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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Low socioeconomic conditions, malnutrition, chronic alcoholism, and ASD with left to right shunt are contributing factors to the development of pulmonary amebiasis. Although no age is exempt, it commonly occurs in patients aged 20 to 40 years, with an adult male to female ratio of 10:1. Children rarely develop thoracic amebiasis: when it does occur there is an equal sex distribution. The infection usually spreads to the lungs by extension of an amebic liver abscess. Infection may pass to the thorax directly from the primary intestinal lesion through hematogenous spread, however. Lymphatic spread is one possible route. Inhalation of dust containing cysts and aspiration of cysts or trophozoites of E histolytica in the lungs are some other hypothetical routes. The lung is the second most common extraintestinal site of amebic involvement after the liver. Usually the lower lobe, and sometimes the middle lobe of the right lung, are affected, but it may affect any lobe of the lungs. The patient develops fever and right upper quadrant pain that is referred to the tip of the right shoulder or in between the scapula. Hemophtysis is common. The diagnosis of thoracic amebiasis is suggested by the combination of an elevated hemidiaphragm (usually right), hepatomegaly, pleural effusion, and involvement of the right lung base in the form of haziness and obliteration of costophrenic and costodiaphragmatic angles. Infection is usually extended to the thorax by perforation of a hepatic abscess through the diaphragm and across an obliterated pleural space, producing pulmonary consolidation, abscesses, or broncho-hepatic fistula. Empyema develops when a liver abscess ruptures into the pleural space. Rarely, a posterior amebic liver abscess can burst into the inferior vena cava and develop an embolism of the inferior vena cava and thromboembolic disease of the lungs with congestive cardiac failure or corpulmonale. Diagnosis by finding E histolytica in stool specimens is of limited value. In a limited number of cases amebae might be found in aspirated pus or expectorated sputum. "Anchovy sauce-like" pus or sputum may be found. Presence of bile in sputum indicates that the pus is of liver origin. Serological tests are of immense value in diagnosis. Liver enzymes are usually normal and neutrophilic leucocytosis may or may not be found. ESR is invariably elevated. Anti-amebic antibodies can be detected by ELISA, IFAT, and IHA. Amebic antigen can be detected from serum and pus by ELISA. Detection of Entamoeba DNA in pus or sputum may be a sensitive and specific method. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung. A single drug regimen with metronidazole with supportive therapy usually cures patients without residual anomalies. Aspiration of pus from empyema thoracis may be needed for confirmation and therapeutic purposes. The pericardium is usually involved by direct extension from the amebic abscess of the left lobe of the liver, sometimes from the right lobe of the liver, and rarely from the lungs or pleura. An initial accumulation of serous fluid due to reactive pericarditis followed by intrapericardial rupture may develop either (1) acute onset of severe symptoms with chest pain, dyspnea, and cardiac tamponade, shock, and death, or (2) progressive effusion with thoracic cage pain, progressive dyspnea, and fever. Chest radiograph, ultrasound examination, and CT scan usually confirm the presence of a liver abscess in continuity with the pericardium and fluid within the pericardial sac with or without the fistulous tract. Echocardiography may demonstrate fluid in the pericardial cavity. Patients should be cared for in the ICU and ambecides should be started without delay. Pericardiocentesis usually confirms the diagnosis and improves the general condition of the patient. Aspiration of the accumulated fluid should be performed urgently in cardiac tamponade; repeated aspiration may be needed. Surgical drainage should be done if needed. Acanthamoeba, a free-living ameba, may also infect the lungs in the form of pulmonary nodular infiltration and pulmonary edema in association with amebic meningoencephalitis in immunocompromised patients. It usually spreads to the meninges of the brain by way of the blood from its primary lesion in the lung or skin. Early diagnosis and institution of treatment may be life saving for these patients. A literature review shows that HIV/AIDS patients are not prone to infection with E histolytica. It is now clear that there are an increasing number of HIV-seropositive patients among amebic liver abscess patients, however, which suggests that although the incidence of intestinal infection is not high among HIV-seropositive or AIDS patients they are more susceptible to an invasive form of the disease.
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PMID:Thoracic amebiasis. 1209 41

