SciELO - Scientific Electronic Library Online

 
vol.96 número5 índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Revista Española de Enfermedades Digestivas

versión impresa ISSN 1130-0108

Rev. esp. enferm. dig. v.96 n.5 Madrid mayo 2004

 

CLINICOPATHOLOGICAL CONFERENCE


Fever, pain in right hypochondrium and liver mass with central calcification

A. Cuadrado, J. Crespo, J. Cabriada and F. Pons-Romero

General Surgery Department. Hospital Universitario Marqués de Valdecilla. Santander, Spain


Cuadrado A, Crespo J, Cabriada J, Pons-Romero F. Fever, pain in right hypochondrium and liver mass with central calcification. Rev Esp Enferm Dig 2004; 96: 331-343.


Recibido: 10-11-03.
Aceptado: 24-11-03.

Correspondencia: Fernando Pons Romero. Servicio de Aparato Digestivo. Hospital Universitario Marqués de Valdecilla. Avenida de Valdecilla, s/n. 39008 Santander.


Closed clinical case. Clinicopathological conference. Departments of Gastroenterology of Hospital Universitario Marqués de Valdecilla (Santander), Hospital Universitario de Basurto (Bilbao), and Hospital Universitario de Galdácano (Galdácano, Biscay).

 

CASE REPORT

A 59-year-old woman presents with a 2-month standing episode of dull, sustained pain in the right hypochondrium that bears no relation to food ingestion or movement, in association with a 4 kg weight loss; pain severity had increased four days before admission, which was associated with (evening) fever of up to 38.5 ºC. Her epidemiological and family history was unremarkable, and no toxic habits were present. A mild hypercholesterolemia that had been diagnosed three years earlier and was under control using dietary management was the only remarkable item in her medical history, and the patient was on no medication on admission. History taking unveiled no other symptoms. Physical examination revealed a blood pressure of 120/80 mm/Hg, a heart rate of 80 bpm, and an axillary temperature of 36.6 ºC. There was mild skin pallor and slight malaise, and no adenopathies were found on palpation. The examination of the cardiovascular, respiratory, neurologic, and musculoskeletal systems was normal; only the abdominal exploration yielded positive findings: tenderness in the right hypochondrium with no peritoneal signs, and tender, smooth-edge, right-lobe hepatomegaly at 5 cm below the costal margin with no bruits.

The following laboratory parameters were of note: erythrocyte sedimentation rate (ESR), 57 mm/h; red-bood cells count, 3.78 x 1012/L; hemoglobin, 11.5 g/dL; hematocrit, 35.4%; mean corpuscular volume, 80 fl; serum iron, 13 µg/dL; ferritin, 47 ng/mL; transferrin saturation ratio, 6%. Total and differential white-cell count, platelet count, and prothombin activity were normal. The patient had mildly altered liver function tests: AST, 58 U/L; ALT, 44 U/L; GGT, 78 U/L, and alkaline phosphatase, 157 U/L, with normal glucemia, creatinine, BUN, uric acid, sodium, potassium, total calcium, total bilirubin, lactate dehydrogenase, cholesterol, ceruloplasmin, alpha-1 antitrypsin, triglycerides, and total protein values. Urine sediment was normal, as were a posteroanterior chest radiograph and electrocardiogram (ECG). Hepatitis B virus surface antigen as well as hepatitis A and C antibodies and human immunodeficiency virus antibody were negative. Serology tests for hydatidosis, amebiasis, syphilis and cytomegalovirus were negative, and serial hemocultures were sterile. Circulating antibodies (anti-smooth muscle, antimitochondrial, antinuclear) were negative, and alpha-fetoprotein, carcinoembryonic antigen (CEA), and CA 19.9 concentrations were also normal.

Abdominal ultrasonography revealed a solid hypoechoic lesion with central calcification in the right hepatic lobe (7 cm in greater diameter). Computerized tomography (CT) scans confirmed the findings on sonography. Finally, a fine-needle aspiration biopsy (FNAB) was performed, which revealed a predominantly mononuclear infiltrate with isolated plasma cells and fibroblasts, as well as calcium deposits. No microorganisms were identified by conventional culture from samples sent to the microbiology laboratory.

