Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a phase II study, 38 previously untreated patients with metastatic colorectal carcinoma were treated with continuous intravenous infusion of 5-fluorouracil (5-FU) 750 mg/m2 daily for 5 days, followed by weekly bolus 5-FU at 750 mg/m2 and subcutaneous interferon (IFN) at 9 million units three times per week. Of 35 evaluable patients, nine (26%) achieved a partial response (95% confidence limit, 11% to 41%), with a median response duration of 7.5 months (range, 4.4 to 17+ months). Seven patients (20%) had a minor response, and 10 (28%) had stable disease. The median length of survival was 13 months (range, 2 to 19+ months). The most common toxicities observed were stomatitis (52%) and diarrhea (43%). Neurotoxicity was seen in 34% of patients and consisted of gait disturbance, dizziness, confusion, memory loss, and dementia. Because of toxicity, 84% of patients required a reduction of the IFN dose by at least 50%, and 63% required reduction of 5-FU by at least 25%. We conclude that while the combination of 5-FU and IFN in patients with advanced colorectal carcinoma has some activity, the regimen is toxic and the observed response rate (26%) is not substantially superior to alternative 5-FU programs.
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PMID:Alfa-2A interferon and 5-fluorouracil for advanced colorectal carcinoma: the Memorial Sloan-Kettering experience. 155 42

Preclinical data showed that the cytotoxic effects of 5-fluorouracil (5-FU) are augmented by interferon (IFN). In a small study, 13 of 17 patients with advanced colorectal cancer responded to a regimen of 5-FU with IFN. Using the same dose and schedule as in this pilot study, 38 previously untreated patients with metastatic colorectal carcinoma were treated with continuous intravenous (IV) infusion of 5-FU 750 mg/m2 daily for 5 days, followed by weekly bolus 5-FU at 750 mg/m2 and subcutaneous IFN at 9 million units three times per week. Of 35 evaluable patients, nine (26%) had a partial response (95% confidence limit, 11% to 41%), with a median response duration of 7.5 months (range, 4.4 to greater than 11.7 months). Seven patients (20%) had a minor response, and ten (28%) had stable disease. The most common toxicities observed were stomatitis (52%) and diarrhea (43%). Neurotoxicity was seen in 34% of patients and consisted of gait disturbance, dizziness, confusion, memory loss, and dementia. Because of toxicity, 84% of patients required a reduction of the IFN dose by at least 50%, and 63% required reduction of the 5-FU dose by at least 25%. Although the combination of 5-FU and IFN in patients with advanced colorectal carcinoma has some activity, the regimen was toxic, and the observed response rate (26%) was not substantially superior to alternative 5-FU programs.
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PMID:Interferon alpha-2a and 5-fluorouracil for advanced colorectal carcinoma. Assessment of activity and toxicity. 224 87

Thallium poisoning is one of the most complex and serious toxicities known to man. The symptomatology of its toxicity is usually nonspecific due to the multi-organ involvement. The initial symptoms of thallium poisoning may include fever, gastrointestinal problems, delirium, convulsions and coma. Symptoms may appear rapidly, but more commonly the acute toxicity subsides to be replaced by a gradual development of mild gastrointestinal disturbances, polyneuritis, encephalopathy, tachycardia, skin eruptions, stomatitis, atrophic changes of the skin, nail changes (Mee's lines), and skin hyperesthesia (mainly in the soles of the feet and the tibia). Degenerative changes of the heart, liver and kidney, subarchanoid hemorrhage, bone marrow depression, and increased radiopacity of the liver may also occur. Development of psychotic behavior with hallucinations and dementia has also been reported. In humans the most characteristic sign of thallium toxicity is alopecia which usually appears in cases when death is delayed for 15-20 days. Other signs and symptoms may develop at any stage of toxicity. The current therapy for thallium poisoning is the use of prussian blue and potassium chloride. Potassium therapy is probably the single most effective agent in the treatment of thallium poisoning. Further research, however, is needed to find an optimal antidote for thallium.
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PMID:Thallium poisoning: a review. 633 55

The follow-up of an important number of patients during the last three decades has shown a substantial difference between the clinical description of pellagra in the 40's (the triad: dermatitis, diarrhea, dementia) and its clinical aspects today: sun-exposed teguments revealing erythema and rapidly becoming pigmented and parchment like, dried, parched lips, angular stomatitis, lead like sclera fine cornea vascularization; gastro-intestinal disturbances: constipation, unjustified diarrhea, strange migratory abdominal feelings accompanied by ubiquitous dysesthesias. Other characteristics of this form of disease are: unexpressive look, continuously concerned, thoughtful, anxious or frowning, labile mind, headaches, insomnia. Villager's neurosis sometimes may be considered, in an appropriate clinical context, as a facet of nutritional deficiency. It is considered that the "classical" features of pellagra have changed due to: protein ingestion slightly below the lowest normal limit, decrease of strenuous physical activity and some associated diseases (frequently gastrointestinal disorders, chronic alcoholism).
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PMID:Particular features of clinical pellagra. 792 Mar 32