Ultrasonography is the first line imaging investigation in patients with jaundice, right upper quadrant pain, or hepatomegaly. Most patients with jaundice have parenchymal or obstructive jaundice. A 56-year old man was admitted to the Institute of Digestive Diseases, Belgrade, with severe pains in the epigastrium, vomiting, icteric coloration of sclera, white stools and dark urine. The symptoms had developed 5 days after a Billroth II resection. The functional liver test indicated a pronounced cholestasis. Real-time ultrasonography showed in the projection of the pancreas head, a clear bordered unechogenic oval formation, with a size of 40 x 35 mm. This finding indicated a possibility of an afferent loop obstruction, accompanied by consecutive obstructive icterus due to compression on the common bile duct. Ultrasonographic examination was followed by surgical reintervention. With the development of noninvasive imaging, transcutaneous ultrasonography, computed tomography and magnetic resonance imaging, the diagnosis of pancreatic and other cysts in upper abdomen is usually straightforward. The important ultrasonographic characteristic of empty organs, compared to cysts and pseudocyts, is a change in the morphology and size of organs after a specific time interval. Air bubbles in the organs lumen are like mobile reflectors, and they are an important sign in identifying segments of the gastrointestinal tract.
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PMID:Jaundice after Billroth II resection. A case report. 1236 42

Migration of Ascaris lumbricoides into the gallbladder is rare, unlike ascariasis of the bile duct, and, when it does occur, treatment is generally by endoscopic or surgical extraction. We describe a case of the successful treatment of gallbladder ascariasis with conservative therapy. A 44-year-old Korean man was admitted because of nausea and right upper quadrant pain that did not respond to medical control and had worsened 1 day before admission. Abdominal ultrasonography showed a long, linear, moving echogenic structure in the distended lumen of the gallbladder, but no abnormal dilation of the bile duct. Computerized tomography showed a linear soft-tissue density in the dependent portion of the gallbladder. The patient presented with eosinophilia, and abnormal liver function results, but no fever or hepatomegaly. Based on these findings, and presuming a diagnosis of gallbladder ascariasis, we administered antiparasitic medication (albendazole 400 mg/day for 1 day). Seven days later, we obtained one adult female A. lumbricoides from the feces. The symptoms were fully resolved, and no moving structure could be visualized in the gallbladder by ultrasonography. We recommend that initial therapy for gallbladder ascariasis should involve conservative treatment, unless an associated disease is present or a complication arises.
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PMID:Successful elimination of Ascaris lumbricoides from the gallbladder by conservative medical therapy. 1237 53

Amebic liver abscess should be suspected in travelers returning from endemic areas or in immunocompromised patients who present with fever, right upper quadrant pain, hepatomegaly, and a liver lesion on an imaging study. Rapid initiation of therapy without serologic confirmation of infection, if necessary, is important to minimize complications. Metronidazole is given orally or intravenously for 14 days. The drug is generally well tolerated and leads to resolution of symptoms in most patients within 2 to 3 days. It is effective against luminal cysts in only 50% of patients and, therefore, must be followed by a course of treatment with paromomycin (Humatin; Parke-Davis, Morris Plains, NJ) or another luminal antiamebic agent to eradicate the parasite. Image-guided drainage of an amebic liver abscess is indicated in patients who do not respond to antimicrobial therapy or who are at risk of abscess rupture. Surgery is reserved for patients with a ruptured abscess. Although medical therapy is generally successful in the treatment of infection caused by Entamoeba histolytica, the development of potent vaccines will be needed for worldwide eradication of disease attributable to E. histolytica.
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PMID:Amebic Liver Abscess. 1240 81

