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)

Fourteen patients with the diagnosis of leukemia and one with lymphoma developed systemic candidiasis. Involvement of the liver (15 patients), spleen (nine patients), and kidney (five patients) was diagnosed by clinical, CT, and pathologic findings. The CT findings ranged from low-density lesions (11 livers, nine spleens, and five kidneys) to hepatomegaly or hepatosplenomegaly. All livers and three kidneys had positive biopsy findings for Candida. Two patients with diffuse splenic lesions underwent splenectomy and were proven to have candidiasis. During a 1 year follow-up, two patients developed hepatic calcifications and one developed renal calcifications. In proper clinical setting, CT should be done for simultaneous evaluation of the liver, spleen, and kidneys. These studies, when positive, are useful to guide percutaneous or open biopsy and to follow the results of therapy. However, regardless of the hepatic CT finding, biopsy should be obtained to establish the diagnosis and begin proper treatment.
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PMID:CT findings in hepatosplenic and renal candidiasis. 330 88

Forty patients with brucellosis were hospitalized and clinical and laboratory findings of patients were recorded, treatment regimens were discussed. Twenty-five of the patients were males and 15 of the patients were females. Leukopenia 21.62%, anemia 27.02% and ESR elevation 83.87% were found. Fever and exhaustion were present all of the patients. Arthralgia, nonproductive cough, gastrointestinal symptoms, headache and night sweating were the other common symptoms. Hepatomegaly, splenomegaly, hepatosplenomegaly and ronchus were imported physical examination findings. First choice treatment solution was tetracycline-streptomycin combination and this combination succeed 89.19 in percent. Relapses were treated with rifampicin.
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PMID:[Brucellosis: clinical and laboratory findings and treatment in 40 patients]. 344 17

We determined the clinical and biological correlates of coagulopathy in a large series of patients with untreated childhood acute leukemia. Twenty-five of 805 children with acute lymphoblastic leukemia (ALL) (3.1%) and 27 of 195 with acute myeloid leukemia (AML) (13.8%) met any two of three requirements for a coagulation disorder: fibrinogen level less than 150 mg/dL; fibrin degradation products greater than 10 micrograms/mL; and prolongation of prothrombin time (PT) greater than 12 seconds, activated partial thromboplastin time (PTT) greater than 45 seconds, or thrombin time (TT) greater than 18 seconds. Patients with ALL complicated by abnormal coagulation were more likely to be boys and to have a T-cell immunophenotype, a high leukocyte count, a mediastinal mass, leukemic involvement of the CNS, hepatosplenomegaly, and L2 blast cell morphology. These features were highly interrelated, with only T-cell markers and CNS involvement achieving independent significance in a multivariate logistic regression model. Hepatomegaly, blast cell morphological subtype (French-American-British [FAB] M3, M4, and M5) and age less than 2 years were each associated with coagulopathy in patients with AML, although age failed to retain importance after logistic regression analysis. The presence of coagulopathy at diagnosis of ALL did not influence the rate of remission induction (P = .55). By contrast, only 14 of 27 children with coagulopathy at diagnosis of AML achieved a complete remission (CR), compared with 129 of 168 other patients who lacked this complication (P = .003). After multivariate analysis, coagulopathy remained independently associated with failure to attain remission in AML (P = .02). Fatal hemorrhagic complications arising in the CNS or lungs accounted for nine of the 13 induction failures in this group. The presence or absence of coagulopathy had no discernible influence on treatment outcome among patients with either ALL or AML who attained a CR. Laboratory evidence of a coagulation defect may be useful in identifying patients with AML who have a greater risk of induction failure and, hence, require close surveillance and intensive replacement therapy to prevent fatal hemorrhagic complications.
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PMID:The clinical and biological correlates of coagulopathy in children with acute leukemia. 352 66

