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)

A two-month-old female presented with hepatomegaly 5 cm below the right costal margin. Resection of a 6 cm hepatic mass demonstrated an infantile hemangioendotheliom (IHE). This documents for the first time the ultrastructural features of an IHE of the liver. Ultrastructural examination showed large numbers of vascular channels of varying sizes lined by abnormal endothelial cells. An incomplete basal lamina separated the endothelial cells from the extracellular material and there were no associated pericytes. The intervascular area contained abundant collagen fibers, fibrils, and cells ultrastructurally similar to fibroblasts. The relationship of structure to certain clinical features of this lesion is discussed.
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PMID:Ultrastructure of infantile hemangioendothelioma of the liver. 67 53

A case of a ruptured haematoma of the liver with intra-abdominal bleeding is reported. The 26-year old primigravida was admitted in the 31st week of gestation because of a HELLP syndrome. She presented additional symptoms, that are considered typical for a HELLP syndrome, complicated by a ruptured haematoma of the liver: severe right upper-quadrant pain, decrease of haemoglobin content, enlarged liver with structural irregularities and free fluid in the abdominal cavity as examined by sonography. During Caesarean section, a subcapsular haematoma of the liver, combined with a 5 cm laceration of the organ surface, was found. The defect was closed with collagen gauze and clotted with fibrin. Additionally the liver was compressed by abdominal compression towels, which were removed 2 days later. The postoperative development was, in the main, complication free.
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PMID:[Manifestations of ruptured liver hematoma as a severe complication of HELLP syndrome]. 186 Jun 64

Adenosine administration was tested in rats with carbon tetrachloride-induced hepatic fibrosis and was able to partially prevent the enlargement of liver and spleen induced by the toxin. This amelioration of the hepatomegaly was accompanied by a 50% reduction of the liver collagen deposition and preservation of content of glycosaminoglycans. A stimulated hepatic collagenase activity is apparently the mechanism for reduction of collagen accumulation. These effects were associated with a striking improvement in liver function. Adenosine treatment did not modify the late hepatotoxic effect of the carbon tetrachloride; however, the stimulatory effect of the nucleoside on energy state appeared to counteract the drastic decreases in adenine nucleotides, ATP, ATP/ADP ratio and energy charge elicited by the hepatotoxin. Moreover, a possible beneficial action of enhanced hepatic oxygenation caused by the vasodilator properties of adenosine cannot be ruled out. Regardless of the mechanism, adenosine seems to change the cellular response to the injury induced by the hepatotoxin.
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PMID:Adenosine partially prevents cirrhosis induced by carbon tetrachloride in rats. 239 Oct 66

A 77-year-old woman had variceal bleeding related to systemic mastocytosis. Physical examination revealed minimal ascites and mild hepatomegaly noted 11 years before. Liver function tests were nearly normal. Because of early recurrent bleeding, a mesocaval shunt was performed. Wedged liver biopsy showed a moderate fibrosis of portal tracts and massive mast cell infiltration within portal tracts and sinusoids. Perisinusoidal collagen deposition was demonstrated ultrastructurally. We suggest that systemic mastocytosis be added to the list of diseases related portal hypertension with perisinusoidal fibrosis. As there is currently no specific treatment, a portocaval shunt should be discussed.
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PMID:[Systemic mastocytosis disclosed by rupture of esophageal varices]. 268 73

Peripheral blood cholyglycine and procollagen-III-peptide were measured in 22 Zairean patients with hepatomegaly caused by S. mansoni before and after treatment with praziquantel. Circulating T-cell subsets and cutaneous in vivo delayed type hypersensitivity were assessed; serum neopterin and beta 2-microglobulin served as indicators for macrophage/lymphocyte activation. The results were compared to age and sex matched patients with S. mansoni infection limited to the intestinal tract and schistosomiasis free controls with equal socioeconomic background. Abnormal serum cholyglycine and neopterin levels and alterations of circulating T-cell subset frequencies were associated with hepatomegaly in schistosomiasis. Normalization of these parameters reflected a regression of egg-induced immunopathology as early as two months after specific chemotherapy. Serum procollagen-III-peptide concentrations rose significantly after treatment, suggesting release of propeptide previously incorporated without cleavage into tissue collagen. The combination of these biochemical and immunological parameters may allow assessment of the pathophysiological mechanisms responsible for liver disease in individual patients.
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PMID:Liver involvement in human schistosomiasis mansoni. Regression of immunological and biochemical disease markers after specific treatment. 290 28

