Revive Her Drive

Improving Your Sex Life

Get Instant Access

Baldwin, G. C., Roth, M. D., & Tashkin, D. P. (1998). Acute and chronic effects of cocaine on the immune system and the possible link to AIDS. Journal of Neu-roimmunology, 83, 133-138.

Baldwin, G. C., Tashkin, D. P., Buckley, D. M., Park, A. N., Dubinett, S. M., & Roth, M. D. (1997). Marijuana and cocaine impair alveolar macrophage function and cyto-kine production. American Journal of Respiratory and Critical Care Medicine, 156(5), 1606-1613.

Cabral, G. A., & Dove Pettit, D. A. (1998). Drugs and immunity: Cannabinoids and their role in decreased resistance to infectious disease. Journal ofNeuroimmu-nology, 83, 116-123.

Costenbader, K. H., & Karlson, E. W. (2006). Cigarette smoking and autoimmune disease: What can we learn from epidemiology? Lupus. 15, 737-745.

Diaz, L. E, Montero A., Gonzaels-Gross, M., Vallejo, A. I., Romeo, J., & Marcos, A. (2002). Influence of alcohol consumption on immunological status: A review. European Journal of Clinical Nutrition, 56(Suppl. 3), S50-S53.

Hutchinson, D., Shepstone, L., Moots, R., Lear, J. T., and Lynch, M. P. (2001). Heavy cigarette smoking is strongly associated with rheumatoid arthritis (RA), particularly in patients without a family history of RA. Annals of Rheumatic Disease, 60, 223-227.

Janeway, C. A., Travers, P., Walport, M., & Shlomchik, M. (2001). Immunobiology: The immune system in health and disease. New York, NY: Inside North America-Garland Publishing.

Johnson, T. R, Knisely, J. S., Christmas, J. T., Schnoll, S. H., & Ruddy, S. (1996). Changes in immunologic cell surface markers during cocaine withdrawal in pregnant women. Brain, Behavior, and Immunity, 10(4), 324-336.

Karlix, J. L., Behnke, M., Davis-Eyler, F., Wobie, K., Adams, V., et al. (1998). Cocaine suppresses fetal immune system. Pediatric Research, 44(1), 43-46.

King, B. L., Tsai, S. C., Gyrga, M. E. (2003). Detection of chromosomal instability on paired breast surgery and ductal lavage specimens by interphase fluorescence in situ hybridization. Clinical Cancer Research, 9, 15091516.

Klein, T. W, Friedman, H., & Specter, S. (1997). Marijuana, immunity and infection. Journal ofNeuroimmu-nology, 83, 102-115.

Klein, T. W., Lane, B., Newton, C. A., & Friedman, H. (2000). The cannabinoid system and cytokine network. Experimental Biology and Medicine, 225, 1-8.

Kumar, R., Perez-Casanova, A. E., Tirado, G., Noel, R. J., Torres, C., Rodriguez, I., et al. (2005). Increased viral replication in Simian Immunodeficiency Virus/Simian-HIV-infected Macaques with self-administering model of chronic alcohol consumption. Journal of Acquired Immune Deficiency Syndrome, 39(4), 386-390.

MacGregor, R. R. (1986). Alcohol and immune defense. Journal of the American Medical Association, 256, 1474-1479.

Madigan, M. T., Martinko J. M., & Parker, J. (2003). Brock Biology of Microorganisms. Upper Saddle River, NJ: Prentice Hall.

Pellegrino, T., & Bayer, B. M. (1998). In vivo effects of cocaine of immune function. Journal of Neuroimmu-nology, 83, 139-147.

Prescott, S. L. (2008). Effects of early cigarette smoke exposure on early immune development and respiratory disease. Pediatric Respiratory Reviews, 9, 3-10.

Roy, S., Wang, J., Kelschenbach, J., Koodie, L., & Martin, J. (2006). Modulation of immune function by morphine: Implications for susceptibility to infection. Journal of Neuroimmune Pharmacology, 1, 77-89.

Szabo, G. (1997). Alcohol's contribution to compromised immunity. Alcohol Health & Research World, 21(1), 30-38.

Tashkin, D. P., Baldwin, G. C., Sarafian, T., Dubinett, S., & Roth, M. D. (2002). Respiratory and immunologic consequences of marijuana smoking. Journal of Clinical Pharmacology, 42, 71S-81S.