Alzheimer's disease is characterized by deposition of beta-amyloid peptide (Abeta) into plaques in the brain, leading to neuronal toxicity and dementia. Human immunodeficiency virus type 1 (HIV-1) infection of the central nervous system can also cause a dementia, and amyloid deposition in the central nervous system is significantly higher in HIV-1-infected individuals compared with uninfected controls. Here we report that Abeta fibrils stimulated, by 5-20-fold, infection of target cells expressing CD4 and an appropriate coreceptor by multiple HIV-1 isolates but did not permit infection of cells lacking these receptors. Abeta enhanced infection at the stage of virus attachment or entry into the cell. Abeta fibrils also stimulated infection by amphotrophic Moloney leukemia virus, herpes simplex virus, and viruses pseudotyped with the envelope glycoprotein of vesicular stomatitis virus. Other synthetic fibril-forming peptides similarly enhanced viral infection and may be useful in gene delivery applications utilizing retroviral vectors. These data suggest that Abeta deposition may increase the vulnerability of the central nervous system to enveloped viral infection and that amyloidogenic peptides could be useful in enhancing gene transfer by enveloped viral vectors.
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PMID:Stimulation of enveloped virus infection by beta-amyloid fibrils. 1211 88

Pellagra is a nutritional wasting disease attributable to a combined deficiency of tryptophan and niacin (nicotinic acid). It is characterized clinically by four classic symptoms often referred to as the four Ds: diarrhea, dermatitis, dementia, and death. Prior to the development of these symptoms, other nonspecific symptoms insidiously manifest and mostly affect the dermatological, neuropsychiatric, and gastrointestinal systems. A review of the literature reveals several case reports describing pellagra in patients with anorexia nervosa. The most common features of pellagra in patients with anorexia nervosa are cutaneous manifestations such as erythema on sun-exposed areas, glossitis, and stomatitis. Health care providers might consider a trial of 150-500 mg niacin if anorexic patients exhibit these cutaneous findings. Pellagra can be diagnosed if cutaneous symptoms resolve within 24-48 hours after oral niacin administration. To further corroborate a diagnosis of pellagra in anorexic patients, specific 24-hour urine tests for niacin metabolites and 5-hydroxy-indole-acetic acid could be run prior to treatment with niacin being instituted. Other factors, such as mycotoxins, excessive dietary leucine intake (although not in anorexia), estrogens and progestogens, carcinoid syndrome, and various medications, might also lead to the development of pellagra. Although pellagra appears to be a rare, yet possible secondary complication of anorexia nervosa, it should be considered in the work-up of patients who exhibit cutaneous manifestations subsequent to sunlight exposure.
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PMID:Pellagra may be a rare secondary complication of anorexia nervosa: a systematic review of the literature. 1277 63

The balance between astrocyte and microglia neuroprotection and neurotoxicity defines the tempo of neuronal dysfunction during HIV-1-associated dementia (HAD). Astrocytes maintain brain homeostasis and respond actively to brain damage by providing functional and nutritive neuronal support. In HAD, low-level, continuous infection of astrocytes occurs, but the functional consequences of this infection are poorly understood. To this end, human fetal astrocytes (HFA) and monocyte-derived macrophages (MDM) were infected with HIV-1DJV and HIV-1NL4-3 (neurotropic and lymphotropic strains respectively) and a pseudotyped Vesicular Stomatitis Virus (VSV/HIV-1NL4-3) prior to intracranial injection into the basal ganglia of severe combined immunodeficient mice. Neuropathological and immunohistochemical comparisons for inflammatory and neurotoxic activities were performed amongst the infected cell types at 7 or 14 days. HIV-1-infected MDM induced significant increases in Mac-1, glial fibrillary acidic protein, ionized calcium-binding adapter molecule 1, and proinflammatory cytokine RNA and/or protein expression when compared with HSV/HIV-1- and HIV-1-infected HFA and sham-operated mice. Levels of neuron-specific nuclear protein, microtubule-associated protein 2, and neurofilament antigens were reduced significantly in the brain regions injected with human MDM infected with HIV-1DJV or VSV/HIV-1. We conclude that HIV-1 infection of astrocytes leads to limited neurodegeneration, underscoring the early and active role of macrophage-driven neurotoxicity in disease.
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PMID:Neuropathologic and neuroinflammatory activities of HIV-1-infected human astrocytes in murine brain. 1670 72