Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-dose continuous infusion 5-fluorouracil (LDCI-FU) was administered to 28 women with advanced breast carcinoma. Daily doses ranged from 175 to 250 mg/m2. The LDCI-FU was delivered continuously until the appearance of toxicity and was reinstituted at a 20% dose reduction after toxicity completely resolved. Patients with a median age of 56 years and a median performance status of 60% (Karnofsky) had been previously treated with combination chemotherapy. Complete responses were observed in two patients with soft tissue metastases. Thirteen patients experienced partial responses with a median duration of response of 4+ months. Partial responses were predominantly observed in soft tissue disease; however, five patients with visceral metastases experienced partial tumor regression. Median survival for the study group was 4+ months. Hormonal receptor status did not predict response to LDCI-FU. Toxicities included stomatitis, ten patients; hand-foot syndrome, eight patients; mild leukopenia, two patients; moderate thrombocytopenia, two patients; diarrhea, three patients; ataxia, three patients. Catheter-related toxicities of sepsis and/or thrombosis occurred in six patients. Because of the demonstrated activity in previously treated patients (53% response rate), LDCI-FU should be investigated in combination chemotherapy regimens in untreated breast cancer patients.
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PMID:Low-dose continuous infusion 5-fluorouracil. Evaluation in advanced breast carcinoma. 291 20

A number of verotoxin-producing Escherichia coli strains isolated from sporadic cases of hemorrhagic colitis in the United States over the last 5 yr were shown to belong to serogroups other than O157:H7-the serotype originally implicated in this disease. Experimental infection of gnotobiotic piglets with five such strains (0111:NM, 0145:NM, 045:H2, 04:NM, and Ound:NM) caused diarrhea resulting from mucosal lesions in the cecum and colon that were indistinguishable from those previously described in piglets infected with E. coli O157:H7. This suggests that, as with other categories of pathogenic E. coli, several serotypes cause hemorrhagic colitis in humans. The five E. coli strains that were compared with one O157:H7 strain and with an enteropathogenic calf strain (serotype 05:NM) caused a spectrum of disease ranging from moderate diarrhea (O157:H7) to severe illness (including septicemia and death) (0111:NM). Characteristic lesions, which were identical for all seven pathogenic strains, included bacterial attachment, effacement of the microvillus border, and dissolution of the cell membranes of surface and glandular epithelium, resulting in complete cell destruction. Some piglets exhibited neurologic signs of convulsions and ataxia. It is concluded that a number of E. coli serotypes, in addition to O157:H7, fulfill the present limited criteria for enterohemorrhagic E. coli, which include association with hemorrhagic colitis, production of one or more verotoxins, possession of a large plasmid (50-70 megadaltons), and induction of distinct mucosal lesions in the large bowel of gnotobiotic piglets.
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PMID:Studies in gnotobiotic piglets on non-O157:H7 Escherichia coli serotypes isolated from patients with hemorrhagic colitis. 327 73

Morphological changes of the thymus, tonsils, lymph nodes, spleen, and other organs in two observations of severe combined insufficiency (SCIN) in infants of the first year of life are described. In both cases there was hypoplasia of the thymus with the lack or occasional thymic bodies and poor content of thymocytes in the lobules. In one infant, hypoplasia of the thymus was combined with intestinal angiomatosis which suggested the syndrome of ataxia-teleangiectasia. In the other infant, SCIN was associated with severe granulocytopenia of the Kostman type. In this case epithelial cells of the lobules formed adenomatous structures. Both infants died with sepsis developing against the background of SCIN.
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PMID:[Hypoplasia of the thymus gland in children]. 686 Jan 70

The present study examines the effect of acute liver failure induced by a single intraperitoneal (i.p.) injection of D-galactosamine-HCl (3 g/kg) on somatostatin (SS) binding and levels in the rat frontoparietal cortex and hippocampus. Neurobehavioural changes were evaluated by the method of Zieve et al. [(1984) J. Lab. Clin. Med., 104:655-664]. The rats were decapitated as soon as they reached neurobehavioural stage I or II. In stage I, rats had lethargy and in stage II they showed mild ataxia, mainly in the hind limbs. The administration of D-galactosamine elevated serum transaminase levels (mean peak level 2,242 IU/1) but hypoglycemia, gross cerebral edema, or signs of sepsis were not detected in any of the animals studied. In addition, D-galactosamine did not affect somatostatin-like immunoreactivity (SSLI) levels in either brain area in any of the experimental groups as compared to the control groups. The rats sacrificed in stage I showed no change in the number or affinity of specific 125I-Tyr11-somatostatin (125I-Tyr11-SS) receptors in synaptosomes from the frontoparietal cortex and hippocampus. The rats sacrificed in stage II showed a decrease in the number of specific 125I-Tyr11-SS receptors in synaptosomes from both brain areas, with no change in receptor affinity. Binding studies were also conducted on synaptosomes from the frontoparietal cortex and hippocampus of rats that received D-galactosamine but did not develop acute liver failure and consequently did not develop neurobehavioural changes. The SS receptors in these synaptosomes did not change in comparison with controls, indicating that the D-galactosamine was not directly responsible for the changes in the cerebral SS receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain somatostatin receptors in a rat model of acute liver failure. 757 Mar 44