Wallace, C. L., & Watson, R. R. (1990). Immunomodulation by tobacco. In R. R. Watson (Ed.), Drugs of abuse and immune function. Boca Raton, FL: CRC Press.

Wang, J., Barke, R. A., Charboneau, R., & Roy, S. (2005). Morphine impairs host immune response and increases susceptibility to Streptococcus pneumoniae lung infection. Journal of Immunology, 174, 426-434.

Watson, R. R., & Witten, M. (2001). Environmental tobacco smoke. Boca Raton, FL: CRC Press.

Watzl, B., & Watson, R. R. (1990). Immunomodulation by cocaine: A neuroendocrine mediated response. Life Sciences, 46, 1319-1329.

Yahya, M. D., & Watson, R. R. (1987). Minireview: Immunomodulation by morphine and marijuana. Life Sciences, 41, 2503-2510.

Ronald R. Watson Felina Marie Cordova


The liver is the largest internal organ of the human body, normally weighing about 3.3 pounds (1.5 kg). It occupies the right upper quadrant of the abdominal cavity just below the diaphragm. As befitting its anatomical prominence, its function is essential to maintain life. Surgical removal of the entire liver from any animal (including humans) would result in the animal's falling into a coma shortly thereafter and then dying. The absence of a certain critical mass of functioning liver tissue is incompatible with life. While the human liver has a remarkable resilience and regenerative capacity after injury or illness, this is true only up to a certain point. If illness damages the liver beyond the point of no return, the person dies.

The liver has a multitude of complex functions and is justly called the laboratory of the human body. It secretes a digestive juice called bile into the intestine, called bile; it produces a number of essential proteins, clotting factors, and fatty substances; it stores and conserves energy-producing sugars; it detoxifies both internally produced and external toxins and drugs that would otherwise be poisonous to the human organism—just to name some of its important functions.

What can seriously jeopardize this very important organ and consequently the well-being and survival of the individual? For one, there are dis-eases—both congenital and acquired—over which a person has little or no control, such as some genetically determined and developmental abnormalities, circulatory liver problems, certain tumors, and infections. A very large part of hepatology (the technical term to describe the study and treatment of liver diseases) is, however, devoted to liver problems created by a peculiar human behavior—the abuse of alcohol and drugs. Whereas discussions as to whether alcoholism and drug abuse are truly self-inflicted problems elicit a variety of opinions, the liver disease that results from substance abuse in a given individual could have been avoided if the substance-abusing behavior had not occurred. Beyond the psychosocial consequences of substance abuse, diseases of the liver (and brain) represent the major complications of alcohol and drugs. The morbidity (disease incidence) and mortality (death incidence) from alcoholic and drug-induced liver injury are very high. In the scientific literature, it is well established that the mortality from alcoholic liver disease is correlated with per capita alcohol consumption; in fact, the prevalence of alcoholism in a given society has been calculated from liver mortality statistics. While alcohol is a direct liver toxin, most of the other commonly abused psychoactive substances are generally not known to affect the liver directly to a great extent. Their major contribution to liver morbidity and mortality is via exposing people to viral hepatitis, a potentially fatal disease.

alcoholic liver diseases

This section discusses the range of alcoholic liver diseases. The interrelationship between them is illustrated in Figure 1.

Alcoholic Fatty Liver. Fat accumulation in the liver is an almost universal response to excessive

Figure 1. Interrelationships between various forms of alcoholic liver disease. Illustration by GGS Information Services. Gale, Cengage Learning

alcohol consumption. It occurs in the majority of heavy drinkers. How and why fat accumulates in liver cells is complicated and not completely understood; however, its presence may be observed. If a piece of biopsied liver tissue from an alcoholic is examined under the microscope, the observer will see that many liver cells are loaded with big bubbles consisting of fat, almost totally occupying the cell. In most cases, this fatty change does not matter much as far as the patient's health is concerned. It is an almost invariable response to too much alcohol consumption and an early warning. The person who has nothing worse than an alcoholic fatty liver may not feel sick at all, and only if a biopsy is done can the fatty liver be diagnosed. The doctor may feel an enlarged liver by palpation (pushing on the abdomen to feel the internal organs), which may be a bit tender. The laboratory test may show a slight elevation in the blood of some liver enzymes, best known by their initials: SGOT (or AST) and SGPT (or ALT). These enzymes are elevated because some of them tend to leak out of the fatty liver cells into the blood.