Amebiasis can be considered the most aggressive disease of the human intestine, responsible in its invasive form for clinical syndromes, ranging from the classic dysentery of acute colitis to extra-intestinal disease, with emphasis on hepatic amebiasis, unsuitably named amebic liver abscess. Found worldwide, with a high incidence in India, tropical regions of Africa, Mexico and other areas of Central America, it has been frequently reported in Amazonia. The trophozoite reaches the liver through the portal system, provoking enzymatic focal necrosis of hepatocytes and multiple micro-abscesses that coalesce to develop a single lesion whose central cavity contains a homogeneous thick liquid, with typically reddish brown and yellow color similar to "anchovy paste". Right upper quadrant pain, fever and hepatomegaly are the predominant symptoms of hepatic amebiasis. Jaundice is reported in cases with multiple lesions or a very large abscess, and it affects the prognosis adversely. Besides chest radiography, ultrasonography and computerized tomography have brought remarkable contributions to the diagnosis of hepatic abscesses. The conclusive diagnosis is made however by the finding of Entamoeba histolytica trophozoites in the pus and by the detection of serum antibodies to the amoeba. During the evolution of hepatic amebiasis, in spite of the availability of highly effective drugs, some important complications may occur with regularity and are a result of local perforation with extension into the pleural and pericardium cavities, causing pulmonary abscesses and purulent pericarditis, respectively The ruptures into the abdominal cavity may lead to subphrenic abscesses and peritonitis. The treatment of hepatic amebiasis is made by medical therapy, with metronidazole as the initial drug, followed by a luminal amebicide. In patients with large abscesses, showing signs of imminent rupture, and especially those who do not respond to medical treatment, a percutaneous drainage must be performed with either ultrasound or computerized tomography guidance. Surgical drainage by laparotomy is reserved to patients with secondary infections.
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PMID:Hepatic amebiasis. 1295 80

A 30-year-old woman presented with hepatomegaly and an audible hepatic bruit at 24 weeks gestation. Non-contrast MRI demonstrated an exophytic 12.6 x 7.8 x 12.8 cm mass arising from the right lobe of the liver with a central scar, suggestive of focal nodular hyperplasia (FNH). Conservative management included monthly abdominal ultrasound examinations until the time of delivery, to assess growth of the mass and monitor for risk of rupture. Seven weeks post partum the patient experienced severe right upper quadrant pain. A CT angiogram of the liver demonstrated a stable mass with no evidence of bleed or rupture and multiple hypervascular masses throughout the liver. Surgical resection of the dominant lesion was performed. Histological examination of the lesion confirmed FNH. The patient is now 22 months post surgery with radiographic evidence of stable multifocal FNH.
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PMID:Symptomatic focal nodular hyperplasia during pregnancy: a case report. 1511 79

Budd-Chiari Syndrome (BCS) refers to hepatic venous outflow obstruction, resulting in simultaneous occurrence of hepatic congestion and portal hypertension, leading to a typical clinical triad consisting of right upper quadrant pain, hepatomegaly and ascites. Contrary to Asia and Africa, where BCS is caused primarily by an obstructing membranous web, BCS in the western world is considered a thrombotic complication of an underlying hypercoagulable state. Recognition of the contribution of hypercoagulability as a causative factor in BCS, has led to acknowledgement of the importance of anti-coagulant therapy in BCS. Indeed, a conservative approach consisting of diuretics and anti-coagulant therapy is considered an appropriate treatment strategy for the BCS patient, in the absence of significant hepatic insult. However, once disease progression is noted, based on clinical symptoms, hepatic laboratory disturbance or histological evidence of irreversible hepatic damage, a definite invasive treatment should be applied. The specific procedure to be used is dependent upon the extent of hepatic insult and the anatomical characteristics of the venous obstruction in any individual patient. In the absence of significant hepatic damage, one may employ surgical shunting or invasive roentgenic measures, such as TransJugular Intrahepatic Porto-Systemic Shunt procedure, for the decompression of the portal system. Alternatively, in cases of a single localized obstruction, one may use balloon angioplasty with stent insertion. In contrast, upon evidence of significant hepatic damage, liver transplantation becomes necessary. To date, numerous studies report excellent results regarding the success of liver transplantation for patients with advanced BCS disease accompanied by significant hepatic damage.
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PMID:[Budd-Chiari syndrome: updated treatment modalities]. 1519 Aug 52

Amoebic liver abscesses are by far the most common extra-intestinal manifestation of invasive amoebiasis. The classical clinical picture consists of fever, right upper quadrant pain and hepatomegaly. Ultrasound and serology make an early diagnosis possible. Amoebic liver abscesses usually appear singly and are normally situated in the right lobe of the liver. This case report refers to a white Belgian woman, living in an endemic area for amoebiasis, presenting with 25 amoebic liver abscesses, who did not improve clinically despite appropriate anti-amoebic therapy, is described. Only percutaneous drainage of the larger abscesses led to clinical recovery. Amoebic abscess aspiration and evacuation under ultrasonographic guidance is of limited risk, but in experienced hands may enhance clinical recovery, particularly in patients with large abscesses not responding to conservative medical treatment. Aspiration of large abscesses (> 5 cm) is rarely necessary but should be considered if there is no clinical improvement after 3 days of nitroimidazole treatment with amoebicides.
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PMID:A case of multiple amoebic liver abscesses: clinical improvement after percutaneous aspiration. 1598 2

