Health Maintenance in Liver Disease and Cirrhosis


Brand names



Hepatitis A



1440 EL.U in 1 mL IM

50 U in 1 mL IM

0, 6–12 months

Hepatitis B


Recombivax HB

20 mig in 1 mL IM

10 mig in 1 mL IM

0, 1, 6 months

Hepatitis A/B

Twinrix (Havrix and Engerix-B)

720 EL.U HAV and 20 mig HBsAG in 1 mL IM

0, 1, 6 months

H. influenza



0.5 mL IM



PCV13 (Prevnar 13)

PPSV23 (Pneumovax)

0.5 mL IM

0.5 mL IM

PCV13 followed by PPSV23 in 8 weeks

PPSV23 every 3–5 years




0.5 mL IM

0.5 mL IM

10 Years

The vaccine is only slightly less immunogenic in patients with chronic liver disease than the general population, with seroconversion rate of 93 % [5]. In patients with decompensated cirrhosis conversion rate is 20–50 % compared to 99 % in immunocompetent hosts [6]. One series illustrated that predictors of non-response were the presence of an alcoholic component of liver disease and a worse stage of liver failure [7]. Evidence supports as disease worsens response to HAV vaccine worsens; therefore, vaccination should be given as early as possible in the disease course of chronic liver disease when the patient has a better chance of achieving seroconversion . To document response, anti-HAV IgG may be assessed 3 months after final vaccination.

Hepatitis B Vaccination

Much like hepatitis A, acute hepatitis B virus (HBV) has been implicated in fulminant hepatitis in patients with chronic liver disease such as those with hepatitis C [8]. Additionally, patients with chronic HBV and HCV co-infection have worse outcomes than patients with either infection alone [9]. One study shows significantly high rates of cirrhosis (95 % vs. 48 %) and hepatocellular carcinoma (63 % vs. 15 %).

Similar to the case of HAV, the CDC also recommends vaccination of all patients with chronic liver disease against hepatitis B (Table 7.1). Because the prevalence of previous infection is more than 30 % in patients with chronic liver disease, it is cost effective to screen patients prior to vaccination [10]. Patients should be tested for immunity and if negative should be given three doses at 0, 1, and 6 months. Immunogenicity is diminished in cirrhotic patients. The proportion of antibody response is 40–70 % in cirrhotic patients and 30–50 % in decompensated cirrhotics; this again suggests that vaccination early in the disease course is preferred [11]. Antibody response should be verified 2–3 months after completion of vaccination. For those without a response, a second series will result in immunity in 60 % of patients [12]. If patients are over 18 years of age a combined vaccination for hepatitis A and B is available called Twinrix. This may be used if both vaccinations are indicated.

Influenza Vaccination

Patients with cirrhosis are at high risk for complications of influenza. While influenza is not more common in cirrhotic patients than the general population, it may increase the risk of decompensation by producing TNF alpha, and IL-1 and IL-6 cytokines [13]. One study illustrated that the influenza vaccine reduced the risk of decompensation in cirrhotic patients [14]. The CDC recommends annual influenza vaccination for patients with cirrhosis as soon as the flu season begins in September. While the CDC does not have guidelines about cirrhotic patients receiving live vaccinations, typically the inactivated vaccination is preferred in these patients.

Pneumococcal Vaccination

Patients with chronic liver disease are at higher risk for pneumococcal infection [15]. Patients with cirrhosis have higher rates of mortality during a pneumococcal infection than non-cirrhotic patients. Patients with cirrhosis are more likely to have bacteremia during a pneumococcal infection [16]. For this reason, pneumococcal vaccination is recommended in all cirrhotic patients. In 2010 the CDC guidelines recommended adults who had not previously received PCV13 pneumococcal conjugate vaccine (PCV13) or pneumococcal polysaccharide vaccine (PPSV23) should receive a dose of PCV13 first, and followed by a dose of PPSV23 at least 8 weeks later. A second PPSV23 dose is recommended 5 years after the first PPSV23 dose. Patients who previously have received ≥1 doses of PPSV23 should be given a PCV13 dose ≥1 year after the last PPSV23 dose was received.

Question Two: Should I Be Evaluated for Bone Disease If I Have Liver Disease?

Answer: The majority of patients with liver disease should be evaluated with bone densitometry for low bone density. There is a high prevalence of bone disease in patients with liver disease. This is particularly true in cholestatic liver disease such as primary biliary cirrhosis, alcohol-related liver disease, or cirrhosis of any etiology. Additionally, fat-soluble vitamin levels such as vitamin D are often low, which can contribute to osteopenia and osteoporosis.

Vitamin D Deficiency

The prevalence of vitamin D deficiency is 60 % in cirrhotic patients and as high as 96 % at the time of liver transplantation [17]. Despite the high prevalence of vitamin deficiency, osteomalacia (defective bone mineralization with subsequent softening of the bones) is rare but osteoporosis and osteopenia are not uncommon. Low vitamin D has been associated with low bone mineral density, hip fracture, and high bone turnover and contributes to osteoporosis in patients with chronic liver disease. A recent study by Venu et al. showed insufficient vitamin D in 83 % of cirrhotic patients [18]. Osteopenia or osteoporosis was noted in 45 and 18 % of cirrhotic patients, respectively; of those patients with osteoporosis, 100 % had vitamin D deficiency. Etiology of liver disease (including cholestatic etiology versus other) was not predictive of who developed vitamin D deficiency.

