hepatitis_hund

Smitsom leverbetændelse

Hvad er smitsom leverbetændelse hos hunde?

Smitsom leverbetændelse er en infektion med en virus, som kaldes adenovirus. Adenovirus findes over hele verden og er yderst smitsom. Ud over hunde kan også ulve, coyote-hunde og bjørne blive smittet.

Hvad er symptomerne på smitsom leverbetændelse?

• Feber
• Apati
• Nedsat appetit
• Øget tørst
• Øjenbetændelse
• Mavesmerter
• Opkast

Hvordan kan din dyrlæge stille diagnosen smitsom leverbetændelse?

Hundens symptomer vil give dyrlægen en idé om, at leveren bør undersøges yderligere. Dyrlægen vil tage en blodprøve, fordi mængden af visse enzymer i blodet fortæller noget om leverskadens omfang. Den egentlige diagnose stilles på baggrund af en vævsprøve ( biopsi ) fra leveren. Hvis der er adenovirus i en prøven, har hunden smitsom leverbetændelse.

Hvordan behandles smitsom leverbetændelse?

Da hunde med hepatitis ofte er meget syge, kræver de væskebehandling via drop , flydende ernæring via drop og eventuelt en blodtransfusion. Behandling med antibiotika, smertestillende medicin og en leverdiæt kommer ofte også på tale.

Hvordan er fremtiden for din hund, hvis den har smitsom leverbetændelse?

Smitsom leverbetændelse er farlig for alle hunde, men sygdommen er især dødelig for unge hunde. Det er vigtig, at hunden kommer til dyrlæge hurtigt, så den kan komme under behandling, hvis man har mistanke om leverbetændelse.

Hvorfor får hunde smitsom leverbetændelse?

Smitten med adenovirus sker via urin, afføring eller spyt fra hunde, der har virussen. Adenovirus kan ligge i omgivelserne i flere uger og være smitsom. Virussen kan dog dræbes af desinfektion med en 1-3% klorinopløsning.

Man kan forebygge leverbetændelse ved at lade sin hund vaccinere årligt.

Hvad er risikoen for, at din hund får leverbetændelse?

På grund af den udbredte vaccination af hunde i dag, er smitsom leverbetændelse blevet en sjælden sygdom. Vaccinerne giver en næsten 100% effektiv beskyttelse.

Hvilke racer er særligt udsatte for at få smitsom leverbetændelse?

Ingen racer er særligt disponerede for leverbetændelse.

Anden viden om smitsom leverbetændelse:

10 til 14 dage efter den indledende fase i infektionen får 25% af de overlevede hunde en blåfarvning af hornhinden i begge øjne (blue-eye). Det skyldes, at proteiner fra hundens immunforsvar lægger sig i hornhinden. Blåfarvningen forsvinder af sig selv hos de fleste hunde.

Gulsot er ikke en egentlig sygdom, men derimod et symptom. Det er en gammel betegnelse for en tilstand, hvor huden og slimhinderne bliver gule. Gulfarvningen finder sted, fordi der sker en ophobning a…

Leverkræft er en sygdom, hvor nogle celler i leveren begynder at vokse ukontrolleret. Det fører mange gange til knuder og nedsat kapacitet i leveren. Hvad er symptomerne på leverkræft? Nedsat spi…

Leversvigt er en alvorlig tilstand, hvor leverens funktion er stærkt nedsat. Den egentlige årsag til leversvigt kan være bakterieinfektion, virusinfektion, forgiftning eller cancer. Leveren er et vigt…

Foder til nyre- eller hjertelidelser

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Tilskudsfoder til hunde og katte ved kronisk nyresvigt

Vi sender faglig information, tips og tricks og gode tilbud 2-4 gange om måneden. Nye abonnenter får en rabatkode på 10% til webshoppen.

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Indholdet på Netdyredoktor.dk er udelukkende til informationsbrug. Disse informationer må på ingen måde kompensere eller erstatte den professionelle rådgivning og behandling, som gives af en autoriseret dyrlæge. Læs afsnittet om juridisk information og ansvarsfraskrivelse samt cookiepolitik .

Vores familiedyr er altid overladt til menneskers omsorg, både hvad angår pleje, sundhed og sygdom.

Det forpligter både dig som dyreejer og os som veterinærsygeplejersker og dyrlæger. Vi er med i et kompetent netværk, hvor vi altid kan trække på hinandens ekspertise. På den måde får dit dyr altid den bedste behandling.

Myasthenia Gravis Associated with Acute Hepatitis E Infection in Immunocompetent Woman

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To the Editor: Hepatitis E virus (HEV) is a common cause of acute hepatitis in developing countries. The course of acute hepatitis E is usually benign, except in pregnant women and in immunocompromised patients, who are prone to a lethal or chronic outcome of the disease. Since 2001, hepatitis E has been emerging in industrialized countries, and neurologic manifestations such as Guillain-Barré syndrome, brachial neuritis, transverse myelitis, and cranial nerve palsies have been reported in patients with acute or chronic forms of the disease (1–6). Most cases with neurologic manifestations have been characterized by infection with genotype 3 HEV. Data are not available to indicate whether this association between HEV infection and neurologic manifestations is related to a specific antigenic stimulus provided by HEV or is linked to the more comprehensive assessment for such neurologic conditions that is available in industrialized countries or to a reporting bias. We report a case of HEV infection in an immunocompetent woman who had muscle-specific kinase (MuSK) antibody–positive myasthenia gravis associated with HEV replication.

