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Amebic liver abscess.

Abstract: Amebic liver abscess is the most common extraintestinal manifestation of infection with Entamoeba histolytica, and it is associated with significant morbidity and mortality. In this article the most recent available information is reviewed relating to epidemiology, pathogenesis, presentation, diagnosis, and treatment. We reviewed thousands of cases of amebic liver abscess in the medical literature and present that information as it pertains to mortality, gender, anatomic location of abscesses, and clinical signs and symptoms.

Key Words: amebiasis, amebic liver abscess, Entamoeba histolytica, hepatic abscess


Amebiasis is a parasitic infection caused by Entamoeba histolytica, an organism that lives up to its formidable name by the invasion of colonic tissue leading to amebic colitis and amebic liver abscess (ALA). Known since classical times, the infection was linked to amebae by Fedor Aleksandrovich Losch in 1875. (1) Despite our long experience with the disease, amebiasis continues to be an international problem, and is a major contributor to the diarrheal deaths of children in developing countries, as well as causing significant morbidity and mortality in adults. (2) ALA is the most common extraintestinal manifestation of infection by E histolytica. (3) As a result of increasing international travel and changing patterns of immigration, physicians in the United States face more cases of amebiasis, including patients with ALA. The purpose of this article is to highlight the salient features of hepatic amebiasis and review its treatment.


Historically, amebic infection has been estimated to be present in approximately 12% of the world population and in up to 50% of the population in tropical and subtropical regions including Mexico, Central and South America, India, Southeast Asia, as well as eastern and southern Africa. (4,5) It is now known that many of these individuals are infected with a morphologically identical but genetically dissimilar organism, Entamoeba dispar. (6-8) E dispar is a nonpathogenic species that has never been shown to cause symptomatic disease, even in individuals with severe immunosuppression, such as those with acquired immunodeficiency syndrome (AIDS). (9) The previous inability to differentiate among Entamoeba species has limited epidemiologic information on E histolytica, but now more widespread diagnostic tests are available to clearly distinguish E histolytica from E dispar. (1,8,10) Studies have now indicated that asymptomatic infection with Entamoeba species is most commonly due to E dispar, but there are still known to be large numbers of people infected with E histolytica who remain asymptomatic, and in some regions, most cases of asymptomatic infection are due to E histolytica. (1) Available epidemiologic studies, specific for E histolytica, demonstrate that infection rates may still be as high as 55% in endemic areas such as Bangladesh, although symptomatic infection rates are less than one-half that number. (11) Although the exact incidence is not clearly defined, it is known that 40,000 to 100,000 people die annually as a result of amebiasis. (12)

Poverty facilitates infection because of deficiencies in sanitation and hygiene, suboptimal sewer systems, deficient fertilization practices, and irrigation with untreated water, all of which facilitate the ingestion of infective E histolytica cysts. Studies during outbreaks have identified that interruptions in water supply, decreases in water pressure, and increased water consumption are associated with high infection rates. (13) Other factors associated with enhanced transmission include cramped living conditions such as long-term institutions and prisons (14) and male homosexuality, (15) although subsequently it has been found that many of these individuals have colonization by the intestinal commensal E dispar. (16) In developed countries, amebic infection should be suspected in patients who have recently traveled to endemic areas, especially those who stayed in the endemic area for more than 1 month, (17) and in immigrants from countries with high rates of infection. (18) However, not all cases of amebiasis in nonendemic areas are related to travel or immigration as several reports have demonstrated. (13,19,20) Patients who are at higher risk of fatal outcomes due to invasive amebiasis include individuals with malnutrition, infants, pregnant and postpartum women, and patients receiving corticosteroids. (4,21)

ALA develop in less than 1% of patients infected with E histolytica, but this still represents a large number of patients. (22) One study from a single hospital in Vietnam identified more than 1,200 cases of ALA during an 8-year period. (23) The epidemiology of ALA is similar to that of amebiasis in general, except that it may occur in short-term travelers (24) and that men aged 18 to 50 are disproportionately affected, typically reported as a ratio of males to females of approximately 10:1. (3,25,26) In our review of more than 8,800 cases of ALA, we found that males accounted for 86% of cases of ALA, as demonstrated in Table 1. The underlying reason for the huge gender difference is not clear, but several theories have been postulated: heavy alcohol consumption in men, (20) hormonal effects in premenopausal women that may modulate infection, (49) and a possible protective effect of iron deficiency anemia among menstruating women. (51)


