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Injurious immune reactions may be evoked not only by exogenous environmental antigens skin care vitamins purchase 20gr benzac, but also by endogenous tissue antigens acne treatments that work order generic benzac online. Some of these immune reactions are triggered by homologous antigens that differ among individuals with different genetic backgrounds skin care mario badescu buy generic benzac 20gr on line. Transfusion reactions and graft rejection are examples of immunologic disorders evoked by homologous antigens acne aid soap buy 20 gr benzac visa. Another category of disorders skin care professionals buy 20gr benzac visa, those incited by self-, or autologous, antigens, constitutes the important group of autoimmune diseases (discussed later). These diseases arise because of the emergence of immune responses against self-antigens. Hypersensitivity diseases can be classified on the basis of the immunologic mechanism that mediates the disease (Table 6-2). This classification is of value in distinguishing the manner in which the immune response ultimately causes tissue injury and disease, and the accompanying pathologic alterations. Prototypes of each of these immune mechanisms are presented in the subsequent sections. Antibodies may also interfere with cellular functions and cause disease without tissue injury. The leukocytes that are recruited (neutrophils and monocytes) produce tissue damage by release of lysosomal enzymes and generation of toxic free radicals. Immediate (Type I) Hypersensitivity Immediate, or type I, hypersensitivity is a rapidly developing immunologic reaction occurring within minutes after the combination of an antigen with antibody bound to mast cells in [20] [21] individuals previously sensitized to the antigen. These reactions are often called allergy, and the antigens that elicit them are allergens. Immediate hypersensitivity may occur as a systemic disorder or as a local reaction. The systemic reaction usually follows injection of an antigen to which the host has become sensitized. The nature of local reactions varies depending on the portal of entry of the allergen and may take the form of localized cutaneous swellings (skin allergy, hives), nasal and conjunctival discharge (allergic rhinitis and conjunctivitis), hay fever, bronchial asthma, or allergic gastroenteritis (food allergy). The immediate, or initial, response is characterized by vasodilation, vascular leakage, and depending on the location, smooth muscle spasm or glandular secretions. These changes usually become evident within 5 to 30 minutes after exposure to an allergen and tend to subside in 60 minutes. Because mast cells are central to the development of immediate hypersensitivity, we first review some of their salient characteristics and then discuss the immune mechanisms that underlie [22] this form of hypersensitivity. The immediate vascular and smooth muscle reaction to allergen develops within minutes after challenge (allergen exposure in a previously sensitized individual), and the late-phase reaction develops 2 to 24 hours later. B, C, Morphology: the immediate reaction (B) is characterized by vasodilation, congestion, and edema, and the late phase reaction (C) is characterized by an inflammatory infiltrate rich in eosinophils, neutrophils, and T cells. Figure 6-13 Activation of mast cells in immediate hypersensitivity and release of their mediators. Thus, the recruited cells amplify and sustain the inflammatory response without additional exposure to the triggering antigen. It is now believed that this late-phase inflammatory response is a major cause of symptoms in some type I hypersensitivity disorders, such as allergic asthma. Therefore, treatment of these diseases requires the use of broad-spectrum anti-inflammatory drugs, such as steroids. A final point that should be mentioned in this general discussion of immediate hypersensitivity is that susceptibility to these reactions is genetically determined. The term atopy refers to a predisposition to develop localized immediate hypersensitivity reactions to a variety of inhaled and ingested allergens. The basis of familial predisposition is not clear, [27] but studies in patients with asthma reveal linkage to several gene loci. To summarize, immediate (type I) hypersensitivity is a complex disorder resulting from an IgE-mediated triggering of mast cells and subsequent accumulation of inflammatory cells at sites of antigen deposition. The clinical features result from release of mast-cell mediators as well as the accumulation of an eosinophilrich inflammatory exudate. With this consideration of the basic mechanisms of type I hypersensitivity, we turn to some conditions that are important examples of IgE-mediated disease. Systemic Anaphylaxis Systemic anaphylaxis is characterized by vascular shock, widespread edema, and difficulty in breathing. In humans, systemic anaphylaxis may occur after administration of foreign [28] proteins. Extremely small doses of antigen may trigger anaphylaxis, for example, the tiny amounts used in ordinary skin testing for various forms of allergies. Within minutes after exposure, itching, hives, and skin erythema appear, followed shortly thereafter by a striking contraction of respiratory bronchioles and respiratory distress. Vomiting, abdominal cramps, diarrhea, and laryngeal obstruction follow, and the patient may go into shock and even die within the hour. The risk of anaphylaxis must be borne in mind when certain therapeutic agents are administered. Although patients at risk can generally be identified by a previous history of some form of allergy, the absence of such 210 a history does not preclude the possibility of an anaphylactic reaction. Local Immediate Hypersensitivity Reactions Local immediate hypersensitivity, or allergic, reactions are exemplified by so-called atopic allergy. About 10% of the population suffers from allergies involving localized reactions to common environmental allergens, such as pollen, animal dander, house dust, foods, and the like. Specific diseases include urticaria, angioedema, allergic rhinitis (hay fever), and some forms of asthma, all discussed elsewhere in this book. The familial predisposition to the development of this type of allergy has been mentioned earlier. The antigenic determinants may be intrinsic to the cell membrane or matrix, or they may take the form of an exogenous antigen, such as a drug metabolite, that is adsorbed on a cell surface or matrix. In either case, the hypersensitivity reaction results from the binding of antibodies to normal or altered cell-surface antigens. Three different antibody-dependent mechanisms involved in this type of reaction are depicted in Figure 614 and described next. Most of these reactions involve the effector mechanisms that are used by antibodies, namely the complement system and phagocytes. Opsonization and Complementand Fc Receptor-Mediated Phagocytosis the depletion of cells targeted by antibodies