A 33-year-old woman was hospitalized in France for subacute asthenia and intermittent symptoms including dysarthria, dysphagia, muscle weakness, and diplopia. She had no family history of autoimmune disease and no notable personal medical history; she had not received any recent vaccinations and had not traveled outside France during the previous year. Physical examination showed no pyramidal, vestibular, or cerebellar syndromes, and all tendon reflexes were typical.

On admission, the patient’s liver function tests showed elevated alanine transaminase (190 UI/L). Test results were within reference ranges for aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, and creatine kinase levels. Antibody tests were negative for hepatitis B virus, hepatitis C virus, HIV, human T-lymphotropic viruses 1 and 2, and Treponema pallidum, but testing for cytomegalovirus and Epstein-Barr virus showed previous exposure. Serum samples were positive for HEV IgM (index 11) and negative for HEV IgG (index 0.71) by Adaltis microplate ELISA (EIAgen; Adaltis, Casalecchio Di Reno, Italy). HEV RNA was detected in serum and fecal samples by using HEV reverse transcription PCR (RT-PCR) (Ceeram, La Chapelle sur Erdre, France) on the SmartCycler II instrument (Cepheid, Sunnyvale, CA, USA). Sequencing studies showed that the HEV strain belonged to genotype 3f.

Brain magnetic resonance imaging results were normal, and results for analysis of cerebrospinal fluid were normal (leukocytes <5 cells/µL, glucose 3.2 mmol/L, protein 38 mg/dL, HEV RT-PCR negative). A nerve conduction study, performed even though the patient was not symptomatic, did not find any abnormality. Pharmacologic testing with prostigmine (0.5 mg intravenously) did not result in symptom improvement. Computed tomography scan of the mediastinum showed no thymoma. Test results for anti-acetylcholine receptor antibodies were negative; however, results were positive for MuSK antibodies (18.7 U/mL by radioimmunoassay; RSR Ltd., Cardiff, Wales, UK). These data, combined with physical examination, confirmed the diagnosis of myasthenia gravis.

Given this association of myasthenia and acute HEV infection, we suspected the potent role of HEV infection in the neurologic symptoms. Therapy was started with ribavirin (1,000 mg/day for 1 month) and intravenous immunoglobulin (IVIG) (1 g/kg/d for 2 days). Alanine transaminase levels rapidly decreased, and after 3 months, test results for HEV IgM and HEV RT-PCR in serum were negative. IVIG treatment relieved symptoms in the short term, but symptoms returned 15 days after treatment ended, requiring continuation of IVIG every 4 weeks for 6 months. Four months after the last infusion of IVIG, the patient reported mild 4-limb fatigability after exercise, but results of objective neurologic examination were normal. Results for MuSK antibodies were still positive, and treatment with azathioprine (150 mg/d) was started. Three weeks later, the patient required another infusion of IVIG for difficulty in swallowing, dyspnea, and 4-limb weakness, but she was free of symptoms for the remaining 5 months of follow-up.

In conclusion, we describe a case of anti-MuSK myasthenia gravis associated with acute HEV in a young, immunocompetent patient in France. Because myasthenia gravis with MuSK antibodies is rare (≈10% of myasthenia gravis cases) (7), the potential role of HEV infection as a trigger of autoimmune disorders should be investigated. Some cases of anti-MuSK myasthenia gravis associated with HIV (8) or Epstein-Barr virus (9) infections have been reported. Nevertheless, our findings do not enable us to draw conclusions regarding causality. Our observation might suggest a coincidental temporal association between HEV infection and myasthenia gravis or a triggering of autoimmunity by HEV. Moreover, anti-MuSK myasthenia gravis is usually characterized by a rapidly progressive course with moderate to severe symptoms (7). The initial unusually benign clinical course in this patient might be explained by the effect of early ribavirin treatment or, more likely, by a particular type of MuSK antibodies (10).

Aude Belbezier, Alban Deroux, Françoise Sarrot-Reynauld , Sylvie Larrat, and Laurence Bouillet

