyzed by microsomal and mitochondrial systems. The role of coenzyme Q in resistance to free radical damage acquired with endurance training. The role of ascorbate in antioxidant protection of biomembranes: Interaction with vitamin E and coenzyme Q. An analysis of the role of coenzyme Q in free radical generation and as an antioxidant. Elevation of tissue coenzyme Q (ubiquinone) and cytochrome c concentrations by endurance exercise in the rat. Lipoic acid favors thiolsulfinate formation after hypochlorous acid scavenging: a study with lipoic acid derivatives. Antioxidative role of ocular melanin pigment in the model of lens induced uveitis. Antioxidant properties of pyridoxine and its derivatives: Quenching of singlet oxygen. Biochemical and toxicological properties of the oxidation products of catecholamines. Enhanced antioxidant activity after chlorination of quercetin by hypochlorous acid. Reaction of ascorbate with the tocopheroxyl radical in micellar and bilayer membrane systems. Protection against superoxide and hydrogen peroxide in synovial fluid from rheumatoid patients. Lipoxygenase/H2O2-catalyzed oxidation of dihydroxyindoles: Synthesis of melanin pigments and study of their antioxidant properties. Autoxidation of drugs: Prediction of degradation impurities from results of reaction with radical chain initiators. Autoxidation of tetrazepam in tablets: Prediction of degradation impurities from the oxidative behavior in solution. Decrease in the antioxidant capacity of red blood cells in children with celiac disease. Formation of novel bioactive metabolites from the reactions of pro-inflammatory oxidants with polyphenolics. Natural histidine-containing dipeptide carnosine as a potent hydrophilic antioxidant with membrane stabilizing function. Protection by ubiquinone and ubiquinol against lipid peroxidation in egg yolk phosphatidylcholine liposomes. Interaction of flavonoids with ascorbate and determination of their univalent redox potentials: A pulse radiolysis study. Reduced risk of colon cancer with high intake of vitamin E: the Iowa women’s health study. Hypoxanthine and xanthine concentrations determined by high performance liquid chromatography in biological fluids from patients with xanthinuria. The 21-aminosteroid inhibitors of lipid peroxidation: Reactions with lipid peroxyl and phenoxyl radicals. Clinical and biochemical correlations in mitochondrial myopathies treated with coenzyme Q10. Identification and quantitation of glutathione in hepatic protein mixed disulfides and its relationship to glutathione disulfide. Protection by organotellurium compounds against peroxynitrite-mediated oxidation and nitration reactions. Up-regulation of protein chaperones preserves viability of cells expressing toxic Cu/Zn-superoxide dismutase mutants associated with amyotrophic lateral sclerosis. Redox and addition chemistry of quinoid compounds and its biological implications. Thioredoxin: A multifunctional regulatory protein with a bright future in technology and medicine. The pecking order of free radicals and antioxidants: lipid peroxidation, tocopherol, and ascorbate. Recent developments in trace element metabolism and function: Newer roles of selenium in nutrition. Peroxide removal by selenium-dependent and selenium independent glutathione peroxidases in hemoglobin-free perfused rat liver. Dietary carotenes, vitamin C and vitamin E as protective antioxidants in human cancers. High-performance liquid chromatographic method for the quantification of anthranilic and 3-hydroxyanthranilic acid in rat brain dialysate. Comparison of different analytical methods for assessing total antioxidant capacity of human serum. Antioxidant and pro-oxidant behavior of flavonoids: Structure-activity relationships. A note on distribution of plasma levels of ascorbic acid and dehydroascorbic acid. Determination of vitamin E in microsamples of serum by liquid chromatography with electrochemical detection. Reversal of age-related increase in brain protein oxidation, decrease in enzyme activity, and loss in temporal and spatial memory by chronic administration of the spin-trapping compound N-tert-butyl-nitrone. Vitamin C protects against and reverses specific hypochlorous acid and chloramine-dependent modifications of low-density lipoprotein. A high-performance liquid chromatographic assay for reduced and oxidized glutathione in embryonic, neonatal, and adult tissue using a porous graphite electrochemical detector. Pramipexole reduces reactive oxygen species production in vivo and in vitro and inhibits the mitochondrial permeability transition produced by the Parkinsonian neurotoxin methylpyridinium ion. Measurement of vitamin E in serum and plasma by high performance liquid chromatography and electrochemical detection. The concentrations of xanthine and hypoxanthine in cerebrospinal fluid as therapeutic guides in hydrocephalus. Catechol estrogen metabolites and conjugates in different regions of the prostate of Noble rats treated with 4-hydroxyestradiol: Implications for estrogen induced initiation of prostate cancer. Molecular origin of cancer: Catechol estrogen-3,4-quinones as endogenous tumor initiators. Neurochemical changes in the rat brain after intraventricular administration of tryptamine-4,5-dione. Vitamin C suppresses oxidative lipid damage in vivo, even in the presence of iron overload. Determination of 15N isotopic enrichment and concentrations of allantoin and uric acid in urine by gas chromatography/mass spectrometry. Evaluation of plasma low molecular weight antioxidant capacity by cyclic voltammetry. Determination of six indolic compounds, including melatonin, in rat pineal using high-performance liquid chromatography with serial fluorometric-electrochemical detection. L-ascorbic acid quenching of singlet delta molecular oxygen in aqueous media: Generalized antioxidant property of vitamin C. Antioxidant activities of some tryptophan metabolites: possible implication for inflammatory diseases. Oxidation of 3-hydroxyanthranilic acid to the phenoxazinone cinnabarinic acid by peroxyl radicals and by compound I of peroxidases and catalases. Inhibition by interferon-gamma of human mononuclear cell-mediated low-density lipoprotein oxidation. Efficacy of dietary d-alpha-tocopherol and dl-tocopheryl acetate for weanling pigs. A modified catalase assay suitable for a plate reader and for the analysis of brain cultures. Scavenging effect of silipide, a new silybin phospholipid complex, on ethanol-derived free radicals. The risk of developing lung cancer associated with antioxidants in the blood: Ascorbic