Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine cases have been presented in detail to illustrate some of the varied causes of sudden neurological deficit in childhood: arteriovenous malformation, cryptic hamartoma, berry aneurysm, mycotic aneurysm, intraspinal arteriovenous malformation, brain tumor, migraine, arteritis, and multiple sclerosis. The Boston Children's Hospital experience with aneurysms and intracranial arteriovenous malformation has been summarized. It is noteworthy that a cutaneous hemangioma overlay one cranial and one intraspinal arteriovenous malformation. One small but deep cerebral arteriovenous malformation apparently destroyed itself after its second hemorrhage. Not only have multiple sclerosis and a brain tumor mimicked a vascular lesion, but a series of vascular accidents was misdiagnosed first as multiple sclerosis then as a thalamic tumor. The many possible causes of childhood strokes has been thoroughly cataloged in the Report of the Joint Committee for Stroke Facilities in 1973 (11). Children may be more susceptible to strokes because of congenital abnormalities such as congenital heart disease, hemophilia, and sickle cell anemia, or by diseases which more commonly occur in this age group, such as leukemia. The likelihood of brain abscess in cyanotic congenital heart disease is stressed. Arteriographic studies in our series have been safe; however, there have been reports of probable worsening of symptoms in children with multiple cerebral occlusive lesions in the presence of homocystinuria.
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PMID:Strokes in children. 98 45

Conclusions drawn from the post-mortem examination of 226 subjects who died of cerebral haemorrhage are presented. There were slightly more women than men (53%) in the series. Arterial hypertension (68%) was the main cause of death, while renal disease, leukaemia, angioma of the pons, and embolism due to bacterial endocarditis were also observed. The most frequently noted sites are listed. Since cerebral haemorrhage follows the rupture of one or more already damaged deep arteries, as assessment was made of the part played by vascular lesions. 13 cases due to leukaemia and 35 to rupture of aneurysms of the polygon of Willis were discarded. In only 20 cases out of 138 in which convincing microscopic evidence of the vascular situation could be obtained was there an absence of significant alterations. The remaining cases consisted of serious hyalinosis (56%), fibrinoid necrosis (13%), and siderocalciosis (12%). An account is also given of the special pathogenetic conditions applicable to cerebral haemorrhage associated wtih serious gastrointestinal haemorrhage or recent myocardial infarct.
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PMID:[Pathogenesis of cerebral hemorrhage considered in the light of objective lesions in the arteries of the brain (in 226 cases studied by autopsy)]. 119 33

We previously reported that the expression of thrombomodulin on the MEG-01, a cell line from human megakaryoblastic leukemia, was increased by agents that increase intracellular cAMP. In this paper we examine the effect of these agents on cultured human umbilical vein endothelial cells (HUVEC) and mouse hemangioma cells. Incubation of the cells with 3 mM dibutyryl cAMP (dbcAMP) increased functionally active thrombomodulin by about 2-fold on HUVEC and 4-fold on hemangioma cells. This effect was observed from 1 hour after the incubation and continued up to 24 hours. Dot hybridization of mRNA demonstrated a dose dependent increase in thrombomodulin mRNA in response to dbcAMP. Treatment of HUVEC with 20 microM forskolin or 100 microM isobutylmethylxanthine (IBMX) also increased cell-surface thrombomodulin on HUVEC. These agents prevented the interleukin I (IL-I) or tumor necrosis factor (TNF)-induced decrease in thrombomodulin on HUVEC. These data suggest that the expression of thrombomodulin on HUVEC and mouse hemangioma cells may be regulated by intracellular cAMP level.
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PMID:Increased expression of thrombomodulin on the cultured human umbilical vein endothelial cells and mouse hemangioma cells by cyclic AMP. 170 10

Fifty-nine cases of nontraumatic splenic disease were reviewed to evaluate the roles of clinical findings, computed tomography, ultrasound, and radionuclide scanning in diagnosis and management. Patient groups included lymphoma (30 patients), infarct (11 patients), abscess (9 patients), cyst (5 patients), hemangioma (3 patients), and hamartoma (1 patient). In no case were clinical findings alone sufficient to diagnose a splenic lesion. Clinical and laboratory manifestations were nonspecific in all groups. Moreover, no radiologic study reliably diagnosed splenic lymphoma or leukemia. All other focal splenic lesions were consistently diagnosed noninvasively. Cross-sectional imaging was more useful than radioisotope scanning, and often provided adjunctive diagnosis of extrasplenic pathology. The superior detail, spatial resolution, and sensitivity of computed tomography made it the single most valuable diagnostic modality.
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PMID:Nontraumatic focal lesions of the spleen: assessment of imaging and clinical evaluation. 218 77