E histolytica is transmitted via the fecal-oral route and is generally acquired by the ingestion of contaminated food and water containing the infective cysts. Venereal transmission through oral-anal contact is also of concern. (17) The infective cyst contains four nuclei, measures 9 to 25 [micro]m in diameter, and is resistant to gastric secretions and other gastrointestinal enzymes. Excystation occurs in the small bowel, where a total of eight trophozoites are formed by nuclear and cytoplasmic division. Trophozoites localize in the colon, are 10 to 20 [micro]m in diameter, and are very sensitive to gastric acidity; they undergo rapid degeneration outside the body (Fig. 1). To complete the cycle, trophozoites encyst into mononucleate cysts that undergo two consecutive nuclear divisions to produce the infecting tetranucleate cyst that is then shed in the feces by "healthy" hosts or convalescent patients. (55) The cysts remain infective for up to 8 days in temperatures ranging from 28 to 34[degrees]C, or up to 30 days at temperatures of 10[degrees]C. Cysts are resistant to chlorine but are susceptible to iodine, acetic acid, or temperatures above 68[degrees]C, and can be removed by using sand filtration. (56)

Trophozoites infest the large intestine, where they actively feed on bacteria and fecal material. Invasive disease occurs when they penetrate the colonic mucosal barrier. The adhesion of trophozoites to the colonic wall seems to be mediated by the parasite cell surface galactose/N-acetylgalactosamine (GalNAc) lectin. (57-59) This lectin is a complex heterodimer comprising a 170-kDa subunit joined to a 35/31-kDa subunit via a disulfide bond and is associated with another 150-kDa protein. (60,61) After successfully adhering to the colonic mucosa, the next step is invasion. Invasion occurs through a series of mechanisms that are incompletely understood but seem to involve a family of small peptides termed amebapores, which have the capacity to puncture lipid bilayers, disrupt the barrier function of the mucosal epithelium, and form a portal of entry into the host. (62) Trophozoites also kill host cells by inducing apoptosis, (63,64) thought to be due in part to the activity of caspases, particularly caspase 3, although the initiating signal is unknown. (61) Apoptosis seems to be quickly followed by phagocytosis of the dying cells, which is believed to limit inflammation and thus limit the host response. (65) The cellular destruction created by this sequence of events classically extends into the submucosa and then propagates laterally, forming a flask-shaped ulceration. (1)


Hepatic infection results from trophozoites entering the portal venous system, or rarely by direct extension, but lymphatic spread is not thought to occur. (66,67) Hepatic infection occurs most commonly in the right hepatic lobe, presumably because this area receives most of the blood draining the cecum and ascending colon. (68) In the current review, isolated left lobe abscesses were seen in approximately 15% of cases, whereas right and left lobes were involved in 12% of cases, as shown in Table 1. Experimental animal studies demonstrate the dilation of hepatic sinusoids containing amebae surrounded by polymorphonuclear leukocytes (PMNs) within 3 hours after embolization of trophozoites into the mesenteric-splanchnic circulation. Twenty-four hours later, a large number of lysed PMNs are seen with adjacent hepatocyte necrosis. Seven days later extensive necrosis is seen, with minimal inflammation. (69) In vivo and in vitro animal studies have demonstrated that these PMNs have a role both in the formation of ALA and in host defense. Lysis of the PMNs is thought to release cytotoxic mediators that further extend the cellular damage beyond that which is immediately adjacent to the trophozoites. (69,70) In murine models, PMNs are an important part of host defense, (71,72) and this may be related to the production of interferon-[gamma] and inducible nitric oxide synthase. (73) In humans, ALA may initially develop as microabscesses that coalesce into a single lesion, with a variable size ranging from less than 1 cm to giant lesions that may replace up to 90% of the organ. (67,74) The abscess in humans is comprised of a core of dead hepatocytes and cellular debris with a surrounding rim containing connective tissue, trophozoites, and inflammatory cells. (1)