A diagnostic exploration was performed.

DIFFERENTIAL DIAGNOSIS

Dr. Antonio Cuadrado. In summary, this is about a 59-year-old woman with an unremarkable medical history who presents with a subacute episode consisting of pain in the right hypochondrium and fever, in association with dissociated cholestasis. Imaging techniques reveal the presence of a lesion within the right hepatic lobe. In view of these data, we considered a differential diagnosis of liver masses in the setting of a patient with a chronic-subacute episode in which the finding of a central calcification on ultrasonography/CT may be considered a "guiding" sign. In this sense, radiographic findings should be reviewed before going any further.

Dr. Carlos Juanco. Abdominal ultrasounds revealed a solid hypoechoic lesion exhibiting a hyperechoic central area with posterior acoustic shadowing, which was located within the right hepatic lobe and was 7 cm in greater diameter. Echographic characteristics suggested a centrally calcified solid mass, and the remaining parenchyma was normal. CT showed a hypointense heterogeneous lesion with central calcification. Absence of hypervascularization in the involved area, presence of unaffected adjacent parenchyma, and central calcification should all be emphasized.

Dr. Antonio Cuadrado. In this context, the differential diagnosis of a liver mass must include primary benign and malignant tumors, metastatic tumors, lymphomas, pseudotumoral lesions, and non-tumoral lesions. The solid character of the lesion excludes a cystic nature. On the other hand, liver calcifications are relatively uncommon and may result from both benign and malignant tumors, as well as inflammatory and infectious conditions. So, more than 100 potential causes of calcification exist, and most of them are rare or exceptional. All this further complicates differential diagnosis. Tables I-III list conditions included in the differential diagnosis of liver masses, with a particular emphasis in those where calcium deposition has been described.


In the presence of a case just as this one is, where a liver mass and a general syndrome stand out, a diagnosis that must be ruled out is that of a tumor. Detecting any underlying liver conditions would be most relevant here, since in the presence of an already established chronic hepatopathy or cirrhosis hepatocellular carcinoma (HCC) is the most commonly diagnosed malignancy. This diagnosis is highly unlikely in our case, as neither the patient's medical history nor the absence of clinical or laboratory disturbances support it. On the other hand, the possibility that an HCC will develop in a non-cirrhotic liver is extremely low in our setting. However, fibrolamellar hepatocellular carcinoma, a variant of HCC that usually develops in non-cirrhotic livers, may present as an abdominal mass that is sometimes painful and may include (central) calcifications in one third of patients (1,2); furthermore, this tumor may develop secondary infection, which results in episodical fever as is the case with our patient (3). Anyway, this is a relatively rare (6-25% of all HCCs) tumor that develops in younger, usually female patients in their 20s-40s (in contrast with our patient), with histologic characteristics that are not consistent with those revealed by FNAB. Other primary malignancies to be considered include peripheral cholangiocarcinoma, angiosarcoma and primary lymphoma of the liver. The former is a glandular tumor arising in intrahepatic bile ducts that commonly associates with alpha-1 antitrypsin deficiency, congenital liver fibrosis, Caroli's disease, sclerosing cholangitis, thorium dioxide (Thorotrast) exposure, or Clonorchis sinensis infestation; it affects older adults and commonly presents with prominent jaundice (4). None of these characteristics occur in our patient, which excludes this diagnosis with great probability. Similarly, a diagnosis of angiosarcoma or malignant hemangioendothelioma, the most common mesenchymal malignancy of the liver, may be reasonably ruled out; the latter is a highly malignant, extremely rare hypervascular tumor that develops in advanced old age and is associated with exposure to Thorotrast, arsenic, polyvinyl chloride or anabolic steroids; in addition, it may be a complication of neurofibromatosis (1,3). An absence of consistent epidemiologic factors, progressive liver failure with jaundice, increased malaise, and consistent radiographic (most commonly multiple defects) or pathologic data rules out this diagnosis. On the other hand, primary liver lymphoma, an unusual, predominantly B-cell variant of lymphoma, may mimic a liver abscess, and patients with a liver mass, pain and episodic fever have been reported as having hypodense images on CT (3,5). Primary non-Hodgkin lymphoma of the liver is an uncommon, nearly always aggressive neoplasm that is usually seen on CT scans as multiple low-density lesions (6). On the other hand, primary liver involvement in Hodgkin's disease is an uncommon event that usually exhibits an infiltrating pattern with multiple (occasionally single) well-defined, big-sized, low-density lesions, in contrast with the findings in our patient (6,7). Other malignant tumors are readily excluded because of a variety of reasons: epithelioid hemangioendothelioma (rare mesenchymal tumor that usually manifests as a multinodular lesion involving the whole liver in a diffuse way), hepatoblastoma (exceptional following the third year of life, with elevated alpha fetoprotein in 90% of patients), non-differentiated sarcoma (extremely rare, usually in children, very aggressive, survival below 2 months, characteristic histology) (4,8). Hepatic metastases are the most common malignancies involving the liver, and they have a 30-fold increased frequency versus primary tumors. Gastric, colonic and pancreatic adenocarcinomas represent more than 40% of liver metastatic disease cases, and colorectal cancer is the most common cause of liver metastasis (2,6). A pattern of dissociated cholestasis, as in this case, may be consistent with metastatic disease; on the other hand, calcifications may develop in, say, colon, breast, thyroid and bronchopulmonary tumors (4). However, a lack of suspicion of an extrahepatic primary neoplasm, the presence of a single lesion instead of a multiple one, and the finding of a hypoechoic lesion on ultrasounds exclude this option (1,3).