is, to a large extent, because the cells are coated (opsonized) with molecules that make them attractive for phagocytes. When antibodies are deposited on the surfaces of cells, they may activate the complement system (if the antibodies are of the IgM or IgG class). Complement activation generates byproducts, mainly C3b and C4b, which are deposited on the surfaces of the cells and recognized by phagocytes that express receptors for these proteins. In addition, cells opsonized by IgG antibodies are recognized by phagocyte Fc receptors, which are specific for the Fc portions of some IgG subclasses. The net result is the phagocytosis of the opsonized cells and their destruction (Fig. Complement activation on cells also leads to the formation of the membrane attack complex, which disrupts membrane integrity by "drilling holes" through the lipid bilayer, thereby causing osmotic lysis of the cells. This form of antibody-mediated cell injury does not involve fixation of complement but instead requires the cooperation of leukocytes. Cells that are coated with low concentrations of IgG antibody are killed by a variety of effector cells, which bind to the target by their receptors for the Fc fragment of IgG, and cell lysis proceeds without phagocytosis. Clinically, antibody-mediated cell destruction and phagocytosis occur in the following situations: (1) transfusion reactions, in which cells from an incompatible donor react with and are opsonized by preformed antibody in the host; (2) erythroblastosis fetalis, in which there is an antigenic difference between the mother and the fetus, and antibodies (of the IgG class) from the mother cross the placenta and cause destruction of fetal red cells; (3) autoimmune hemolytic anemia, agranulocytosis, and thrombocytopenia, in which individuals produce antibodies to their own blood cells, which are then destroyed; and (4) certain drug reactions, in which antibodies are produced that react with the drug, which may be attached to the surface of erythrocytes or other cells. Complementand Fc Receptor-Mediated Inflammation When antibodies deposit in extracellular tissues, such as basement membranes and matrix, the resultant injury is because of inflammation and not because of phagocytosis or lysis of cells. The deposited antibodies activate complement, generating byproducts, such as C5a (and to a lesser extent C4a and C3a), that recruit neutrophils and monocytes. The leukocytes are activated, they release injurious substances, such as enzymes and reactive oxygen intermediates, and the result is damage to the tissues (Fig. It was once thought that complement was the major mediator of antibody-induced inflammation, but knockout mice lacking Fc receptors also show striking reduction in these reactions. It is now believed that inflammation in antibody-mediated (and immune complex-mediated) diseases is because of both complement and Fc receptor[29] dependent reactions. Antibody-mediated inflammation is the mechanism responsible for tissue injury in some forms of glomerulonephritis, vascular rejection in organ grafts, and other diseases (Table 6-4). As we shall discuss in more detail below, the same reaction is involved in immune complex-mediated diseases. Antibody-Mediated Cellular Dysfunction In some cases, antibodies directed against cell-surface receptors impair or dysregulate function without causing cell injury or inflammation. For example, in myasthenia gravis, antibodies reactive with acetylcholine receptors in the motor end-plates of skeletal muscles impair neuromuscular transmission and therefore cause muscle weakness (Fig. In pemphigus vulgaris, antibodies against desmosomes disrupt intercellular junctions in epidermis, leading to the formation of skin vesicles. In this disorder, antibodies against the thyroid-stimulating hormone receptor on thyroid epithelial cells stimulate the cells, resulting in hyperthyroidism. The toxic 211 Figure 6-14 Schematic illustration of the three major mechanisms of antibody-mediated injury. A, Opsonization of cells by antibodies and complement components and ingestion by phagocytes. B, Inflammation induced by antibody binding to Fc receptors of leukocytes and by complement breakdown products. Examples of immune complex disorders and the antigens involved are listed in Table 6-5. Immune complex-mediated diseases can be generalized, if immune complexes are formed in the circulation and are deposited in many organs, or localized to particular organs, such as the kidney (glomerulonephritis), joints (arthritis), or the small blood vessels of the skin if the complexes are formed and deposited locally. Systemic Immune Complex Disease Acute serum sickness is the prototype of a systemic immune complex disease; it was at one time a frequent sequela to the administration of large amounts of foreign serum. Patients with diphtheria infection were being treated with serum from horses immunized with the diphtheria toxin. Von Pirquet noted that some of these patients developed arthritis, skin rash, and fever, and the symptoms appeared more rapidly with repeated injection of the serum. Von Pirquet concluded that the treated patients made antibodies to horse serum proteins, these antibodies formed complexes with the injected proteins, and the disease was due to the antibodies or immune complexes. In modern times the disease is infrequent, but it is an informative model that has taught us a great deal about systemic immune complex disorders. The first phase is initiated by the introduction of antigen, usually a protein, and its interaction with immunocompetent cells, resulting in the formation of antibodies approximately a week after the injection of the protein. These antibodies are secreted into the blood, where they react with the antigen still present in the circulation to form antigen-antibody complexes. In the second phase, the circulating antigen-antibody complexes are deposited in various tissues. The factors that determine whether immune complex formation will lead to tissue deposition and disease are not fully understood, but two possible influences are the size of the immune complexes and the functional status of the mononuclear phagocyte system: • Large complexes formed in great antibody excess are rapidly removed from the circulation by the mononuclear phagocyte system and are therefore relatively harmless. The most pathogenic complexes are of small or intermediate size (formed in slight antigen excess), which bind less avidly to phagocytic cells and therefore circulate longer. In addition, several other factors, such as charge of the immune complexes (anionic versus cationic), valency of the antigen, avidity of the antibody, affinity of the antigen to various tissue components, three-dimensional (lattice) structure of the complexes, and hemodynamic factors, influence the tissue deposition of complexes. Because most of these influences have been investigated with reference to deposition of immune complexes in the glomeruli, they are discussed further in Chapter 20.

