Cases reported "Liver Abscess, Amebic"

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1/9. Gastric perforation of a left lobe amoebic liver abscess.

    liver abscess is the most common extra-intestinal manifestation of invasive amoebiasis. Perforation of the abscess is a potential life-threatening complication. We report a case where perforation into the stomach was successfully managed conservatively. The initial diagnosis in this case was made by gastroscopy and biopsy. To our knowledge, only five cases of gastric perforation of an amoebic liver abscess have been reported in the English literature. In none of these cases was the diagnosis established by histology of gastric biopsy specimens.
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2/9. Defective production of reactive oxygen intermediates (ROI) in a patient with recurrent amebic liver abscess.

    Previously, we reported the case of a man in the fourth decade of life afflicted with three independent episodes of amebic liver abscesses over a period of 4 years. Previous evidence has indicated that the cellular immune response is involved in protection against recurrent invasive amebic infection, and macrophage-mediated effector mechanisms appear important for host resistance to entamoeba histolytica infection. The aim of the present work was to investigate locomotor activity and oxidative burst function of peripheral mononuclear cells of this individual after healing of the third amebic liver abscess. A locomotion assay using Boyden chemotaxis chambers and the respiratory burst evaluated by chemiluminescence were performed in both mononuclear phagocytes (MPs) and polymorphonuclear (PMN) leukocytes. Levels of salivary IgA and serum IgG anti-amebic antibodies were followed during 48 months after the second amebic liver abscess. Results obtained showed a deficiency in MP but not in PMN leukocyte respiratory burst. respiratory burst is a major microbicidal mechanism in MP leukocytes; this also has been considered as a host resistance strategy against E. histolytica. It may be at least one risk factor in our patient that was responsible for recurrence of amebic liver abscess.
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3/9. Missed diagnosis of amoebic liver abscess: a case for forward clinical reasoning.

    BACKGROUND: Increasingly, a wrong diagnosis is made and wrong investigations and treatment ordered, because the doctor uses one or two symptoms to jump into a premature conclusion, without consideration of the totality of a patient's presentation. This is not forward clinical reasoning. Forward clinical reasoning is based on a systematic approach to patient's problems. The objective of this paper is to use a real case to illustrate the pitfall in ignoring forward clinical reasoning and how forward clinical reasoning serves the physician's and patient's interest better. METHOD/RESULT: The case of a 3 year old who had amoebic liver abscess but was wrongly diagnosed and treated for lobar pneumonia with pleural effusion is highlighted. The sequence for forward clinical reasoning is used to show how the right diagnosis could have been arrived at. CONCLUSION: The correct diagnosis following sequential forward clinical reasoning saves time, money and life.
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4/9. Histopathological diagnostics of liver amoebiasis in cambodia.

    Results of histopathological examination of a solitary chronical amoebic abscess in the liver of a patient from cambodia are described. The abscess was at a proliferously reparative phase and entamoeba histolytica was detected at the border between the necrosis and inner wall of abscess, as well as in the proper non-specific granulation tissue of the inner layers of abscess capsule. A differential diagnosis of the amoebic abscess from similar parasitary or pseudoparasitary liver lesions and differential diagnosis of amoebae in histological sections are given. For orientation examinations of the liver tissue for the presence of amoebae the authors recommend the impregnation after Grocott and staining with Goldner's trichrome for a more detailed evaluation of histological sections.
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5/9. Amoebic lung abscesses. A case report.

    A case of multiple amoebic lung abscesses without indication of direct extension from a subclinical liver abscess, which delayed correct diagnosis, is reported. Severe constitutional symptoms, life-threatening haemoptysis and large pulmonary lesions were the prominent clinical manifestations. The response to metronidazole was dramatic. It is postulated that haematogenous spread was responsible. The rarity of this form of amoebiasis is evident on published reports.
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6/9. Amebic liver abscess: 1966-1976.

    A 10-year retrospective analysis of 15 patients with amebic liver abscess is reviewed and represents a continuation of the previous 2-decade experience at our institution (37 patients). Records were studied to determine the population affected, presenting symptoms, physical and laboratory findings, type and response to therapy. Most patients were rural males of lower socioeconomic status in the third to fifth decade of life. They presened as a febrile illness with abdominal pain for an average of 2 1/2 months duration. Significanct physical abnormalities were tender hepatomegaly (93%), right-sided pulmonary changes (40%), and fever (66%). All patients had abnormal liver scan, positive amebic serology, and hypoalbuminemia. All patients promptly responded to amebicidal therapy except one whose therapy was delayed. Clinical suspicion, liver scanning, serologic testing, and response to therapy are the keys to diagnosis.
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7/9. Sonography in the diagnosis and management of hepatic amebic abscess in children.

    Hepatic amebic abscess is a potentially fatal infection which is difficult to diagnose in children. Sonography is an ideal non-invasive imaging tool which can prove invaluable in the diagnosis and management of hepatic amebic abscess. Sonographic findings should suggest the correct diagnosis in most instances. This allows prompt initiation of therapy, forestalling life-threatening complications. Sonography is also an extremely useful non-invasive means of following response to therapy in children with hepatic amebic abscesses.
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8/9. Fulminant amebiasis: a clinical evaluation.

    Two patients with fulminant amebic colitis with colon perforation and concomitant liver abscess were collected over the last 5 years. One patient underwent emergency laparotomy to treat amebic cecal perforation. Diverted ileostomy saved his life. The ileostomy was successfully reversed 6 months later. The other patient underwent 4 laparotomies with more invasive procedures in less than 1 month due to sequential complications of amebiasis. colon resection with enterostomy miraculously allowed him to survive. In comparison with the latter, who underwent more aggressive surgery and experienced more catastrophic complications, the former with conservative surgery had a smoother clinical result. Thus, conservative operation for colon perforation due to amebiasis is recommended. Besides, thanks to the alertness of doctors, the favorable age of the patients, the advent of new antiamebic and antimicrobial agents, excellent hyperalimentation, the great improvement in medical facilities and postoperative care, the two critical patients eventually survived after several operations, and had a better outcome as compared with the high mortality rate of 87.5% in our hospital 2 decades earlier.
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9/9. Amebic liver abscess in infancy: case report and review.

    Amebic liver abscess (ALA) is uncommon in the united states and is potentially lethal when acquired during the first year of life. The clinical course of ALA in a 10-month-old infant is presented and the characteristics of 18 previously described cases of infants with ALA from the united states are reported; this infant population (including our patient) is compared with a population of adults with ALA. In contrast to the initial signs in adults, those in infants are nonspecific and include fever, hepatomegaly, anemia, and elevated levels of transaminases. colitis may occur in infants, but results of examinations for ova or parasites are usually negative. On presentation the amebic serology for one-third of infants with ALA is negative. The clinical course of ALA in infants is usually fulminant and is associated with a mortality rate of nearly 50%.
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