When examining a solid nodule in a patient with no liver disease or neoplasm, its differential diagnosis must include benign liver tumors and other pseudotumoral lesions (9). Solid nodules are more common in young women, and the lesion is usually benign when no underlying liver disease is present. Hemangiomas are the most common bening focal lesion of the liver, and may be seen in up to 4-7% of adult patients (2,9). Liver function tests are normal, and they result in symptoms only very rarely, except for local complications; on the other hand, ultrasonography reveals a homogeneous hyperechogenic mass with mild posterior acoustic shadowing, and CT scans show a globular, contrast-filled hypodense mass extending from the periphery towards the center (2). None of these features is consistent with those reported for our patient. Focal nodular hyperplasia is an uncommon lesion that develops between the third and fifth decades of life, with a higher frequency in women; even extensive lesions are always virtually asymptomatic, as they never undergo necrosis, bleeding or spontaneous rupture (10). No characteristic lesions are revealed by CT scans or ultrasounds, although central scarring is common. Hepatic adenoma is a rare lesion that mainly affects women of childbearing age, and it only develops in high-risk groups (women on contraceptives, and exceptionally men on anabolic agents or patients with glycogen storage disease) (9).

Other benign pseudotumoral lesions include, for example, nodular regenerative hyperplasia, a condition that is seen relatively often in autopsies, and which is characterized by diffusely spread nodules in the liver with no fibrotic component; in 80% of patients this is associated with another disease, most commonly rheumatoid arthritis or Felty's syndrome, but also hyperviscosity, myeloproliferative disorders in transplanted livers or in response to drugs, particularly anabolic steroids and cytotoxic agents (11). Inflammatory pseudotumor is a rare condition that may be mistaken for a tumor. It develops particularly in young males, who present with intermittent fever, abdominal pain, jaundice, vomiting and diarrhea. In approximately 50% of patients leukocytosis, increased ESR, and polyclonal hyperglobulinemia develop. Given the aforementioned epidemiologic characteristics both conditions may be safely excluded.

Vascular disorders such as hematoma, portal thrombosis or hepatic artery aneurysm may manifest as focal lesions and even become calcified; however, their radiographic recognition is pretty straightforward.

