Cirrhosis: Vitamin K Deficiencies
Vitamin K and Liver Disease
,The liver stores vitamins and minerals to be used as needed including all the fat-soluble vitamins;(A, B12, D, E and K). .
Vitamin K is a fat-soluble organic compound that the body needs to remain healthy. Although bacteria in the human intestine make some vitamin K, it is not nearly enough to meet the body's needs, so people must get most of their vitamin K from foods in their diet.
Hepatitis C Cirrhosis; Vitamin K Deficiencies
.
The liver needs vitamin K to make factors that regulate blood clotting
.
Vitamin K deficiency is extremely rare in healthy people. It can, however, occur in individuals who have significant liver damage or disease disorders that interfere with the absorption of nutrients from the intestine. .
Liver disease (cirrhosis) causes a decrease in bile salt synthesis, leading to impaired absorption and Vitamin K deficiency. The liver makes a number of coagulation (clotting) factors including prothrombin and fibrinogen. Most of these require the presence of vitamin K to function normally. Vitamin K, as a fat-soluble vitamin, in turn requires bile salts to be absorbed properly by the body. If the liver is impaired and does not produce enough bile this will have an effect on the capacity to clot blood; increasing the risk of bleeding.
..,. 1-Vitamin K is necessary for the formation of prothrombin and other blood-clotting factors in the liver, and it also plays a role in bone metabolism.
.,2-A form of the vitamin is produced by bacteria in the colon and can be utilized to some degree.
,Tell Me More About These Blood-clotting Factors Prothrombin and Fibrinogen
Prothrombin
Role of Vitamin K in Blood Coagulation Process
Vitamin K is necessary for the synthesis prothrombin in the liver. If vitamin k is inadequate in the diet or is not absorbed in the intestine, blood clotting or coagulation process becomes inefficient.
Role of Vitamin K in Blood Coagulation Process
Vitamin K is necessary for the synthesis prothrombin in the liver. If vitamin k is inadequate in the diet or is not absorbed in the intestine, blood clotting or coagulation process becomes inefficient.
Fibrinogen
Fibrinogen, also called serum fibrinogen, plasma fibrinogen and factor I, is a protein produced by the liver. Fibrinogen helps stop bleeding by helping the formation of blood clots. During normal blood clotting, fibrinogen is broken down by an enzyme called thrombin into short fragments of fibrin. Thrombin also activates a substance called Factor XIII. Factor XIII helps weave the fibrin fragments (see picture) into a complex lattice, closing off injured blood-vessel walls. Blood platelets attach to the fibrin fragments, clumping together to form blood clots and stop bleeding.
What Are The Symptoms associated with vitamin K deficiency ?
Symptoms Signs and symptoms associated with vitamin K deficiency include; Easy bruising, oozing from the nose or gums; excessive bleeding from wounds, punctures, injections, and surgical sites; heavy menstrual periods; bleeding from the gastrointestinal tract; blood in the urine and/or stool and an increased prothrombin time (prothrombin is a coagulation factor).
What Else Causes Vitamin K Deficiency ?
In adults additional causes of the vitamin deficiency is associated with low dietary intake of Vitamin K due to chronic illness, malnutrition, alcoholism, multiple abdominal surgeries, long-term parenteral nutrition, malabsorption, parenchymal liver diseases such as cirrhosis secondary to viral hepatitis, cholestatic disease, cystic fibrosis, inflammatory bowel disease, and drugs (eg, antibiotics [cephalosporin], Coumadin, salicylates, anticonvulsants, certain sulfa drugs) are some of the common causes of Vitamin K deficiency. Groups that may suffer from secondary vitamin K deficiency include bulimics, or those on stringent diets.
What Are Some Vitamin K Interactions?
.As for healthy adults no complications are expected from vitamin K, especially when most of the vitamin K comes from dietary sources. However, pregnant and breastfeeding women should avoid taking vitamin K. People with liver disease should not take Vitamin K supplements. .People who are taking blood-thinning drugs, especially warfarin (Coumadin), should discuss their vitamin K needs with their healthcare provider. They may need to restrict their intake of vitamin K. The purpose of blood-thinning drugs is to keep the blood from forming clots in the veins and arteries. Since vitamin K helps blood to clot, high levels of vitamin K in the diet may work against blood-thinning drugs and reduce their effect. Individuals taking these drugs are encouraged to keep their daily intake of vitamin K steady at or slightly below the IA level. In addition, they should have their international normalized ratio (INR) and prothrombin time (PT), both measures of blood clotting potential, checked regularly.