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In the mildest forms acne wallet cheap 20 gr benzac otc, significant inflammation is limited to acne video buy 20 gr benzac portal tracts and consists of lymphocytes skin care coconut oil buy 20 gr benzac otc, macrophages acne y clima frio polar purchase benzac in united states online, occasional plasma cells skin care collagen 20 gr benzac sale, and rare neutrophils or eosinophils. Liver architecture is usually well preserved, but smoldering hepatocyte necrosis throughout the lobule may occur in all forms of chronic hepatitis. In all forms of chronic hepatitis, continued interface hepatitis and bridging necrosis are harbingers of progressive liver damage. At first, only portal tracts exhibit increased fibrosis, but with time, periportal septal fibrosis occurs, followed by linking of fibrous septa between lobules (bridging fibrosis). Continued loss of hepatocytes and fibrosis results in cirrhosis, with fibrous septae and hepatocyte regenerative nodules. This pattern of cirrhosis is characterized by irregularly sized nodules separated by variable but mostly broad scars (Fig. Historically, this pattern of cirrhosis has been termed postnecrotic cirrhosis, but it should be noted that the term "postnecrotic cirrhosis" has been applied to all forms of cirrhosis in which the liver shows large, irregular-sized nodules with broad scars, regardless of etiology. Autoimmune hepatitis, hepatotoxins (carbon tetrachloride, mushroom poisoning), pharmaceutical drugs (acetaminophen, methyldopa), and even alcohol (discussed later) may give rise to a cirrhotic liver with irregular-sized large nodules. In some cases that come to autopsy, the inciting cause of the so-called postnecrotic cirrhosis cannot be determined at all ("cryptogenic cirrhosis"). In essence, the morphology of the end-stage cirrhotic liver is neither helpful in determining the basis of the liver injury, nor can it be easily related to any specific set of clinical circumstances. Patients may experience spontaneous remission or may have indolent disease without progression for many years. Conversely, some patients have rapidly progressive disease and develop cirrhosis within a few years. Fulminant Hepatitis When hepatic insufficiency progresses from onset of symptoms to hepatic encephalopathy within 2 to 3 weeks, it is 900 Figure 18-17 Diagrammatic representations of the morphologic features of acute and chronic hepatitis. Bridging necrosis (and fibrosis) is shown only for chronic hepatitis; bridging necrosis may also occur in acute hepatitis (not shown). A, Liver parenchyma showing hepatocytes with diffuse granular cytoplasm, so-called ground glass hepatocytes. Figure 18-19 Acute viral hepatitis showing disruption of lobular architecture, inflammatory cells in the sinusoids, and hepatocellular apoptosis (arrow). Figure 18-20 Chronic viral hepatitis due to hepatitis C virus, showing portal tract expansion with inflammatory cells and fibrous tissue and interface hepatitis with spillover of inflammation into the adjacent parenchyma. Portal tracts and terminal hepatic veins are closer together than normal, owing to necrosis and collapse of the intervening parenchyma. However, individual genetic differences in the hepatic metabolism of xenobiotics through activating and detoxification pathways play a major role in individual susceptibility to "predictable" hepatotoxins. Many other xenobiotics, such as sulfonamides, methyldopa, and allopurinol, cause idiosyncratic reactions. Reye syndrome, a potentially fatal syndrome of mitochondrial dysfunction in liver, brain, and elsewhere, occurs predominantly in children who are given acetylsalicylic acid (aspirin) for the relief of virus-induced fever. This disease, which features extensive accumulation of fat droplets within hepatocytes (microvesicular steatosis), is exceedingly rare. A causal relationship with use of salicylates was never established, but a national campaign in the 1970s and 1980s warning against the use of aspirin in children with febrile illness might have served to break the Reye syndrome epidemic. Drug-induced liver disease is usually followed by recovery upon removal of the drug. Exposure to a toxin or therapeutic agent should always be included in the differential diagnosis of liver disease. The interrelationships among hepatic steatosis, hepatitis, and cirrhosis are shown, along with a depiction of key morphologic features at the morphologic level. Figure 18-24 Alcoholic liver disease: macrovesicular steatosis, involving most regions of the hepatic lobule. B, Eosinophilic Mallory bodies are seen in hepatocytes, which are surrounded by fibrous tissue (H&E). A, the characteristic diffuse nodularity of the surface reflects the interplay between nodular regeneration and scarring. A hepatocellular carcinoma is present as a budding mass at the lower edge of the right lobe (lower left of figure). B, the microscopic view shows nodules of varying sizes entrapped in blue-staining fibrous tissue. Parenteral iron overload •••••••Transfusions ••••••••••Long-term hemodialysis ••••••••••Aplastic anemia ••••••••••Sickle cell disease ••••••••••Myelodysplastic syndromes ••••••••••Leukemias •••••••Iron-dextran injections ••••B. Ineffective erythropoiesis with increased erythroid activity ••••••• Thalassemia •••••••Sideroblastic anemia •••••••Pyruvate kinase deficiency ••••C. Increased oral intake of iron •••••••African iron overload (Bantu siderosis) ••••D. Chronic liver disease •••••••Chronic alcoholic liver disease •••••••Porphyria cutanea tarda [4] In white populations of northern European extraction, the frequency of the C282Y mutation is estimated at 6. However, the penetrance of this disorder is only about 20% in patients with the homozygous C282Y mutation, so the genetic condition does not lead to disease in all individuals. It may be recalled that the total body content of iron is tightly regulated, as the limited daily losses of iron are matched by gastrointestinal absorption. In hereditary hemochromatosis, regulation of intestinal absorption of dietary iron is lost, leading to net iron accumulation of 0. The disease manifests itself typically after 20 gm of storage iron have accumulated. The TfR-Tf-iron complex is endocytosed into the crypt enterocyte; acidification of the endosome releases iron into the regulatory iron pool of the crypt cell. This is a