acid, carotenoids, tocopherol, selenium, and total peroxyl radical absorbing capacity. Glutathione and ascorbate during ischemia and post-ischemia reperfusion in rat brain. The relationship of intracellular iron chelation to the inhibition of regeneration of human ribonucleotide reductase. Structure-activity relationship and classification of flavonoids as inhibitors of xanthine oxidase and superoxide scavengers. Protective effects of melatonin in zymosan-activated plasma-induced paw inflammation. N-acetylcysteine: Pharmacological considerations and experimental and clinical applications. The failure of aerosolized superoxide dismutase to modify pulmonary oxygen toxicity. Oxidative stress and abnormal cholesterol metabolism in patients with adult respiratory distress syndrome. Melatonin counteracts lipid peroxidation induced by carbon tetrachloride but does not restore glucose-6-phosphatase activity. Protection of Chinese hamster ovary cells from paraquat mediated cytotoxicity by a low molecular weight mimic of superoxide dismutase. Decreased total antioxidant capacity of normal lipid hydroperoxide concentrations in sera of critically ill patients. Oxidation of melatonin by singlet molecular oxygen produces N1-acetyl-N2-formyl-5-methoxykynurenine. Tissue injury by reactive oxygen species and the protective effects of flavonoids. Analysis of hepatic reduced glutathione, cysteine, and homocysteine by cation-exchange high-performance liquid chromatography with electrochemical detection. Desferrioxamine inhibition of the hydroxyl radical like reactivity of peroxynitrite: Role of the hydroxamic groups. Total homocysteine level in plasma: High performance liquid chromatographic determination with electrochemical detection and glassy carbon electrode. Determination of dehydroascorbic acid using high-performance liquid chromatography with coulometric electrochemical detection. Isocratic reversed-phase liquid chromatography of all-trans-retinoic acid and its major metabolites in new potential supplementary test systems for development toxicology. Will the “good fairies” please prove to us that vitamin E lessens human degenerative disease? Bilirubin, formed by activation of heme oxygenase-2, protects neurons against oxidative stress injury. Microdialysis of melatonin in the rat pineal gland: Methodology and pharmacological applications. Parasympathetic inhibition of pineal indole metabolism by prejunctional modulation of noradrenaline release. Exogenous melatonin entrains rhythm and reduces amplitude of endogenous melatonin; An in vivo microdialysis study. Microdialysis reveals dynamics of coupling between noradrenaline release and melatonin secretion in conscious rats. Anethole dithiolethione prevents oxidative damage in glutathione depleted astrocytes. Melatonin in edible plants identified by radioimmunoassay and by high-performance liquid chromatography-mass spectrometry. Micronutrients measurement quality assurance program: helping participants use interlaboratory comparison exercise results to improve their long-term measurement performance. Buckminsterfullerenol free radical scavengers and apoptotic death of cultured cortical neurons. The relationship between redox properties and superoxide dismutase mimetic activities. Retinoic acid causes an anterioposterior transformation in the developing central nervous system. Oxidative reactivity of the tryptophan metabolite 3-hydroxyanthranilate, cinnabarinate, quinolinate and picolinate.

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As described in the text, these normally controlled processes may be dysregulated by endobiotics and xenobiotics as well as during pathologic processes, such as carcinogenesis. Humans do genes are the homeobox genes that determine the body plan dur not respond with hepatocellular and peroxisomal proliferation to ing early ontogenesis. Chloracne, metabolism of endobiotics and xenobiotics by inducing overex as this multiple dermal lesion has been called inappropriately, pression of relevant enzymes. Dioxin-induced hamartomas ﬁbrates induce lipoprotein lipase and enzymes involved in fatty appear in the epidermis and are characterized by (1) nonmalig acid oxidation. This accounts for marked species differences in the solute carriers (Saurat et al. Genes of several xenobiotic their role in development of dioxin-induced dermal hamartomas metabolizing enzymes may be activated by these chemicals. It has been hypothesized that thalidomide (or its hydrolysis increased abundance in the liver induces hepatocellular prolifera product) exerts teratogenic effect in the embryo by intercalating to tion. Another chemical proliferation on Wy-14,643 treatment, supporting a causative rela feature of thalidomide that may account for impaired Sp1-mediated tionship between these events. In histone modiﬁcations (eg, acetylation, methylation) inﬂuences the addition, glucocorticoids can also upregulate the transcription of transcriptional activity of the adjacent gene. Overexpression of the Bim protein, at both transcrip methylation (hypermethylation) silences genes, whereas decreased tional and translational levels, may be the principal mechanism of methylation (hypomethylation) permits their activation. The vast that are turned on by these systems and that in turn control the majority of genes in both germ cells (ie, the sperm and the egg) transcriptional activity of genes that determine the fate of cells by similarly undergo or avoid epigenetic alterations (eg, methylation inﬂuencing mitosis and/or apoptosis. Mitogenic signal For example, the insulin-like growth factor-2 gene, which encodes ing molecules thus induce cell proliferation. Because the genomically imprinted kinase inhibitor proteins (eg, p15, p21, and p57), which mediate its genes have only a single active copy, they are especially susceptible antimitotic effect (Johnson and Walker, 1999) (see Fig. Dysregulation of imprinting can range well as the proapoptotic protein Bim (see Fig. The Wnt–β-catenin and Hh–Gli systems during early development, as in the preimplantation mammalian are especially important in certain proliferative processes, such as embryo, the genome (except for the imprinted genes) undergoes embryogenesis, development of adult stem cells as well as progeni extensive demethylation, and appropriate patterns of cytosine meth tor cells, tissue regeneration after injury, and oncogenesis. During this are in fact phosphorylating enzymes (ie, receptor protein tyrosine period (embryonic 11–15 days in the rat), the androgen receptor and kinases). Importantly, these effects were transferred through