In addition to interfering with blood-thinning drugs mentioned above, vitamin K may interact with the following:
Some broad-spectrum antibiotics (antibiotics that kill a wide variety of bacteria) may decrease the amount of vitamin K2 produced in the intestines. . Aspirin (salicylates) taken in high doses over a long time may increase the body's need for vitamin K.
Cholestyramine (Questran) and mineral oil may decrease vitamin K absorption.
Quinine may increase the body's need for vitamin K
Orlistat (Xenical, Alli) is likely to decrease Vitamin K absorption.
Olestra, a compound that reduces fat absorption, decreases the absorption of vitamin K. The FDA requires all foods containing olestra to be fortified with the fat-soluble vitamins A, D, E, and K.
What Are The Symptoms associated with vitamin K deficiency ?
Symptoms Signs and symptoms associated with vitamin K deficiency include; Easy bruising, oozing from the nose or gums; excessive bleeding from wounds, punctures, injections, and surgical sites; heavy menstrual periods; bleeding from the gastrointestinal tract; blood in the urine and/or stool and an increased prothrombin time (prothrombin is a coagulation factor).
What Else Causes Vitamin K Deficiency ?
In adults additional causes of the vitamin deficiency is associated with low dietary intake of Vitamin K due to chronic illness, malnutrition, alcoholism, multiple abdominal surgeries, long-term parenteral nutrition, malabsorption, parenchymal liver diseases such as cirrhosis secondary to viral hepatitis, cholestatic disease, cystic fibrosis, inflammatory bowel disease, and drugs (eg, antibiotics [cephalosporin], Coumadin, salicylates, anticonvulsants, certain sulfa drugs) are some of the common causes of Vitamin K deficiency. Groups that may suffer from secondary vitamin K deficiency include bulimics, or those on stringent diets.
What Are Some Vitamin K Interactions?
.As for healthy adults no complications are expected from vitamin K, especially when most of the vitamin K comes from dietary sources. However, pregnant and breastfeeding women should avoid taking vitamin K. People with liver disease should not take Vitamin K supplements. .People who are taking blood-thinning drugs, especially warfarin (Coumadin), should discuss their vitamin K needs with their healthcare provider. They may need to restrict their intake of vitamin K. The purpose of blood-thinning drugs is to keep the blood from forming clots in the veins and arteries. Since vitamin K helps blood to clot, high levels of vitamin K in the diet may work against blood-thinning drugs and reduce their effect. Individuals taking these drugs are encouraged to keep their daily intake of vitamin K steady at or slightly below the IA level. In addition, they should have their international normalized ratio (INR) and prothrombin time (PT), both measures of blood clotting potential, checked regularly.
In addition to interfering with blood-thinning drugs mentioned above, vitamin K may interact with the following:
Some broad-spectrum antibiotics (antibiotics that kill a wide variety of bacteria) may decrease the amount of vitamin K2 produced in the intestines. . Aspirin (salicylates) taken in high doses over a long time may increase the body's need for vitamin K.
Cholestyramine (Questran) and mineral oil may decrease vitamin K absorption.
Quinine may increase the body's need for vitamin K
Orlistat (Xenical, Alli) is likely to decrease Vitamin K absorption.
Olestra, a compound that reduces fat absorption, decreases the absorption of vitamin K. The FDA requires all foods containing olestra to be fortified with the fat-soluble vitamins A, D, E, and K.
Natural Sources For Vitamin K
There are two common forms of vitamin K: phylloquinone (vitamin K1) is the main dietary form of the vitamin K group. Rich sources of vitamin K include spinach, kale, broccoli, brussels sprouts, watercress, swiss chard, avocado, parsley (two tablespoons of parsley contain 153% of the recommended daily amount of vitamin K) , kiwifruit and some oils, including soybean, cottonseed, canola and olive. Vitamin K2 make up the rest which is produced primarily in the large intestine, is also found in meat, eggs and cheeses.
.The Nutrition Source Vitamin K .
Vitamin K helps make four of the 13 proteins needed for blood clotting. Its role in maintaining the clotting cascade is so important that people who take anticoagulants such as warfarin (Coumadin) must be careful to keep their vitamin K intake stable.