Among non-tumoral origins of liver masses infection is particularly relevant (Table III), with pyogenic abscess as its major representative. Bile duct infection is the most common etiology, and in most cases develops in patients of advanced old age with an underlying bile tract disease. Otherwise their origin is portal, arterial or by contiguity. No primary etiology is unveiled in up to 50% of cases (12). Clinically, infection usually has an insidious onset consisting of febrile syndrome, malaise and dull pain in the right hypochondrium for weeks or months. Physical examination may reveal tender hepatomegaly; jaundice, ascites, spleno-megaly and other portal hypertension signs are uncommon. Laboratory tests commonly demonstrate anemia, leukocytosis with neutrophilia, increased ESR, and elevated AP and GGT, and less commonly elevated bilirubin and a slight increase in transaminases; blood cultures may identify a causative microorganism in up to 50% of cases. Ultrasonography is the initial diagnostic modality of choice, and may detect lesions as small as 1 cm in diameter (13,14). Aspirates obtained under sonographic control are positive in 90% of cases. Contrast-enhanced CT scans are more sensitive in the detection of small abscesses, extrahepatic collections, air, and calcifications (15). Liver abscesses usually appear as hypodense structures on CT, and may have a contrast-filled halo in up to 20% of patients (12). The clinical-laboratory-radiographic picture of our patient is consistent with that of a liver abscess, with no hints of a primary cause and negative microbiology for both ultrasound-guided aspirates and blood cultures; furthermore, the central calcification suggests an old disease (16). All this indicates the possibility of an abscess by an uncommon agent.

Both in miliary tuberculosis (more commonly) and biliary tuberculosis, the liver may become affected by this pathogen. Similarly, localized forms have been described (17). The former condition is part of a generalized disease, and results from mycobacterial dissemination in the blood through the hepatic artery. It may difussely involve the liver, or this organ may develop focal lesions in the form of tubercles and abscesses. It usually progresses with no symptoms and is difficult to diagnose (17). In its local form, the liver is the only organ that becomes affected in the body, and the prevelence of this is small in clinical practice. It may manifest as single or multiple nodules by the name of tuberculomas or as a hepatic tuberculous abscess. Abscesses result from caseous degeneration in tuberculomas, and harbor abundant acid- and alcohol-fast bacilli inside. Calcification may occur in tuberculomas. Hepatobiliary forms are least common. Clinically they manifest as pain in the right hypochondrium, fever and a constitutional syndrome, and cholangitis episodes may develop. Painful hepatomegaly and dissociated cholestasis stand out, with highly increased alkaline phosphatase levels. Diagnosis is difficult; a biopsy sample is essential for a histologic and microbiologic study of the lesion, and both conventional blood culture and polymerase chain reaction are needed. Tuberculin testing was not carried out in our case, but this is merely a marker for infection, not active disease. Although our clinical and radiographic data are consistent with those of a tuberculous abscess, we believe this is not the case with this patient in view of its low frequency and the following facts: absence of data suggesting any underlying immunosuppression (negative HIV serology), no history of direct contact with patients suffering from active tuberculosis, absence of extrahepatic involvement, unremarkable histology, and negative culture.

The liver is involved in all forms of syphilis, a condition that must be included in the differential diagnosis of obscure liver disease given its increased incidence and varied clinical expressions. Secondary syphilis includes hepatitis in 1 to 50% of patients, and miliary granulomas develop in parallel with a maculopapular rash of the palms and soles; generalized lymphadenopathies also develop in almost all patients. Gumma may be single or multiple, and usually develop in the right lobe; these are the characteristic lesions of liver involvement in tertiary syphilis. This rare condition usually entails no symptoms and is associated with positive serology; histologic involvement includes aseptic necrosis, granulomas and spirochetes (13); hence syphilis is ruled out as a diagnosis.

