Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019214 (hepatosplenomegaly)
 4,408 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The 11 cases of malaria admitted to Kaohsiung Medical College Hospital in the past 10 years were analyzed to assess the characteristics of patients who acquired malaria parasite infection. Nine of the patients contracted malaria in Southeast Asia. Two men had received antimalarial chemoprophylaxis before they went abroad and another two men relapsed after antimalarial treatment. The initial symptoms and signs were nonspecific, including fever, chills, abdominal pain and hepatosplenomegaly. Seven patients responded well to the antimalarial regimens. Two persons developed meningeal malaria. Resistance to chloroquine and primaquine and even to quinine was noted in another two cases. Hypoglycemia was diagnosed in one of latter two patients who developed heavy parasitemia (26%), acute renal failure and died 5 days after treatment. Peripheral blood smear examination is a simple and quick method to make a diagnosis in any suspicious case. Resistance to chloroquine and primaquine is not uncommon, especially in those who acquired the infection in Southeast Asia. Changing to more potent agents and aggressive management in complicated cases is necessary.
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PMID:Clinical experience on malaria. 205 63

Castleman's disease (also called giant lymph node hyperplasia or angiofollicular lymph node hyperplasia) is a clinicopathological entity of unknown etiology. Two histologic patterns of lymph nodes are classically recognized: the hyaline-vascular and plasma-cell variants. Recently, multicentric Castleman's disease has emerged as a separate clinical entity manifested primarily by generalized lymphadenopathy and systemic manifestations, such as thrombocytopenia, hemolytic anemia, hepatosplenomegaly, altered liver function tests, central nervous system alterations, and autoimmune manifestations. A number of renal alterations have been described in association with the two pathological variants of Castleman's disease, but thrombotic microangiopathy has been previously reported only once in a patient with Castleman's disease. No renal biopsy was performed in that patient, although there was evidence of renal dysfunction. We report two cases of biopsy-proven renal thrombotic microangiopathy associated with multicentric Castleman's disease. In addition to having lymph node pathology characteristic of Castleman's disease, both patients presented with generalized lymphadenopathy and systemic manifestations, including acute renal failure, hypergammaglobulinemia, anemia, thrombocytopenia, and hypoalbuminemia. Autoantibodies were present in both patients, including antiphospholipid antibodies in one patient. The renal biopsies, examined by light, immunofluorescence, and electron microscopy, were diagnostic for renal thrombotic microangiopathy. The simultaneous development of two rather uncommon syndromes, multicentric Castleman's disease and renal thrombotic microangiopathy, suggests a possible link between Castleman's disease and renal thrombotic microangiopathy. Furthermore, we propose that the production of autoantibodies, in particular antiphospholipid antibodies, may lead to the development of thrombotic microangiopathy in some patients with multicentric Castleman's disease.
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PMID:Renal thrombotic microangiopathy associated with multicentric Castleman's disease. Report of two cases. 766 Dec 75

Renal lymphoma is commonly secondary to lymphomatous infiltration of the kidneys in disseminated lymphoma and advanced stage IV disease. We describe a 57-year-old white woman presenting with an acute renal failure due to a bilateral "primary" B-cell lymphoma infiltration of the kidneys. The diagnosis of the lymphoma was made by renal biopsy. The striking feature observed was a destructive infiltration of the kidney by a malignant B-cell lymphoma that left the renal capsule intact, without any sign of secondary localization on the hilar regions. Physical examination did not reveal any peripheral lymphadenopathy or hepatosplenomegaly. A bilateral infiltration of both kidneys was the only feature shown by computed tomography and renal angiography. This case raises the question of the occurrence of a primary B-cell lymphoma in a nonlymphoid organ, which was diagnosed by renal biopsy at a time when the development was exclusively renal in origin.
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PMID:Primary bilateral B-cell renal lymphoma: a case report and review of the literature. 794 15