If a person stops drinking, the fat disappears from the liver cells, the swelling subsides, and the AST and ALT levels become normal. The two-way arrow in the diagram of Figure 1 indicates that fatty liver is reversible with abstinence, and the condition may fluctuate back and forth between normal and fatty liver with abstinence and drinking, respectively. Thus, fatty liver in itself is not likely a serious situation; it is an early warning that the liver does not respond well to alcohol and that its condition may worsen. There was a time when fatty liver was regarded as a precursor of the end-stage liver disease called cirrhosis (indicated by the broken arrow and question mark on Figure 1), but most physicians do not now believe that this direct connection exists.

Alcoholic Hepatitis. Alcoholic hepatitis is a potentially more serious form of alcoholic liver disease. A certain proportion of alcoholics, in addition to accumulating fats in their livers when drinking, will develop inflammation (hepatitis means liver inflammation) consisting of an accumulation of white blood cells, the death (necrosis) of some of the liver cells, and the presence of some very characteristic material called Mallory bodies. Again, all these changes can be seen under the microscope in a biopsied piece of tissue.

The clinical picture of alcoholic hepatitis varies. At one extreme is the person who feels perfectly well and only the biopsy could indicate that something is wrong. At the other extreme is the dying patient with a swollen and painful liver, jaundice (a yellowing of the entire body from bile pigment leaking into the blood), fever, and disturbed consciousness. Between these extremes are people with varying degrees of illness; for example, with or without some jaundice, with or without pain and fever. The white blood cell count is usually elevated. The bilirubin (bile pigment) level may be elevated in patients who have turned yellow (a pale to deep mustard). The liver enzymes are higher than normal in the blood because they leak out of the inflamed liver cells. However, these values are not as high as in viral hepatitis. In alcoholic hepatitis AST (SGOT) is higher than ALT (SGPT). This finding helps to distinguish alcoholic hepatitis from viral hepatitis, which is difficult to do at times. In viral hepatitis not only are the absolute enzyme values higher, but the ratio is reversed: ALT is higher than AST.

Thus, the outcome of alcoholic hepatitis can be death (worst scenario) or recovery (best scenario), as shown on Figure 1. Even if the patient does not die in a given episode, repeated episodes of drinking and alcoholic hepatitis can lead to the last stage of alcoholic liver disease: cirrhosis.

Alcoholic Cirrhosis. In terms of histology (tissue damage) alcoholic cirrhosis is an end-stage disease: a cirrhotic liver cannot become normal. In Figure 1, there is no arrow between cirrhosis and normal liver. Clinically, cirrhosis is a serious disease, potentially fatal, but not inevitably so. Alcoholism, while not its only cause, is by far the most common. Under the microscope a cirrhotic liver shows a disorganized architecture: the dead (necrotic) liver cells have been replaced by scar tissue. The liver tries to repair itself. In a somewhat haphazard fashion it attempts to produce new liver tissue in the form of nodules, which are separated from each other by scar tissue. These newly formed liver nodules may indeed sustain liver function and thus life for a time, but at a price: the liver's blood circulation is mechanically compressed. Thus, pressure increases in the blood vessels leading to the liver. Some of these overloaded blood vessels, especially those on the border of the stomach and esophagus (called esophageal varices), can rupture at any time, causing a major hemorrhage.

Patients in the cirrhotic stage of alcoholic liver disease present their symptoms in various ways. Some of them look quite normal; only the biopsy will reveal the presence of cirrhosis. Others are jaundiced, the yellow color from bile pigment leaking out of the damaged liver into the blood, thus staining the skin and the whites of the eyes. Still others have large fluid accumulations in their extremities (edema) or in their abdominal cavity (ascites). The latter may make these patients— men or women—look like they are nine months pregnant. Some may vomit blood because of the hemorrhaging. In most advanced cases, there is just not enough functioning liver tissue left; the liver no longer can perform its laboratory function, and the person slips into a coma and may die. When cir-rhotic patients are examined by doctors, their livers do not feel smooth but bumpy from the nodules that have formed. At first the liver may be swollen and enlarged, but in the later stages it shrinks. The ultrasound picture suggests a patchy, disorganized liver architecture. The spleen may enlarge from the increased pressure in the blood vessels. The liver enzymes (AST and ALT) may be moderately

Cirrhosis of the liver. Nucleus Medical Art/Phototake

elevated as in other forms of alcoholic liver disease, but this elevation has no prognostic importance. More ominous signs pointing toward severely compromised liver functions are the following: a decrease in blood level of albumin (an important protein manufactured by the liver), deficiency in blood-clotting factors that are also made in the liver, and the presence of anemia (low hemoglobin and red blood cell count).