kinase Akt to the membrane for activation. These adverse transgenerational effects on reproduction cor branches (Morgensztern and McLeod, 2005). Arsenite-induced oxidative stress (Lynn tion, which is carried out by protein phosphatases. As discussed earlier, by attacking protein Rac pathway to the neighboring Nox, which also resides in the thiolate groups and converting them into sulfenic acid groups, plasma membrane. The thiol-oxidizing agent diamide (which cular smooth muscle cells (Bokoch and Knaus, 2003). It Effect Xenobiotics that facilitate phosphorylation of signal trans is to be noted, however, that acute high-dose exposure to microcys ducers often promote mitosis and tumor formation. These chemicals acid is the underlying cause of the diarrhetic shellﬁsh poisoning. Protein kinases may also be activated tive and prolife signaling, because via the above pathways, growth by interacting proteins that had been altered by a xenobiotic. Some signal transduction pathways from cell membrane receptors to signal-activated nuclear transcription factors that inﬂuence transcription of genes involved in cell-cycle regulation. The symbols of cell membrane receptors are numbered 1 to 8 and some of their activating ligands are indicated. Several xenobiotics that are indicated in the ﬁgure may dysregulate the signaling network. In addition, these pathways regulating gene expression not only determine the fate of cells but also control certain aspects of the ongoing cellular activity. The Wnt signaling—a proliferative pathway especially important in embryogenesis, stem cell and progenitor cell development, and carcinogenesis. Wnt ligands are a secreted proteins covalently modiﬁed by palmitoylation and glycosylation. The disruption of E-cadherin–β-cat complexes causes an increase in β-cat mediated transcription of Wnt-responsive genes. In contrast, stabilization of the E-cadherin–β-cat complex brings about reduced β-cat-mediated Wnt signaling. Chemicals that inﬂuence Wnt signaling may interfere with embryonic development, cell proliferation, and carcinogenesis. The hedgehog (Hh) signaling—a proliferative pathway especially important in embryogenesis, stem cell and progenitor cell development, and car cinogenesis. They act in autocrine, paracrine, or endocrine manner through their membrane receptor Patched (Ptch), which is the key inhibitor of Hh signaling in the unligated form (Katoh and Katoh, 2008). In the absence of Hh (as in the left side of the ﬁgure) Ptch impedes the Hh pathway by inhibiting the activity of Smoothened (Smo), a positive regulator of signaling. According to the model presented in the ﬁgure, Ptch is a sterol pump that exports sterols (cholesterol or an oxysterol), thereby removing these activator molecules from Smo and making Smo idle. The repression of Smo by Ptch incapacitates the downstream Hh effectors, the glioma-associated family of transcription factors (Gli). Binding of Hh to Ptch (as in the right side of the ﬁgure) abrogates its sterol-exporting activity; therefore, the sterol can activate Smo. Thereafter the active Gli accumulates in the cell, translocates into the nucleus, and binds to its target genes. Chemicals that activate or inhibit Smo (shown in the left and right sides of the ﬁgure, respectively) may interfere with embryonic development. For example, the plant alkaloid cyclopamine inhibits Smo and causes cyclopia, a birth defect, in lambs. Smo inhibitors are potentially anticarcinogenic, whereas Smo activa tors may promote carcinogenesis by increased Hh signaling. The proliferative Wnt signaling is pituitary hormone secretion and, in turn, the peripheral gland. Toxicants can adversely affect ongoing cellular activity signal transduction with proliferative effect. By disrupting the E-cadherin/β-catenin complex in the skeletal, cardiac, and smooth muscle cells. Altered regulation of neural and/or muscle activity is the basic Chemically Altered Signal Transduction with Antiproliferative mechanism of action of many drugs and is responsible for toxicities Effect Turning off the increased proliferative signaling after cell associated with drug overdosage, pesticides, and microbial, plant, injury may compromise replacement of injured cells. As neurons are signal tion has been made from a study on cultured Hepa 1–6 cells that transducing cells, the inﬂuence of chemicals on neurons is seen not exhibited the following, seemingly consequential alterations on only on the neuron affected by the toxicant but also on downstream exposure to acetaminophen (follow the path in Fig. Thus, tetrodotoxin, which tion of Raf → diminished degradation of IκB → diminished bind blocks voltage-gated Na+ channels (item 7 in Fig. Alteration in Neurotransmitter Levels Chemicals may alter Offsetting the Hh–Gli pathway (Fig. This the convulsive effect of hydrazine and hydrazides (eg, isoniazid) severe cephalic malformation was observed in the offspring of sheep is due to their ability to decrease the synthesis of the inhibitory grazing in a ﬁeld where Veratrum californicum grew. Reserpine causes its several tains the steroidal alkaloid cyclopamine, which is an inhibitor of adverse effects by inhibiting the neuronal storage of norepineph Smoothened, a positive regulator of Hh signaling (Chen et al. This simpliﬁed scheme depicts major cellular signaling mechanisms that are operational in many neurons and muscle and exocrine cells. Fast signaling is initiated by the opening of ligand gated Na+/Ca2+ channels (1, 2). The resultant cation inﬂux decreases the inside negative potential (ie, evokes depolarization) and thus triggers the opening of the voltage-gated Na+ and Ca2+ channels (7, 8). The signal is terminated by channels and transporters (eg, 9, 10) that remove cations from the cells and thus reestablish the inside negative resting potential (ie, cause repolarization) and restore the resting Ca2+ level. Fast signaling can be suppressed by opening the ligand-activated Cl− or K+ channels (3–6), which increases the inside negativity (ie, induces hyperpolarization) and thus counteracts opening of the voltage-gated Na+ and Ca2+ channels (7, 8). Encircled positive and negative signs indicate activation and inhibition, respectively. A hypertensive crisis can occur with the combined is due to inhibition of acetylcholine release from motor neurons and use of tricyclic antidepressants and monoamine oxidase inhibitors, the lacking stimulation of the acetylcholine receptors at the neuro drugs that block different mechanisms of norepinephrine elimina muscular junction (receptor 1 in Fig. Inhibition of the neuronal reuptake