sensing mechanism for the systemic iron balance, as increased levels of circulating iron bound to transferrin will lead to an increased iron regulatory pool in enterocytes. As small intestinal crypt cells are the progenitors of villus absorptive cells, these cells are preprogrammed to absorb dietary iron regardless of the systemic iron overload. Whatever the actions of iron, they are reversible in cells that are not fatally injured, and removal of excess iron during therapy promotes recovery of tissue function. The most common causes of secondary hemochromatosis are the hemolytic anemias associated with ineffective erythropoiesis, discussed in Chapter 13. In these disorders, the excess iron may result not only from transfusions, but also from increased absorption. The crypt epithelial cell is the precursor cell of the mature absorptive enterocyte on the tip of the villus, through migration up the villus axis. Hepatocellular iron deposition is blue in this Prussian blue-stained section of an early stage of the disease, in which parenchymal architecture is normal. Periodic acid-Schiff stain of the liver, highlighting the characteristic red cytoplasmic granules. The major conditions causing it are (1) cholangiopathies, primarily biliary atresia (discussed later) and (2) a variety of disorders causing conjugated hyperbilirubinemia in the neonate, collectively referred to as neonatal hepatitis. Neonatal cholestasis and hepatitis are not specific entities, nor are the disorders necessarily inflammatory. Instead, the finding of "neonatal cholestasis" should evoke a diligent search for [38] recognizable toxic, metabolic, and infectious liver diseases, the more common of which are listed in Table 18-10. Once identifiable causes have been excluded, one is left with the syndrome of "idiopathic" neonatal hepatitis, which shows considerable clinical overlap with biliary atresia. Affected infants have jaundice, dark urine, light or acholic stools, and hepatomegaly. Variable degrees of hepatic synthetic dysfunction may be identified, such as hypoprothrombinemia. Thus, liver biopsy is critical in distinguishing neonatal hepatitis from an identifiable cholangiopathy. The morphologic features of neonatal hepatitis are: • Lobular disarray with focal liver cell necrosis • Panlobular giant cell transformation of hepatocytes and formation of hepatocyte "rosettes": radially arrayed hepatocytes • Prominent hepatocellular and canalicular cholestasis • Mild mononuclear infiltration of the portal areas • Reactive changes in the Kupffer cells • Extramedullary hematopoiesis this predominantly parenchymal pattern of injury may blend imperceptibly into a ductal pattern of injury, with bile ductular proliferation and fibrosis of 913 portal tracts. Specific features that point toward a particular etiology include the inclusions of cytomegalovirus, or fatty change with cirrhosis in galactosemia and tyrosinemia. Electron microscopy may be helpful, for example, by showing phospholipid whorls in Neimann-Pick disease. Despite the long list of disorders associated with neonatal cholestasis, most are quite rare. Differentiation of biliary atresia from nonobstructive neonatal cholestasis assumes great importance, since definitive treatment of biliary atresia requires surgical intervention, whereas surgery may adversely affect the clinical course of a child with other disorders. Fortunately, discrimination can be made with clinical data, without or with liver biopsy, in about 90% of cases. Intrahepatic Biliary Tract Disease In this section, we discuss three disorders of intrahepatic bile ducts: secondary biliary cirrhosis, primary biliary cirrhosis, and primary sclerosing cholangitis, (summarized in Table 18-11). Secondary biliary cirrhosis is a condition resulting most often from uncorrected obstruction of the extrahepatic biliary tree. Primary biliary cirrhosis is a destructive disorder of the intrahepatic biliary tree. Primary sclerosing cholangitis involves both the extrahepatic and intrahepatic biliary tree. It should also be noted (although not discussed here) that intrahepatic bile ducts are frequently damaged as part of more general liver disease, as in drug toxicity, viral hepatitis, and transplantation—both orthotopic liver transplantation and graft-versus-host disease after bone marrow transplantation. The most common cause of obstruction in adults is extrahepatic cholelithiasis (gallstones, described later), followed by malignancies of the biliary tree or head of the pancreas and strictures resulting from previous surgical procedures. Obstructive conditions in children include biliary atresia, cystic fibrosis, choledochal cysts (a cystic anomaly of the extrahepatic biliary tree, see later), and syndromes in which there are insufficient intrahepatic bile [39] ducts (paucity of bile duct syndromes). The initial morphologic features of cholestasis were described earlier and are entirely reversible with correction of the obstruction. However, secondary inflammation resulting from biliary obstruction initiates periportal fibrosis, which eventually leads to hepatic scarring and nodule formation, generating secondary biliary cirrhosis. Subtotal obstruction may promote secondary bacterial infection of the biliary tree (ascending cholangitis), which aggravates the inflammatory injury. The end-stage obstructed liver exhibits extraordinary yellow-green pigmentation and is accompanied by marked icteric discoloration of body tissues and fluids. The histology is characterized by coarse fibrous septae that subdivide the liver in a jigsaw-like pattern. Embedded in the septa are distended small and large bile ducts, which frequently contain inspissated pigmented material. There is extensive proliferation of smaller bile ductules and edema, particularly at the interface between septa (formerly portal tracts) and the parenchyma. Cholestatic features in the parenchyma may be severe, with extensive feathery degeneration and formation of bile lakes. However, once regenerative nodules have formed, bile stasis 914 Figure 18-30 Biliary cirrhosis. Sagittal section through the liver demonstrates the fine nodularity and bile staining of end-stage biliary cirrhosis. A portal tract is markedly expanded by an infiltrate of lymphocytes and plasma cells. The granulomatous reaction to a bile duct undergoing destruction (florid duct lesion) is highlighted by the arrowheads.