References

1. Cheung MC , Maguire J , Carey I , Wendon J , Agarwal K . Review of the neurological manifestations of hepatitis E infection. Ann Hepatol . 2012 ; 11 : 618 – 22 . PubMed
2. Peri AM , Milazzo L , Meroni L , Antinori S . Radiculoneuropathy associated with acute hepatitis E. Dig Liver Dis . 2013 ; 45 : 963 – 4 . DOIPubMed
3. GeurtsvanKessel CH . Islam Z, Mohammad QD, Jacobs BC, Endtz HP, Osterhaus AD. Hepatitis E and Guillain-Barré syndrome. Clin Infect Dis . 2013 ; 57 : 1369 – 70 . DOIPubMed
4. Scharn N , Ganzenmueller T , Wenzel JJ , Dengler R , Heim A , Wegner F . Guillain-Barré syndrome associated with autochthonous infection by hepatitis E virus subgenotype 3c. Infection . 2014 ; 42 : 171 – 3 . DOIPubMed
5. Despierres LA , Kaphan E , Attarian S , Cohen-Bacrie S , Pelletier J , Pouget J , Neurologic disorders and hepatitis E, France, 2010. Emerg Infect Dis . 2011 ; 17 : 1510 – 2 . PubMed
6. Kamar N , Bendall RP , Peron JM , Cintas P , Prudhomme L , Mansuy JM , Hepatitis E virus and neurologic disorders. Emerg Infect Dis . 2011 ; 17 : 173 – 9 . DOIPubMed
7. Evoli A , Padua L . Diagnosis and therapy of myasthenia gravis with antibodies to muscle-specific kinase. Autoimmun Rev . 2013 ; 12 : 931 – 5 . DOIPubMed
8. Kurokawa T , Nishiyama T , Yamamoto R , Kishida H , Hakii Y , Kuroiwa Y . Anti-MuSK antibody positive myasthenia gravis with HIV infection successfully treated with cyclosporin: a case report. Rinsho Shinkeigaku . 2008 ; 48 : 666 – 9 . DOIPubMed
9. Bhibhatbhan A , Kline G , Vincent A , Toth C . Anti-MuSK myasthenia gravis presenting with Epstein-Barr virus–associated mononucleosis and immune-mediated diabetes mellitus. Muscle Nerve . 2007 ; 36 : 264 – 6 . DOIPubMed
10. Zouvelou V , Stamboulis E , Skriapa L , Tzartos SJ . MuSK-Ab positive myasthenia: not always grave. J Neurol Sci . 2013 ; 331 : 150 – 1 . DOIPubMed

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Please use the form below to submit correspondence to the authors or contact them at the following address:

Françoise Sarrot-Reynauld, Clinique Universitaire de Médecine Interne, Pôle Pluridisciplinaire de Médecine, Centre Hospitalier Universitaire de Grenoble, CS10217, 38043 Grenoble Cedex, FranceFrançoise Sarrot-Reynauld, Clinique Universitaire de Médecine Interne, Pôle Pluridisciplinaire de Médecine, Centre Hospitalier Universitaire de Grenoble, CS10217, 38043 Grenoble Cedex, France

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Impfschädigung beim Hund

Impfen mit Verstand

Die Dunkelziffer der Impfschäden ist sehr groß und oftmals ist der direkte Zusammenhang zwischen Impfung und Erkrankung nicht eindeutig zu erkennen da der Ausbruch der Krankheit über mehrere Monate nach der Impfung erst erfolgt. Die direkten Nebenwirkungen einer Impfung wie Husten, Abgeschlagenheit, Erbrechen und die häuftigste, die Ohrenentzündung lässt sich jedoch recht schnell erkennen.

All dies wird hervorgerufen durch die Schwächung des Immunsystems nach erhaltener Impfung. Besonders Welpen sind davon betroffen und der spätere Besitzer, der sich über eine angehende Ohrenentzündung wundert weiß oft nicht, dass diese von erhaltener Grundimmunisierung kommt. In schlimmen Fällen reagieren Welpen oftmals nach Impfungen, die in den ersten Lebenswochen durchgeführt werden mit Schüttelfrost, Bewegungs- und Gleichgewichtsstörungen, Zittern und Krämpfen. Dies zeigt sich erstmals zwischen dem 8. und dem 13. Tag nach erhaltener Impfung. In diesem Stadium der Schädigung sei gesagt, geht es bereits um Leben und Tod.

- Staupe: wird mit einem Lebendimpfstoff gespritzt. Nach der Grundimmunisierung und einer Auffrischung nach ca. einem Jahr hält dieser Schutz mindestens 15 Jahre.

- Parvo: auch hier wird ein Lebendimpfstoff verabreicht. Schutzdauer auch hier 15 Jahre.

- Hepatitis: Lebendimpfstoff, Schutzdauer wie bei Staupe und Parvo.

Zwingerhusten (Parainfluenza Virus): Die Schutzdauer beträgt hier 3 Jahre, der Impfstoff versagt nachweislich jedoch relativ häufig. Diese Impfung ist deshalb umstritten da der Krankheitsverlauf nach Ansteckung relativ harmlos und gut behandelbar ist.

Zwingerhustenerreger (Bordetella bronchiseptica): Impfschutz 1 Jahr wobei auch hier der Impfstoff regelmäßig versagt.

Zeckenimpfung: Eine Impfung, gegen die von Zecken übertragenen Borrelien. Der Impfstoff schützt nur gegen einen kleinen Teil der bekannten Borrelienerreger. Hundehalter beobachteten nach erhaltener Impfung sogar epileptische Anfälle.

Leptospirose:Dieser Impfstoff ist besonders für Welpen und Junghunde unverträglich. Dieser Impfstoff bietet noch dazu nur gegen 2 Arten dieser Viren einen Schutz.

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Rabies Titer Blood Test

Rabies Titer Blood Test

The Rabies Titer test is used to evaluate a person’s immunity to Rabies. This test screens for antibodies capable of neutralizing the Rabies virus. This Rabies Titer test, also known as the RFFIT, is considered the gold standard of Rabies blood tests by the World Health Organization and Advisory Committee on Immunization Practices. It is more accurate than ELISA testing for Rabies which may provide a person with false positives for immunity.