Non-alcoholic steatohepatitis (NASH) is one of the most common liver disorders. This is highly prevalent in obese and diabetic subjects. Persons with central obesity are at particular risk. Other clinical predictors are age more than 40-50 years and hyperlipidemias, but none of these factors is invariable for causation of NASH. Other reported associations are, celiac disease, Wilson's Disease and few other metabolic diseases. Drugs, particularly amiodarone, tamoxifen, nucleoside analogues and methotrxate have also been linked to NASH. The disease is evenly distributed in both sexes but advanced disease is more common in women. Ethnic variation exists and African Americans are less affected than Hispanic Americans. Specific clinical features of NASH are infrequent. Patients usually come to clinical attention by elevated liver enzymes found on routine evaluation but on history, about two third of patients will admit to have mild fatigue and about half will report right upper quadrant pain. Rarely, patient may present with a complication of cirrhosis. Physical examination may reveal hepatomegaly and splenomegaly. Research in last few years has stressed that development of steatosis, stetohepatitis, fibrosis with subsequent cirrhosis are most probably the result of insulin resistance. Therefore, clinical features may reflect existence of insulin resistance. Obesity, particularly central obesity is most important of these. Patients may have sleep apnea syndrome. Hypertension and manifestations of diabetes mellitus like polyuria, polydypsia, and neurological deficits may occur. Patients may have varying combination of obesity, diabetes, hyperlipidemia, hypertension and impaired fibrinolysis (syndrome X). Children with insulin resistance may show acanthosis nigricance. Patients with polycystic ovary syndrome, which consists of insulin resistance, diabetes, obesity, hirsutism, oligo or polymenorrha and hyperlipidemia may have NASH. Other rare manifestations of insulin resistance, which can be seen in patients of NASH are lipomatosis, lipoatrophy/lipodystrophy and panniculitis. Most other rare conditions known to cause NASH like peroxisomal diseases, mitochondialpathies, Weber-Christian disease, Mauriac syndrome, Madelung's lipomatosis and abetaliopprotenemia also have insulin resistance. This is believed that primary defect underlying insulin resistance is impairment in postreceptor pathways (through tyrosine kinase activity) of insulin action. Primary defect in insulin receptors appear uncommon. This results in down regulation of insulin receptor substance 1 (IRS-1) signaling by excess free fatty acids. In muscle, activated IRS-1 promotes translocation of glucose transporter protein 4 (GLUT4) to cell membrane. As a result, monocyte glucose uptake by GLUT4 increases glucose disposal from blood and reduced need for insulin. PKC-0 is a likely candidate as serine kinase in muscle regulated by fatty acids that can impair the activation of IRS-1. Insulin resistance is usually evaluated by fasting insulin levels, Quantitative Insulin Check Index (QUICKI) and Homeostasis Model Assessment of Insulin Resistance (HOMA), C-peptid/insulin ratio oral glucose tolerance test and hyper insulinemic euglycemic clamp. The clamp technique is considered the gold standard.
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PMID:Insulin resistance and clinical aspects of non-alcoholic steatohepatitis (NASH). 1619 20

Budd-Chiari syndrome is a rare condition resulting from outflow obstruction of the liver. This syndrome due to a pyogenic abscess is rarely documented in the English literature. Here a male patient with acute Budd Chiari syndrome is presented. A 21-year-old male patient was admitted to the hospital because of severe right upper quadrant pain, jaundice, hepatomegaly and fever. The examination of liver by computerized tomography and ultrasound revealed a large lesion 120 x l00 mm in size located in the right lobe of liver, which was compressing the inferior vena cava, the right and middle hepatic veins. Twenty-three days after percutaneous catheter drainage and medical treatment, the patient was discharged with complete healing. Although many disorders including malignant diseases can cause Budd-Chiari Syndrome, a pyogenic liver abscess compressing the inferior vena cava, and hepatic veins leading to acute Budd-Chiari syndrome has been rarely reported in English medical literature. Patients presenting with abdominal pain, hepatomegaly, and ascites should be carefully evaluated from this point of view.
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PMID:Acute Budd-Chiari syndrome resulting from a pyogenic liver abscess. 1620 Nov 17


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