Host Immunity

Serum antiamebic antibodies to E histolytica appear in patients who develop invasive amebiasis. Studies performed in Mexico (75) and India (76) suggest that the presence of antibodies is associated with a lower rate of developing invasive disease, whereas more recent studies demonstrate that reinfection may occur at rates similar to the background population. (23) In patients with ALA, antibodies develop by the seventh day into the illness and may persist for as long as 10 years. (77) These IgA antibodies are directed at the GalNAc lectin and demonstrate in vitro evidence of the inhibition of adherence to the colonic epithelium. The development of these antibodies does not seem to halt the progression of disease. (78) Antiamebic secretory IgA have been described in saliva, serum, breast milk, and feces of patients with invasive amebiasis. (79-82) In a study in Bangladesh, mucosal IgA antibodies in children were associated with a short-lived acquired resistance to E histolytica infection. (11,83,84)

Innate resistance has been shown in children who lack serum antiparasite IgG. (11) Although this seems counterintuitive, similar findings have been demonstrated in other infectious diseases including leishmaniasis and leprosy; a suggested similarity among the diseases is a protective proinflammatory T helper 1 (Th1) cytokine response among asymptomatic patients. (11) Another recent study showed that asymptomatic patients infected with E histolytica had higher serum levels of interferon-[gamma], a cytokine related to the Th1 profile. (85) The same study demonstrated significantly higher levels of interleukin 4 associated with a Th2 cytokine profile among patients with invasive amebiasis. (85) These findings may partially explain why, although ALA occurs in patients with AIDS, (86,87) the incidence is not necessarily increased in patients with AIDS.

Cell-mediated immunity is also of importance in the host response to E histolytica infection. Macrophages exhibit cytotoxicity through nitric oxide and through cofactors hydrogen peroxide ([H.sub.2][O.sub.2]) and superoxide ([O.sub.2.sup.-]). (88) Recently, a patient was described with a dysfunction in the production of reactive oxygen intermediates, and who has had three episodes of ALA within a 4-year period, underscoring the role of macrophages in host defense. (89) T lymphocytes isolated from animals immunized with amebic lysates and from patients with invasive disease develop a proliferative response and kill trophozoites in vitro. (90,91) Lymphokine production is associated with enhanced macrophage and neutrophil killing of amebae. (92) However, depressed T-cell activity has been observed during acute amebiasis, possibly secondary to a parasite-induced factor. (93)

Clinical Manifestations

ALA usually presents with high fever, chills, and right upper quadrant abdominal pain of less than 10 days' origin. In nonendemic regions such as the United States, patients usually report travel to an endemic area in the last 2 to 5 months, with a median of 3 months. Ninety-five percent of these patients will present within 5 months, although much longer lags in time (up to 12 yr) have been reported. (94) Table 2 lists the results of our review of the literature and the frequency with which we found various signs and symptoms. By far the most common clinical manifestations, abdominal pain was reported in 92% of patients and fever in 90% of patients. Pain may radiate to the shoulder, subscapular area, or epigastrium (more commonly in abscesses involving the left lobe) and may have a pleuritic quality on deep inspiration. Anorexia and weight loss were reported in 47% and 39% of the patients, respectively. A recent history of diarrhea is reported in 23% of the patients. Interestingly, a history of moderate-to-heavy alcohol consumption was obtained in 40% of the 750 patients for which that information was available. The level of consumption is not listed or clearly defined in most of the studies, but this does suggest that it may predispose patients to ALA. The average duration of symptoms in the review of cases seemed to be longer in the early studies, typically reported as months, to less than 2 weeks in most of the more recent studies. A subset of patients will have a subacute and indolent presentation (>2 wk) with fatigue, night sweats, weight loss, and hepatomegaly as the predominant presentation. (34) Lastly, a recent Vietnamese study has suggested that subclinical cases of asymptomatic ALA may occur, further widening the continuum of hepatic amebiasis. (97)

On examination, 78% of patients will have abdominal tenderness and 62% will demonstrate hepatomegaly. Clinical jaundice is present in 22% of the patients, which is higher than typically reported. Even when considering cases published from 1990 to the present, the number is no less. Cullen sign has been described in ALA, even without rupture into the peritoneum. (98) On pulmonary auscultation, rales may be heard over the right lower lobe and signs of a pleural effusion may be present. These signs occur most commonly as a result of atelectasis and a serous pleural effusion, and do not necessarily represent transdiaphragmatic erosion of the abscess with subsequent rupture into the pleural cavity.