Amebic abscess results from liver parenchymal invasion by Entamoeba histolytica trophozoites from the colon via the portal vein. This diagnosis is suspected in those who have traveled to an endemic area. In comparison to pyogenic abscess, amebic abscess more commonly presents with an acute episode including local pain in the right hypochondrium and fever, which may be intermittent on occasion. Both jaundice and extradigestive symptoms are infrequent. A history of blood-containing diarrhea is described in less than 10% of patients, and a latency of years may come between intestinal infection and liver involvement. Laboratory findings match those discussed for pyogenic abscess, as imaging studies do as well (12). They are more commonly found in the right hepatic lobe near the diaphragm, usually as single lesions. Conventional serologic tests cannot differentiate between acute and chronic infection, and so they must be interpreted within their clinical context, since they may stay abnormally high for years following recovery or cure (13). However, amebic abscess is unlikely when tests are negative. On the other hand, the chocolate-like looks of the material collected by abscess puncture is characteristic, and the parasite may be often identified therein. The absence of consistent epidemilogic data, negative serology, absence of characteristic aspect, and lack of positive culture reasonably rule out a diagnosis of amebic abscess.

Regarding liver hidatidosis, a zoonosis brought about by the developing larva of Echinococcus granulosus, which is prevalent around the Mediterranean region, this condition may cause fever and nonspecific abdominal discomfort; however, most commonly it manifests as an asymptomatic abdominal mass or liver enlargement found on routine examination (18). Radiography and serology are vital diagnostic tools. In up to one fourth of infected patients plain, radiographs may demonstrate ring-shaped calcifications; the sensitivity and specificity of ultrasonography and CT are high for diagnosis confirmation, and these reveal a cyst-like image that is either simple or has multiple loculations and septa, which correspond to daughter vesicles (2,12). In 30% of patients there is eosinophilia above 7%; regarding serologic tests, both ELISA and indirect hemagglutination may be used in the diagnosis with a sensitivity of 90%, although false negative results may occur (12). Hemagglutination is the most reliable serologic test for diagnosis, with a sensitivity and specificity of 90 and 95%, respectively (19). A negative serology, and absence of epidemiologic data and eosinophilia, as well as non-characteristic radiographs exclude this diagnosis.

Another rare parasitosis that relates to the ingestion of water plants such as water cress, cattle breeding, and trekking is liver fascioliasis, an endemic condition in some areas of Northern Spain (19). Liver granulomas may be seen, but the presence of epidemiologic antecedents, a clinical picture consistent with choledocholithiasis or cholangitis, often marked eosinophilia (it may account for up to 80% of leucocytes), and positive serology and feces or fluid tests help confirm this diagnosis (12).

Infestation by Estrongiloides estercolaris is common in tropical areas and usually asymptomatic; it may become symptomatic depending upon parasite load and host immunosuppression status though (12). Liver involvement manifests as jaundice and cholestatic disturbances, and diagnosis is based on larvae identification in feces or intestinal biopsy samples, although serologic tests are also available.

Fungal infections of the liver may present with fever, altered liver function tests, and radiographic images resembling those encountered in the present case; however, they occur in immunocompromised patients, which is not the case with our patients.

Liver involvement by brucellosis is common and develops in 50% of patients, given the affinity of Brucella for the reticuloendothelial system. A self-limited increase in tran-saminases commonly develops in the acute stage, its histologic substrate being a nonspecific, reactive granulomatous hepatitis (20). Necrosis and suppuration in the form of single or multiple liver abscesses (brucellomas or pseudotumoral necrotizing granulomas) has been rarely described with an incidence of 0.2%, and 40 cases have been included in the literature from 1904 to 2002, many of them in Spain. In such cases of brucellosis, liver involvement is rarely the presentation form, as it commonly remains latent and becomes a feature of the chronic disease (21). In a review of 14 cases of brucellar abscess, fever was the most common symptom and affected almost all patients (22); this fever was variable in duration (between 5 days and 5 months), was most commonly associated with profuse sweating without chills or shivering, and did not subside using conventional antipyretics and antibiotics (22). In this series two thirds of patients had prolonged, overall insidious pain in the right hypochondrium. Other symptoms included asthenia, anorexia and weight loss in up to 67% of patients (16). Hepatomegaly develops in 67% of patients. From the laboratory standpoint, most significant disturbances include increased ERG with values above 100 in 50% of cases, and normocytic, normochromic anemia in half of the patients, with no leukocytosis or leukopenia, and a normal or slightly neutrophilic differential count (22). As regards liver function tests, the most commonly described disturbance is an increase in cholestasis-dependent enzymes with values 4- to 5-fold above normality in 50% of cases, generally with no increased bilirubin or transaminases. Ultrasonography and CT images are characteristic. They show a pseudotumoral, most commonly single, hypoechoic, hypodense, heterogeneous lesion with one or more calcium deposits in its center (21). CT findings most commonly depict a hypodense area, and often one or more saccular, loculated forms, a heterogeneous mass, and 1 or more calcifications (21). The presence of central calcification(s) is a very common finding, particularly in long-staying involvement, which should alert on the possibility of an abscess by Brucella (22). Finally, the diagnosis is based in most cases on compatible clinical and radiographic manifestations, and positive Brucella serology, since organism cultures are uncommon in prolonged cases (22). In view of the aforementioned clinical and radiographic findings, we believe that Brucella serology is the diagnostic test of choice.