In 20 patients with hepatic or hepatosplenic schistosomiasis and 82 individuals infected with S. mansoni, but without liver enlargement, serum parameters reflecting the fibrotic process and hemodynamic alterations as well as immunomodulation were examined. Included as controls were 35 age- and sex-matched healthy individuals from the study region in Northeast Brazil. Peripheral blood cholylglycine levels in patients with hepatomegaly, reflecting the spillover of portal blood into the systemic circulation, were elevated 12-fold over values of patients without liver involvement. Procollagen-III-peptide, a cleavage product of collagen synthesis, was elevated in patients with hepatomegaly (P less than 0.001) but normal in uncomplicated cases. Immunomodulation was assessed by in vivo delayed hypersensitivity to recall antigens and by serum beta 2-microglobulin and neopterin, substances released in the context of lymphocyte activation. Neopterin, predominantly a macrophage product, was elevated most strikingly in hepatomegalic cases (P less than 0.001). The possible interrelation between altered immune responses and excess fibrogenesis is discussed.
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PMID:Liver involvement in human schistosomiasis mansoni. Assessment by immunological and biochemical markers. 313 58

Sixty-one patients with essential thrombocythemia (ET) were followed from 1974 through 1987 at the Medizinische Poliklinik. Fifty-one patients (84%) presented with thromboembolic complications, and eight patients (13%) with hemorrhages. In seven patients (12%), a thrombocytosis was detected accidentally. Disturbances of the microcirculation (67%), mainly of the fingers and toes (53%), were the most frequent thromboembolic symptoms. The mean age of all patients was 58 years (male patients, 61 years; female patients, 56 years). The average platelet count at diagnosis was 897,000/microliter. The average maximal platelet count was 1.231 X 10(6)/microliter (range, 500,000/microliter to 4 X 10(6)/microliter). Seventy-two percent had a moderate leukocytosis (average, 12,400/microliter), 34% a splenomegaly, 29% a hepatomegaly. Signs of hypermetabolism were infrequent, lactate dehydrogenase (LDH) and uric acid elevations, if present, were moderate. Bleeding time and viscosity were normal in most patients. Spontaneous platelet aggregation was increased in 81% of patients (n = 40). Platelet aggregation studies with the aggregation inducing substances adenosine diphosphonate (ADP), platelet activating factor (PAF), thrombin, collagen, and adrenalin showed hypoaggregation in most patients. Adrenalin-induced aggregation distinguished best between ET-patients and reactive thrombocytosis showing hypoaggregation in all ET-patients tested (n = 16) and in none of 22 controls. Bone marrow studies were performed in 57 patients. The histologic studies (done in 49 patients) were consistent with a chronic myeloproliferative disorder in all cases. In 41 cases (84%) the picture of a megakaryocytic myelosis was found, in 12 of these a granulocyte-rich form of megakaryocytic myelosis. Cytologic studies only (eight patients) did not differentiate ET well from reactive thrombocytosis. Platelet aggregation studies and bone marrow histology may be of help in the diagnosis of difficult cases of thrombocytosis. The Philadelphia status was negative in all cases studied (14 patients). Fourteen patients died. The causes of death were thromboembolic complications in probably 11 and acute leukemia in two patients. The probability of 10-year survival is 64% after a mean follow-up time of approximately 5 years. It appears that considering the average age of ET patients at diagnosis, life expectancy is close to normal.
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PMID:Essential thrombocythemia. Clinical characteristics and course of 61 cases. 336 70