Rupture into the peritoneum with resulting peritonitis is seen in 2 to 7% and occurs most often with left-sided abscesses. Other complications include rupture of the abscess into the chest with the development of pleuropulmonary amebiasis in 10 to 20% of cases; of these patients, 50% will have an abnormal chest with elevation of the right hemidiaphragm. (99,100) These patients may present with cough, pleuritic chest pain, and dyspnea. Amebic empyema may develop, and occasionally erosion into a bronchus will be associated with expectoration of brown, thick sputum. (99,101) Abscesses located in the left hepatic lobe may rupture into the pericardium, causing pericarditis or tamponade. (102) Other organs and structures in which ALAs may rupture include the duodenum, colon, bile ducts, portal vein, inferior vena cava, hepatic artery, mediastinum, and retroperitoneal space. (4,74,103-106) Finally, infection may disseminate distally, presumably via hematogenous spread, to include cutaneous and central nervous system infection. (95,107) In extremely rare cases, isolated cutaneous infection has been described. (108)

Laboratory Features

Table 3 lists the laboratory characteristics of the cases reviewed. Leukocytosis was commonly seen with average white blood cell count of 15.6, without eosinophilia. The serum alkaline phosphatase was elevated in 76% of the cases, but typically the serum bilirubin and the aspartate transaminase levels are only minimally elevated. Hypoalbuminemia with an average albumin of 2.8 is also seen. Stool examinations for amebae were found to be poor tests, with only 12% of patients demonstrating evidence of amebic infection. Amebae were more commonly isolated from abscess material (42%), but most of this information is derived from older studies when drainage was more commonplace. Other reports state that trophozoites are found under microscopy in up to 85% of cases, with a much higher percentage reported in endemic regions and with dedicated observation of the aspirated material. (109,110)

Antibodies develop in 90 to 100% of patients with ALA and become detectable at 7 to 10 days after the onset of symptoms. (4,77) The available assays to detect antibodies to E histolytica include indirect hemagglutination, latex agglutination, indirect immunofluorescence, counterimmunoelectrophoresis, gel diffusion, complement fixation, and enzymelinked immunosorbent assay. Indirect hemagglutination and enzyme-linked immunosorbent assay are widely used because of their high sensitivity as demonstrated in a recent study from Kuwait, which reported sensitivities of 99% and 97.9% and specificities of 99.8% and 94.8% respectively. (53) The value of these diagnostic tests in the setting of acute disease in endemic areas is less because they remain positive for many years. (4,94,111,112) To distinguish recent from remote infection, counterimmunoelectrophoresis and gel diffusion are more appropriate because they remain positive for only 6 to 12 months after the onset of infection. (113,114) Newer polymerase chain reaction tests are being used on ALA aspirates and stool samples, and this diagnostic technique will likely become increasingly important in endemic regions to identify acute infections and to differentiate between E histolytica and E dispar. (115,116)

Radiographic Features

Chest Roentgenography. Abnormalities, seen on average in 59% of patients, include an elevated right hemidiaphragm (Fig. 2), atelectasis, and right pleural effusion. (74,99,117,118)

Ultrasonography. Ultrasonography is the preferred imaging technique for the detection of amebic abscess because of its lower cost, noninvasiveness, and availability. It can also guide needle aspiration for diagnostic and therapeutic purposes. The classic ultrasonographic appearance is of a round or oval homogenous hypoechoic lesion with well-defined borders, typically located near the surface of the liver. However, early lesions may be hyperechoic in relation to the surrounding parenchyma when solid necrotic material is present. As the necrosis liquefies, the center of the lesion becomes progressively hypoechoic. (42,74,119) The ability to differentiate sonographically between pyogenic liver abscess and ALA was significant in one blinded study, but clinically it is not believed to be sufficient for diagnosis. (120)