Sphingomyelinosis (spm), an autosomal recessive mutation in mice originally occurred in the C57BL/KsJ inbred strain. Spm/spm mice of this genetic background show striking hepatosplenomegaly with a marked accumulation of sphingomyelin and cholesterol due to a deficiency of sphingomyelinase. However, in spm/spm mice of C57BL/6J and DBA/2J backgrounds, hepatosplenomegaly was not pronounced in spite of marked elevation of hepatic lipid concentrations. The lifespan of C57BL/6J-spm/spm and DBA/2J-spm/spm mice was shorter than that of C57BL/KsJ-spm/spm mice. This appeared to be associated with the comparatively rapid rise in hepatic lipid concentrations, which in turn might be related to the absence of hepatomegaly. Histological study revealed the formation of massive foam cell clusters in the livers and spleens of C57BL/KsJ-spm/spm mice, whereas in the case of C57BL/6J-spm/spm and DBA/2J-spm/spm mice, diffusely scattered foam cells were found. These findings suggest that the functions of reticuloendothelial system (RES) play a crucial role in the development of hepatosplenomegaly in response to lipid accumulation.
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PMID:A mouse model for Niemann-Pick disease. Influence of genetic background on disease expression in spm/spm mice. 355 64

Forty-one black patients aged 21 to 75 years with hepatic tuberculosis diagnosed at liver biopsy were studied prospectively. The liver varied in size and consistency and was tender in 44 per cent of patients. Abdominal symptoms, weight loss, pyrexia, hepatomegaly, splenomegaly and anaemia were absent in 54, 39, 37, 5, 68 and 27 per cent of patients respectively. Twenty-two per cent of chest radiographs were normal. Liver function tests were of little diagnostic value and hepatic imaging techniques often gave normal results. Acid-fast bacilli, caseation and coexistent liver disease were detected in 59, 51 and 37 per cent of patients respectively. Since there was no consistent clinical pattern a high index of suspicion is necessary if this disease is to be detected in communities in which tuberculosis is endemic. In patients with unexplained hepatomegaly or hepatosplenomegaly or pyrexia of unknown origin liver biopsy provides the only means of making this diagnosis.
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PMID:A prospective study of hepatic tuberculosis in 41 black patients. 365 66

Two- to three-week-old mice homozygous for the recessive oc gene had negligible numbers of marrow cells but possessed no significant spleno- and hepatomegaly. They also maintained normal numbers of blood cells except for monocytes, which were significantly lower. Additionally, they had reduced numbers of total cells and resident macrophages in the peritoneum, as determined by cell counts in the peritoneal lavage fluid. The frequency of spleen colony-forming units (CFU-S) in the spleens of oc/oc mice was the same as that in the spleens of normal littermate control mice. These oc/oc CFU-S showed essentially similar differentiation patterns as CFU-S of control mice. Also, a few CFU-S could be detected in livers of oc/oc mice. On the other hand, the frequency of cells that formed macrophage colonies in a four-day liquid-culture system in the presence of colony-stimulating activity was significantly reduced in oc/oc mice and abnormalities were observed in the formation of the adherent (stromal) layers by oc/oc spleen cells in liquid cultures. Numbers of fibroblastoid cell colonies in these layers were reduced and, moreover, cultures demonstrated a marked decrease in the number of macrophages both within and outside the fibroblastoid cell colonies. Transplants of spleen and thymus cells of oc/oc mice into lethally irradiated +/? recipients induced oc/oc-like lesions. They included peritoneal macrophage deficiency, marrow deficiency, as well as hepatosplenomegaly. This suggests a hemopoietic stem cell and not microenvironmental defect in this particular type of osteopetrosis. The murine mutant characterized in this study may be useful in studies of cellular interactions during blood and bone formation and in studies of the mononuclear phagocyte system.
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PMID:Congenital murine osteopetrosis inherited with osteosclerotic (oc) gene: hematological characterization. 375 33

