اولین مارکر هپاتیت B : HBsAg حتی زود تر ازترانس آمینازها و بروز علایم بالینی و طی مرحله زردی یا دوره فعال بیماری و پس از آن در سرم، قابل شناسایی باقی می ماند.
در هپاتیت مزمن B : HBsAg بیش از 6 ماه ، HBeAg بیش از 3 ماه و آنزیمها، بیلی روبین و گلبولین بیش از6-12 ماه بالا باقی می مانند.
ارتباط معکوسی بین غلظت HBsAg و شدت صدمه کبدی وجود دارد.
تیتر HBsAg در افراد دچار سرکوب ایمنی در بالاترین میزان، در بیماری مزمن کبدی کمتر و در بیماران هپاتیت حاد برق آسا در حد بسیار پایینی قرار دارد.
Hepatitis C
Breast feeding does not increase the risk of HCV infection between an infected mother and her infant.
IG is ineffective in preventing hepatitis C and is no longer recommended for postexposure prophylaxis in cases of perinatal, needle stick, or sexual exposure.
For stable, monogamous sexual partners, sexual transmission of hepatitis C is unlikely, and sexual barrier precautions are not recommended.
For persons with multiple sexual partners or with sexually transmitted diseases, the risk of sexual transmission of hepatitis C is increased, and barrier precautions (latex condoms) are recommended
No special precautions are recommended for babies born to mothers with hepatitis C, and breast feeding does not have to be restricted.
آسیت، ادم محیطی و علائم انسفالوپاتی --› پیش آگهی بد بیماری هپاتیت A و B
PT طولانی، آلبومین سرم پایین، هیپوگلیسمی، افزایش شدید بیلی روبین --› بیماری شدید سلول کبدی
بیمارانی که علائم فوق را دارند باید سریعا در بیمارستان بستری شوند.
هپاتیت E در زنان حامله ، 10-20 % مرگ و میر دارد.
هپاتیت A دو پاترن دارد:1- Relapsing hepatitis،2- نوع کلستاتیک
هپاتیتA خودمحدود بوده ، مزمن نمی شود.
هپاتیت C : همراهی با کرایوگلبولینمی مختلط اساسی (می تواند منجر به لنفوم سلول B شود) – لیکن پلان- پورفیری جلدی تاخیری
دوره پرودرومال هپاتیت B : ایجاد بیماری سرم (5-10%) – با علائم: آرتریت، بثورات، آنژیوادم،ندرتاً هماچوری و پروتئینوری- :Δ اندازه گیری آمینوترانسفرازهای بالا- و HBsAg سرم
در هپاتیت مزمن B اندازه گیری HBV-DNA شاخص حساستر و دقیقتری برای همانند سازی ویروس در مقایسه با HBeAg و آنتی HBeAb (نشاندهنده عفونت زایی نسبی) است.
HBeAg یک شاخص کیفی و HBV-DNA یک شاخص کمی برای همانند سازی ویروس است.
عفونت مزمن HBV --› Geround Glass
HDV --› استئاتوز میکرووزیکولر
HEV --› کلستاز قابل توجه
هپاتیت ویروسی--› اجسام کانسیلمن
هپاتیت فولمینانت در--› هپاتیت های B(50%) ,D,E – و نیز هپاتیت A در افراد مسن و بیماری زمینه ای کبد.
هپاتیت فولمینانت: کبد چروکیده، افزایش سریع بیلی روبین، و PT طولانی و انسفالوپاتی
In patients with hepatitis B, testing for anti-HDV is useful under the following circumstances: patients with severe and fulminant diseases,
patients with severe chronic disease,
patients with chronic hepatitis B who have acute hepatitis-like exacerbations,
persons with frequent percutaneous exposures, and
persons from areas where HDV infection is endemic.
TABLE 285-4 Simplified Diagnostic Approach in Patients Presenting with Acute Hepatitis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Chronic Hepatitis
Certain clinical and laboratory features suggest progression of acute hepatitis to chronic hepatitis:
(1) lack of complete resolution of clinical symptoms of anorexia, weight loss, and fatigue and the persistence of hepatomegaly;
(2) the presence of bridging or multilobular hepatic necrosis on liver biopsy during protracted, severe acute viral hepatitis;
(3) failure of the serum aminotransferase, bilirubin, and globulin levels to return to normal within 6 to 12 months after the acute illness; and
(4) the persistence of HBeAg beyond 3 months or HBsAg beyond 6 months after acute hepatitis.
Chronic hepatitis is defined as a hepatic inflammatory process that fails to resolve after 6 months.