Diagnosis by Dr. Antonio Cuadrado: calcified brucellar abscess (brucelloma).

Clinical diagnosis: brucellar hepatic abscess.

Diagnostic test: serum agglutination tests for the detection of Brucella were performed, as well as Coombs' test for Brucella mellitensis and Rose Bengal stain. Agglutination tests were positive at 1:160, Coombs' test was positive at 1:1280, and Rose Bengal was also positive.

DISCUSSION

A pathologist from "Hospital Universitario de Galdácano". Brucellar abscess pathology is characterized by the presence of granulomas with a caseous necrotic center and a perinecrotic ring of epithelioid cells, together with a predominantly mononuclear infiltrate including lymphocytes, plasma cells, and giant multinucleated cells, as well as fibroblasts and fibrous tissue (22). A single major calcification or multiple small confluent calcifications have been described in up to 71% of patients, and the presence of calcifications has been associated with prolonged disease. Our case report is consistent with some of the discussed characteristics, as is the case with the mononuclear infiltrate and calcium deposition. Possibly, the collected sample was not significant enough to include more florid changes (i. e., granulomas).

Dr. Fernando Pons. What is the role played by microbiologic and serologic diagnostic modalities in the diagnosis of this condition? And what about radiography? In summary, what is diagnosis based upon?

Dr. J. Cabriada. Diagnosis is reached in most cases based on clinical and radiographic manifestations, and on positive Brucella serology, since cultures are uncommon in prolonged cases (21,22). However, these organisms grow slowly and may be usually detected between the second and third incubation weeks, and this is why cultures must be kept for some 6 weeks before being deemed sterile. Classically, cultures in a biphasic (Ruiz-Castañeda) or biphasic modified medium have been recommended (23). Using these techniques, cultures become positive in 7 to 21 days on average, but they may take up to 35 days. Biphasic media, however, are not routinely used by laboratories, many of which rely on automated culture systems. This is why suspected brucellosis should be reported to laboratories, so that they may keep cultures in appropriate media for an adequate period of time. On the other hand, the frequency of positive blood cultures decreases in prolonged, insidious cases (24). Most serologic studies in the diagnosis of brucellosis are based on the antibody detection; test tube hemagglutination, complement fixation, Rose Bengal or fast agglutination, anti-Brucella Coomb's test, and ELISA stand out (23). The most widely used test is serum agglutination, which exhibits a good correlation with Rose Bengal. Overall, a single titer > 1:160 in the presence of compatible disease is thought to support this diagnosis (23). The use of Coombs' test is a relevant supplementary contribution to serum agglutination, and a systematic approach with both tests is recommended. A titer equal to or greater than 1/160 is usually significant. If both tests are properly performed and yield negative results, the disease may be almost safely ruled out (24). Quantifying anti-Brucella Igs is possible using ELISA, and this provides a much greater insight into antibody development all along the disease. IgA, IgG and IgM all have a good correlation with serum agglutination, and IgM is most deeply involved during the initial months (24). In contrast with IgM, other Ig titers remain high for a long time, particularly IgG titers, which remain positive for 2-3 years on average. An increase in IgG and to a lesser extent IgA may be identified using ELISA and Coombs' testing, or serum agglutination in one fourth of case, when relapse occurs. Prolonged high serologic titers call for careful assessment. In many cases they are associated with an initial serolo-gic titer above normal that has slowly decreased, or corresponds to a specific localization (24). ELISA has been recently used to quantify anti-cytoplasmic protein antibodies, which seemingly correlate to infection activity. Serologic studies (Rose Bengal, agglutinations, complement fixation, and Coombs' test) yield positive results in almost all patients with brucellar abscess, and these tests become later positive in initially negative cases (22). In the series by Sadia Pérez et al. (2001), titers in correctly followed patients fell in parallel with definite clinical recovery, which was attained using an exclusively drug-based or interventionist therapy (drainage or surgery).