of norepi dysfunction, and neuromuscular abnormalities. Acetyl-choline Skeletal muscle Nicotine Muscle ﬁbrillation, Tubocurarine, lophotoxin Muscle paralysis nicotinic Anatoxin-a and then paralysis α-Bungarotoxin receptor Cytisine α-Cobrotoxin Ind: ChE inhibitors α-Conotoxin Erabutoxin b Ind: botulinum toxin Neurons See above Neuronal activation Pb2+, general anesthetics Neuronal inhibition 2. Virtually all receptors and channels listed occur in multiple forms with different sensitivity to the agents. The α2-adrenergic receptor agonist clonidine induces release also similarities in the responses evoked by agonist/activators on in the brain of β-endorphin, an endogenous peptide that stimulates excitatory receptors and those elicited by antagonists/inhibitors opioid receptors (item 6 in Fig. Thus, glutamate receptor agonists and musca dine intoxication mimics several symptoms of morphine poisoning, rinic receptor agonists cause neuronal hyperactivity in the brain including depressed respiration and pinpoint pupils. It is also apparent that chemicals acting as agonists/activators on Toxicant–Neurotransmitter Receptor Interactions Some inhibitory receptors and those acting as antagonists/inhibitors on chemicals interact directly with neurotransmitter receptors, includ excitatory receptors may exert similar effects. In the absence of other actions, (ie, neuronal nicotinic acetylcholine receptor and glutamate recep agonists and activators mimic, whereas antagonists and inhibi tors; see items 1 and 2, respectively, in Fig. For example, the neuronal barbiturates, benzodiazepines, general anesthetics, and alcohols nicotinic acetylcholine receptor is extremely sensitive to inhibition are activators (Narahashi, 1991). Thus, all these chemicals cause by lead ions, whereas the muscular nicotinic receptor subtype is not inhibition of central nervous system activity, resulting in sedation, (Oortgiesen et al. Other chemicals that produce neurotrans general anesthesia, coma, and ultimately blockade of the medullary mitter receptor–mediated toxicity are listed in Table 3-5. Toxicant–Signal Transducer Interactions Many chemicals alter neuronal and/or muscle activity by acting on signal transduction Dysregulation of the Activity of Other Cells While many sign processes. In contrast, chemicals that block voltage-gated Ca2+, which may have toxicological signiﬁcance. Many exocrine secretory cells are controlled by muscarinic the Na+ channels are also important in signal transduction in sen acetylcholine receptors (item 11 in Fig. Salivation, lacrima sory neurons; therefore, Na+-channel activators evoke sensations tion, and bronchial hypersecretion after organophosphate insecti and reﬂexes, whereas Na+-channel inhibitors induce anesthesia. In contrast, this explains the reﬂex bradycardia and burning sensation in the blockade of these receptors contributes to the hyperthermia charac mouth that follow the ingestion of monkshood, which contains the teristic of atropine poisoning. Kupffer cells, resident macrophages Na+-channel activator aconitine, as well as the use of Na -channel+ in the liver, secrete inﬂammatory mediators (see Fig. Because Kupffer cells possess glycine receptors, that is, glycine-gated Cl− channels (item 4 in Fig. Such inter efﬂux may prolong excitation, as occurs with the blockade of Ca + 2+ vention alleviates ethanol-induced liver injury (Yin et al. The arachidonic acid metabolite 20-hydroxy-5,8,11,14 + 2+ + cemic agents for diabetic patients. The antihypertensive diazoxide acts in tant decrease in renal cortical blood ﬂow may underlie the neph + the opposite fashion on K channels and impairs insulin secretion. Several drugs with such an effect (eg, aste tural and functional integrity as well as provide supportive func mizole, cisapride, grepaﬂoxacin, terfenadine) have been withdrawn tions for other cells. Glycosides from digitalis and other plants inhibit + + by chemicals, resulting in a toxic response. The resultant rise in the intracellular anisms of Toxic Cell Death For survival, all cells must synthe concentration of Ca2+ enhances the contractility and excitability of size endogenous molecules; assemble macromolecular complexes, cardiac muscle. Lithium salts, although used therapeuti these functions, especially the energy-producing function of mito cally, have the potential to produce hyperreﬂexia, tremor, convul chondria and protein synthesis controlling function of the genome, sions, diarrhea, and cardiac arrhythmias (Hardman et al. In the across the inner membrane; and (5) return of protons across the following discussion, these events and the chemicals that may cause inner membrane into the matrix space down an electrochemical gra them are individually characterized. These chemicals are execute death by activating catabolic processes that bring about an divided into 5 groups (Table 3-6). Substances in class A interfere ordered disassembly and removal of the cell, called apoptosis. Class C agents interfere with oxygen delivery to nance both as a chemical for biosynthesis and as the major source of the terminal electron transporter, cytochrome oxidase. It is utilized in numerous biosynthetic reactions, activating that cause hypoxia ultimately act at this site. These pumps phenol import protons into the mitochondrial matrix, dissipating the maintain conditions essential for various cell functions. Arrows with letters A to D point to the ultimate sites of action of 4 cat egories of agents that interfere with oxidative phosphorylation (Table 3-6). For simplicity, this scheme does not indicate the outer mitochondrial membrane and that protons are extruded from the matrix space along the electron transport chain at 3 sites. Gluconeogenesis (critical in renal tubular cells): coenzyme A depletors (see below) 3. Fatty acid oxidation (critical in cardiac muscle): hypoglycin, 4-pentenoic acid, 4-ene-valproic acid 4. Depletors of coenzyme A (CoA) (a) Thiol-reactive electrophiles: 4-(dimethylamino)phenol, p-benzoquinone (b) Drugs enzymatically conjugated with CoA: salicylic acid (the metabolite of aspirin), valproic acid 8. Chemicals inhibiting oxygenation of Hb: carbon monoxide, methemoglobin-forming chemicals 4. Multisite inhibitor drugs: phenformin, propofol, salicylic acid (when overdosed) E. The increased conversion of pyruvate to lactate also may contribute to the acidosis. Terminally, the intracellular pH rises, increasing phospholipase activity, and this contributes to irreversible membrane damage (ie, 2+ Figure 3-17. Sustained Rise of Intracellular Ca2+ Intracellular Ca2+ levels are highly regulated (Fig.