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Correspondence to: Dr Vidyut Bhatia acne diet benzac 20 gr line, Apollo Center for Advanced Pediatrics acne 911 zit blast buy cheap benzac on-line, Indraprastha Apollo Hospital skin care 30 years old buy generic benzac 20 gr, New Delhi 110 076 acne-fw13c order benzac no prescription, India acne diagram order benzac master card. Late referral and lack of management practices in major centers in India, and to identify precise etiological diagnosis are reasons for poor outcome in various problems in effective diagnosis and ways to improve the substantial number of cases in India. Current problems faced in different areas were better awareness among the pediatricians, obstetricians and discussed and possible remedial measures were identified. The primary care physicians on early recognition, prompt evaluation ultimate aim would be to achieve results comparable to the and referral to regional centers. Process: Eminent national faculty members were invited to Recommendations: Early recognition, prompt evaluation and participate in the process of forming a consensus statement. Inclusion of stool/urine color charts in well baby specific issues, which were reviewed by two other members. Considering the was organized; presentations, ensuing discussions, and need for specific expertise and the poor outcome in subopinions expressed by the participants were incorporated into optimally managed cases, referral to regional centers is the final draft. Objectives: To review available published data on the subject Keywords: Cholestatic jaundice, Neonate, Practice guidelines. Conjugated with pediatric gastroenterology units should follow a hyperbilirubinemia in a neonate is defined as a serum uniform protocol of evaluation, and third, the direct/conjugated bilirubin concentration greater than 1. It is important to note that the diazo method of A number of steps including a public campaign on estimating bilirubin, that is still practiced in many Indian ‘Yellow alert’ and educational programs at pediatric centers, tends to overestimate the direct fraction at lower meetings were since held to address the key issues [2,3]. The group however felt that the above the algorithm put in place in 2001 was followed at almost mentioned definition has to be retained since it is an all major centers, until newer advances were reported. Although appropriate center for further investigations and cholestasis is known to occur in babies with early onset treatment at the earliest [1]. Yet simultaneous screening should be done infants with deranged liver function tests, particularly for metabolic causes. Galactosemia, a treatable cause, uncorrected coagulopathy, require urgent referral to rule may be present even in babies with culture proven sepsis. A recent publication with jaundice, and this leads to parents and physicians exhaustive workup has shown that Pi-Z and Pi-S alleles underestimating the seriousness of the problem [3]. Many responsible for alpha-1 antitrypsin deficiency may be rare health care professionals also have a misconception that in our population [7]. Enlarging the scope of the ‘yellow Etiologic Factor N-1008* (%) N-420#(%) alert’ to include the whole country through visual and Obstructive causes print media would also be beneficial. The Group recommended urine and stool color assessment Biliary atresia 34 30 (minimum 3 stool samples) by the mother and physician Choledochal cysts 4 5 in a stool color card incorporated in all well baby cards Hepatocellular causes (Indian Academy of Pediatrics and the Government of Infections 17 18 India cards). The group also felt that the Taiwanese experience with stool color cards (subsequently Metabolic causes 4 12 replicated in other countries) should be possible in India Miscellaneous 2 3 as well [21]. Unknown etiology 30 31 Persistent cholestasis from any cause leads to liver Ductal paucity 3 1 damage and cirrhosis. Also, the outcome of Kasai portoenterostomy #Data from the largest single series (7). Improved outcome is also noted in centers disorders, and diseases that are managed medically from with a higher case load [24]. However in the transaminases are sensitive indicators of hepatocellular light of recent publications and better laboratory support, injury, but lack specificity and prognostic value. High modifications are required in the evaluation and alkaline phosphatase levels can be seen in biliary management protocol. Fructose mucosal lining with an indistinct wall or irregular/lobular challenge test can make the child very ill and is now contour) [19], no contraction of the gallbladder after oral obsolete. Markedly raised serum required (5-7 days) for priming before the scan, ferritin and uncorrected coagulopathy are suggestive of especially in patients who are referred late, is a limitation. In bile plugs in ducts, fibrosis and lymphocytic infiltrates in breastfed infants, breastfeeding should be encouraged the portal tracts. Essential fatty acids should constitute 2biopsy must be interpreted by an experienced pathologist 3% of the energy provided. Vegetable protein at 2-3 g/kg/ in conjunction with the clinical profile and results of the d is recommended [34]. Infants with cholestasis require supplementation with fat-soluble vitamins administered orally as water-soluble In galactosemia, urine is positive for non-glucose preparations. Suggested daily vitamin and mineral reducing substances while the infant is on lactose feeds. Depending markedly prolonged, intramuscular injections should be on severity and response to previous agent, add-on drug avoided. Appropriate antibiotics depending on till 3 months after resolution of jaundice [35]. There is no role for steroids in Surgery gives excellent results for choledochal cysts and idiopathic neonatal hepatitis. Elemental iron Oral 5-6 mg/kg/d • Ultrasound, isotope scan and liver biopsy Adapted from Ref. Special formulae may have a role in select Liver Transplantation, the standard therapy for cases. Of the 355 transplants in children Conference in memory of their son Kunwar Viren Oswal. Inborn errors of metabolism in infancy: a guide Interpreting conjugated bilirubin levels in newborns. Guideline for the evaluation of program on 5-year outcome of biliary atresia in Taiwan. Lampela H, Ritvanen A, Kosola S, Koivusalo A, Rintala R, with chronic liver disease in North India. Usefulness of a scoring system in the prognostic factors associated with biliary atresia in interpretation of histology in neonatal cholestasis. Tyrosinemia type I—diagnostic issues and prenatal liver failure in infants and children: Consensus statement of diagnosis. India’s first successful pediatric liver mManagement of cholestasis in infants and children. Screening and outcomes in biliary Risk Factors, and Outcomes of 755 Patients Listed for atresia: summary of a National Institutes of Health Liver Transplantation. Cholecystoappendicostomy for progressive familial Outcome of live donor liver transplantation in Indian intrahepatic cholestasis. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the Italian Copyright Law in its current version, and permission for use must always be obtained from Springer. Product liability: the publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. Cover design: Simona Colombo, Milan Typesetting: Compostudio, Cernusco s/N (Milan) Printing and binding: Arti Grafiche Nidasio, Assago (Milan) Preface to the Second Edition the practicing radiologist is continually challenged to update his/her competencies so as to deliver state-of-the-art radiological care. Nowhere is this truer than in the rapidly evolving world of magnetic resonance imaging, where innovations in both technology and diagnostic pharmaceuticals have dramatically altered the landscape of practice. This information is vital for decisions as to the appropriate course of treatment for a given patient. For completion, comparison is also made with the typical enhancement behavior of lesions on alternative diagnostic imaging modalities, namely ultrasound and computed tomography. The chapters included in the first edition have been enriched with the most recent information available in the literature, and by the inclusion of many additional images; the opportunity to directly observe the characteristic features of the lesions under discussion represents a very efficient learning tool for practicing radiologists. Finally, an entire chapter is dedicated to comparing the available contrast agents for imaging of specific liver lesions (Chapter 8). This information is essential in transplant patients and can also contribute to reducing overall health-care costs by reducing the number of imaging studies and avoiding unnecessary surgery. The editors owe a debt of gratitude to the contributors to this book for sharing their extensive knowledge with the wider radiology community. Indeed, this kind of academic-industrial partnership is what helps us provide the best care for our patients. We hope readers find the contents of this book beneficial, and we welcome feedback on how we might continue to facilitate the transfer of essential knowledge in the radiological community. The absence of ionizing radiation, unparalleled soft tissue contrast, inherent multiplanar capability and high temporal resolution in dynamic gadolinium-enhanced imaging are major advantages over other imaging techniques. The increase in differences in signal intensity between normal hepatic parenchyma and hypoor hypervascular neoplastic tissues is discussed, as are the specific enhancement patterns observed in different phases of perfusion following gadolinium administration. Chapter three presents a detailed overview of the histological classification of focal and diffuse liver pathologies, focusing on the essential needs of radiologists. Specifically, flow charts and tables for the differential diagnoses of liver lesions are presented, thereby consolidating in a single source the charts and tables found in a multiplicity of books and articles on abdominal and hepatobiliary imaging. All benign and malignant primary liver lesions are presented from the most common such as hemangioma or hepatocellular carcinoma to the rarest such as nodular regenerative hyperplasia or epithelial hemangioendothelioma. The sections on secondary liver lesions cover not only metastases and lymphoma, but also inflammatory and parasitic lesions. Where appropriate, the imaging features observed with other techniques (computed tomography and ultrasound) are presented for comparison. Their respective institutions, the University Clinic of Homburg-Saar, Germany, the University Hospital of Brescia, Italy, and the Mass. This truly international effort has produced a fully-encompassing source for radiologists anywhere with current and practical information. I predict that this book will influence the way we practice liver imaging: the protocols will be improved, the differential diagnosis charts will be copied and pinned up in reading rooms in many departments and overall it will have a beneficial impact. Schneider, Grazioli and Saini with the certainty that you will enjoy their material and information. Clinic for Diagnostic and Interventional Clinic for Diagnostic and Interventional Radiology Radiology University Hospital of Saarland University Hospital of Saarland 66421 Homburg/Saar, Germany 66421 Homburg/Saar, Germany Luigi Grazioli, M. Department of Radiology Clinic for Diagnostic and Interventional University of Brescia Radiology Piazzale Spedali Civili 1 University Hospital of Saarland 25023 Brescia, Italy 66421 Homburg/Saar, Germany Sanjay Saini, M. World Wide Medical Affairs Department of Radiology Bracco Imaging SpA University of Brescia Via E. Folli 50 Piazzale Spedali Civili 1 Milan, Italy 25023 Brescia, Italy Peter Fries, M. Clinic for Diagnostic and Interventional Clinic for Diagnostic and Interventional Radiology Radiology University Hospital of Saarland University Hospital of Saarland 66421 Homburg/Saar, Germany 66421 Homburg/Saar, Germany Maria Pia Bondioni, M. Department of Radiology Emory Healthcare University of Brescia the Emory Clinic, Inc. Johnston, Gianni Chiappella and Patrizia Andreoni for their precious support in the preprint processes of copyediting and typesetting, respectively, and Alexandra Davies and John R. Disclaimer: the publisher and authors of «Swiss Essentials in During the daily clinical routine as well as during the preparation for Gastroenterology» assume no obligation to update the publication specialist exams or student courses, it became evident that a suitable, and no responsibility or warranty with respect to the timeliness, compact reference book comprising relevant decision-making accuracy, and completeness of the information, and rejects any gastroenterological facts was lacking. No liability is accepted for data usually needs to be sourced from original publications, any damage or loss arising from the use of this information. Our aim was to speed up and simplify this time-consuming process with «Swiss Essentials in Gastroenterology». The outcome of our work is currently only available in this print version, as we believe in the effectiveness of the «white coat pocket guide book» even in the era of «apps» and the Internet.