This test is typically ordered by people who work with animals and have an occupational risk of exposure to Rabies. This test may also be used to evaluate the effectiveness of post exposure treatment for Rabies.

The Rabies Titer test is run at the Kansas State University Rabies Laboratory, one of only two commercial laboratories recognized by the Center for Disease Control for performing the test. As a result, turnaround time for this test can be up to 4 weeks.

Note: Result turn around times are an estimate and are not guaranteed. Our reference lab may need additional time due to weather, holidays, confirmation/repeat testing, or equipment maintenance.

This test is not available in the state of FLORIDA Customers testing in Florida have the option of ordering an alternative test, the Rabies RFFIT Test. This test uses the same methodology and is performed at a lab recognized by the CDC for providing Rabies testing. For more information on the CDC's guidelines regarding the methodologies for Rabies testing, please see the link below.

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Hepatic Fibrosis

By Jesse M. Civan, MD, Assistant Professor and Medical Director, Liver Tumor Center, Thomas Jefferson University Hospital

• Fibrosis and Cirrhosis

Hepatic fibrosis is overly exuberant wound healing in which excessive connective tissue builds up in the liver. The extracellular matrix is overproduced, degraded deficiently, or both. The trigger is chronic injury, especially if there is an inflammatory component. Fibrosis itself causes no symptoms but can lead to portal hypertension (the scarring distorts blood flow through the liver) or cirrhosis (the scarring results in disruption of normal hepatic architecture and liver dysfunction). Diagnosis is based on liver biopsy. Treatment involves correcting the underlying condition when possible.

In hepatic fibrosis, excessive connective tissue accumulates in the liver; this tissue represents scarring in response to chronic, repeated liver cell injury. Commonly, fibrosis progresses, disrupting hepatic architecture and eventually function, as regenerating hepatocytes attempt to replace and repair damaged tissue. When such disruption is widespread, cirrhosis is diagnosed.

Various types of chronic liver injury can cause fibrosis (see Table: Disorders and Drugs That Can Cause Hepatic Fibrosis). Self-limited, acute liver injury (eg, acute viral hepatitis A), even when fulminant, does not necessarily distort the scaffolding architecture and hence does not cause fibrosis, despite loss of hepatocytes. In its initial stages, hepatic fibrosis can regress if the cause is reversible (eg, with viral clearance). After months or years of chronic or repeated injury, fibrosis becomes permanent. Fibrosis develops even more rapidly in mechanical biliary obstruction.

Disorders and Drugs That Can Cause Hepatic Fibrosis

Disorders with direct hepatic effects

Certain storage diseases and inborn errors of metabolism

Alpha-1 antitrypsin deficiency

Copper storage diseases (eg, Wilson disease)

Glycogen storage diseases (especially types III, IV, VI, IX, and X)

Iron-overload syndromes (hemochromatosis)

Lipid abnormalities (eg, Gaucher disease)

Peroxisomal disorders (eg, Zellweger syndrome)

Congenital hepatic fibrosis

Bacterial (eg, brucellosis)

Parasitic (eg, echinococcosis)

Viral (eg, chronic hepatitis B or C*)

Nonalcoholic steatohepatitis (NASH)

Primary biliary cirrhosis

Primary sclerosing cholangitis

Disorders affecting hepatic blood flow

Hepatic veno-occlusive disease †

Portal vein thrombosis

Drugs and chemicals

Scarring due to prior liver surgery

Bile duct strictures due to impacted gallstones

*Most common causes.

† Sometimes caused by pyrrolizidine alkaloids, present in herbal products such as bush teas.

Pathophysiology

Activation of the hepatic perivascular stellate cells (Ito cells, which store fat) initiates fibrosis. These and adjacent cells proliferate, becoming contractile cells termed myofibroblasts. These cells produce excessive amounts of abnormal matrix (consisting of collagen, other glycoproteins, and glycans) and matricellular proteins. Kupffer cells (resident macrophages), injured hepatocytes, platelets, and leukocytes aggregate. As a result, reactive O₂ species and inflammatory mediators (eg, platelet-derived growth factor, transforming growth factors, connective tissue growth factor) are released. Thus, stellate cell activation results in abnormal extracellular matrix, both in quantity and composition.

Myofibroblasts, stimulated by endothelin-1, contribute to increased portal vein resistance and increase the density of the abnormal matrix. Fibrous tracts join branches of afferent portal veins and efferent hepatic veins, bypassing the hepatocytes and limiting their blood supply. Hence, fibrosis contributes both to hepatocyte ischemia (causing hepatocellular dysfunction) and portal hypertension. The extent of the ischemia and portal hypertension determines how the liver is affected. For example, congenital hepatic fibrosis affects portal vein branches, largely sparing the parenchyma. The result is portal hypertension with sparing of hepatocellular function.

Symptoms and Signs

Hepatic fibrosis itself does not cause symptoms. Symptoms may result from the disorder causing fibrosis or, once fibrosis progresses to cirrhosis, from complications of portal hypertension. These symptoms include variceal bleeding, ascites, and portosystemic encephalopathy. Cirrhosis can result in hepatic insufficiency and potentially fatal liver failure.