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Even in the same family chronic gastritis forum buy misoprostol pills in toronto, two individuals carrying the same mutant genes may have some signs and symptoms in common gastritis diet restrictions buy misoprostol discount, whereas their other disease manifestations may be quite different gastritis patient handout discount misoprostol 100mcg on-line, depending on which tissues or organs happen to gastritis diet 3121 order cheapest misoprostol and misoprostol be affected gastritis diet �� buy 200 mcg misoprostol with amex. The challenge to gastritis not healing generic misoprostol 200mcg with visa the clinician caring for these families is to not miss very subtle signs of a disorder in a family member and, as a result, either mistake mild expressivity for lack of penetrance or infer that the individual does not have the disease-causing genotype. Pedigrees Single-gene disorders are characterized by their patterns of transmission in families. To establish the pattern of transmission, a usual first step is to obtain information about the family history of the patient and to summarize the details in the form of a pedigree, a graphical representation of the family tree, with use of standard symbols (Fig. An affected individual through whom a family with a genetic disorder is first brought to the attention of the geneticist. The person who brings the family to attention by consulting a geneticist is referred to as the consultand; the consultand may be an affected individual or an unaffected relative of a proband. A family may have more than one proband, if they are ascertained through more than one source. Brothers and sisters are called sibs or siblings, and a family of sibs forms a sibship. Relatives are classified as first degree (parents, sibs, and offspring of the proband), second degree (grandparents and grandchildren, uncles and aunts, nephews and nieces, and half-sibs), or third degree. If the proband is the only affected member in a family, he or she is an isolated case (see Fig. If an isolated case is proven to be due to new mutation in the proband, it is referred to as a sporadic case. When there is a definitive diagnosis based on comparisons to other patients, well-established patterns of inheritance in other families with the same disorder can often be used as a basis for counseling, even if the patient is an isolated case in the family. Thus, even when a patient has no similarly affected relatives, it may still be possible to recognize that the disorder is genetic and determine the risk to other family members. Although there is no uniform system of pedigree notation, the symbols used here are according to recent recommendations made by professionals in the field of genetic counseling. The proband has nine first-degree relatives (her parents, siblings, and offspring), nine second-degree relatives (grandparents, uncles and aunts, nieces and nephews, and grandchildren), two third-degree relatives (first cousins), and four fourth-degree relatives (first cousins once removed). Examining a pedigree is an essential first step in determining the inheritance pattern of a genetic disorder in a family. There are, however, a number of situations that may make the inheritance pattern of an individual pedigree difficult to discern. The inheritance pattern in a family with a lethal disorder affecting a fetus early in pregnancy may be obscure because all that one observes are multiple miscarriages or reduced fertility. Conversely, for phenotypes with variable age of onset, an affected individual may have unaffected family members who have not yet reached the age at which the mutant gene reveals itself. In addition to reduced penetrance or variable expressivity that may mask the existence of relatives carrying the mutant genotype, the geneticist may lack accurate information about the presence of the disorder in relatives or about family relationships. Finally, with the small family size typical of most developed countries today, the patient may by chance alone be the only affected family member, making determination of any inheritance pattern very difficult. Mendelian Inheritance the patterns of inheritance shown by single-gene disorders in families depend chiefly on two factors: Whether the chromosomal location of the gene locus is on an autosome (chromosomes 1 to 22), on a sex chromosome (X and Y chromosomes), or in the mitochondrial genome. Whether the phenotype is dominant (expressed when only one chromosome carries the mutant allele) or recessive (expressed only when both chromosomes of a pair carry mutant alleles at a locus) Autosomal, X-Linked, and Mitochondrial Inheritance the different patterns of transmission of the autosomes, sex chromosomes, and mitochondria during meiosis result in distinctive inheritance patterns of mutant alleles on these different types of chromosome (see Chapter 2). Mutant alleles on an X chromosome, however, are not distributed equally to sons and daughters. Males pass their Y chromosome to their sons and their X to their daughters; they therefore cannot pass an allele on the X chromosome to their sons and always pass the allele to their daughters (unless it is at one of the pseudoautosomal loci; see Chapter 6). Because mitochondria are inherited from the mother only, regardless of the sex of the offspring, mutations in the mitochondrial genome are not inherited according to a mendelian pattern. Autosomal, X linked, and mitochondrial inheritance will be discussed in the rest of the chapter that follows. Dominant and Recessive Traits Autosomal Loci As classically defined, a phenotype is recessive if it is expressed only in homozygotes, hemizygotes, or compound heterozygotes, all of whom lack a wild-type allele, and never in heterozygotes, who do have a wild-type allele. In contrast, a dominant inheritance pattern occurs when a phenotype is expressed in heterozygotes as well as in homozygotes (or compound heterozygotes). For the vast majority of inherited dominant diseases, homozygotes or compound heterozygotes for mutant alleles at autosomal loci are more severely affected than are heterozygotes, an inheritance pattern known as incompletely dominant (or semidominant). Very few diseases are known in which homozygotes (or compound heterozygotes) show the same phenotype as heterozygotes; in such cases, the disorder is referred to as a pure dominant disease. Finally, if phenotypic expression of both alleles at a locus occurs in a compound heterozygote, inheritance is termed codominant. The difference between the A and B antigen is which of two different sugar molecules makes up the terminal sugar on a cell surface glycoprotein called H. When the red blood cells lack antigen A, the serum contains anti-A antibodies; when the cells lack antigen B, the serum contains anti B. Formation of anti-A and anti-B antibodies in the absence of prior blood transfusion is believed to be a response to the natural occurrence of A-like and B-like antigens in the environment. X-Linked Loci For X-linked disorders, a condition expressed only in hemizygotes and never in heterozygotes has traditionally been referred to as an X-linked recessive, whereas a phenotype that is always expressed in heterozygotes as well as in hemizygotes has been called X-linked dominant. Because of epigenetic regulation of X-linked gene expression in carrier females due to X chromosome inactivation (introduced in Chapters 3 and 6), it can be difficult to determine phenotypically if a disease with an X-linked inheritance pattern is dominant or recessive, and some geneticists have therefore chosen not to use these terms when describing the inheritance of X-linked disease. Strictly speaking, the terms dominant and recessive refer to the inheritance pattern of a phenotype rather than to the alleles responsible for that phenotype. Similarly, a gene is not dominant or recessive; it is the phenotype produced by a particular mutant allele in that gene that shows dominant or recessive inheritance. Autosomal Patterns of Mendelian Inheritance Autosom al Recessive Inheritance Autosomal recessive disease occurs only in individuals with two mutant alleles and no wild-type allele. Such homozygotes must have inherited a mutant allele from each parent, each of whom is (barring rare exceptions that we will consider later) a heterozygote for that allele. When a disorder shows recessive inheritance, the mutant allele responsible generally reduces or eliminates the function of the gene product, a so-called loss-of-function mutation. For example, many recessive diseases are caused by mutations that impair or eliminate the function of an enzyme. The remaining normal gene copy in a heterozygote is able to compensate for the mutant allele and prevent the disease from occurring. However, when no normal allele is present, as in homozygotes or compound heterozygotes, disease occurs. Disease mechanisms and examples of recessive conditions are discussed in detail in Chapters 11 and 12. Three types of matings can lead to homozygous offspring affected with an autosomal recessive disease. The most common mating by