Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purulent pericarditis, though rare in developed countries, is not uncommon in developing countries. However, the type of pericardial drainage required and the risk of subsequent constrictive pericarditis has not been clearly defined. Thirty children between the ages of 3 months and 12 years with a diagnosis of purulent pericarditis were studied retrospectively. Pericardial effusion was confirmed in all by echocardiography and the diagnosis of bacterial pericarditis was based on aspiration of purulent fluid with leucocytosis and high proteins. Purulent pericarditis was a part of the disseminated sepsis in 25 (83%) children. Fever was present in all, hepatomegaly in 28 and breathlessness in 25, whereas muffled heart sounds, raised JVP and pericardial rub were found in only 18, 16 and 7, respectively. The ECG was abnormal in only 16 children. Staphylococcus aureus was the causative organism in 24 (96%). Open surgical drainage was done in 26 children, 23 of whom underwent anterior pericardiectomy. Two children died of disseminated sepsis. None of the 21 who returned for follow-up for periods of between 4 and 24 months had any long-term sequelae.
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PMID:Purulent pericarditis: clinical profile and outcome following surgical drainage and intensive care in children in Chandigarh. 1071 33

Primary pericardial disease is rare in children. The clinical features usually reflect limited venous return and cardiac output. Tuberculous pericarditis is the leading cause of pericardial disease in developing nations. A definitive diagnosis in children is frequently difficult and the manifestations are protean. We report a 10-month-old girl with fibrinofibrous pericarditis that manifested as constrictive pericarditis with prolonged fever, hepatomegaly, edema, and poor appetite. Echocardiography showed a solid mass that originated from the thickened pericardium and compressed the whole heart. In contrast, computed tomography revealed pericardial thickening with fluid collection. The symptoms and signs dramatically improved after surgical pericardiectomy. Pathologic analysis confirmed the diagnosis of tuberculous fibrinofibrous pericarditis. The patient received a 1-year course of antituberculosis therapy and has remained symptom free for 2 years. We suggest that a discrepancy between echocardiography and computed tomography (CT) findings might indicate a diagnosis of fibrinofibrous pericarditis.
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PMID:Fibrinofibrous pericarditis mimicking a pericardial tumor. 1074 49

The principal viruses implicated in pericarditis are enteroviruses. Cytomegalovirus pericarditis is quite rare and has been reported in immunocompromised patients with acquired immunodeficiency syndrome, malignant neoplasm or organ transplantation. We report a three-month-old male infant who suffered from cough and rhinorrhea for two weeks. He developed shortness of breath for three days, and fever for one day, prior to admission. Physical examination revealed tachycardia, tachypnea, pale conjunctiva, hepatomegaly, and a muffled heart sound without significant murmur. Chest radiography showed marked enlargement of the cardiac silhouette. Echocardiography demonstrated a large amount of pericardial effusion with impaired diastolic ventricular function. After pericardial drainage and supportive treatment, the fluid gradually disappeared. Viral culture of the pericardial fluid and serologic data confirmed a cytomegalovirus infection. Cytomegalovirus pericarditis should be included in the differential diagnosis of pericardial effusion in a young infant.
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PMID:Cytomegalovirus pericarditis with cardiac tamponade in a young infant. 1086 55

We report a retrospective study of 115 hospitalized non-immunocompromised adults with proved or presumed diagnosis of cytomegalovirus infection. Clinical symptoms were fever (95%), constitutive symptoms (80%), joint and muscle pain (41%), shivering (32%), abdominal pain (26%), non-productive cough (20%), cutaneous eruption (20%), and diarrhea (10%). Examination found hepatomegaly (25%), splenomegaly (23%), cutaneous rash (20%), adenopathy (19%), pharyngitis (9%), jaundice (3%) or signs of meningeal irritation (1%). Seventeen patients had a gastrointestinal form (hepatitis, jaundice, colitis, antral gastritis or cholecystitis), eight had a pattern of hemopathy, two interstitial pneumonitis, two pericarditis, two immune thrombocytopenic purpura, two a polymyalgia rheumatica-like pattern, one thrombotic thrombocytopenic purpura, one cutaneous vasculitis and one meningoencephalitis. Sixty-four percent of the patients had atypical lymphocytosis. Hepatocellular injury occurred in 90% of the patients. Nineteen of the patients had biological immune abnormalities. Cytomegalovirus infection should be mainly suspected in any patient with persistent fever, isolated or associated with signs of poor specificity, or in some patients with visceral manifestations of initially unknown origin.
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PMID:Clinical and laboratory findings of cytomegalovirus infection in 115 hospitalized non-immunocompromised adults. 1147 69