Sometimes blood tests and/or noninvasive imaging tests

Sometimes liver biopsy

Hepatic fibrosis is suspected if patients have known chronic liver disease (eg, chronic viral hepatitis C and hepatitis B [see Table: Characteristics of Hepatitis Viruses], alcoholic liver disease) or if results of liver function tests are abnormal; in such cases, tests are done to check for fibrosis and, if fibrosis is present, to determine its severity (stage). Knowing the stage of fibrosis can guide medical decisions. For example, screening for hepatocellular carcinoma and for gastroesophageal varices is indicated if cirrhosis is confirmed, but it is generally not indicated for mild or moderate fibrosis. Also, if liver biopsy does not detect advanced fibrosis in patients with hepatitis C, many clinicians defer treatment with interferons because they anticipate that more effective, less toxic drugs will be available.

Tests used to stage fibrosis include noninvasive imaging tests, blood tests, liver biopsy, and newer tests that assess liver stiffness.

Noninvasive imaging tests include conventional ultrasonography, CT, and MRI and should include cross-sectional views. These tests can detect evidence of cirrhosis and portal hypertension, such as splenomegaly and varices. However, they are not sensitive for moderate or even advanced fibrosis if splenomegaly and varices are absent. Although fibrosis may appear as altered echogenicity on ultrasonography or heterogeneity of signal on CT, these findings are nonspecific and may indicate only liver parenchymal fat.

New technologies can increase the accuracy of ultrasonography and MRI for detecting fibrosis or early cirrhosis; they include ultrasound elastography, magnetic resonance elastography, and acoustic radiation force impulse imaging. For these tests, acoustic vibrations are applied to the abdomen with a probe. How rapidly these vibrations are transmitted through liver tissue is measured—an indication of how stiff (ie, fibrosed) the liver is.

Liver biopsy remains the gold standard for diagnosing and staging hepatic fibrosis and for diagnosing the underlying liver disorder causing fibrosis. However, liver biopsy is invasive, resulting in a 10 to 20% risk of minor complications (eg, postprocedural pain) and a 0.5 to 1% risk of serious complications (eg, significant bleeding). Also, liver biopsy is limited by sampling error and imperfect interobserver agreement in interpretation of histologic findings. Thus, liver biopsy may not always be done.

Blood tests include commercially available panels that combine indirect markers (eg, serum bilirubin) and direct markers of hepatic function. Direct markers are substances involved in the pathogenesis of extracellular matrix deposition or cytokines that induce extracellular matrix deposition. These panels are best used to distinguish between 2 levels of fibrosis: absent to minimal vs moderate to severe; they do not accurately differentiate between degrees of moderate to severe fibrosis. Therefore, if fibrosis is suspected, one approach is to start with one of these panels and then do liver biopsy only if the panel indicates that fibrosis is moderate to severe.

Which tests are done may depend on the degree of clinical suspicion, based on clinical evaluation, including liver function test results. For example, noninvasive blood tests may be used to determine whether biopsy is indicated; in some of these cases, imaging tests may not be needed.

Treatment of cause

Because fibrosis represents a response to hepatic damage, primary treatment should focus on the cause (removing the basis of the liver injury). Such treatment may include eliminating hepatitis B virus or hepatitis C virus in chronic viral hepatitis, abstaining from alcohol in alcoholic liver disease, removing heavy metals such as iron in hemochromatosis or copper in Wilson disease, and decompressing bile ducts in biliary obstruction. Such treatments may stop the fibrosis from progressing and, in some patients, also reverse some of the fibrotic changes.

Treatments aimed at reversing the fibrosis are usually too toxic for long-term use (eg, corticosteroids, penicillamine ) or have no proven efficacy (eg, colchicine ). Other antifibrotic treatments are under study. Simultaneous use of multiple antifibrotic drugs may eventually prove most beneficial. Silymarin, present in milk thistle, is a popular alternative medicine used to treat hepatic fibrosis. It appears to be safe but to lack efficacy.

Key Points

Self-limited, acute liver injury (eg, due to acute viral hepatitis A), even when fulminant, tends not to cause fibrosis.

The most common causes of hepatic fibrosis are hepatitis B and C and alcohol abuse.

Fibrosis does not cause symptoms unless it progresses to cirrhosis.

Liver biopsy, although imperfect, is the gold standard diagnostic test.

Noninvasive testing, including ultrasound elastography and magnetic resonance elastography, is becoming increasingly important.

Treat the cause of fibrosis.

Last full review/revision January 2016 by Jesse M. Civan, MD

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Leverbetændelse (hepatitis)

Leverbetændelse (hepatitis) kan have mange forskellige årsager. Ofte skyldes det infektioner, men alkohol samt visse lægemidler og sygdomme kan også forårsage leverbetændelse.

Hvad er leverbetændelse? 

Man skelner mellem:

• Akut leverbetændelse, som er den sygdom der opstår kort tid efter smitten. Både hepatitis A, B og C kan give akut leverbetændelse. Hepatitis C dog sjældent.
• Kronisk leverbetændelse, som er den sygdom der opstår, hvis smitten forbliver i leveren i mere end 6 måneder. Kun hepatitis B og C kan blive kronisk. Hepatitis A bliver aldrig kronisk.