Computed Tomography. Computed tomography (CT) may be more sensitive for smaller lesions, particularly if helical CT is used. Otherwise, it generally does not add further specific information when compared with ultrasonography. On CT imaging, amebic abscesses appear as a hypodense avascular liver mass with well-defined margins and alternating hypodense and hyperdense halos after contrast administration (Fig. 3). Extrahepatic extension of the lesion, when present, may be another indicator that the lesion is amebic in origin. (40,74)

Magnetic Resonance Imaging. Amebic abscess appears as a high-signal intensity on T2-weighted images. The area around the abscess, adjacent to the parenchyma, may appear hyperintense or hypointense, corresponding to areas of edema and hypervascularity interspersed with areas of thrombosis. This modality is very sensitive but lacks specificity because the above changes may be seen in certain tumors and in pyogenic abscesses. Magnetic resonance imaging may have a limited role in patients with renal insufficiency. (121,122)



Scintigraphy. Nuclear scanning with Technetium Tc 99m displays a photopenic area. Gallium scanning may be useful in distinguishing amebic abscess from pyogenic liver abscess in patients with a negative serology or an atypical clinical presentation. Amebic abscesses, as opposed to pyogenic abscesses, do not contain leukocytes within the cavity; therefore, on scanning, ALA appears as a cold spot. (4,68,74) One retrospective study demonstrated 100% sensitivity in scintigraphy and ultrasonography in identifying focal liver lesions in patients with ALA, but further distinguishing between ALA, pyogenic abscess, and malignancy reduced the sensitivity. (123)

Differential Diagnosis

The diagnosis of liver abscess secondary to E histolytica has to be considered in patients with risk factors for developing the disease (eg, those who have recently traveled, immigrants), in those with a history of diarrheal illness or dysentery, and in those with positive amebic serology. The principal clinical entities that have to be distinguished from ALA include pyogenic liver abscess, echinococcal cyst, and hepatic tumors. (124)

Patients with pyogenic liver abscess are more likely to be older, have significant comorbidities such as diabetes, and have a history of recent biliary disease and/or surgery. Clinically they tend to have a more protracted course and severe disease with hepatomegaly; they tend to have more frequent elevations in serum bilirubin, alkaline phosphatase, and transaminases; and they tend to have positive blood cultures. (3) Patients with pyogenic abscesses also are more likely to have multiple lesions on imaging, but multiple lesions occurred in 38% of patients with ALA in this review (Table 1), and as many as nine distinct lesions have been reported. (125) Patients with ALA usually have positive serology as outlined above.

Echinococcal lesions are typically asymptomatic and seen more frequently in patients from regions endemic to sheep and, to a lesser degree, cattle herding. Eosinophilia occurs in as many as 40% of patients, and differentiating characteristics on imaging may include the following: calcifications, the presence of "daughter" cysts, and communications with the biliary system, (124,126) although the radiographic appearance is in rare instances misleading. (127)

Malignant hepatic tumors such as hepatoma may rarely present as cystic lesions and should be considered in cirrhotic patients and in patients emigrating from the Far East, where hepatomas are more common due to the higher incidence of liver flukes and viral hepatitis. Serum [alpha]-fetoprotein levels may be elevated, and further differentiation can be accomplished with the use of imaging techniques such as ultrasonography and "three-phase" CT, in which the hepatoma enhances during the arterial phase of contrast administration. (126,128) Metastatic lesions should be considered in the appropriate clinical setting.