Dr. Carlos Juanco. Regarding radiographic findings, some series have reported usually single, irregular calcifications in the right hypochondrium on plain abdomen x-rays from up to 60% of patients (22). Radiographically, Brucella-induced liver abscesses are usually hypodense single masses with heterogeneous contents and irregular borders in the right hepatic lobe that exhibit single gross calcifications in both sonographic images and CT scans; their typical sonographic description is that of a centrally-calcified hypoechoic lesion with acoustic shadowing (16,22). In fact, the presence of calcification at the abscess center is a common fact, particularly in prolonged cases; hence, such calcification should alert on the possibility of brucellar abscess (22). In this sense ultrasonography, CT and magnetic resonance imaging provide significant diagnostic information (21). Lesions vary in size (3-10 cm). Occasionally, they are multiple and are associated with splenic abscess or calcification.

Dr. Benito de las Heras. How was the patient treated and followed? Has radiographic follow-up been considered after treatment? Any serologic monitoring?

Dr. J. Cabriada. Conservative therapy was initially administered using two combined antibiotics: doxicillin (100 mg/12 hours) and rifampicin (600 mg/día) for 3 months, a combination used in a number of successful treatments that has been suggested as initial therapy (22). In our patient, the outcome was favorable, and fever as well as general symptoms disappeared in 15 to 30 days. Radiographic follow-up at 6 months after treatment onset demonstrated no abscess and a persistent central calcification, an outcome similar to that described in other series (22). Serologic titers gradually decreased in a significant way.

Dr. Victor Orive. Are there any other therapeutic alternatives?

Dr. Javier Crespo. Optionally, streptomycin could be used instead of rifampicin. Puncture-drainage can also be performed with diagnostic and therapeutic aims. If the patient's outcome does not get any better in a prudential time of, say, 4 to 6 weeks, or if it worsens during treatment, or if symptoms return after therapy is discontinued, abscess evacuation should be considered using either open surgery or puncturing under the guidance of an imaging modality, the latter option being more reasonable as it is less aggressive (22). Anyway, antibiotic therapy should be continued for an undetermined period of time that might well oscillate from 2 to 3 months.

REFERENCES

1. Kew MC. Hepatic tumors and cysts. En: Feldman M, Scharchmidt BF y Sleisenger MH, eds. Gastrointestinal and Liver Disease. Philadelphia: W.B. Saunders; 1998. p. 1364-87.

2. Cacho Acosta G, Lledó Navarro JL, González Martín JA, et al. Protocolo diagnóstico de la lesión ocupante de espacio hepática. Medicine 2000; 8 (12): 644-6.

3. Scully RE, Mark EJ, McNeely W, et al. A 32-year-old woman was admitted to the hospital because of left subcostal pain, bouts of fever, and a mass in the left hepatic lobe. Case records of the Massachusetts General Hospital. N Engl J Med 1996; 334: 176-82.

4. Sherlock S, Dooley J. Malignant liver tumours. En: Sherlock S, Dooley J, eds. Diseases of the liver and biliary system. 11th ed. Oxford: Blackwell Science, 2002. p. 537-61.

5. Wu MS, Lin JT, Yang PM, et al. Hepatic lymphoma mimicking liver abscess: report of a case and review of the literature. J Formos Med Assoc 1993; 92: 263-6.

6. Scully RE, Mark EJ, McNeely WF, et al. A 22-year-old man was admitted to the hospital because of a hepatic mass. Case records of the Massachusetts General Hospital. N Engl J Med 2000; 343: 1553-60.