far is between two unaffected heterozygotes, who are often referred to as carriers. However, any mating in which each parent has at least one recessive allele can produce homozygous affected offspring. The transmission of a recessive condition can be followed if we symbolize the mutant recessive allele as r and its normal dominant allele as R. Autosomal Recessive Inheritance the wild-type allele is denoted by uppercase R, a mutant allele by lowercase r. The chance of inheriting two recessive alleles and therefore being affected is thus × or 1 in 4 with each pregnancy. The 25% chance for two heterozygotes to have a child with an autosomal recessive disorder is independent of how many previous children there are who are either affected or unaffected. The proband may be the only affected family member, but if any others are affected, they are usually in the same sibship and not elsewhere in the kindred (Fig. Sex-Influenced Autosomal Recessive Disorders Because males and females both have the same complement of autosomes, autosomal recessive disorders generally show the same frequency and severity in males and females. Some autosomal recessive diseases demonstrate a sex-influenced phenotype, that is, the disorder is expressed in both sexes but with different frequencies or severity. For example, hereditary hemochromatosis is an autosomal recessive phenotype that is 5 to 10 times more common in males than in females (Case 20). Affected individuals have enhanced absorption of dietary iron that can lead to iron overload and serious damage to the heart, liver, and pancreas. The lower incidence of the clinical disorder in homozygous females is believed to be due to their lower dietary iron intake, lower alcohol usage, and increased iron loss through menstruation. Gene Frequency and Carrier Frequency Mutant alleles responsible for a recessive disorder are generally rare, and so most people will not have even one copy of the mutant allele. Because an autosomal recessive disorder must be inherited from both parents, the risk that any carrier will have an affected child depends partly on the chance that his or her mate is also a carrier of a mutant allele for the condition. Thus knowledge of the carrier frequency of a disease is clinically important for genetic counseling. The presence of such hidden recessive genes is not revealed unless the carrier happens to mate with someone who also carries a mutant allele at the same locus and the two deleterious alleles are both inherited by a child. It may also, however, be an overestimate, because it includes mutations in many genes that are not known to cause disease. Consanguinity Because most mutant alleles are generally uncommon in the population, people with rare autosomal recessive disorders are typically compound heterozygotes rather than true homozygotes. One well-recognized exception to this rule occurs when an affected individual inherits the exact same mutant allele from both parents because the parents are consanguineous. Finding consanguinity in the parents of a patient with a genetic disorder is strong evidence (although not proof) for the autosomal recessive inheritance of that condition. For example, the disorder in the pedigree in Figure 7-5 is likely to be an autosomal recessive trait, even though other information in the pedigree may seem insufficient to establish this inheritance pattern. Consanguinity is more frequently found in the background of patients with very rare conditions than in those with more common recessive conditions. This is because it is less likely that two individuals mating at random in the population will both be carriers of a very rare disorder by chance alone than it is that they would both be carriers because they inherited the same mutant allele from a single common ancestor. In contrast, in more common recessive conditions, most cases of the disorder result from matings between unrelated persons, each of whom happens by chance to be a carrier. The genetic risk to the offspring of marriages between related people is not as great as is sometimes imagined. For marriages between first cousins, the absolute risks of abnormal offspring, including not only known autosomal recessive diseases but also stillbirth, neonatal death, and congenital malformation, is 3% to 5%, approximately double the overall background risk of 2% to 3% for offspring born to any unrelated couple (see Chapter 16). Consanguinity at the level of third cousins or more remote relationships is not considered to be genetically significant, and the increased risk for abnormal offspring is negligible in such cases. The incidence of first-cousin marriage is low (≈1 to 10 per 1000 marriages) in many populations in Western societies today. However, it remains relatively common in some ethnic groups, for example, in families from rural areas of the Indian subcontinent, in other parts of Asia, and in the Middle East, where between 20% and 60% of all marriages are between cousins. C h a r a cte r istics o f A u to so m a l R e ce ssiv e I n h e r ita n ce. An autosomal recessive phenotype, if not isolated, is typically seen only in the sibship of the proband, and not in parents, offspring, or other relatives. This is especially likely if the gene responsible for the condition is rare in the population. Autosomal Dominant Inheritance More than half of all known mendelian disorders are inherited as autosomal dominant traits. For example, adult polycystic kidney disease (Case 37) occurs in 1 in 1000 individuals in the United States. Other autosomal dominant disorders show a high frequency only in certain populations from specific geographical areas: for example, the frequency of familial hypercholesterolemia (Case 16) is 1 in 100 for Afrikaner populations in South Africa and of myotonic dystrophy is 1 in 550 in the Charlevoix and Saguenay–Lac Saint Jean regions of northeastern Quebec. The burden of autosomal dominant disorders is further increased because of their hereditary nature; when they are transmitted through families, they raise medical and even social problems not only for individuals but also for whole kindreds, often through many generations. The risk and severity of dominantly inherited disease in the offspring depend on whether one or both parents are affected and whether the trait is a pure dominant or is incompletely dominant. There are a number of different ways that one mutant allele can cause a dominantly inherited trait to occur in a heterozygote despite the presence of a normal allele. Denoting D as the mutant allele and d as the wild-type allele, matings that produce children with an autosomal dominant disease can be between two heterozygotes (D/d) for the mutation or, more frequently, between a heterozygote for the mutation (D/d) and a homozygote for a normal allele (d/d). Autosomal Dominant Inheritance the mutant allele causing dominantly inherited disease is denoted by uppercase D; the normal or wild-type allele is denoted by lowercase d. In the population as a whole, then, the offspring of D/d by d/d parents are approximately 50% D/d and 50% d/d. Of course, each pregnancy is an independent event, not governed by the outcome of previous pregnancies. Thus, within a family, the distribution of affected and unaffected children may be quite different from the theoretical expected ratio of 1 : 1, especially if the sibship is small. Typical autosomal dominant inheritance can be seen in the pedigree of a family with a dominantly inherited form of hereditary deafness (Fig. B, Pedigree showing inheritance of achondroplasia, an incompletely dominant (or semidominant) trait. C, Pedigree showing a sporadic case of thanatophoric dwarfism, a genetic lethal, in the proband (arrow). In medical practice, homozygotes for dominant phenotypes are not often seen because matings that could produce homozygous offspring are rare. Again denoting the abnormal allele as D and the wild-type allele as d, the matings that can produce a D/D homozygote might theoretically be D/d by D/d, D/D by D/d, or D/D by D/D. In the case of two heterozygotes mating, three fourths of the offspring of a D/d by D/d mating will be affected to some extent and one fourth unaffected. Pure Dominant Inheritance As mentioned earlier, very few human disorders demonstrate a purely dominant pattern of inheritance. Even Huntington disease (Case 24), which is frequently considered to be a pure dominant because the disease is generally similar in the nature and severity of symptoms in heterozygotes and homozygotes, appears to have a somewhat accelerated time course from the onset of disease to death in homozygous individuals compared with heterozygotes. Most achondroplasia patients have normal intelligence and lead normal lives within their physical capabilities. A pedigree of a mating between two individuals heterozygous for the most common mutation that causes achondroplasia is shown in Figure 7-6B. Sex-Limited Phenotype in Autosomal Dominant Disease As discussed earlier for the autosomal recessive condition hemochromatosis, autosomal dominant phenotypes may also demonstrate a sex ratio that differs significantly from 1 : 1.