The mainstay of therapy is metronidazole, which is effective in eliminating the intestinal and extraintestinal infection. (22,129) The standard dose is 750 mg orally three times daily, or 500 mg intravenously every 6 hours for 7 to 10 days, with oral administration being the preferred route. Table 4 demonstrates the current recommendation for therapy. (130,131) A shorter duration of therapy has been shown to be efficacious with metronidazole, and other nitroimidazoles such as tinidazole or ornidazole are effective; however, the latter agents are not available in the United States. (132) After treatment with metronidazole, patients should be given a course of another agent to treat the luminal carrier state that occurs in 40 to 60% of patients. This can be accomplished by treatment with either iodoquinol, paromomycin, or diloxanide furoate. (133-135) Some authors have suggested that critically ill patients or patients not responding to metronidazole receive emetine or chloroquine in addition to metronidazole, but these drugs have a high incidence of side effects and their use should be limited to special circumstances. (4,24,109) Pharmacologic therapy alone is adequate in more than 85% of cases. (54,68) No documented resistance to metronidazole by E histolytica has been observed clinically, but there have been experiments demonstrating resistance related to inducing increased superoxide dismutase activity in vitro. (136,137)

The indications for percutaneous drainage include large ALA in which rupture is believed to be imminent, abscesses in the left hepatic lobe at risk for rupturing into the pericardium, and treatment failure in which fever and pain persist for 3 to 5 days after the initiation of therapy. (52,138,139) It should be noted that even large (>5 cm) uncomplicated ALA typically respond to medical therapy. (54) Surgical drainage has been replaced by percutaneous drainage in most cases; it is rarely performed and should be reserved for those lesions that are large, at high risk of rupture, and not accessible for percutaneous drainage. (17,74) Abscess fluid obtained should be sent for Gram stain and culture to rule out bacterial superinfection, which would require more aggressive drainage techniques. Complications arising from aspiration include bleeding, bacterial superinfection, peritoneal leakage, and injury to adjacent structures. (4,109,138,139)


Clinical response to nitroimidazole therapy is rapid and complete in the majority of cases, and the remainder of patients with ALA usually recover after drainage. ALA usually resolves within 6 months, and serial imaging studies are not necessary for follow-up as long as the patient is responding satisfactorily to therapy. Occasionally there is some variability in radiographic resolution of ALA: in some cases they have been shown to increase in size during the first few weeks of successful therapy, and 10% of patients may still have an abnormal ultrasound at 12 months. (17) Mortality secondary to uncomplicated ALA is generally less than 1%, although it may be higher in developing countries. (4,17,74,140) Overall mortality in this review was 5.9%, which is not appreciably different even when considering reports published only from 1990 to the present (Table 1). One prospective study identified several variables associated with increased mortality:

* bilirubin >3.5 mg/dL

* albumin <2.0 g/dL

* multiple abscesses

* volume of abscess >500 mL

* encephalopathy

In addition, there seemed to be an association between high ethanol intake and mortality in that population. (48) There was another retrospective study that identified diabetes mellitus, dyspnea, and elevated right hemidiaphragm or pleural effusion on chest radiograph as poor prognostic markers. (46)


Instituting public health measures such as health education, adequate sanitation, and a clean water supply are imperative in preventing amebic infection. Boiling can safely disinfect water; however, low-dose iodine and chlorine are ineffective against cysts. It is important that travelers to endemic areas follow enteric precautions and be mindful of contamination of water both from tap sources and bottled sources, and on fresh fruits and vegetables such as lettuce. (17,141) Modifications in sexual practices that involve fecal-oral contact should be stressed to at-risk groups such as male homosexuals. (141) Finally, special attention is needed among institutionalized populations, especially people with mental retardation, to improve hygiene and identify cases of infection early. (142)

Development of an effective vaccine to prevent amebic infection would be a tremendous public health breakthrough, but the availability of a successful vaccine does not seem likely in the near future. Several potential antigen-based vaccines have been tested on animals, including the serine-rich E histolytica protein (SREHP), the E histolytica Gal/GalNAc-specific lectin, the 29-kDa cysteine-rich E histolytica antigen, the amebapore protein, and the cysteine proteinase. (143,144) Of these, the Gal/GalNAc-specific lectin currently seems to hold the most promise, based on animal studies, the fact that intestinal antilectin IgA antibodies confer protection, and the ongoing modification of such vaccines including a DNA vaccine. (145,146)
Table 1. Gender, mortality, and location of abscesses

Variable Average (%) Range (%) Number of Sources (ref. no.)