, Researchers have demonstrated that vitamin K is also involved in building bone. Low levels of circulating vitamin K have been linked with low bone density, and supplementation with vitamin K shows improvements in biochemical measures of bone health. A report from the Nurses' Health Study suggests that women who get at least 110 micrograms of vitamin K a day are 30 percent less likely to break a hip than women who get less than that. Among the nurses, eating a serving of lettuce or other green, leafy vegetable a day cut the risk of hip fracture in half when compared with eating one serving a week. Data from the Framingham Heart Study also shows an association between high vitamin K intake and reduced risk of hip fracture in men and women and increased bone mineral density in women.
People who do not regularly eat a lettuce salad or green, leafy vegetables are likely to be deficient in their intake of vitamin K; national data suggests that only about one in four Americans meets the goal for vitamin K intake from food.
Hepatitis C ; Vitamins And Liver Disease
Excessive amounts of some vitamins may be an additional source of stress to the liver that must act as a filter for the body
.Fat soluble vitamins (especially vitamins A, D, and E) can accumulate in the liver, and if taken in "megadose" quantities may damage even normal livers. Vitamin A is perhaps the most toxic of this group with accidental overdosages causing fulminant liver failure. For this reason, no more than standard recommended daily allowances (RDA's) of vitamins A, D and E are suggested for those with liver disease, regardless of the cause. Vitamin K is also a fat soluble vitamin, supplements of Vitamin K generally are not taken, nor are they recommended.
.Be careful with dietary supplements
.
Iron and Vitamin C
Some people with hepatitis C, particularly those with cirrhosis, have above-average levels of iron in their body. Too much iron can damage organs.
If these people take multivitamin/mineral pills, they should take the ones without iron. These pills usually are marketed as formulas for men or adults over 50. These people also should avoid taking large doses of vitamin C because vitamin C helps the body absorb iron. .
Vitamin A
Vitamin A, if taken in doses larger than the recommended 10,000 IU, can harm the liver. Vitamin A is even more toxic in someone who drinks alcohol.
You won't get too much vitamin A from food, but be careful taking routine dietary supplements with high doses. There's a non-toxic form of vitamin A, present in many fruits and vegetables, called beta-carotene. If you take vitamin A supplements, look for those with beta-carotene.
Vitamin D
Vitamin D is important for health in normal amounts (such as diets with plenty of milk). The body also can make vitamin D when exposed to sunlight. Taking supplements of 800 IU of vitamin D daily may help people with poor diets or long winter seasons, or those who are housebound. Supplements with doses greater than 2,000 IU should not be taken. .
Vitamin E
Researchers are looking into ways that vitamin E can reduce risk of many diseases. But, current medical opinion is that the amount of vitamin E in a well-balanced diet is the safest amount to take. .
Avoid supplements with doses greater than 400 IU. At high doses, vitamin E can thin the blood. This can be a problem for some people, so never take high-dose supplements without first talking to your doctor.
.
Vitamin K
Vitamin K is involved in blood clotting. It is present in the diet mostly in green vegetables. It also is produced by bacteria in the intestines. As mentioned above Vitamin K supplements are not generally used, or recommended.
Cirrhosis
Author: David C Wolf, MD, FACP, FACG, AGAF, Medical Director of Liver Transplantation, Westchester Medical Center, Professor of Clinical Medicine, Division of Gastroenterology and Hepatobiliary Diseases, Department of Medicine, New York Medical College
Contributor Information and Disclosures
Updated: Mar 9, 2011
Excerpt;
See Full Text at Medscape
Nutrition
.Many patients complain of anorexia, which may be compounded by the direct compression of ascites on the GI tract. Care should be taken to ensure that patients receive adequate calories and protein in their diets. Patients frequently benefit from the addition of commonly available liquid and powdered nutritional supplements to the diet. Only rarely can patients not tolerate proteins in the form of chicken, fish, vegetables, and nutritional supplements. Institution of a low-protein diet in the fear that hepatic encephalopathy might develop places the patient at risk for the development of profound muscle wasting.
The practice guideline for alcoholic liver disease published by the American Association for the Study of Liver Diseases (AASLD) and the American College of Gastroenterology in 2010 recommends aggressive treatment of protein calorie malnutrition in patients with alcoholic cirrhosis. Multiple feedings per day, including breakfast and a snack at night, are specified.42
Adjunctive therapies
Zinc deficiency commonly is observed in patients with cirrhosis. Treatment with zinc sulfate at 220 mg orally twice daily may improve dysgeusia and can stimulate appetite. Furthermore, zinc is effective in the treatment of muscle cramps and is adjunctive therapy for hepatic encephalopathy.