Causes of Death in Cirrhosis. Ascites (fluid accumulation in the abdomen) is very uncomfortable and unsightly but by itself usually does not kill, unless infection develops, which is always a threat. Generally, cirrhosis compromises the immune system, rendering cirrhotic alcoholics susceptible to all sorts of potentially overwhelming infections. Portal hypertension is also a serious complication of the cirrhotic fibrosis. The obstruction to portal vein flow through the liver results in the development of other vein channels to accommodate the return of blood from the abdominal organs, which ordinarily flows through the portal vein. The result is the development of varices (enlarged, engorged veins) in the stomach and esophagus. These enlarged, thin-walled veins are prone to rupture, leading to one of the most serious complications of cirrhosis of the liver—bleeding varices. This constitutes an emergency and calls for immediate intervention in the form of measures to control the bleeding. A variety of therapies are available, all of which have been employed with a varying degree of success that depends on the severity of the hemorrhage and the skill and experience of the physician. Once the bleeding has been controlled, the patient should be considered for an appropriate permanent venous shunt procedure whereby venous blood bypasses the liver. Finally, total decompensation of liver cell function may cause coma and death.

The good news is that even when there is irreversible cirrhosis at the tissue level, death may not be inevitable. Survival depends mainly on two factors: luck and alcohol abstinence. Abstaining alcoholics with cirrhosis can stabilize and survive on what's left of their liver tissue without necessarily and relentlessly progressing to one of the fatal outcomes.

Risk Factors for Alcoholic Liver Disease. There are no certain answers to the question ofwho is likely to get alcoholic liver disease. Fatty liver is an almost universally predictable response to heavy alcohol consumption, but this by itself is seldom a serious problem. A smaller number of people develop alcoholic hepatitis and still fewer (variously estimated in different populations between 5 percent and 25 percent of alcoholics) end up with cirrhosis. Considering the large number ofalcoholics in the general population, the minority who develop cirrhosis still represent large numbers; cirrhosis is one of the leading causes of all deaths.

Still, why do some alcoholics develop alcoholic hepatitis and cirrhosis, while others who drink equally heavily do not? The amount of alcohol consumption and the length of time of heavy drinking is certainly one risk factor. Gender may be another: women's livers generally are more vulnerable to the effects of alcohol than those of men, given equal alcohol exposures. Chronic viral infection, especially chronic Hepatitis C infection, has been shown to be another risk factor. Finally, there may be a genetically determined but still unclarified individual susceptibility, which may explain why some people never get cirrhosis; why some do after many years of alcoholism; and why still others get cirrhosis at a young age or after a relatively short drinking career.

Prognosis and Treatment. The issues of prognosis and treatment cannot be separated. The cornerstone of treatment is complete abstinence from alcohol. Achieving abstinence can arrest the progression of liver disease, even in established cirrhosis; continued drinking leads to deterioration and death.

One therapeutic issue relating to alcoholism is relevant to liver disease. The drug disulfiram (Anta-buse) is sometimes prescribed to reinforce abstinence. Its unpleasant, sometimes severe interaction with alcohol is a deterrent against drinking. Since disul-firam (as so many other drugs) has been occasionally reported to produce liver toxicity of its own, the presence of alcoholic liver disease is sometimes regarded as a relative contraindication against prescribing disulfiram. Some clinicians believe, however, that liver toxicity caused by alcohol far outweighs any risk that may be caused by disulfiram. Another drug used to treat alcohol dependence, naltrexone (Revia, Vivitrol), can also cause liver injury when given in excessive doses. Its use in patients with active liver disease requires careful consideration by the prescribing physician. Another drug for the maintenance of abstinence, acamprosate (Campral), does not have the disadvantage of the other two agents. Its elimination is dependent on the kidney, rather than the liver, and can be used to reinforce abstinence even in individuals with mild-to-moderate liver impairment.