Male gender 86 69.5-100 8,819 18, 20, 25, 27-44, 46-54
Mortality 5.9 0-33 3,530 25, 31, 33-35, 37-39,
 44, 46-52, 54
 lesions 37.7 15-43 3,347 20, 25, 27, 29, 33-35,
 37, 39, 40, 42-49
 Left lobe 14.6 5-35 3,785 20, 25, 33, 35, 37, 39,
 54, 42-44, 46-49, 52,
 Bilateral 12.4 2.5-38 1,062

Table 2. Clinical signs, symptoms, and laboratory features of ALA (a)

 of cases
 Average Range reviewed (b)

Symptoms and signs
 Weight loss (%) 39 11-83 871
 Anorexia (%) 47 23-89 499
 Abdominal pain (%) 92 73-100 1,701
 Diarrhea (%) 23 12-40 1,426
 Fever (%) 90 72-100 2,192
 Jaundice (%) 22 5-50 1,630
 Hepatomegaly (%) 62 20-100 1,539
 Abdominal tenderness (%) 78 40-100 1,424
Laboratory tests
 Stool cysts/trophozoites (%) 12 4-30 4,908
 Amebae in cyst aspirate (%) 42 30-76 1,402
 Hemoglobin level (g/dL) 12.1 10.2-12.8 229
 Hematocrit (%) 34.7 29.8-37.5 223
 Alkaline phosphatase ([%] 76 65-91 589
 > 120 U/L)
 Total bilirubin (g/dL) 1.4 0.8-2.4 509
 Albumin (g/dL) 2.8 2.3-3.4 404
 Aspartate aminotransferase 1.7 1.0-2.5 459
 (Times upper limit of normal)
 Cholesterol (mg/dL) 149 109-158 128
 Erythrocyte sedimentation rate 91 91 26

(a) ALA, amebic liver abscess.
(b) Sources: 18, 20, 25, 27-30, 32-39, 43-51, 95, 96.

Table 3. Treatment of ALA (a)

Drug Adult dosage Side effects

Metronidazole 750 mg tid X 7-10 days ~10%: headache,
 dizziness, nausea,
 anorexia, vomiting
 <1%: ataxia, seizures,
 peripheral neuropathy,
 reaction with alcohol,
 metallic taste, vaginal
Tinidazole 2 g/d divided tid X 3 days Similar to
 metronidazole, but
 typically better
-followed by-
Iodoquinol 650 mg tid X 20 days Optic neuritis with
 long-term use;
 generally well
Paromomycin 25-35 mg/kg/d divided tid 1-10%: diarrhea,
 X 7 days nausea, vomiting,
 abdominal cramps,
 <1%: headache, vertigo,
 eosinophilia, rash,
 pruritus, ototoxicity
Diloxanide furoate 500 mg tid X 10 days Flatulence, nausea,
 vomiting, pruritus,

(a) ALA, amebic liver abscess.


We are indebted to Dr. Peter G. Pappas for reproduction of CT scans from his personal collection.

Accepted September 12, 2003.

Copyright [c] 2004 by The Southern Medical Association



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* Amebic liver abscess is the most common extraintestinal manifestation of amebiasis.

* Diagnosis is made on the basis of imaging and serologic examination in the proper clinical setting.

* Treatment with metronidazole is usually curative; however, complications do occur.

* Prevention is achieved only through adequate hygiene; there is currently no vaccine.

Christopher D. Wells, MD, and Miguel Arguedas, MD

From the Department of Internal Medicine, and the Division of Gastroenterology and Hepatology, UAB Liver Center, Department of Internal Medicine, University of Alabama at Birmingham, Birmingham, AL.

Reprint requests to Miguel Arguedas, MD, Division of Gastroenterology and Hepatology, UAB Liver Center, Department of Internal Medicine, University of Alabama at Birmingham, MCLM 281, 1530 Third Avenue S., Birmingham, AL 34294-0005. Email:
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Title Annotation:Review Article
Author:Arguedas, Miguel
Publication:Southern Medical Journal
Date:Jul 1, 2004
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