Ten of 18 children in a highly inbred Arab kindred suffered from either ataxia telangiectasia (AT) or a variant syndrome consisting of ataxia, microcephaly, and congenital cataract (AMC). Four of the nine afflicted children were treated in our unit when they developed lymphomas (both Hodgkin's and non-Hodgkin's including Burkitt's). They were given chemotherapy (either standard COMP or low-dose ABV/CVPP). The children with non-Hodgkin's lymphomas died of sepsis after receiving full-dose COMP. Low-dose ABV/CVPP brought about a 20-month remission in one child with nodular sclerosing Hodgkin's lymphoma and both AT and AMC, but she developed a preleukemic syndrome and her parents refused further treatment; she too died. A fourth child, also with nodular sclerosing Hodgkin's lymphoma, is currently in complete remission after ABV/CVPP. Treatment of lymphomas in patients with AT is extraordinarily difficult and has potential side effects so grave as to necessitate careful monitoring and individualized protocols.
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PMID:Ataxia telangiectasia and lymphoma: an indication for individualized chemotherapy dosing--report of treatment in a highly inbred Arab family. 762 85

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26

The patient first noticed general muscle stiffness at the age of 36. Two years later, she suffered from a tonic-clonic seizure which brought her to a hospital for the first time. Choreoathetoid movement, ataxia and cognitive deficit were apparent. At the age of 44, tonic-clonic seizures became more frequent and she was admitted to our hospital as being status epilepticus. After the cessation of clinical seizures, she became appllic. Gradual increase of atrophic changes in cerebrum, cerebellum and brain stem were observed by MRI and CT. Hematological study showed that she had abnormal hemoglobin, Hb Takamatsu. Four of her five children were clinically examined; all of them showed abnormal EEG findings; three being mentally retarded and had clinical generalized convulsive seizures; two had hemoglobinopathy (Hb Takamatsu). The patient died from sepsis at the age of 50 and the autopsy was carried out. The brain weighed 930 gram. Histological findings confirmed the diagnosis of dentato-rubro-pallido-luysian atrophy; neuronal loss accompanied by gliosis in dentate nuclei, red nuclei, lateral part of globus pallidus, and subthalamic nuclei. The coincidence of the hereditary traits of two independent diseases, DRPLA and familial hemoglobinopathy (Hb Takamatsu) suggests closeness of their genetic loci.
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PMID:[A familial case of DRPLA diagnosed by an autopsy associated with hemoglobinopathy (Hb Takamatsu)]. 825 33

Sensory ataxia in inorganic germanium intoxication is rare. A 63-year-old housewife had taken inorganic germanium preparations at a dosage of 36 mg a day for about 6 years (total dose about 80 g). She subsequently developed difficulty in writing and gait disturbance with peripheral neuropathy and renal involvement. Germanium, which is not usually detected in the non-germanium user, was accumulated in her hair and nails, permitting a diagnosis of inorganic germanium intoxication. The peripheral neuropathy and renal injury were not reversible after discontinuing the preparation. Pneumonia and sepsis then supervened and the patient died. Autopsy findings showed degeneration and loss of the dorsal root ganglion cells and degeneration of the dorsal column of the spinal cord. Two previously reported cases presented with ataxia. These patients took germanium for long periods and/or large quantities like our case. It was supposed that sensory ataxia was induced by chronic and dose dependent toxicity of inorganic germanium.
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PMID:Germanium intoxication with sensory ataxia. 858 90

Onion bulb formations involving cranial nerves are an unusual pathologic feature. We report the postmortem neuropathologic findings in a 69-year-old man with a longstanding neuropathy characterized by progressive muscle weakness, sensory ataxia and multiple cranial nerve abnormalities. Electrodiagnostic testing disclosed features of an acquired demyelinating polyneuropathy. Treatment with corticosteroids and plasmapheresis resulted in no change in his neurologic status, and the patient died after repeated episodes of pneumonia and sepsis. Autopsy showed widespread onion bulb formation in cranial nerves III, IV, V, VI, X, XI and XII, anterior and posterior spinal nerve roots, dorsal root ganglia and multiple peripheral nerves, some of which also had foci of epineurial perivascular inflammation. Muscle sections revealed severe neurogenic atrophy. This case demonstrates that, in longstanding acquired demyelinating neuropathy, the cranial nerves also undergo repetitive cycles of demyelination and remyelination resulting in severe weakness of the bulbar musculature and histologic features of hypertrophic neuropathy.
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PMID:Severe cranial nerve involvement in longstanding demyelinating polyneuropathy: a clinicopathologic correlation. 883 44

Two siblings manifested a neuro-haematologic syndrome characterised by low birth weight, failure to thrive, chronic persistent tongue ulceration, severe truncal ataxia and pancytopenia without either telangiectasia or chromosomal instability. One sibling died from sepsis and the cerebellum demonstrated reduced cellularity of the molecular and granular layers with relative preservation of Purkinje cells and minimal gliosis. A surviving sibling has shown haematologic progression to a myelodysplastic disorder. There was no evidence of any chromosomal instability following exposure of fibroblasts and lymphocytes to irradiation. Monosomy-7 was not present in the surviving sibling. We suspect that these two patients represent another example of the rare Hoyeraal-Hreidarsson syndrome and we are currently engaged in very close monitoring of the surviving sibling for evidence of any karyotypic abnormality.
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PMID:Familial cerebellar hypoplasia and pancytopenia without chromosomal breakages. 1002 49


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