Other treatment techniques beyond abstinence have been proposed to aid in recovery from alcoholic liver damage. In the late 1980s, a Toronto research group reported the beneficial effect of propylthiouracil (PTU). PTU is a drug normally used for the treatment of thyroid disease, but by reducing oxygen demand in the body (including in the liver), it might help to repair the damage caused by alcohol. The early results were promising but have not been confirmed by other researchers. Other drugs, such as corticosteroids (to decrease inflammation) or colchicine (to decrease scar formation) have dubious value.

There are relatively effective treatments available for some of the complications of alcoholic liver disease that enable patients to survive and thus begin their abstinence program. Fluid accumulation in the extremities (edema) or in the abdomen (ascites) can he helped by diet modifications (salt restriction), water-removing drugs (diuretics), albumin infusion, or tapping the abdomen with a needle to withdraw fluid.

Infections can be treated with antibiotics. The brain syndrome associated with liver failure (so-called hepatic encephalopathy or, in severe cases, hepatic coma) can improve with dietary means (protein restriction) or some drugs (e.g., neomycin, lactulose). Potentially or actually bleeding esophageal varicose veins can be obliterated by sclerotherapy, a procedure in which certain injections are delivered through a gastroscope (a tube inserted through the mouth that makes it possible to visualize the stomach). Risk of bleeding can be lessened by beta-blocking (heart-rate slowing) drugs or some surgical procedures to decrease pressure.

Finally, there is the possibility of liver transplantation. If all else fails, a successful liver transplant cures alcoholic liver disease. Apart from the general problems of donor matching and supply, some people have raised objections to offering transplantation for alcoholic liver disease on ethical grounds, claiming that the condition is self-inflicted. This is not an acceptable objection and goes against medical ethics. Well-motivated recovering alcoholics are entitled as much as anybody else to a life-saving procedure. In fact, studies have shown that the dramatic and heroic nature of this operation may be an extremely powerful motivator for future abstinence by liver recipients. Numerous successful transplants have been carried out on alcoholics.

drugs and the liver

Although many drugs in medicinal use may be toxic to the liver, most of the psychoactive drugs that people tend to abuse are not known to be particularly harmful. Occasional liver damage has been reported with solvent sniffing and cocaine use, but this is not a common problem. Narcotics (opioids), anti-anxiety, and other sedative drugs (such as barbiturates), marijuana, and hallucinogens do not usually cause liver injury.

There are, however, several relevant secondary issues concerning drug abuse and the liver. For one, a damaged liver (for example, from alcohol or hepatitis) results in poor tolerance of sedatives, because good liver function is necessary to eliminate sedatives properly. Impaired liver function can therefore result in an exaggerated sedative effect. Conversely, some sedatives, notably barbiturates (which were often abused in the past and sometimes still are), actually stimulate (induce) certain liver enzymes, which can result in increased elimination (i.e., decreased effect) of another therapeutically necessary drug. For example, a barbiturate user (or abuser) may have poor effect from a clotting pre-ventative (anti-coagulant) drug that is necessary in heart disease or after a stroke. Some drugs do the opposite: they inhibit liver enzymes. For example, the anti-ulcer drug cimetidine (Tagamet), which has no psychoactive effect per se, can cause such enzyme inhibition. If a person at the same time also happens to use or abuse a sedative, the sedative can have an exaggerated effect. Generally speaking, the normal liver transforms or inactivates drugs to less active or harmless forms. A notable and important exception is acetaminophen, one of the most commonly used medications against pain and fever (e.g., the various Tylenol preparations). The liver can transform acetaminophen into a toxic metabolite that can cause a potentially lethal liver injury. Generally, this does not happen at ordinary therapeutic acetaminophen dose levels. In the case of an acetaminophen overdose, however, such severe liver toxicity can occur that a person will die within days. Most of such overdoses are, of course, suicide attempts.