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The incidence of the refeeding syndrome among reports have noted this complication during nutritional these patients was 10% chronic gastritis gerd buy discount misoprostol 100mcg online. Among the seven deaths gastritis healing diet misoprostol 200 mcg low price, ve rehabilitation of patients with eating disorders were attributed to gastritis tips order misoprostol 200 mcg mastercard multisystem failure secondary to gastritis diet �� buy 200 mcg misoprostol fast delivery [19 gastritis diet �� purchase misoprostol cheap online,20 gastritis treatment dogs misoprostol 100mcg online,21,22]. Notably, caloric intake noted the risk of Wernicke–Korsakoff’s syndrome from was signi?cantly higher on day 1 among patients who thiamine de?ciency in patients with anorexia nervosa. This illustrates the importance of ongoing monitoring for refeeding syndrome to prevent neurological derange There is also likely to be a risk of refeeding syndrome ments in this population. Several studies have demonstrated the onset Another case report demonstrated acute hypoxic respir of hypophosphatemia with this regimen, which may atory failure in a bulimic female due to severe hypophos represent an unacknowledged form of the refeeding phatemia (phosphorus <1 mg/dl) [23]. The speci?c amount of glucose required to induce the condition is unknown; however, clinicians Whitelaw et al. Patients were assessed for anticipated Pathophysiology risk of refeeding syndrome and prescribed varying caloric A thorough understanding of the refeeding syndrome regimens. Caloric prescription was reduced for one requires a description of the physiology of different patient suspected to be at high risk for refeeding syn nutritional states [27]. These hormonal alterations account for the most likely to develop hypophosphatemia and were the electrolyte and uid shifts that are seen in the syndrome. The Starvation authors reiterated the need for clinical trials comparing Liver glycogen is depleted within 24 h of entering a various caloric regimens to determine the risk of refeed fasting state. The major hormonal shift during starvation Copyright © Lippincott Williams & Wilkins. Starved state During the initial stages of starvation, urinary nitrogen is very high as a result of the conversion of amino acids to glucose. With prolonged starvation past 10 days, the brain shifts its primary metabolic source to fat in the form of ketone bodies. Without this shift, the loss of lean body mass from Abrupt introduction of nutrition muscle catabolism would be fatal in less than 1 month. Fed state Shift of hormonal milieu With the reintroduction of nutrition, particularly carbo -Increase insulin hydrate, to individuals who have had a metabolic adap tation to starvation, there is a dramatic shift in macro -Decrease glucagon nutrient metabolism. Although ordinary meals are associated with this shift in the hormonal Initial derangements milieu, starved patients have different metabolic charac -Electrolyte abnormalities teristics that place them at risk for developing the refeed ing syndrome. The severity of these uctuations largely depends on the severity of malnutrition and electrolyte depletion experienced prior to the refeeding period. Several physiologic alterations can be observed as a result of these metabolic changes and are outlined as follows [28]. Clinical implications -Weakness Hypophosphatemia -Organ failure the most prominent electrolyte abnormality of the -Arrhythmias refeeding syndrome is hypophosphatemia [8,9,17,29– 31]. The starved state leads to a total body loss of phosphorus; however, serum levels may still be normal. The abrupt introduction of a carbo hydrate diet shifts energy metabolism to an anabolic is a reduction of insulin combined with a relative increase state. The primary sources of energy substrates increase, which causes intracellular migration of phos during starvation are fat and protein. Furthermore, phosphorus is also required for protein and hydrolysis of triglycerides provides necessary structural incorporation into phospholipids, nucleopro precursors for hepatic gluconeogenesis, which provide a teins and nucleic acids. There is also incorporation of source of glucose for hematologic and neurologic cells. During prolonged starvation, there are additional mech Hypokalemia anisms to produce glucose and conserve substrates. This yields less attributed to the reintroduction of carbohydrate and the Copyright © Lippincott Williams & Wilkins. There is typically a (a) diaphragm fatigue, whole-body reduction of potassium during starvation, (b) respiratory failure, and which accentuates the problems of hypokalemia during (c) prolonged ventilatory weaning. Depletion of magnesium during the refeeding process is (6) Immunologic: multifactorial. As with phosphorus and potassium, there (a) immune suppression, and is a total body depletion of magnesium during starvation. Serum levels may be deceptively normal due to concur (7) Neurologic: rent dehydration. Weakness Hyperglycemia Muscular weakness is commonly seen in the refeeding Upon reintroduction of carbohydrate to a patient experi syndrome. Thisweaknesscanbesynergisticwithweakness encing starvation, gluconeogensis is initially suppressed. It is mainly However, as refeeding continues, glucocorticoid circula driven by electrolyte aberrations, primarily hypophospate tion increases leading to exacerbation of hyperglycemia. Sodium retention and uid imbalance Arrhythmia the hyperinsulinemic response to carbohydrate in the Both hypomagnesaemia and hypokalemia are associated starved patient causes decreased renal excretion of with cardiac arrhythmias [35]. The retention of sodium and water as potentially lethal ventricular arrhythmias [36,37]. This enzyme is required for ef?cient of?oading Vitamin and mineral de?ciencies may already be present of oxygen to peripheral tissues. As a result, even in the in a patient experiencing starvation from prolonged presence of normal gas exchange, delivery of oxygen to inadequate intake [34]. Limited thiamine Cardiac dysfunction stores can be utilized early in the refeeding process. The introduction of adequate nutrition places signi?cant metabolic stress on marginalized myocardium. The already poorly functioning heart may be unable to handle Clinical implications the additional volume from the uid retention associated There are a number of clinical consequences to the with the refeeding syndrome [7,39,40]. Most of these are the result of tion represented the causes of death among prisoners in electrolyte shifts and vitamin depletion. The characteristics of the refeeding syndrome are as follows: Respiratory failure Hypophosphatemia is a well known mediator of diaphrag (1) Electrolyte abnormalities: matic fatigue. The refeeding syndrome can lead to new (a) hypokalemia, respiratory failure or prolonged ventilator weaning [8,23]. The (3) Cardiac: remaining thiamine is used up very rapidly after the (a) heart failure, and introduction of a glucose source. The anemia associated with refeeding syndrome is multi Recent guidelines in electrolyte replacement are summar factorial. Intravenous replacement is is also an inability to shift metabolic demands to increase preferred initially in critically ill patients to avoid issues red cell production. In our hospital, we have had success utilizing a combination of intravenous and enteral phos Infection phorus replacement inadults. NaPhosas prescribed Infectious complications can be seen with the refeeding by electrolyte