7. Thiele DL, Eigenbrodt EH. Hepatic manifestations of systemic dis-ease and other disorders of the liver. En: Feldman M, Scharchmidt BF, Sleisenger MH, eds. Gastrointestinal and Liver Disease. Philadelphia: W.B. Saunders, 1998. p. 1388-403.

8. Bruix J, Llovet M, Bru C. Carcinoma hepatocelular y otros tumores hepáticos primarios. En: Berenguer J, Bruguera M, García-Bengoechea M, Rodrigo L, eds. Tratamiento de las enfermedades hepáticas y biliares 2ª ed. Madrid: Elba, 2000. p. 247-55.

9. Xiol X. Estudio del nódulo hepático aislado. Gastroenterología y hepatología continuada 2003; 2 (4).

10. Martín L, Rodríguez C, Correro F. Tumores hepáticos benignos. En: Berenguer J, Bruguera M, García-Bengoechea M, Rodrigo L, eds. Tratamiento de las enfermedades hepáticas y biliares. 2ª ed. Madrid: Elba, 2000. p. 239-45.

11. Sherlock S, Dooley J. Nodules and benign liver lesions. En: Sherlock S, Dooley J, eds. Diseases of the liver and biliary system. 11th ed. Oxford: Blackwell Science, 2002. p. 527-35.

12. Chung RT, Friedman LS. Liver abscess and bacterial, parasitic, fungal, and granulomatous liver disease. En: Feldman M, Scharchmidt BF, Sleisenger MH, eds. Gastrointestinal and Liver Disease. Philadelphia: W.B. Saunders, 1998. p. 1170-88.

13. Sherlock S, Dooley J. The liver in infections. En: Sherlock S, Dooley J, eds. Diseases of the liver and biliary system. 11th ed. Oxford: Blackwell Science, 2002. p. 495-526.

14. Alfonso V, Rayón M. Granulomatosis hepática e infecciones hepáticas no víricas. En: Berenguer J, eds. Gastroenterología y hepatología. 2ª ed. Barcelona: Doyma Libros, 1994. p. 752-7.

15. Saini S. Imaging of the hepatobiliary tract. N Engl J Med 1997; 336 (26): 1889-94.

16. Cosme A, Barrio J, Ojeda E, et al. Sonographic findings in Brucellar hepatic abscess. J Clin Ultrasound 2001; 29 (2): 109-11.

17. Maroto N, Ponce M. Tuberculosis y aparato digestivo. Gastroenterol Hepatol 2003; 26 (1): 34-41.

18. Hidalgo M, Castillo MJ, Eymar JL. Hidatidosis hepática. Abscesos hepáticos. En: Berenguer J, Bruguera M, García-Bengoechea M, Rodrigo L, eds. Tratamiento de las enfermedades hepáticas y biliares. 2ª ed. Madrid: Elba, 2000. p. 301-10.

19. Martin J, Berenguer J. Hidatidosis y fasciolasis hepáticas. En: Berenguer J, ed. Gastroenterología y hepatología. 2ª ed. Barcelona: Doyma Libros, 1994. p. 794-803.

20. Cervantes F, Bruguera M, Carbonell J, et al. Liver disease in brucellosis. A clinical and pathological study of 40 cases. Postgrad Med J 1982; 58: 346-50.

21. Sisteron O, Souci J, Chevallier P, et al. Hepatic abscess caused by Brucella: US, CT and MRI findings. Case report and review of the literature. J Clin Imaging 2002; 26: 414-7.

22. Sadia Pérez D, Cea-Calvo L, Aguado García JM, et al. Absceso hepático por Brucella. Descripción de un caso y revisión de la literatura. Rev Clin Esp 2001: 201: 322-6.

23. Everett ED. Brucellosis. UpToDate, 2001. Disponible en: www.uptodate.com. (800)998-6374. (781) 237-4788.

24. Ariza J. Brucelosis. En: Farreras P, Rozman C, ed. Medicina Interna. 14ª ed. Madrid: Harcourt, 2000. p. 2610-5.