The clinical, radiological and hepatic histological features of 51 patients with hepatobiliary fibropolycystic disease were reviewed. Many of the patients had more than one of the diseases; the combination of both congenital hepatic fibrosis (CHF) and Caroli's disease was most striking. Twelve patients with CHF (50% male) presented at 6 +/- 2 years of age (mean +/- SEM) with hepatosplenomegaly or variceal bleeding. Their main problems were recurrent variceal bleeds and renal disease. Polycystic kidneys and renal stones were present in 79% and chronic renal failure in 30%. Six of the 8 patients with Caroli's disease were male (75%) and presented later (aged 37 +/- 8 years) with hepatomegaly or cholangitis. Recurrent cholangitis developed in most (7/8) and 2 had polycystic kidneys. Twelve patients had a combination of CHF and Caroli's disease presenting with hepatosplenomegaly, bleeding or cholangitis. As in Caroli's disease, most (83%) were male, but the age of presentation (15 +/- 4 years), and the incidence of polycystic kidneys (42%) and renal failure (8%) was intermediate between CHF and Caroli's disease. In these patients, bleeds always predated cholangitis. Histologically, acute cholangitis was superimposed on the changes of CHF. Adult polycystic liver disease (10 patients) presented later (43 +/- 3 years) in females (90%) with pain, a mass or incidentally; polycystic kidneys were present in 33%. Microhamartomas (10 patients), which were usually incidental findings, were diagnosed latest (50 +/- 6 years). Three choledochal cysts were seen. The hazard of cancer in these diseases was reflected by 2 bile duct cancers and 1 pancreatic cancer (incidence 6%). This study has confirmed that hepatobiliary fibropolycystic diseases form part of a family and are often associated together. However, the diseases are of greatly differing severity and the prognosis in an individual patient is determined by the fibropolycystic diseases present.
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PMID:Hepatobiliary fibropolycystic diseases. A clinical and histological review of 51 patients. 395 71

A 28-year-old woman was admitted six months before her death because of abdominal pain, anemia and hepatosplenomegaly. Clinical diagnosis by biopsy examination was primary hepatic angiosarcoma. The autopsy revealed about 700 ml of bloody ascites. The spleen weighed 510 g, and was completely replaced by dark grayish-red tumors. The enlarged liver was 6,560 g and revealed multiple tumor nodules. Microscopically, the tumor cells formed irregular vascular spaces. Factor VIII-related antigens were stained in the tumor cells. Zonula adherens was observed also by electron microscopic observation.
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PMID:[An autopsy case of primary splenic hemangiosarcoma]. 407 65

Three children developed acute veno-occlusive disease of the liver following combination chemotherapy for acute myelocytic leukemia. The clinical presentation was similar in all three, with acute onset of hepatomegaly and thrombocytopenia in the absence of significant transaminasemia or icterus. In all three patients, radionuclide imaging with technetium-99m sulfur colloid showed hepatosplenomegaly, decreased liver uptake, and increased splenic activity. The results of liver biopsy established the diagnosis, revealing marked centrilobular congestion with hemorrhage into the spaces of Disse, atrophy of central hepatic cords, and edema of the walls of the central and sublobular veins. Each patient showed marked improvement following temporary cessation of chemotherapy. The diagnosis of veno-occlusive disease is suggested by the triad of: (1) clinical signs and symptoms; (2) scintigraphic findings; and (3) temporal relationship to chemotherapy.
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PMID:Veno-occlusive disease of the liver in children following chemotherapy for acute myelocytic leukemia. 657 67

Schistosoma mekongi is a newly recognized species of Schistosoma that is closely related to Schistosoma japonicum and is pathogenic to humans. Like the other forms of schistosomiasis in which the parasites reside in the mesenteric vasculature, S. mekongi infection has hepatosplenomegaly and portal venous hypertension as its most common serious sequelae. Schistosomiasis, although endemic in certain areas of Southeast Asia, has not been recognized as a health problem in Asian refugees who are currently entering the United States. In the present study 12 Laotian immigrants with S. mekongi infection were examined. The clinical, laboratory, and parasitologic findings in these patients are discussed. The diagnosis was made by examination of stool specimens in 11 patients and rectal biopsy specimens in one patient. All patients were asymptomatic, although the six youngest children had hepatomegaly. It is suggested that specific serologic tests may be useful in screening Asian refugees for infection with Schistosoma.
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PMID:Infection with Schistosoma mekongi in Southeast Asian refugees. 731 Jan 75


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