Pruritus is a common complaint in both cholestatic liver diseases (eg, primary biliary cirrhosis) and in noncholestatic chronic liver diseases (eg, hepatitis C). Although increased serum bile acid levels once were thought to be the cause of pruritus, endogenous opioids are more likely to be the culprit pruritogen. Mild itching complaints may respond to treatment with antihistamines and topical ammonium lactate.
Cholestyramine is the mainstay of therapy for the pruritus of liver disease. Care should be taken to avoid coadministration of this organic anion binder with any other medication, to avoid compromising GI absorption. Other medications that may provide relief against pruritus include antihistamines (eg, diphenhydramine, hydroxyzine), ursodeoxycholic acid, ammonium lactate 12% skin cream (Lac-Hydrin, Westwood-Squibb Pharmaceuticals, Inc,; Princeton, NJ), doxepin, and rifampin. Naltrexone, an opiate (an opioid antagonist), may be effective but is often poorly tolerated. Gabapentin is an unreliable therapy. Patients with severe pruritus may require institution of ultraviolet light therapy or plasmapheresis.
Some male patients suffer from hypogonadism. Patients with severe symptoms may undergo therapy with topical testosterone preparations, although their safety and efficacy is not well studied. Similarly, the utility and safety of growth hormone therapy remains unclear.
Patients with cirrhosis may develop osteoporosis. Supplementation with calcium and vitamin D is important in patients at high risk for osteoporosis, especially patients with chronic cholestasis, patients with primary biliary cirrhosis, and patients receiving corticosteroids for autoimmune hepatitis. The discovery of decreased bone mineralization upon bone densitometry studies also may prompt institution of therapy with an aminobisphosphonate (eg, alendronate sodium).
Regular exercise, including walking and even swimming, should be encouraged in patients with cirrhosis, lest the patient slip into a vicious cycle of inactivity and muscle wasting. Debilitated patients frequently benefit from formal exercise programs supervised by a physical therapist. Patients with chronic liver disease should receive vaccination to protect them against hepatitis A. Other protective measures include vaccination against influenza and pneumococci.
Drug hepatotoxicity in the patient with cirrhosis
The institution of any new medical therapy warrants the performance of more frequent liver chemistries. Indeed, patients with liver disease can ill afford to have drug-induced liver disease superimposed on their condition. Medications associated with drug-induced liver disease include NSAIDs, isoniazid, valproic acid, erythromycin, amoxicillin/clavulanate, ketoconazole, chlorpromazine and ezetimibe.
Hepatic 3-methylglutaryl coenzyme A (HMG Co-A) reductase inhibitors are frequently associated with mild elevations of alanine aminotransferase (ALT) levels. However, severe hepatotoxicity is reported infrequently.43 The literature suggests that statins can be used safely in most patients with chronic liver disease.44 Certainly, liver chemistries should be followed frequently after the initiation of therapy.
In a study of the effects of statins in 58 patients with primary biliary cirrhosis, Rajab and Kaplan concluded that statin use is safe in patients with this condition.45 Individuals in the study were on statins for a median period of 41 months, with ALT levels measured every 3 months. The authors found that these levels did not increase, being slightly elevated when statin treatment began and normal by the last follow-up analysis. Patients did not complain of muscle pain or weakness, and serum cholesterol levels fell by 30%.
The use of analgesics in patients with cirrhosis can be problematic. Although high-dose acetaminophen is a well-known hepatotoxin, most hepatologists permit the use of acetaminophen in patients with cirrhosis at doses up to 2000 mg/d. NSAID use may predispose patients with cirrhosis to develop GI bleeding. Patients with decompensated cirrhosis are at risk for NSAID-induced renal insufficiency, presumably because of prostaglandin inhibition and worsening of renal blood flow. Opiate analgesics are not contraindicated but must be used with caution in patients with preexisting hepatic encephalopathy on account of their potential to worsen underlying mental function.
Aminoglycoside antibiotics are considered obligate nephrotoxins in patients with cirrhosis and should be avoided.
Low-dose estrogens and progesterone appear to be safe in the setting of liver disease.
.The Nutrition Source Vitamin K .
Vitamin K helps make four of the 13 proteins needed for blood clotting. Its role in maintaining the clotting cascade is so important that people who take anticoagulants such as warfarin (Coumadin) must be careful to keep their vitamin K intake stable.