Symptomer på leverbetændelse 

Akut leverbetændelse, hvad enten det er hepatitis A, B eller C - giver altid følgende typiske symptomer:

• kvalme
• madlede
• træthed
• trykken i maven under ribbenene på højre side
• ondt i leddene
• lidt feber

Efter nogle dage/uger kan man få:

• gulsot (huden og det hvide i øjnene bliver gult)
• lys afføring
• meget mørk urin
• evt. hudkløe.

Inkubationstid for leverbetændelse

• Ved hepatitis A: 2-6 uger
• ved hepatitis B: 6-26
• ved hepatitis C: 3-20 uger.

Medicinsk forebyggelse af hepatitis A

Medicinsk forebyggelse af hepatitis B

Hepatitis B kan forebygges med vaccination både hos voksne og nyfødte:

• Voksne skal have 3 doser vaccine. Anden dosis gives ca. 1 mdr. efter første dosis, 3. dosis ca. 6 mdr. efter første dosis. Vaccinen virker hos de fleste (raske, voksne) i mindst 20 år og, såfremt der er udviklet antistof, målt 1 måned efter den sidste vaccination, formentlig livslangt. Virkningen kan være mindre effektiv hos svage eller syge personer.
• Nyfødte børn, hvis mødre har kronisk hepatitis B, skal have vaccinen sammen med hepatitis B immunglobulin ved fødslen og efter 1, 2 og 12 måneder. Cirka 5 % af børn, født af kvinder med kronisk hepatitis B, viser sig at være smittede trods ovenstående vaccination.

Medicinsk forebyggelse af hepatitis C

Årsager til leverbetændelse

Efter smitten formerer virus sig i levercellerne. Det fremkalder en modreaktion fra kroppens immunforsvar, og der opstår leverbetændelse. Denne reaktion har det formål at udrydde virus. Det lykkes ofte, men ikke altid. Hvis virus ikke udryddes, vil leverbetændelse blive kronisk.

Risiko for kronisk leverbetændelse

• Hepatitis A: Bliver aldrig kronisk.
• Hepatitis B: Bliver kronisk hos 5 % af smittede voksne, 5-10 % af smittede børn og 90 % af smittede nyfødte.
• Hepatitis C: Bliver kronisk hos cirka 60 % af alle smittede.

Smittemåder

Hepatitis A

• Smitter via afføring. Enten ved direkte kontakt eller via forurenede drikke- eller madvarer

Hepatitis B

• Ubeskyttet sex
• Blod
• Fra en smittet mor til hendes nyfødte barn
• Yderst sjældent ved tæt ikke-seksuel kontakt i familier og institutioner, fx ved kontakt med blod fra små sår. Smitte sker ikke ved almindelig social kontakt.

Hepatitis C

• Blod
• Ubeskyttet sex
• Sjældent fra en smittet mor til hendes nyfødte barn

Hvad kan man selv gøre?

Hepatitis A

• Hold generel god hygiejne. Vær særlig omhyggelig med håndvask og køkkenhygiejne, hvis et medlem af husstanden har hepatitis A
• Spis og drik fornuftigt under rejse til områder i verden, hvor hygiejnen er dårlig
• Overvej vaccination ved fx: rejse til områder, hvor hepatitis A er hyppig; en i husstanden har hepatitis A; modtagelse af adoptivbarn fra områder, hvor hepatitis A er hyppig; kronisk hepatitis C eller stofmisbrug, idet hepatitis A kan have alvorligt forløb i disse grupper

Hepatitis B

• Undgå ubeskyttet sex
• Del ikke sprøjter og kanyler med andre
• Del ikke tandbørste eller barbergrej med en smittet
• Overvej vaccination ved fx: en i husstanden har kronisk hepatitis B; en i institutionen (vuggestue, børnehave eller botilbud) har kronisk hepatitis B; en fast seksualpartner har kronisk hepatitis B; stofmisbrug; mange skiftende sexpartnere (især homoseksuelle mænd); hospitalsansatte med hyppig blodkontakt; altid til børn født af mødre med hepatitis B.

Hepatitis C

• Del ikke sprøjter og kanyler med andre
• Del ikke tandbørste eller barbergrej med en smittet

Hvis man er smittet

• Spis en varieret og sund kost, som man har lyst til.
• Ved akut hepatitis bør alkohol helt undgås, indtil man føler sig rask, og blodprøverne er normale.
• Ved kronisk hepatitis C bør alkoholindtag så vidt muligt undgås, idet alkohol forværrer forløbet af sygdommen.

Hvor udbredt er leverbetændelse? 

I Danmark lever skønsmæssigt 11.000 personer med kronisk hepatitis B og 21.000 personer med kronisk hepatitis C.

Eksempler på personer med særlig stor risiko for at have eller få hepatitis B:

• Personer, der har ubeskyttet sex med mange partnere
• Børn, hvis mødre har kronisk hepatitis B
• Mænd, der har sex med mænd
• Seksualpartnere til personer med kronisk hepatitis B
• Hustandsmedlemmer til personer med kronisk hepatitis B
• Personer, der kommer fra områder i verden, hvor forekomsten af hepatitis B er høj (Asien, Afrika og Sydamerika)
• Stofmisbrugere (nuværende eller tidligere)
• Personer med kronisk hepatitis C eller HIV infektion
• Personer med skrumpelever

Eksempler på personer med særlig stor risiko for at have eller få hepatitis C:

• Stofmisbrugere (nuværende eller tidligere)
• Mænd, der har sex med mænd
• Personer med uforklarlig forhøjelse af levertal (ALAT)
• Personer med hæmofili (blødersygdom)
• Personer, der har fået blodtransfusion, før man begyndte at teste donorblod i 1991
• Personer, der har fået blod, er blevet opereret eller har fået injektioner under ophold i lande, hvor den hygiejniske standard er dårlig
• Børn, hvis mødre har kronisk hepatitis C.