Chorioangioma is the most common tumor of the placenta. However, a large one complicated with hydrops fetalis is rare. We report a patient who had hydrops fetalis associated with placental chorioangioma. The clinical manifestations included generalized edema, coagulopathy, thrombocytopenia, anemia, hypoproteinemia and hepatosplenomegaly. The hospital course was complicated with acute renal failure and repeated pneumonia. The patient died on the 54th day of life due to persistent lung atelectasis and hypovolemic shock. The pathophysiology and management of the complications of hydrops fetalis with chorioangioma are discussed.
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PMID:Hydrops fetalis due to placental chorioangioma: report of one case. 915 71

Granulomatous reactions caused by foreign bodies have been described in drug abusers, in subjects exposed to occupational pollutants, and more rarely, in association with the use of prosthetic devices. We describe a 62-year-old patient with multiorgan parenchymal granulomatosis caused by inorganic debris of unknown origin. The patient presented with fever, hepatosplenomegaly, progressive cholestasis, and acute renal failure. Liver and kidney biopsies showed the presence of noncaseating epithelioid giant-cell granulomas containing scattered polarizable particles. Similar particles were also present in stools. Studies by innovative scanning electron microscopy and energy-dispersive microanalytical techniques showed that the particles isolated in liver, kidney, and stools were made by feldspars, the main component of porcelain. No occupational or environmental exposure to these materials could be identified in this patient and the only reliable source of the porcelain debris turned out to be constituted by 2 dental bridges evidently worn because of a possible inappropriate construction, malocclusion, and bruxism. The porcelain of the dental prostheses had the same elemental spectrum of the particles isolated from stool specimens and liver-kidney granuloma. After identification of the dental prostheses as the most likely source of ceramic debris, and after their removal, the particles from stool specimens disappeared. The patient was then treated with steroids leading to a remission of the clinical symptoms and a decrease in granulomatous inflammatory reaction in both liver and kidney. This is the first report suggesting that a foreign body systemic granulomatosis can be associated with worn dental prostheses.
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PMID:Liver and kidney foreign bodies granulomatosis in a patient with malocclusion, bruxism, and worn dental prostheses. 1167 17

A 37-year-old man had a sore throat and pyrexia since January 1999. He was treated at a nearby hospital, but not improved. Jaundice was indicated there, and the patient was referred transferred to our hospital, where he was admitted for treatment with a diagnosis of severe acute hepatitis with acute renal failure. Thereafter the patient was revealed to have had a past history of heavy drinking, and he underwent the treatment with a diagnosis of acute fulminant hepatitis due to hepatitis A virus (HAV). He showed a tendency toward improvement. During the course, however, viral associated hemophagocytic syndrome (VAHS) developed. Various treatments were conducted, but it was not improved, and the patient died on Hospital Day 66. On pathologic autopsy, remarkable hepatosplenomegaly associated with marked bone marrow abnormalities compatible with VAHS was observed. Aspergillus abscesses were also observed in many organs, and they were considered as an adverse reaction to potent immunosuppressive therapy. Since there have been only a few reports on HAV-related VAHS, discussing VAHS related to HAV, the present case was considered valuable.
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PMID:Hemophagocytic syndrome associated with fulminant hepatitis A: a case report. 1271 21

We report a case of a 22 years old type 1 diabetic man with a history of weight loss, weakness, anorexia, fever and recurrent urinary tract infection since February 2001. In April 2001, he presented anuria due to obstructive acute renal failure. Hepatosplenomegaly and lymphadenopathy were absent at physical examination. Laboratory tests revealed a high level of gamma globulin (53.4 g/l) and anaemia (haemoglobin 7.7 g/100 ml) without leukopenia and thrombocytopenia. CT scan showed multiple retroperitoneal lymphadenopathies causing compression of the two ureters, hydro-ureter associated with hydronephrosis, hepatosplenomegaly and multiple pulmonary nodes. Lymphadenopathies, anaemia, high level of gamma globulin, high titres of anti-leishmanial antibodies and the excellent outcome after treatment with meglumine antimoniate (Glucantime) confirmed visceral leishmaniasis. This report documented an unusual clinical presentation of Visceral leishmaniasis in a diabetic patient.
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PMID:[Obstructive acute renal failure revealing visceral leishmaniasis in a diabetic patient]. 1272 15