, Researchers have demonstrated that vitamin K is also involved in building bone. Low levels of circulating vitamin K have been linked with low bone density, and supplementation with vitamin K shows improvements in biochemical measures of bone health. A report from the Nurses' Health Study suggests that women who get at least 110 micrograms of vitamin K a day are 30 percent less likely to break a hip than women who get less than that. Among the nurses, eating a serving of lettuce or other green, leafy vegetable a day cut the risk of hip fracture in half when compared with eating one serving a week. Data from the Framingham Heart Study also shows an association between high vitamin K intake and reduced risk of hip fracture in men and women and increased bone mineral density in women.
People who do not regularly eat a lettuce salad or green, leafy vegetables are likely to be deficient in their intake of vitamin K; national data suggests that only about one in four Americans meets the goal for vitamin K intake from food.
Hepatitis C ; Vitamins And Liver Disease
Excessive amounts of some vitamins may be an additional source of stress to the liver that must act as a filter for the body
.Fat soluble vitamins (especially vitamins A, D, and E) can accumulate in the liver, and if taken in "megadose" quantities may damage even normal livers. Vitamin A is perhaps the most toxic of this group with accidental overdosages causing fulminant liver failure. For this reason, no more than standard recommended daily allowances (RDA's) of vitamins A, D and E are suggested for those with liver disease, regardless of the cause. Vitamin K is also a fat soluble vitamin, supplements of Vitamin K generally are not taken, nor are they recommended.
.Be careful with dietary supplements
.
Iron and Vitamin C
Some people with hepatitis C, particularly those with cirrhosis, have above-average levels of iron in their body. Too much iron can damage organs.
If these people take multivitamin/mineral pills, they should take the ones without iron. These pills usually are marketed as formulas for men or adults over 50. These people also should avoid taking large doses of vitamin C because vitamin C helps the body absorb iron. .
Vitamin A
Vitamin A, if taken in doses larger than the recommended 10,000 IU, can harm the liver. Vitamin A is even more toxic in someone who drinks alcohol.
You won't get too much vitamin A from food, but be careful taking routine dietary supplements with high doses. There's a non-toxic form of vitamin A, present in many fruits and vegetables, called beta-carotene. If you take vitamin A supplements, look for those with beta-carotene.
Vitamin D
Vitamin D is important for health in normal amounts (such as diets with plenty of milk). The body also can make vitamin D when exposed to sunlight. Taking supplements of 800 IU of vitamin D daily may help people with poor diets or long winter seasons, or those who are housebound. Supplements with doses greater than 2,000 IU should not be taken. .
Vitamin E
Researchers are looking into ways that vitamin E can reduce risk of many diseases. But, current medical opinion is that the amount of vitamin E in a well-balanced diet is the safest amount to take. .
Avoid supplements with doses greater than 400 IU. At high doses, vitamin E can thin the blood. This can be a problem for some people, so never take high-dose supplements without first talking to your doctor.
.
Vitamin K
Vitamin K is involved in blood clotting. It is present in the diet mostly in green vegetables. It also is produced by bacteria in the intestines. As mentioned above Vitamin K supplements are not generally used, or recommended.
Cirrhosis
Author: David C Wolf, MD, FACP, FACG, AGAF, Medical Director of Liver Transplantation, Westchester Medical Center, Professor of Clinical Medicine, Division of Gastroenterology and Hepatobiliary Diseases, Department of Medicine, New York Medical College
Contributor Information and Disclosures
Updated: Mar 9, 2011
Excerpt;
See Full Text at Medscape
Nutrition
.Many patients complain of anorexia, which may be compounded by the direct compression of ascites on the GI tract. Care should be taken to ensure that patients receive adequate calories and protein in their diets. Patients frequently benefit from the addition of commonly available liquid and powdered nutritional supplements to the diet. Only rarely can patients not tolerate proteins in the form of chicken, fish, vegetables, and nutritional supplements. Institution of a low-protein diet in the fear that hepatic encephalopathy might develop places the patient at risk for the development of profound muscle wasting.