We isolated a field strain of avian hemangioma retrovirus (AHV) which induces a cytopathic effect (CPE) on cultured avian and mammalian cells shortly after infection. The kinetics of cell killing were dependent on the multiplicity of infection. The CPE on avian and mammalian cells was independent of virus replication, because UV-irradiated virus led to cell death as well. Biochemical and genetic experiments indicated that AHV env gene products were responsible for the CPE. Partially purified AHV envelope glycoproteins (gp85), but not those of the Rous sarcoma virus Prague C strain, induced a CPE. Rous-associated virus type 1, in which the env region was replaced by the AHV gp85 region, induced a CPE on avian and mammalian cultured cells. Therefore, we suggest that CPE is induced by AHV via interaction between viral gp85 and the cell membrane. This mode of CPE is unique among avian sarcoma-leukemia viruses.
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PMID:Cytocidal effect caused by the envelope glycoprotein of a newly isolated avian hemangioma-inducing retrovirus. 255 Jun 68

The risk of second malignant neoplasm (SMN) was evaluated in 979 children with Hodgkin's disease. This cohort was diagnosed between 1955 and 1979 at one of the institutions of the Late Effects Study Group. Solid tumors, non-lymphocytic leukemia, and non-Hodgkin's lymphoma (NHL) developed in 18, 17, and 3 patients, respectively. The estimated cumulative probability of developing any SMN was 2% at 5 years from diagnosis, 5% at 10 years, and 9% at 15 years. The incidence is ninefold greater than the risk of acquiring cancer in 19 year-olds, the median age at which the diagnosis of SMN was made in this study population. For leukemia and NHL the corresponding probabilities were 1%, 3%, and 4% for the group as a whole but were increased (2%, 6%, and 8%) in patients who had suffered one or more recurrences. In order to analyze the risk of leukemia and NHL associated with alkylating agent chemotherapy, each patient was assigned a score of one for each alkylating agent administered for a 6-month period. Scores of 2, 4, 6, and 8 were associated with probabilities of leukemia or NHL of 2%, 3%, 6%, and 10%, respectively. In a multivariate analysis for leukemia/lymphoma that included AAD score, stage, and splenectomy, the effect of AAD score and splenectomy did not change substantially compared to the univariate results. AAD score remained statistically significant (P = .0001), and splenectomy was of borderline significance (P = .09). Of the 18 solid tumor SMNs, 15 developed within the field of radiation, and one other developed in tissue irradiated 34 years earlier for hemangioma. This study of a large and unselected group of children with Hodgkin's disease who received a variety of therapies demonstrates that children are as likely as adults to develop acute leukemia after alkylating agents and solid tumors in the field of radiation therapy.
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PMID:Second malignant neoplasms following childhood Hodgkin's disease: treatment and splenectomy as risk factors. 258 62

Mortality was studied in 18,357 patients (33% males and 67% females) with skin hemangioma admitted to Radiumhemmet between 1920 and 1959. The treatments of the hemangiomas were performed by radium-226 sources (13,094 patients) or x-ray therapy (2,540 patients). In 2,723 patients no radiotherapy was given. The median age was 6 months for the treated patients and 8 months for the patients not receiving radiotherapy. Between 1920 and 1951 a total of 154 patients were reported dead. The cohort was matched with the Swedish Cause of Death Register between 1952 and 1985. During that period 504 died, in 146 patients the cause of death was cancer or leukemia. The total number of person-years at risk was 587,426. In patients treated with radium-226 or orthovoltage x-rays, 410 deaths occurred (standardized mortality ratio (SMR) = 1.07; ns). In patients given contact therapy 34 deaths occurred (SMR = 0.82; ns) and in the not irradiated group 60 deaths occurred (SMR = 0.78; ns). Patients treated with radium-226 or orthovoltage x-rays had an SMR of 1.34 for all cancers combined (p less than 0.05). For patients treated between 1920 and 1939 the SMR for cancer was 1.53 (p less than 0.05) as compared to an SMR of 1.16 (ns) for those treated between 1940 and 1959.
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PMID:Mortality in a cohort of radiation treated childhood skin hemangiomas. 261 Oct 31