Hvordan udvikler leverbetændelse sig? 

Undersøgelse for leverbetændelse 

Behandling af leverbetændelse

Der er ikke med sikkerhed påvist effekt af medicinsk behandling af akut leverbetændelse. Formålet med behandlingen af kronisk leverbetændelse er at forebygge udvikling af skrumpelever.

Behandling af hepatitis B

Andre navne og stavemåder for leverbetændelse:

Behandling af hepatitis C

Såfremt der forud for behandling var konstateret skrumpelever, skal man til løbende kontrol, idet der forbliver en øget risiko for udvikling af leverkræft, også selvom man er helbredt for selve virusinfektionen.

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Peliosis Hepatis

Introduction: Peliosis Hepatis

Description of Peliosis Hepatis

Peliosis Hepatis: A vascular disease of the LIVER characterized by the occurrence of multiple blood-filled CYSTS or cavities. The cysts are lined with ENDOTHELIAL CELLS; the cavities lined with hepatic parenchymal cells (HEPATOCYTES). Peliosis hepatis has been associated with use of anabolic steroids (ANABOLIC AGENTS) and certain drugs.

Source: MeSH 2007

Peliosis Hepatis: Related Topics

These medical condition or symptom topics may be relevant to medical information for Peliosis Hepatis:

• Peliosis

Hierarchical classifications of Peliosis Hepatis

The following list attempts to classify Peliosis Hepatis into categories where each line is subset of the next.

MeSH 2007 Hierarchy:

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Overview of Hepatic Disease in Small Animals

By Sharon A. Center, BS, DVM, DACVIM, Professor, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University

• Hepatic Disease in Small Animals

The liver performs numerous functions, including but not limited to lipid, carbohydrate, and protein metabolism; storage, metabolism, and activation of vitamins; storage of minerals, glycogen, and triglycerides; extramedullary hematopoiesis; and synthesis of coagulant, anticoagulant, and several acute phase proteins. It also influences immunologic responses and contributes to digestion through synthesis and enterohepatic circulation of bile acids and detoxification of many endogenous and exogenous compounds, toxins, and xenobiotics. Because the liver has a large functional reserve and the ability to regenerate, hepatic injury must be considerable or chronic and recurrent to cause overt hepatic dysfunction or failure.

Active liver injury is accompanied by increased liver enzyme activity, with cytosolic transaminases (ALT, AST) acutely reflecting altered membrane permeability or viability or the phenomenon of membrane blebbing, and membrane-affiliated enzyme induction (alkaline phosphatase [ALP], γ-glutamyl transferase [GGT]) reflecting cholestasis and increased protein transcription (enzyme induction). The liver is predisposed to secondary injury owing to its sentinel position between the systemic circulation and GI tract and because it contains the largest population of fixed macrophages (Kupffer cells) in the body. Macrophage phagocytosis can initiate release of a cascade of inflammatory cytokines, leading to local cellular damage and recruitment of inflammatory infiltrates. The considerable metabolic activity of the liver exaggerates its exposure to noxious products, particularly in the centrilobular region, where high cytochrome p450 activity produces noxious products and adducts. Hepatocytes in this region also are more easily injured by hypoxia. The accumulation of hepatic copper and/or iron can initiate and augment liver injury through oxidative mechanisms.

Clinical signs of liver injury vary depending on the type, mechanism, and chronicity of the insult. Common clinical features may include anorexia, vomiting, diarrhea, weight loss, and fever. With severe, diffuse liver injury, animals may become jaundiced and demonstrate polyuria and polydipsia (PU/PD), coagulation abnormalities, and ascites. Ascites indicates development of portal hypertension and is typically associated with formation of acquired portosystemic shunts (APSSs) and concurrent hypoalbuminemia. Hepatic encephalopathy (HE) develops in acquired liver disease only when diffuse fibrosis and APSSs have developed, in acute fulminant liver failure, or secondary to congenital portosystemic shunts (congenital malformations of the portal vein that shunt portal blood directly to the systemic circulation). Fecal color may change with complete occlusion of bile ducts (acholic or pale-colored feces) or because of increased enteric bilirubin elimination (green fecal color). Hepatomegaly is found with diffuse infiltrative or storage disorders, acute extrahepatic bile duct obstruction (EHBDO), congenital biliary cystic malformations, or passive congestion, whereas microhepatica (small liver) usually reflects portal venous hypoperfusion, diversion of enteric hepatotrophic factors normally delivered in the portal circulation, or the presence of chronic hepatic fibrosis in dogs.