replacement protocols with an additional syndrome [10,29]. These issues likely stem from hyper 1–3 packets of generic sodium phosphate daily) to more glycemia but there may also be intrinsic immunologic rapidly replace phosphorus levels of less than 2 mg/dl back dysfunction. These teams play a critical role in identifying and have gradual introduction and advancement of feeding. It preventing complications associated with refeeding syn is important, especially in critically ill patients, to account drome. Historically, management of refeeding syndrome for all energy and carbohydrate intake sources, such as was largely based upon case reports and clinical experi propofol and intravenous dextrose. As the recognition of refeeding syndrome provision have been described to be 20–75% of estimated improved, guidelines on the management of this syn energy needs in the adult and pediatric populations or drome have evolved but optimal treatment has not been 5–20 kcal/kg/day for adult patients depending on the con?rmed through clinical trials. Electrolyte repletion A complete electrolyte panel should be obtained in Few recommendations exist on the percentage of calories patients at high risk for refeeding syndrome prior to start that should come from carbohydrate versus protein or fat. Caloric intake should increase Monitoring by 10–25% per day or by 200–250 kcal/day after electro Recommendations have been made that heart rate and lytes have stabilized. Clinicians should be especially nutritional therapy to detect cardiac complications from cautious with patients receiving parenteral nutrition, as refeeding syndrome. A retrospective study described a pathway of correcting undernutrition in anorexic patients while also avoiding If symptoms of refeeding syndrome are observed, nutri refeeding syndrome [21 ]. Thirty-three female patients, tional intakes should be reduced or halted until symp aged 22. All patients were given thiamine and a element supplementation that should be administered to B vitamin supplement on day 1 of admission. Furthermore, it is enced a signi?cant increase in body weight while none recommended to continue with 100 mg of enteral experienced laboratory or clinical symptoms of refeeding thiamine daily. This study represents the largest case study high doses of thiamine (500–750 mg) may be warranted known thus far for refeeding of patients with anorexia [19]. In the pediatric patients, thiamine should also be nervosa successfully without symptoms of refeeding replaced, though at a lower dose of 10–25 mg/day initially syndrome. Published guidelines recommend additional micronutri Conclusion In conclusion, the refeeding syndrome remains a signi? ent supplementation in adults [2 ]. This supplement ation includes pyridoxine (vitamin B6), cobalamine cant issue in critically ill patients. Most factors and the clinical signs of the refeeding syndrome is multivitamin–mineral combination pills are likely ade important to optimize outcomes. This can be most effec quate to provide the additional recommended mainten tively accomplished with a multidisciplinary team that is ance doses of these vitamins; however, clinicians should attuned to nutritional needs and metabolic demands of consult with their pharmacy to determine the speci?c this patient population. References and recommended reading Volume Papers of particular interest, published within the annual period of review, have been highlighted as: Consideration should be given to sodium and uid bal of special interest ance when initiating a feeding regimen in a patient at risk of outstanding interest for refeeding syndrome. Some authors have recom Additional references related to this topic can also be found in the Current World Literature section in this issue (p. Refeeding syndrome: treatment hyponatremia should be slowly corrected to avoid per considerations basedoncollectiveanalysisofliteraturecasereports. This review represents extensive guidelines for the prevention and treatment of the outputs, heart rate, and sodium values should be mon refeeding syndrome. Transient hypoxic respiratory failure in a patient with severe hypopho Nutrition 2001; 17:632–637. This study represents the most report of the refeeding syndrome in critically ill patients. This study also provides an excellent description of the morbity and 6 Majumdar S, Dada B. Refeeding syndrome: a serious and potentially mortality of the refeeding syndrome in anorexic patients. Tight glucose control inintensive care units: an update with an emphasis on nutritional issues. Acute respiratory failure due to refeeding syndrome and cose–insulin–potassium therapy. A case report and proposal for altered hypophosphatemia induced by hypocaloric enteral nutrition. Refeeding syndrome: an important aspect of supportive oncol prevent and treat it. Serum phosphate predicts this study evaluated a series of elderly patients and noted the incidence of early mortality in adults starting antiretroviral therapy in Lusaka, Zambia: a hypophosphatemia and infectious complications. When the brakes came off: re-feeding oedema after de?ation of a gastric band – a case report. Refeeding syndrome: awareness is the rst step in preventing nutritiontreatment in Crohn disease. Magnes Res 2010; total parenteral nutrition: a cohort study to determine the incidence of 23:60–72. Enteral nutrition practice recom anorexia nervosa patients suffering from extreme undernutrition. Nutrition Support Core Curriculum: a without the induction of the refeeding syndrome. Acute edema/cutaneous distention syndrome associated with refeeding in a patient with anorexia nervosa. Physician may determine actual individual fuid needs to be either lower or higher than this amount. Elsevier Saunders 2015: 246-249 2 Baseline fuid requirements Initaton and Advancement of Enteral Feeds 1-10 kg 100 mL/kg (from A. Enteral Nutriton Practce Recommendatons, 2009): 10-20 kg 1000 mL + 50 mL/kg for each kg above 10 kg 1. Beginning and advancing enteral feedings in pediatric patents > 20 kg 1500 mL + 20 mL/kg for each kg above 20 kg is guided by clinical judgment and insttutonal practces in the absence of prospectve controlled clinical trials. Generally children are started on an isotonic formula at a rate of 1-2 mL/kg/h for smaller children and 1mL/kg/h for larger Fluid needs based on above formula: children over 35-40 kg. Feedings are advanced to goal calories within 24-48 hours and 2 200 54 2180 then bolus feedings are started, if indicated. Bolus feedings are given via gravity or over a longer period of 5 500 60 2300 tme via an enteral feeding pump. When the plan involves beginning with bolus feedings, a 7 700 64 2380 volume of 2. Bolus feedings can be given over shorter periods of tme by 14 1200 74 2580 gradually increasing the volume infused per hour. At no tme should a bolus feeding be given in a shorter period 18 1400 78 2660 of tme than a child would be expected to consume if given a 20 1500 80 2700 botle feeding. Bolus feedings may be started with 25% of the goal volume 32 1740 92 2940 divided into the desired number of daily feedings. Formula volume may be increased by 25% per day as tolerated, 36 1820 96 3020 divided equally between feedings. Pump-assisted feedings: A full-strength, isotonic formula can 42 1940 102 3140 be started at 1-2 mL/kg/h and advanced by 0. Preterm, critcally ill, or malnourished children who have not 48 2060 108 3260 been fed enterally for an extended period may require a lower 50 2100 110 3300 inital volume of 0.

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