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Stress hematuria occurs afA positive reagent strip (dipstick) in the absence of ter exercise skin care chanel safe 20 gr benzac. Patients with benign familial hematuria (thin basemoglobinuria occurs with hemolysis skin care physicians buy benzac 20 gr fast delivery. It may occur in hemoment membrane nephropathy) have an excellent prognosis but lytic anemias acne before and after purchase genuine benzac online, hemolytic-uremic syndrome acne 8 year old boy cheap benzac 20gr with amex, mismatched must be followed acne under beard order discount benzac online. Nutcracker syndrome is due to carbon monoxide, fava beans, venoms, mushrooms, naphthathe compression of the distal segment of the lef renal vein belene, quinine, and many other substances. Papillary will ofen show fragmented cells, and the reticulocyte count necrosis may result in hematuria in patients with sickle cell may be elevated. Myoglobinuria occurs with rhabdomyolysis afer viral myositis and in children with inborn errors of energy metabolism, Acute postinfectious glomerulonephritis occurs 4 days to 7 ofen afer exercise. The clinical picture as well as elevated 3 weeks afer a febrile illness just with hematuria, but also muscle enzyme levels may aid in distinguishing myoglobinuria with oliguria, edema, and hypertension. If needed, Hgb and myoglobin may be meainfection causing either pharyngitis or impetigo is the most sured in the urine. Laboratory fndings include a decrease in C3 and C4 levels and laboratory evidence of a preceding group A Microscopic hematuria is ofen found on routine screen3 streptococcal infection (Streptozyme, antistreptolysin, antihyaling. If proteinuria is present, the port syndrome is associated with a family history of renal disevaluation is the same as for gross hematuria (see algorithm). Proteinuria suggests glomerular involvemay be due to associated renal cysts and angiomyolipomas. Chapter 163 122 Part V u Genitourinary System particularly in focal segmental sclerosis and membranoproBibliography liferative glomerulonephritis. It may also Pediatrics textbook of pediatric care, Elk Grove Village, Ill, 2009, American be associated with other diseases, such as systemic lupus Academy of Pediatrics, pp 1566–1569. It may also be done by quantitative assessment of proteinuria in ambulatory and recumbent urine specimens. The amount in the ambulatory specimen may vary but is usually 2 to 4 times that of the recumbent specimen. In patients who have persistent asymptomatic proteinuria, Proteinuria is a common laboratory fnding that is ofen a symp4 further evaluation may proceed as in symptomatic patients. It may also be found in normal, healthy It is reasonable to refer even the patient with normal test results children. It is therefore important to distinguish between pathoto a nephrologist, because there are diferent opinions regarding logic and nonpathologic causes of proteinuria. Because this is a transient fnding in a majority of children, it is Patients with proteinuria who are symptomatic (edema, 5 important to retest the urine before making a diagnosis. Trace proteinuria is usually not signifcant; tory of glomerulonephritis or renal failure should have further 11 proteinuria (30 mg/dl) may be signifcant. In most cases, referral to the nephrologist may be repeated and viewed in the context of the urine Sp gr. This evaluation includes assessment of renal function negative results may occur with urine that is too dilute (,1. Nephrotic synand false-positive results may occur with overlong dipstick imdrome consists of proteinuria, hypoalbuminemia, edema, and mersion, alkaline urine, pyuria, bacteriuria, mucoprotein and hyperlipidemia. Total serum protein, albumin, as well as cholesquaternary ammonium compounds, and detergents. Tests for antistreptococcal Quantitative testing for proteinuria is done by a timed 12to antibodies (Streptozyme) as well as complement levels (C3, C4) 24-hour urine collection for protein: less than 4 mg/m2/h is norare done to exclude poststreptococcal glomerulonephritis. The mal, 4-40 mg/m2/h is abnormal, and over 40 mg/m2/h is in the diagnosis of poststreptococcal glomerulonephritis is made in a nephrotic range. An early morning spot testing of urine protein/Cr child with acute nephritic syndrome, evidence of recent strepratio (in mg/dL) correlates well with 24-hour urine protein extococcal infection, and a low C3 level. Antinuclear antibody testing may be considered, especially 2 years; for children 6 months to 2 years, over 0. Minimal change nephrotic syndrome is more common in 6 History should include questions about recent exercise, red boys and usually appears between ages 2 and 6 years. Renal function may be reduced, cholesterol and triglycon awakening, increased abdominal girth, and difculty putting erides are elevated, and serum albumin is decreased. The C3 on shoes, may indicate nephrotic syndrome and should be investilevel is normal. Family history related to renal disease, hematuria, or hypertension should be pursued. This is an increased protein excretion in the upright position only and is less common in younger children. It may Children younger than age 1 with nephrotic syndrome 10 account for as much as 60% of all proteinuria in children and has have a poor prognosis. It is an autosomal Any of the following tests may be performed to test for recessive condition and may occur as failure to thrive due to orthostatic proteinuria. Geme J, et al, editors: Nelson textbook of pediatrics, ed 19, Philadelphia, 2011, Elsevier Saunders. Chapter 162 Features of hyperthyroidism include goiter and eye fnd5 Chapter 34 ings, including proptosis, exophthalmos, and lid lag. Symptoms due to increased catecholamines include palpitations, tachycardia, hypertension, tremor, and brisk refexes. An associated myopathy may cause weakness, periodic paralysis, and heart failure. It Severe anemia, particularly in a newborn, may cause 6 may occur as a result of increased capillary pressure (congestive edema. Kasabach-Merritt syndrome occurs in children with (nephrotic syndrome, burns), decreased intake (malnutrition), large cavernous hemangiomas of the trunk, extremities, or abor impaired lymphatic fow. Trombocytopenia, a microangiopathic hemolytic anemia, and The history and physical examination are very important in 1 ofen a consumptive coagulopathy are present. Arteriovenous malformations may Signs and symptoms specifc to heart failure, liver failure, and also be present within the anomalies, resulting in heart failure. History of burns and the presence of severe and extensive burns reveal the etiology. Vital signs may myopathies there may be lef or right ventricular ischemic indicate a diagnosis; with heart failure there is tachycardia and changes on the electrocardiogram. Electrocardiography is also useful in deterties) is usually present with peripheral edema. Echocardiography is most useful may be seen with lymphedema or thyroid disease (pretibial in assessing ventricular function as well as underlying strucmyxedema). Angioedema is a form of urticaria afecting deeper tissue Congenital heart defects are the most common cause of 2 8 planes, including the skin and subcutaneous tissues. A history of recurrent angioedema may indicate episodic angioedema, which is associated Cardiomyopathy may occur as a result of a number of dis9 with fever and eosinophilia. Dilated cardiomyopathy is characterized by massive sults from a decreased synthesis of C1 esterase inhibitor, occurs cardiomegaly and ventricular dilation. The cause is usually unas sudden attacks of edema ofen precipitated by minor trauma, known. Congenital lymphedema may occur in Turner synthematosus), hyperthyroidism, and metabolic (mitochondrial drome, Noonan syndrome, and Milroy disease. Acquired disorders) and nutritional disease (beriberi, defciency of seleobstruction may be due to tumors, lymphoma, flariasis, nium, taurine, and carnitine). Other causes include disorders of postirradiation fbrosis, and postinfammatory or postsurgical coronary arteries (anomalous origin of lef coronary), and carscarring. Injury to major lymphatic vessels may result in chydiotoxic drugs (doxorubicin, chronic ipecac abuse). Restrictive cardiomyopathies result in Signs and symptoms include tachycardia, tachypnea, syspoor ventricular compliance and inadequate ventricular flling; temic venous congestion (hepatomegaly), and cardiomegaly. Respiratory sympViral myocarditis is most commonly caused by adenovirus toms such as wheezing, rales, and cough may be present, 10 and coxsackievirus B. Other infectious causes include diphtheria, sysor a gallop rhythm may be present. An older child may have temic bacterial infections (sepsis), and Rocky Mountain spotted orthopnea or may experience syncopal symptoms. Heart failure is more likely with large intracranial arterioveMetabolic disorders associated with liver failure include 16 nous fstulas. They are less likely with peripheral arteriovenous hereditary fructose intolerance, and urea cycle defects. Later there is desive jaundice, fetor hepaticus, fever, anorexia, vomiting, and creased growth, decreased stamina, muscle loss, increased susabdominal pain. The edema may mask poor without clinical improvement, hemorrhagic diathesis, and asciweight gain. Infants may present with irritability, lethargy, poor feeding, coarse and discolored, resulting in streaky red or gray hair. Mental status changes are noted with Laboratory fndings include decreased serum albumin, hypoprogression of symptoms. Older children may demonstrate glycemia, hypophosphatemia, and defciency of potassium and asterixis. Signs of vitamin (especially vitamin A) and mineral In liver failure, hypoalbuminemia results in edema, and 13 (zinc) defciencies may be present. Serum aminotransferase levels are elevated early but may decrease as Protein-losing enteropathy may result in edema secondary 18 the patient’s condition deteriorates. Measurement of levels in the stool is monia level is usually elevated, and there may be hypoglycemia, helpful in the diagnosis of protein-losing enteropathy. Causes hypokalemia, hyponatremia, metabolic acidosis, or respiratory include food protein–induced enteropathy and postinfectious alkalosis. Eosinophilic gastroenteritis is another cause; it may be associated with dietary protein hypersensitivity as well Viral hepatitis is a common cause of liver failure. Tere is ofen eosinophilia and an elelikely in children with a combined infection with hepatitis vated serum immunoglobulin (Ig)E. Other viruses that may result in liver failure include severe malnutrition may also present with edema. A careful skin examination should identify characteristic fndings such as cafe-au-lait spots (neurofbromatosis); tubers, ash leaf spots (tuberous sclerosis); hirsutism (congenital adrenal hyperplasia); malar rash (lupus); and purpura (HenochIt is currently recommended that all children older than age 3 Schonlein purpura). Tere may be a heart murmur with absent or include those with a history of prematurity, congenital heart decreased femoral pulses in aortic coarctation, and tachyardisease, renal disease, solid organ transplant, cancer, medicarhythmias with pheochromocytomas. Bruits may indicate use an appropriate-size cuf whose width measures 40% of the aortic or renal arterial disease. Abdominal examination may circumference of the arm, and the cuf bladder length should identify enlarged kidneys. Use of automated devices is acceptable neck, shield chest, low hairline), and Williams syndrome (elfn in newborns and infants when auscultation may be difcult and facies, poor growth, retardation) should be identifed. A complete in settings that require continuous monitoring, such as an infamily history may be helpful in identifying primary or secondary tensive care unit. Electrolytes may be helpful in the diagnosis of hyperaldosteronism History should include ingestion of medications and tox1. Symptoms such as abdominal pain, dysuria, frequency, nocturia, enuresis, hematuria, and Consider further evaluation for comorbidities (lipid pro5 edema may indicate a renal cause. In infants, growth failure, irfle, fasting glucose, polysomnography when indicated).

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