DRUG-INDUCED AND TOXIN-INDUCED HEPATITIS
استروژن،اریترومایسین و کوآموکسی کلاو ، کوتریموکسازول--› کلستاز خالص
کلرپرومازین--› هپاتیت کلستاتیک
متوترکسات--› فیبروز
آلوپورینول، سولفونامید--› گرانولوم
اتانول، کورتون -- آمیودارون، آلوپورینول (تکامل)--› کبد چرب
Table 41-4. Classification of Drug-Induced Liver Disease |
Classic examples include viral hepatitis-like reactions (halothane and isoniazid),
cholestatic hepatitis (chlorpromazine),
granulomatous hepatitis (allopurinol),
chronic hepatitis (methyldopa), and
pure cholestasis without inflammation or hepatocellular necrosis (estrogens and androgens).
Isoniazid, as single-drug prophylaxis against tuberculosis, commonly produces subclinical hepatic injury (20% incidence), as evidenced by raised serum transaminase levels. Thus, the incidence of severe hepatic damage increases with age, such that significant elevation of aminotransferase levels in persons who are more than 35 years of age is an indication for discontinuing the drug.
Phenytoin and carbamazepine have been implicated in an anti-epileptic hypersensitivity syndrome, characterized by a triad of rash, fever, and hepatocellular injury that may lead to fulminant hepatic failure. Lymphadenopathy and a mononucleosis-like picture with atypical lymphocytes may be present. Renal and pulmonary involvement may also occur.
Table 41-5. Causes of Chronic Hepatitis |
سیروز:
متوتروکسات، آمیودارون--› سیروز
Table 43-4. Causes of Ascites |
Low: <1.1 g/dL | |
Peritoneal carcinomatosis | |
Peritoneal tuberculosis | |
Pancreatic and biliary disease | |
Nephrotic syndrome | |
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رویکرد به دیس پپسی
A GU that fails to heal after 12 weeks and a DU that does not heal after 8 weeks of therapy should be considered refractory.
Alarm features include weight loss, vomiting, dysphagia, evidence of anemia, gastrointestinal bleeding, or an abdominal mass or l
زولینگر-الیسون:
The most common causes of hypergastrinemia are:
antrum-dominant H. pylori infection or
achlorhydria related to either decreased intraluminal acid in the setting of atrophic gastritis or antisecretory therapy with PPIs.
Hypergastrinemia may be related to other causes, including:
retained gastric antrum (after ulcer surgery),
massive small bowel resection,
chronic gastric outlet obstruction, and
chronic renal failure.
Therefore, acid hypersecretion, as documented by gastric acid analysis, is necessary for the diagnosis of ZES.
The diagnosis of ZES is made when there is a fasting gastrin >1000 pg/mL in the setting of gastric acid hypersecretion.
In equivocal cases (e.g., gastrin < 1000 pg/mL),à a positive secretin provocative test will confirm the diagnosis.
The secretin test is positive (≥200 pg/mL increase over the preinjection fasting gastrin level) in approximately 90% of patients with ZES and moderately elevated gastrin levels. Basal acid output is elevated (>15 mmol/hr without previous gastric acid-reducing surgery and >5 mmol/hr with prior surgery) in more than 90% of patients with ZES.
The single best imaging test for gastrinoma is somatostatin receptor scintigraphy (SRS), which is more sensitive than any conventional imaging study.
بیماریهای التهابی روده:
Table 36-2. Differentiating Features |
ASCA = anti-Saccharomyces cerevisiae antibodies; pANCA = perinuclear antineutrophil cytoplasmic antibodies; RLQ = right lower quadrant. |
Table 36-3. Treatment Options |
TABLE 285-2 Clinical and Epidemiologic Features of Viral Hepatitis | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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The acute level of these enzymes, however, does not correlate well with the degree of liver cell damage. Peak levels vary from 400 to 4000 IU or more;
Bilirubin levels >340 µmol/L (20 mg/dL) extending and persisting late into the course of viral hepatitis are more likely to be associated with severe disease.
Hepatitis Aپروفیلاکسی پیش و پس از تماس در هپاتیت
Hepatitis A vaccines are approved for use in persons who are at least 2 years old and appear to provide adequate protection 4 weeks after a primary inoculation.
If it can be given within 4 weeks of an expected exposure, such as by travel to an endemic area, hepatitis A vaccine is the preferred approach to preexposure immunoprophylaxis
If travel is more imminent, IG (0.02 mL/kg) should be administered at a different injection site, along with the first dose of vaccine.
When administered before exposure or during the early incubation period, IG is effective in preventing clinically apparent hepatitis.
For postexposure prophylaxis of intimate contacts (household, sexual, institutional) of persons with hepatitis A, the administration of 0.02 mL/kg is recommended as early after exposure as possible; it may be effective even when administered as late as 2 weeks after exposure.
Prophylaxis is not necessary for casual contacts (office, factory, school, or hospital), for most elderly persons, who are very likely to be immune, or for those known to have anti-HAV in their serum.