Acetaminophen itself does not have any psychoactive (mind-altering) properties; thus people do not abuse it to induce euphoria. Many combination narcotic prescription painkillers, however, contain acetaminophen. People seeking narcotic highs from such preparations might inadvertently ingest acetaminophen in large enough quantities to subject themselves to potentially severe liver injury. The person who is overdosing with suicidal intent is more likely to be discovered and brought to quick medical attention than an unintentionally overdosing drug abuser. Unfortunately, the antidote against acetaminophen poisoning, acetylcysteine, is effective only if it is given within a few hours (less than a day) after the ingestion of the drug. By the time acetaminophen poisoning has been suspected, the opportunity for treatment with the antidote may have already passed. An additional issue with acetaminophen is strong evidence of increased risk when alcohol and acetaminophen are combined. In alcoholics, relatively low doses of acetaminophen can cause severe and potentially fatal liver damage.

Viral Hepatitis in Drug Abusers. The major cause of liver damage in those individuals who abuse drugs is not direct toxicity from the drug, but rather from the transmission of viruses from person to person through contaminated needles and syringes. The problem of viral hepatitis, then, is largely that of injecting drug users (IDUs). At least five types of disease-causing hepatitis viruses have been identified, designated by the letters A to E. Of the five, Hepatitis A and E are not particularly associated with injecting drug abuse; but the other three are, and they will be discussed in some detail.

Hepatitis B. Hepatitis B (which used to be called serum hepatitis) is endemic to some parts of the world, such as Southeast Asia, where as many as 10 percent of the population may be infected. In the Western world, IDUs represent the greatest reservoir for Hepatitis B virus. It is transmitted through a direct blood-borne route, such as the following:

1. Contaminated needles and syringes (which drug addicts notoriously did not sterilize in the past).

2. From an infected mother across the placenta and through the umbilical cord of a developing fetus.

3. From accidental needle-stick injuries involving contaminated blood in health care workers.

4. From any blood-to-blood contact occurring during sexual intercourse. At one time blood transfusions were a common source of infection, but screening tests can now identify infected donors.

The symptoms of Hepatitis B infection vary. In its severest form, it can cause general malaise, fever, jaundice, coma, and death. The majority of patients, even with marked jaundice and fever, do not die. Many infected people do not even have an overt illness; they may not feel sick at all or may just have transient, flu-like symptoms. There may be a tender enlargement of the liver. If such people are tested in the laboratory, they have elevated liver enzymes, such as AST (also known as SGOT) and ALT (also known as SGPT), which are usually much higher than the values found in alcoholic liver disease. The bilirubin (bile pigment) level will be high if the person has yellow jaundice. The diagnosis is confirmed when serologic tests are positive for a viral particle called Hepatitis B antigen. Those who recover from the illness and clear the virus from their bodies will develop a protective antibody that will prevent them from becoming infected again. The antibody can be detected in a laboratory test.

The majority of people who get infected with Hepatitis B recover and acquire protective antibodies.

A sizable minority of those who survive, however, perhaps 10 percent, will continue to carry the virus, remaining antigen positive. Some of these individuals will have a chronic liver inflammation that will develop into cirrhosis. The cirrhosis caused by Hepatitis B is essentially similar to alcoholic cirrhosis, with the same consequences and potential complications described above. Moreover, Hepatitis B has the potential to cause liver cancer in some of those who develop cirrhosis. Not only is Hepatitis B in such chronically infected individuals a threat to their own survival, but it is also a source of infection to others, particularly to their needle-sharing partners, to their sexual partners, and to their developing fetuses and newborn babies.

A vaccine to prevent Hepatitis B has been available in the United States since 1982; however, it was not until the introduction of a recombinant form of the vaccine in the early 1990s that universal immunization for all newborns and adolescents became feasible. While most individuals born in the 1990s and many born in the 1980s are now immunized, millions of Americans remain unvaccinated. The Advisory Committee on Immunization Practices (ACIP) recommends that all IDUs be immunized against Hepatitis B infection. Other individuals for whom immunization is strongly recommended include sexually active heterosexuals with more than one sex partner within a six-month period or those who have contracted a sexually transmitted disease; men who have sex with men; persons at occupational risk of infection (e.g., health care professionals); hemodialysis patients; household or close contacts of persons with chronic Hepatitis B viral infection; residents and staff of institutions for the developmental^ disabled; persons with chronic liver disease or human immunodeficiency virus (HIV) infection; and international travelers to areas of the world where Hepatitis B is endemic.