• Hepatic Disease in Small Animals

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Considerations

Considerations for the Titer Testing of Core Canine Vaccines

A report by Ronald D. Schultz, PhD, Dipl. ACVIM, Professor and Chair, Department of Pathobiological Sciences School of Veterinary Medicine – University of Wisconsin-Madison

Background:

The routine administration of vaccines in dogs has been one of the most significant factors in the consistent reduction of serious canine infectious diseases. This approach has resulted in excellent disease control for infections that were once considered important causes of morbidity and mortality.

Although all veterinarians agree vaccines are necessary, the frequency in which they’re given is debated.

Veterinarians need to administer the rabies vaccine as defined by law, but other core vaccines for canine distemper virus (CDV), parvovirus (CPV-2) and canine adenovirus-2 (CAV), are administered more often than necessary. Vaccines are largely safe, and are intended to improve the health and welfare of animals, but when problems do occur and the animal didn’t even need the vaccine, that’s unacceptable. More puppies and kittens need to be vaccinated with the core vaccines because there are many that never get vaccinated. It is known that dogs often maintain protective antibody to CDV, CPV-2, and CAV-1, (from vaccination with CAV-2) for three or more years and numerous experimental studies support this observation. Core vaccines should not be given any more frequently than every three years after the 12 month booster injection following the puppy/kitten series, because the duration of immunity (DOI) is many years and may be up to the lifetime of the pet. In order to ensure the existence of duration of immunity, titer testing may be used.

Titer Testing to Determine Duration of Immunity (DOI):

For canine core vaccines there is excellent correlation between the presence of antibody and protective immunity and there is long DOI for these products.

Antibody tests can be used to demonstrate the DOI after vaccination with core vaccines. Therefore, when antibody is present there should not be a need to revaccinate the dog for the specific disease being tested. If antibody titer is absent (irrespective of the serological test used) the dog should be revaccinated unless there is a medical basis for not so doing.

Currently a significant drawback in performing antibody tests is the cost and the time to obtain results. More often than not, titer testing requires sending blood or serum to a lab which entails a relatively expensive test, with an answer from the lab obtained some days later. For many years a “user friendly” rapid and cost-effective test has been required.

A Concept Change in Titer Testing:

Recently the Canine VacciCehck was approved by the USDA. The Canine VacciCheck is intended to be used as a diagnostic tool to evaluate the antibody response to the core vaccination or infection by Infectious Canine Hepatitis (Canine Adenovirus), Canine Parvovirus and Canine Distemper Virus.

The test is a rapid, simple, reliable and cost-effective “in house” assay and is especially useful to determine if a dog requires additional vaccination. This may save the dog unnecessary vaccination. It can also help determine the vaccination status of a dog with unknown vaccination history to help determine if puppies have received immunity from vaccination, if a sample is collected 2 or more weeks after the last puppy dose at 14 to 16 weeks of age. If the puppy does not have a CDV or CPV-2 titer, it should be revaccinated immediately and does not wait until 1 year of age.

What is also unique about the Canine VacciCheck is that the tests can be individualized. In addition, test results are preserved, with a simultaneous result developed for all three core vaccines per test. This should prove useful for the veterinary clinic, shelter or the veterinary lab alike. Results are available within 20 minutes.

The kit is a “self contained” dot ELISA titer test kit, not needing any reagent preparation. Practitioners therefore have a quick and simple in-house test that can be performed at a reasonable cost to the pet owner.

Illustration of the VacciCheck Kit Comb and Developing Plate

In the past, even though there was an intention by many pet owners and/or veterinarians to carry out titer testing for core vaccines instead of automatically revaccinating, the price of a titer test when compared to a vaccination was often significantly more expensive. Therefore, with the price factor lessened, via the use of VacciCheck, the concept should be that instead of sending reminder cards for vaccines, veterinarians should be sending ‘annual health check’ reminders.

The ‘annual health check’ removes the emphasis from, and client expectations of, annual revaccination. The annual health check may still encompass administration of selected non-core vaccines which should be administered annually, as the DOI for these products is generally one year or less. Neither a titer nor annual vaccination is necessary every year because of the core vaccines’ duration of immunity. However, a blood sample taken yearly from an animal for a titer check is preferential to an unnecessary vaccination as a vaccine may cause harm. Medically, however, I don’t know of any harm that might come from taking a blood sample and doing a titer check. Also, there are many practitioners and owners who need assurance that an animal does have immunity. An antibody test such as the VacciCheck can give them that assurance.

Titer Testing for Puppies:

Antibody assays for CDV, CPV-2 and CAV-1 are the tests of greatest benefit in monitoring immunity, especially after the puppy vaccination series. On completion of the puppy series at 14-16 weeks of age, an animal should have a positive test result, provided the serum sample is collected 2 or more weeks after vaccination. Seronegative animal should be revaccinated and retested 2 or more weeks later. If it again tests negative, the dog should be considered a non-responder that is possibly incapable of developing protective immunity.

In order to confirm the puppy protocol, the Canine VacciCheck can be deemed a cost effective, user friendly and expedient titer test for Hepatitis (Canine Adenovirus), Parvovirus and Distemper.

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Pet Owners

Are you a pet owner rightfully concerned about over-vaccination consequences? Your veterinarians may not know about this affordable and effective alternative.

Bring this one page handout to your Veterinarian and talk to them about titer testing with VacciCheck!

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Featured Video

VacciCheck and antibody titer testing on Animal House Full Episode #1