Imaging procedures have lately become important in pathologic conditions of the spleen, because they are simple to use and do not cause much stress to the patient. Ultrasonography is the method of choice for determination of the position, shape, size and volume of the spleen, and also for the diagnosis of changes within the spleen. Circumscribed lesions cannot be detected by ultrasonography until they have reached a size of 0.5-1.0 cm; the same limit of detection applies for CT, which has approximately the same diagnostic reliability. In the presence of generalized splenic disease (e.g. splenomegaly in myeloid leukaemia) imaging procedures are being used increasingly for staging and for monitoring of the results of treatment. Perhaps in future histochemical determinations made with the aid of core-spin spectroscopy will present a further means of diagnosis without the necessity for biopsy. Angiography was the leading diagnostic technique for spleen conditions for many years, and continues to occupy this place for primary disease of the spleen (aneurysm, arterioportal fistula, haemangioma); it is currently gaining in importance with the advent of therapeutic embolization as an option. For diffuse spleen disease and also for circumscribed lesions, however, it has now been superseded by the non-invasive methods of diagnosis.
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PMID:[Modern imaging procedures in splenic diseases]. 355 34

On a second mail survey (in 1984) concerning radiation-induced cancer following radiotherapy for benign diseases, 86 cases were collected from 95 hospitals in Japan. Adding these to 150 cases collected in the previous survey in 1979, 236 cases were accumulated. This is a report on the analysis of the 236 cases from a clinicopathological viewpoint. Underlying diseases consisted of cervical tuberculous lymphadenitis (125 cases), skin diseases (41 cases), benign thyroid diseases (19 cases), hemangioma (18 cases) and others (33 cases). Radiation-induced cancers, which were defined as cancers originating in the radiation field, including leukemia, consisted of hypopharyngeal cancer (68 cases), skin cancer (61 cases), laryngeal cancer (26 cases), esophageal cancer (23 cases), thyroid cancer (23 cases), salivary gland tumor (8 cases) and others (27 cases). Multiple primary cancers in the radiation field were observed in 7 cases. Average latent period was 28.9 years. It was demonstrated that the older the age at irradiation the shorter the latent period. Based on the population irradiated for benign diseases before 1977, which was collected in the first mail survey, incidence of radiation-induced cancers was estimated to be about 0.9%. The incidence varied with the period of radiotherapy; 1.9% for the period of radiotherapy before 1955, 0.4% for 1956-1965, 0.1% for 1966-1977. Although radiotherapy is now rarely indicated for benign diseases, it was shown in the first mail survey that more than 15,000 cases of benign diseases had been irradiated after 1956. It seems to be reasonable to consider that radiation-induced cancers after radiotherapy for benign diseases may continue to be discovered for several years in the future.
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PMID:[Radiation-induced cancers following radiotherapy of benign diseases: the second mail survey in Japan]. 372 66

Over a period of nine years we observed 52 children with acute neurological symptoms which were caused by a cerebrovascular disease. Fourteen patients had congenital vascular malformations, most frequently AV-angiomas (9 patients). A Sturge-Weber-Syndrome and a venous angioma were found in two cases and one patient had an aneurysm of the middle cerebral artery. Thirty-eight patients had acquired cerebrovascular diseases such as ischaemic infarctions (22), intracranial haemorrhages without vascular malformations (14) and thromboses of the dural sinus (2). The cerebral infraction was a complication of a congenital heart disease in 8 children, two others suffered from chronic renal insufficiency and were on haemodialysis. Two children had a trauma of the internal carotid artery and in one patient a large haemorrhagic infarct was caused by hypernatremic dehydration. In 9 patients (6 females, 3 males) no obvious aetiology of the infarct could be found. However, in most of these cases a nonspecific febrile illness preceded the neurological manifestations. The thrombosis of the dural sinus occurred in a 6-week old previously healthy infant and in a 3-year old boy as a complication of a nephrotic syndrome. Intracranial haemorrhages (without cerebrovascular malformations) occurred in 14 patients, mainly as a complication of haematological diseases (acute lymphatic leukaemia, severe aplastic anaemia, haemophilia A, lupus erythematodes). Four children had spontaneous intracerebral haemorrhages without obvious causes. The prognosis for survival was good in children with infarcts, but persisting neurological deficits were more severe than in children with haemorrhages. At the acute stage the lethality was higher in children with intracranial haemorrhages.
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PMID:[Cerebrovascular diseases in childhood--etiology, clinical aspects and prognosis]. 395 16


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