For travelers to tropical countries, developing countries, and other areas outside standard tourist routes, IG prophylaxis had been recommended, before a vaccine became available!!!. When such travel lasted less than 3 months, 0.02 mL/kg was given; for longer travel or residence in these areas, a dose of 0.06 mL/kg every 4 to 6 months was recommended.
Hepatitis B
We now recognize that many cases of hepatitis B result from less obvious modes of nonpercutaneous or covert percutaneous transmission.
Perinatal transmission occurs primarily in infants born to HBsAg carrier mothers or mothers with acute hepatitis B during the third trimester of pregnancy or during the early postpartum period.
Perinatal transmission is uncommon in
ویروس هپاتیت B پره کور-موتانت: هپاتیت مزمن شدید- سطوح پایین HBV DNA مثبت - HBe Ag منفی - AntiHBe Ab مثبت- نوسانات متناوب در فعالیت نکروز التهابی کبد- شایعترین نوع هپاتیت در مدیترانه و اروپا
Patients with such precore mutants that are unable to secrete HBeAg tend to have severe liver disease that progresses more rapidly to cirrhosis.
They have severe chronic HBV infection and detectable HBV DNA but with anti-HBe instead of HBeAg. These patients were found to be infected with an HBV mutant that contained an alteration in the precore region rendering the virus incapable of encoding HBeAg.
Both “wild-type” HBV and precore-mutant HBV can coexist in the same patient, or mutant HBV may arise late during wild-type HBV infection.
Precore-mutant hepatitis B is now the most frequently encountered form of hepatitis B in Mediterranean countries and in
Characteristic of such HBeAg-negative chronic hepatitis B are lower levels of HBV DNA and periodic fluctuations in hepatic necroinflammatory activity.
اسکیپ موتانت: در اثر جهش HBsAg خاصیت ایمنونیزاسیون اکتیو و پاسیو از بین می رود و افراد را علیرغم ایمن سازی به هپاتیت B مبتلا می سازد.
The second important category of HBV mutants consists of escape mutants, in which a single amino acid substitution, from glycine to arginine, occurs at position 145 of the immunodominant a determinant common to all subtypes of HBsAg. This change in HBsAg leads to a critical conformational change that results in a loss of neutralizing activity by anti-HBs. This specific HBV/a mutant has been observed in two situations, active and passive immunization
Although the precise mode of perinatal transmission is unknown, and although approximately 10% of infections may be acquired in utero, epidemiologic evidence suggests that most infections occur approximately at the time of delivery and are not related to breast feeding.
The likelihood of perinatal transmission of HBV correlates with the presence of HBeAg;
90% of HBeAg-positive mothers but
only 10 to 15% of anti-HBe-positive mothers
transmit HBV infection to their offspring.
In most cases, acute infection in the neonate is clinically asymptomatic, but the child is very likely to become an HBsAg carrier.
Pregnancy is not a contraindication to vaccination.
For unvaccinated persons sustaining an exposure to HBV, postexposure prophylaxis with a combination of HBIG (for rapid achievement of high-titer circulating anti-HBs) and hepatitis B vaccine (for achievement of long-lasting immunity as well as its apparent efficacy in attenuating clinical illness after exposure) is recommended.
For perinatal exposure of infants born to HBsAg-positive mothers, a single dose of HBIG, 0.5 mL, should be administered intramuscularly in the thigh immediately after birth, followed by a complete course of three injections of recombinant hepatitis B vaccine to be started within the first 12 h of life.
For those experiencing a direct percutaneous inoculation or transmucosal exposure to HBsAg-positive blood or body fluids (e.g., accidental needle stick, other mucosal penetration, or ingestion), a single intramuscular dose of HBIG, 0.06 mL/kg, administered as soon after exposure as possible, is followed by a complete course of hepatitis B vaccine to begin within the first week.
For those exposed by sexual contact to a patient with acute hepatitis B, a single intramuscular dose of HBIG, 0.06 mL/kg, should be given within 14 days of exposure, to be followed by a complete course of hepatitis B vaccine.
When both HBIG and hepatitis B vaccine are recommended, they may be given at the same time but at separate sites.
Approximately 80 to 90% of immunocompetent vaccinees retain protective levels of anti-HBs for at least 5 years, and 60 to 80% for 10 years.
Currently, booster immunizations are not recommended routinely, except in immunosuppressed persons who have lost detectable anti-HBs or immunocompetent persons who sustain percutaneous HBsAg-positive inoculations after losing detectable antibody.
Specifically, for hemodialysis patients, annual anti-HBs testing is recommended after vaccination; booster doses are recommended when anti-HBs levels fall below 10 mIU/mL.
TABLE 285-3 Commonly Encountered Serologic Patterns of Hepatitis B Infection | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
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ymphadenopathy.