Low Bone Density

Patients with chronic liver disease exhibit many risk factors for low bone density and osteoporosis. Known risk factors include poor nutrition, steroid use, alcohol intake, and hypogonadism [17]. Cirrhotic patients are not the only patients with liver disease at risk for low bone density. One study showed that alcohol intake was inversely related to bone mineral density in men. Additionally, in 76 men who drank 216 g/day or more for 24 years, 30 % had vertebral fractures regardless of stage of fibrosis on histology [19]. Non-cirrhotic patients with hemochromatosis also have high rates of osteoporosis which seem to correlate with the degree of hepatic iron level.

Patients with non-cirrhotic biliary disease have been examined for increased rates of osteopenia and osteoporosis . The incidence of osteoporosis in primary sclerosing cholangitis (PSC) is between 3 and 32 %. It does not appear that treatment with ursodeoxycholic acid improves bone density in this patient population [20]. According to the American Association for the Study of Liver Disease (AASLD) practice guidelines, bone density should be evaluated with any new PSC diagnosis and at subsequent 2–3-year intervals [21]. The AASLD guidelines also recommend calcium and additional vitamin D to promote calcium absorption in patients with proven osteopenia [21]. Patients with end-stage primary biliary cirrhosis (PBC) have significantly greater risk of osteopenia and osteoporosis than do age-matched and sex-matched controls, although this has been subject to controversy. Recent studies show that PBC patients have a fourfold increased risk of osteoporosis [22]. The American Gastroenterological Association (AGA) guidelines suggest that bone mineral density evaluation should be considered in all patients with PBC at diagnosis, whereas other recommendations limit bone mineral density evaluation to patients with bilirubin greater than three times the upper limit of normal [23, 24]. The AASLD recommends baseline and regular screening every 2–3 years using bone mineral density testing [25]. The AASLD also recommends measuring annual vitamin D levels in patients with advanced disease. In PBC patients with osteoporosis, alendronate has been shown in a randomized controlled trial to significantly improve bone density when compared to placebo. Therefore, AASLD recommends alendronate for osteoporosis, but only if the patient has no known varices or reflux [25].

Cirrhotic patients of all etiologies are at an increased risk for osteoporosis. Prevalence of osteoporosis varies in studies but ranges from 12 to 55 % [26, 27]. Rates of osteoporosis increase with worsening hepatic function reflected by a higher Child’s score and do not seem to correlate with degree of cholestasis. AASLD suggests screening densitometry in all cirrhotic patients and all patients undergoing transplant evaluation [28].

Low bone density and osteoporosis are particularly concerning in liver transplant recipients. In the first 3 months following liver transplantation, bone density falls dramatically [29]. This is a time when patients are limited in their mobility and typically receiving high-dose corticosteroids to prevent rejection. Fracture rates of 15–35 % have been reported, with most fractures occurring within the first 2 years of transplantation. A recent study showed that 25 % of patients have new fracture within the first 6 months after liver transplantation. Another study showed that bone density decreases in the first 6 months and remains low in the femoral neck, but improves to exceed pretransplantation density in the lumbar spine by 2 years [29]. The role of calcineurin inhibitors in bone turnover following transplantation remains controversial. However, long-term steroid use increases the risk for decreased bone mineral density.

Question Three: What Effect Does Coffee Have on My Liver

Answer: Coffee has been shown to be beneficial in many types of liver disease. Increased coffee consumption reduces mortality, decreases progression of nonalcoholic fatty liver disease (NAFLD) , decreases the rate of scarring in the liver and progression to cirrhosis, decreases rate of liver cancer development, and increases treatment response to hepatitis C antiviral interferon-based therapy (Table 7.2).

Table 7.2
Benefits of coffee in liver disease

Decrease in ALT and GGT

Decrease in fibrosis progression in HCV, NASH, and other causes of liver disease

Higher SVR in patients treated for HCV with IFN + RBV

Decreased risk of NAFLD

Decreased risk of HCC in cirrhotic patients

Decreased mortality in alcoholic cirrhosis

All-cause decrease in mortality

IFN interferon, RBV ribavirin

Coffee has been shown to decrease the risk of all-cause mortality and be beneficial in many medical conditions. Numerous studies between 1996 and 2010 have shown an inverse relationship between coffee consumption and liver enzymes including GGT and ALT. A large study of over 12,000 patients completed in Japan showed a strong inverse relationship between coffee consumption and GGT in male alcohol drinkers (P < 0.0001) [30]. The third National Health and Nutrition Examination Survey (NHANES) also found that coffee consumption and caffeine were associated with decrease in ALT in patients who were at high risk for liver disease [31].

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Nov 20, 2017 | Posted by in GASTROENTEROLOGY | Comments Off on Health Maintenance in Liver Disease and Cirrhosis

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