Authors present the case of 15-year-old girl with diagnosed pre T-acute lymphoblastic leukaemia with hyperleukocytosis--at admission 213 x 10(9)/l. At clinical evaluation a major peripheral and abdominal lymphadenopathy, mediastinal mass, hepatosplenomegaly were revealed. After administration of prednisone for two times--11.4 mg/m2/24 h--the features of tumour lysis syndrome rapidly increased. Hyperphosphatemia, hyperkalemia and hyperuricemia resulted in acute renal failure. Renal replacement therapy was introduced with simultaneous application of cytoreduction phase therapy and induction of remission according to New York protocol. Total number of performed hemodialysis sessions was 12. Obtained haematological remission in 8th week of treatment is still present. Renal function remains normal. Remission supportive treatment has been continued according to above-mentioned protocol.
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PMID:[Tumor lysis syndrome in the course of acute lymphoblastic leukemia as the consequence of prednisone monotherapy]. 1464 89

A 52-year-old Japanese man presented with fever spikes, generalized fatigue, anorexia, and anasarca. The patient was referred for the evaluation of fever of unknown origin in association with swelling of cervical, axillary, and inguinal lymph nodes. He also manifested nephrotic syndrome, acute renal failure, hepatosplenomegaly, massive pleural effusion, ascites, disseminated intravascular coagulation, and hypergammaglobulinemia. C-reactive protein was positive and plasma vascular endothelial cell-derived growth factor (VEGF) and serum interleukin-6 levels were markedly elevated. Lymph node biopsy results showed that findings were compatible with Castleman's disease of hyaline vascular type associated with interfollicular plasmacytosis. In conjunction with the clinical findings, a diagnosis of multicentric Castleman's disease was made. The patient underwent renal biopsy because of nephrotic syndrome, and the results showed proliferation of mesangial cells, lobulation of glomeruli, and tram track pattern of the capillary wall without immune complex deposition. Electron microscopy showed widening of the subendothelial space. No electron-dense deposits were present in both mesangial and subendothelial regions. Pathologic features were compatible with glomerular microangiopathy and membranoproliferative glomerulonephritis-like lesions. With corticosteroid therapy, systemic symptoms disappeared; both VEGF and interleukin-6 levels were normalized, and he went into complete remission of nephrotic syndrome. In this article, the role VEGF plays in the pathogenesis of nephrotic syndrome and glomerular microangiopathy is discussed.
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PMID:Multicentric Castleman's disease associated with glomerular microangiopathy and MPGN-like lesion: does vascular endothelial cell-derived growth factor play causative or protective roles in renal injury? 1471 66

A 53-year-old male patient began treatment for systemic exanthema with diaphenylsulfone (DHS) on 21 November 2002. On 18 December 2002, the patient developed a fever and additional systemic erythematous exanthema. Systemic lymphadenopathy, hepatosplenomegaly, leukocytosis (in particular, an increase in the number of atypical lymphocytes) and liver dysfunction followed. After cessation of the DHS treatment on 25 December 2002, acute renal failure occurred and the patient was transferred to Shinshu University Hospital on 4 January 2003. The patient was diagnosed with drug-induced hypersensitivity syndrome (DIHS). Steroid pulse therapy (methylprednisolone 1000 mg/day for 3 days) was given, followed by 60 mg/day of prednisolone. The patient's renal functions recovered and he was taken off hemodialysis therapy. However, the patient relapsed twice despite two sessions of steroid pulse therapy and an increase in the dose of prednisolone to 100 mg/day. Plasma exchange (PE) was carried out to reduce the activity of the disease. With a total of four plasma exchanges, we were able to reduce the dose of prednisolone from 100 mg/day to 60 mg/day without relapse. There were no adverse effects from the plasma exchanges. Plasma exchange should be considered in the treatment with corticosteroid-resistant DIHS with multiple organ lesions.
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PMID:A case of drug-induced hypersensitivity syndrome with multiple organ involvement treated with plasma exchange. 1620 17


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