A 54-year-old man, who had undergone atrial septal defect (ASD) closure 30 years previously, was admitted for exertional dyspnea and chest oppression. He presented with right pleural effusion and hepatomegaly. Hemodynamic characteristics were consistent with constrictive pericarditis caused by multiple cystic lesions anterior to the main pulmonary artery and right ventricle, and severe calcification over the posterior and diaphragmatic sides of the heart. Magnetic resonance imaging was useful for differential diagnosis of the cystic mass and at surgery, it was revealed that the cystic lesions were old hematoma without cells. Pericardiectomy and removal of the calcification were performed safely using an ultrasonic scalpel, without cardiopulmonary bypass, resulting in hemodynamic improvement and relief of his symptoms.
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PMID:Constrictive pericarditis caused by calcification and organized hematoma 30 years after cardiac surgery. 1207 83

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

History and presenting signs and symptoms in 26 Hungarian Gaucher patients are described in order to promote recognition of non-diagnosed patients. Macrophages accumulating glucocerebrosidase due to deficient glucocerebrosidase activity may be present in many organs leading to a wide variety of clinical manifestations. The most common presenting signs and symptoms are splenomegaly, hepatomegaly, hypersplenism with anemia and thrombocytopenia, and bone deterioration. Rare manifestations of Gaucher disease including glomerulonephritis, pericarditis, pericardial calcification, haemorrhagic colitis and amyloidosis are also discussed.
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PMID:[Presenting signs and symptoms in Gaucher disease]. 1243 34

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

In this Grand Round we present a 32-yr-old African man who became severely ill after a 5-month history of weight loss, pyrexia, arthralgia, sweats and rash. He went on to develop pericarditis, pericardial effusion with tamponade, hepatomegaly with abnormal liver function tests, lymphadenopathy, massive proteinuria and required ventilatory, circulatory and renal support. The differential diagnosis was adult onset Still's disease, systemic lupus erythematosus (SLE), infection and lymphoma. Primary infection and lymphoma were excluded and he was treated, with dramatic success, with intravenous immunoglobulins (i.v.IG). Subsequent renal biopsy excluded SLE but confirmed collapsing glomerulopathy. The proteinuria improved dramatically following treatment with mycophenolate mofetil. We discuss some of the difficult diagnostic and management issues raised by this patient and the different uses and mechanisms of action of i.v.IG.
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PMID:Adult onset Still's disease and collapsing glomerulopathy: successful treatment with intravenous immunoglobulins and mycophenolate mofetil. 1503 97

This is the case of a patient who presented with severe right-sided heart failure due to diastolic dysfunction that caused a dilemma of differential diagnosis between restrictive cardiomyopathy and constrictive pericarditis. Restrictive cardiomyopathy was diagnosed based on noninvasive and invasive hemodynamic testing. However, the patient did not respond to therapy and succumbed to worsening heart failure and multiple comorbidities. Clinical features of right heart failure with edema, ascites, jugular venous distention, and tender hepatomegaly are commonly seen in clinical practice. When systolic function is determined to be normal, diastolic causes of heart failure must be ruled out. These include myocardial disorders with a broad range of pathologies leading to restrictive physiology, of which amyloidosis is a prototype. Pericardial disorders leading to diastolic heart failure are usually in the form of constrictive physiology, when pericardial tamponade is ruled out. Differentiation between restrictive and constrictive pathologies is often difficult and requires careful attention to hemodynamic and Doppler echocardiographic features. We report a case of severe right heart failure illustrating some of the complexities in decision-making and the importance of meticulous hemodynamic and ancillary testing in the diagnosis and treatment of this often fatal condition.
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PMID:Constrictive pericarditis versus restrictive cardiomyopathy: challenges in diagnosis and management. 1547 69


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