The purpose of this study was to elucidate the clinical features of right ventricular (RV) dysplasia, a recently described clinical entity characterized by RV myopathic changes and ventricular tachycardia of left bundle branch block morphology. Five cases were reported, in which the diagnosis was established according to the criteria of Marcus. Case 1, a 33-year-old man, was referred to us for evaluation of his paroxysmal ventricular tachycardia of five years duration. Case 2, a 38-year-old man, was admitted because of shock caused by ventricular tachycardia. In both cases, the QRS configurations during ventricular tachycardia were those of the left bundle branch block pattern, and electrocardiograms during sinus rhythm showed T wave inversions in the right precordial leads and late ventricular potentials. Two-dimensional echocardiography, radionuclide angiography and contrast angiography disclosed RV dilatation and dysfunction with normal left ventricular (LV) function. The biopsied myocardium from the right and left ventricles in Case 2 revealed myocytolysis, a paucity of myofibrils and proliferation of collagen fibers. Case 3, a 73-year-old woman began to experience exertional dyspnea since 16 years of age. Her treatment consisted of bed rest, diuretics and digitalis. In December 1983, her New York Heart Association functional class was III, and physical examinations disclosed a Levine III/VI systolic murmur suggestive of tricuspid regurgitation, jugular vein dilatation, hepatomegaly, and pretibial edema. Electrocardiogram showed atrial fibrillation, incomplete right bundle branch block and T wave inversions in the precordial leads. Chest radiograph revealed marked cardiomegaly (cardiothoracic ratio of 92%). Echocardiography, radionuclide angiography and contrast angiography revealed marked RV dilatation, depressed ejection fraction (RV end-diastolic volume index of 342 ml/m2, and RV ejection fraction of 28%). Case 4, a 20-year-old man, was admitted with a chief complaint of palpitation. Case 5, a 19-year-old man, was referred to us for the evaluation of asymptomatic cardiomegaly, and his cardiothoracic ratio was 54%. A 12-lead electrocardiogram showed right bundle branch block and T wave inversions in the right precordial leads. Ambulatory electrocardiography revealed frequent premature ventricular complexes of the left bundle branch block pattern. Echocardiography, radionuclide angiography, and contrast angiography disclosed RV dilatation and dysfunction in both cases, and mild LV dilatation and dysfunction (LV end-diastolic volume index of 149 ml/m2, LV ejection fraction of 48%) in Case 4.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Right ventricular dysplasia: clinical characteristics of five patients]. 383 64

Liver examination performed in seven patients who had renal failure related to light chain deposits demonstrated in all cases the presence of liver light chain deposits. In all of our patients clinical renal involvement antedated the liver disease. The portal areas and the Disse spaces contained a granular material which strongly reacted with antilight chain antiserum (kappa or gamma). In one patient in whom lesions were severe, the sinusoid edge was ruptured and a pelliosis -like lesion was observed. In the five patients who were hemodialyzed for more than several months at the time of discovery of liver deposits, increased amounts of collagen were present in the Disse spaces, and one patient had extensive liver fibrosis by light microscopy. Clinical liver involvement was defined by moderate hepatomegaly in five patients, with ascites in two. A slight increase in phosphatase alkaline activity was frequently observed and bromsulphalein retention was present in two. In one patient liver tests remained entirely normal despite the presence of diffuse kappa light chain deposits.
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PMID:Liver involvement in nonamyloid light chain deposits disease. 642 20

Disturbances of intravenously administered indocyanin green (ICG) elimination are related to the effective circulating blood volume and the amount of binding protein for transportation in blood plasma through the liver because of the narrowed sinusoidal space due to the enlarged liver cells with fullness of confluent fat droplets in the cytoplasma. However, morphologic changes of the liver resulting in disturbances of ICG elimination could not be actually clarified until the present. Therefore, morphologic changes of the liver resulting in delayed ICG elimination in fatty liver, occurring in diabetes mellitus were investigated in contrast with those in fatty liver in non-diabetic, non-alcoholic diseases of the liver. An electron microscopic study of the liver with delayed ICG elimination revealed thickening and amorphous growth of the sinusoidal wall with obscure pores followed by membraneous formation, narrowness of Disse's space, rarefaction of sinusoidal microvilli and proliferation of collagen fibers, in fatty livers derived from both diabetes mellitus and other diseases. The term "intrasinusoidal block" in fatty liver should be utilized on the basis of these electron microscopic features of the liver.
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PMID:Light microscopic and electron microscopic study on morphologic features resulting in the delay of ICG elimination in diabetic and non-diabetic fatty liver. 653 68


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