Liver disease: Early signs you may be missing

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Applied Evidence

Liver disease: Early signs you may be missing

J Fam Pract. 2009 October;58(10):514-521

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References

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TABLE 1
Child-Pugh: Classifying cirrhosis, predicting survival*

	1 point	2 points	3 points
Bilirubin (mg/dL)	<2	2-3	>3
Prothrombin time (INR)	<4 sec (<1.7)	4-6 sec (1.7-2.3)	> 6 sec (>2.3)
Albumin (g/dL)	>3.5	2.8-3.5	<2.8
Ascites	Absent	Mild	Severe
Encephalopathy	Absent	Mild	Severe
INR, international normalized ratio.
* Total the number of points for all 5 indicators (1 point for every answer in column 1, 2 points for every answer in column 2, and 3 points for every answer in column 3). Patients with ≤6 points (Grade A) have an estimated 1-year survival rate of 100%; patients with 7-9 points (Grade B) have an estimated 1-year survival rate of 80%; and patients with ≥10 points (Grade C) have an estimated 1-year surival rate of 45%.
Adapted from: Infante-Rivard C, et al. Hepatology. 1987.¹⁴

Treatment for cirrhosis depends on the cause

Although primary care physicians can often provide most, or all, of the care for those in stable condition, a specialist may be helpful in determining further testing to identify the underlying cause of the cirrhosis, which is essential to determining the most appropriate treatment. What’s more, research has shown that patients with cirrhosis whose care is managed by a primary care physician and a hepatologist have better outcomes than those who are treated by a primary care doctor alone.¹⁸

What to test for?

FAST TRACK

Cirrhosis may have more than 1 contributing factor—obesity and a virus, or chronic alcohol use and metabolic fatty liver, for example.

Tests to determine the cause of cirrhosis are listed in TABLE 2 . For an individual patient, diagnostic tests would be based on the suspected cause. A patient with a family history of hereditary hemochromatosis would be tested for elevated serum ferritin levels and hepatic iron content on liver biopsy sample; the transferrin saturation index would also be obtained, and the patient might be tested for specific gene mutations. A patient who drinks heavily would be tested for elevated gamma-glutamyl transpeptidase and mean corpuscular volume. For someone with obesity, diabetes, and an enlarged liver, standard lab tests, including high-density lipoprotein (HDL) cholesterol, glucose, and triglycerides, may be sufficient.

Keep in mind, however, that cirrhosis may have more than 1 contributing factor—obesity or chronic alcohol use and a virus, for example; alcohol abuse and metabolic fatty liver; or virus and hemochromatosis. Thus, it may require more than 1 type of treatment.

FAST TRACK

Recovering alcohol abusers may not be considered for a liver transplant until they have had 6 months of continuous abstinence.

Alcohol abuse is the cause of 25% of cases of liver cirrhosis, and a contributor to another 25% to 50%.¹⁹ The key treatment here—and an ideal role for a family physician—is to refer the patient to a detoxification and treatment program and provide ongoing monitoring and support. Antiviral treatment may be helpful for a recovering alcoholic who also tests positive for hepatitis B or C virus, but because of potential problems with compliance, some physicians delay therapy until the patient has had at least 6 months of continuous abstinence. Although this is not an absolute criterion, the same period of abstinence may be required before a patient becomes eligible for a liver transplant.

NAFLD/NASH is typically diagnosed on the basis of lab values and physical presentation. For a stable patient, the primary treatment includes lifestyle change—a low-calorie, low-carbohydrate diet and an exercise regimen—and a possible switch to insulin for better glycemic control.

For patients who are not candidates for such targeted treatments, either because their disease is too advanced or they’re unable to tolerate the recommended therapy, numerous pharmaceutical preparations claiming antioxidant or anti-inflammatory properties are available. But only 1—an herbal extract known as silymarin, derived from the milk thistle plant and taken with vitamin E—has been found to have some protective effects.²⁰

TABLE 2
Liver cirrhosis: Common causes, diagnostic tests, and treatments^4,34-38

Cause	Test (result)	Therapy
Alcohol	GGT (↑), MCV (↑)	Abstinence
HBV + delta virus infection	HBsAg (+) HBV-DNA(+) HBc-IgM (+) HDV-RNA (+)	Interferon alpha-2b, nucleoside (lamivudine, telbivudine, entecavir) and nucleotide (adefovir, tenofovir) analogs
HCV infection	HCV-RNA (+)	Interferon + ribavirin
Primary biliary cirrhosis	GGT (↑) Alkaline phosphatase (↑) AMA (+)	Ursodeoxycholate
Autoimmune hepatitis	ANA (+) ASMA (+) LKM (+)	Prednisone, azathioprine
Hemochromatosis	Ferritin (↑) Transferrin saturation index (>45%) Hepatic iron content (↑) HFE gene mutation (C282Y, H63D)	Phlebotomy, chelating agents
Wilson’s disease	Ceruloplasmin (↓) Serum copper (↓) 24h urinary copper excretion (↑)	D-penicillamine, zinc
NAFLD/NASH	HDL cholesterol (↓) Glucose (↑) Triglycerides (↑)	Low-calorie diet, physical activity, insulin-sensitizer drugs or insulin
AMA, antimitochondrial antibody; ANA, antinuclear antibody; ASMA, anti-smooth-muscle antibody; GGT, gamma–glutamyl transpeptidase; HBc-IgM, immunoglobulin M antibody to hepatitis B core antigen; HBsAg, hepatitis B surface antigen; HBV-DNA, hepatitis B virus DNA; HCV-RNA, hepatitis C virus RNA; HDL, high-density lipoprotein; HDV-RNA, hepatitis delta virus RNA; LKM, liver kidney microsomes; MCV, mean corpuscular volume, NAFLD/NASH, nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.