Hepatitis C. Until about 1990, Hepatitis C was called non-A-non-B Hepatitis, because there were viral hepatitis cases that were caused by neither of the two identifiable viruses, A and B. An antibody test can now identify this virus, which is called Hepatitis C. The antibody detected is not a protective antibody, but it is similar to the AIDS (HIV) antibody in that it indicates the presence of the virus. Many cases of viral hepatitis caused by blood transfusions in the past were due to Hepatitis C infection. The antibody test can eliminate this source of transmission, as it is used to screen the donor blood supply.

Injecting drug users, however, remain a major reservoir and source for the spread of this virus. Hepatitis C is transmitted similarly to Hepatitis B—and, for that matter, to HIV—primarily through direct blood-to-blood contact (by contaminated injection paraphernalia) and to a lesser extent, but still possibly, via sex and from mother to fetus. The primary infection very often goes unnoticed. The laboratory tests, in addition to Hepatitis C antibodies, will show elevated ALT and AST levels. Because Hepatitis C is a newly identified virus, its natural history is not yet clear. A fair amount of evidence suggests that chronic hepatitis, eventual cirrhosis, and liver cancer may be an even greater risk with Hepatitis C than it is with Hepatitis B. Some studies in the medical literature indicate that 50 to 80 percent of intravenous drug addicts may be infected with Hepatitis C.

Hepatitis D. Hepatitis D is a very unusual virus, which was originally called delta agent and later renamed Hepatitis D. It is an incomplete virus that can exist only in the presence of Hepatitis B. When the two organisms combine, the outcome is a particularly nasty, potentially lethal hepatitis, both in terms of acute mortality and chronic consequences. Discovered in Italy about 1990, in North America Hepatitis D is known to be primarily harbored by the IDU population.

prevention and treatment of viral hepatitis

Obviously, the best prevention for injection drug users would be to stop injecting drugs. Other, often more realistic prophylactic measures—as with HIV—are the use of sterile (or at least bleached) needles and syringes, needle exchange programs, and condoms for sexual activities.

Immediately after a known or suspected exposure to Hepatitis B, the injection of an antibody preparation known as Hepatitis B immune globulin can prevent illness. A more permanent prophylaxis in high-risk populations is provided by the Hepatitis B vaccine, which gives long-term immunity in previously uninfected individuals. IDUs certainly represent one of these high-risk populations, although the widespread use of the Hepatitis B vaccine in this group raises some obvious logistic dilemmas. As of 2008, there is no passive or active immunization available for Hepatitis C.

During the first decade of the twenty-first century, a number of new agents were introduced for the treatment of chronic Hepatitis B and C infections. Hepatitis C infection can be treated with the combination of two antiviral drugs: pegylated interferon (PegIntron, Pegasys) and ribavirin (Rebetol, Cope-gus). Pegylated interferon must be injected once weekly and can cause severe side effects, including flu-like symptoms, fatigue, irritability and depression. Ribavirin is better tolerated but is ineffective alone and must be used in combination with the interferon. The treatment is given over a period ofmonths; some patients are still not able to clear the virus after a year's therapy. Treatment success depends on a number of factors, including the strain of virus being treated and the patient's ability to tolerate the interferon side effects. Hepatitis B can also be treated with a form of interferon (Intron A), which is successful in eliminating the virus in about half of all patients treated. Two oral agents are also used: lamivudine (Epivir HBV) and adefovir (Hepsera). These drugs can sometimes eliminate the Hepatitis B virus; but even if they do not, when taken long term they can suppress viral replication, potentially preventing liver damage. Finally, as mentioned under alcoholic liver disease, the most radical form of therapy in the end stages is liver transplantation.

See also Needle and Syringe Exchanges and HIV/AIDS; Risk Factors for Substance Use, Abuse, and Dependence: An Overview; Social Costs of Alcohol and Drug Abuse.

Was this article helpful?

0 0
How To Bolster Your Immune System

How To Bolster Your Immune System

All Natural Immune Boosters Proven To Fight Infection, Disease And More. Discover A Natural, Safe Effective Way To Boost Your Immune System Using Ingredients From Your Kitchen Cupboard. The only common sense, no holds barred guide to hit the market today no gimmicks, no pills, just old fashioned common sense remedies to cure colds, influenza, viral infections and more.

Get My Free Audio Book

Post a comment