The practice guideline for alcoholic liver disease published by the American Association for the Study of Liver Diseases (AASLD) and the American College of Gastroenterology in 2010 recommends aggressive treatment of protein calorie malnutrition in patients with alcoholic cirrhosis. Multiple feedings per day, including breakfast and a snack at night, are specified.42
Adjunctive therapies
Zinc deficiency commonly is observed in patients with cirrhosis. Treatment with zinc sulfate at 220 mg orally twice daily may improve dysgeusia and can stimulate appetite. Furthermore, zinc is effective in the treatment of muscle cramps and is adjunctive therapy for hepatic encephalopathy.
Pruritus is a common complaint in both cholestatic liver diseases (eg, primary biliary cirrhosis) and in noncholestatic chronic liver diseases (eg, hepatitis C). Although increased serum bile acid levels once were thought to be the cause of pruritus, endogenous opioids are more likely to be the culprit pruritogen. Mild itching complaints may respond to treatment with antihistamines and topical ammonium lactate.
Cholestyramine is the mainstay of therapy for the pruritus of liver disease. Care should be taken to avoid coadministration of this organic anion binder with any other medication, to avoid compromising GI absorption. Other medications that may provide relief against pruritus include antihistamines (eg, diphenhydramine, hydroxyzine), ursodeoxycholic acid, ammonium lactate 12% skin cream (Lac-Hydrin, Westwood-Squibb Pharmaceuticals, Inc,; Princeton, NJ), doxepin, and rifampin. Naltrexone, an opiate (an opioid antagonist), may be effective but is often poorly tolerated. Gabapentin is an unreliable therapy. Patients with severe pruritus may require institution of ultraviolet light therapy or plasmapheresis.
Some male patients suffer from hypogonadism. Patients with severe symptoms may undergo therapy with topical testosterone preparations, although their safety and efficacy is not well studied. Similarly, the utility and safety of growth hormone therapy remains unclear.
Patients with cirrhosis may develop osteoporosis. Supplementation with calcium and vitamin D is important in patients at high risk for osteoporosis, especially patients with chronic cholestasis, patients with primary biliary cirrhosis, and patients receiving corticosteroids for autoimmune hepatitis. The discovery of decreased bone mineralization upon bone densitometry studies also may prompt institution of therapy with an aminobisphosphonate (eg, alendronate sodium).
Regular exercise, including walking and even swimming, should be encouraged in patients with cirrhosis, lest the patient slip into a vicious cycle of inactivity and muscle wasting. Debilitated patients frequently benefit from formal exercise programs supervised by a physical therapist. Patients with chronic liver disease should receive vaccination to protect them against hepatitis A. Other protective measures include vaccination against influenza and pneumococci.
Drug hepatotoxicity in the patient with cirrhosis
The institution of any new medical therapy warrants the performance of more frequent liver chemistries. Indeed, patients with liver disease can ill afford to have drug-induced liver disease superimposed on their condition. Medications associated with drug-induced liver disease include NSAIDs, isoniazid, valproic acid, erythromycin, amoxicillin/clavulanate, ketoconazole, chlorpromazine and ezetimibe.
Hepatic 3-methylglutaryl coenzyme A (HMG Co-A) reductase inhibitors are frequently associated with mild elevations of alanine aminotransferase (ALT) levels. However, severe hepatotoxicity is reported infrequently.43 The literature suggests that statins can be used safely in most patients with chronic liver disease.44 Certainly, liver chemistries should be followed frequently after the initiation of therapy.
In a study of the effects of statins in 58 patients with primary biliary cirrhosis, Rajab and Kaplan concluded that statin use is safe in patients with this condition.45 Individuals in the study were on statins for a median period of 41 months, with ALT levels measured every 3 months. The authors found that these levels did not increase, being slightly elevated when statin treatment began and normal by the last follow-up analysis. Patients did not complain of muscle pain or weakness, and serum cholesterol levels fell by 30%.
The use of analgesics in patients with cirrhosis can be problematic. Although high-dose acetaminophen is a well-known hepatotoxin, most hepatologists permit the use of acetaminophen in patients with cirrhosis at doses up to 2000 mg/d. NSAID use may predispose patients with cirrhosis to develop GI bleeding. Patients with decompensated cirrhosis are at risk for NSAID-induced renal insufficiency, presumably because of prostaglandin inhibition and worsening of renal blood flow. Opiate analgesics are not contraindicated but must be used with caution in patients with preexisting hepatic encephalopathy on account of their potential to worsen underlying mental function.
Aminoglycoside antibiotics are considered obligate nephrotoxins in patients with cirrhosis and should be avoided.
Low-dose estrogens and progesterone appear to be safe in the setting of liver disease.