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)

Currently available techniques do not enable the clinician to identify which patients with rheumatoid arthritis will respond favorably to chrysotherapy or to predict which patients will develop gold-related complications. Gold concentrations are similar in blood, urine, feces, skin, hair and nails in gold-responders and non-responders, and in gold-toxic and non-toxic patients. However, gold toxicity is a function of dosage schedule; higher than conventional doses increase the prevalence and severity of adverse reactions. Preliminary observations suggest that the frequency of common side-effects (e.g. dermatitis, stomatitis, proteinuria) from oral gold (auranofin) is less than that incurred with intramuscular gold prepartions. The possible genetic predisposition to develop gold toxicity is under investigation.
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PMID:Gold compounds in rheumatoid arthritis: clinical-pharmacokinetic correlates. 11 49

One hundred thirty-eight adults with advanced cancers were treated with Baker's Antifol. The complete response + partial response rate was only 10%. Best responses were obtained in 31 patients with lung adenocarcinoma (complete response + partial response, 13%), in 25 patients with colorectal carcinoma (partial response, 16%), and in 6 patients with renal cell carcinoma (partial response, 50%). Two partial responses occurred in 15 patients with squamous cancer. No significant responses were seen in 27 patients with other adenocarcinomas, 13 with sarcomas, 14 with melanomas, and 8 with miscellaneous tumors. The most frequent toxicities were dermatitis, stomatitis, gastrointestinal symptoms, and mild myelosuppression. The incidence of dermatitis was significantly decreased by shortening the schedule of Baker's Antifol administration from 5 to 3 days. Baker's Antifol has some degree of antitumor activity, and studies of combination of this agent with other effective chemotherapeutic agents are indicated.
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PMID:Phase 2 study with Baker's Antifol in solid tumors. 13 5

Triazinate (Baker's Antifol, NSC 139105) was given to 28 patients as a single agent in the chemotherapy of advanced colerectal carcinoma. The dosage utilized was 250 mg/m2 intravenously, administered daily in three consecutive days. Patients were evaluated at three weeks, six weeks, and then monthly until progression was evident. Various immunologic determinants (i.e., DNCB sensitization, immunoglobulins, recall skin tests, lymphocyte blastogenesis, and circulating lymphocytes, T-cells and B-cells) were obtained prior to treatment and at each re-evaluation. The principal side effects were dermatitis, stomatitis, diarrhea, nausea, somnolence, and leukopenia. There was no discernable effect of Triazinate on the immunologic determinants tested. There was one complete response, and four partial responses, for an objective regression rate of 18%. This study suggests that Triazinate has a definite, though limited, effect on advanced colorectal carcinoma.
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PMID:A phase II study of triazinate (NSC 139105) in advanced colorectal carcinoma. 14 77

Pyrazofurin was administered to 17 patients with refractory acute myelogenous leukemia in 5-day courses every 2-3 weeks. Doses ranged from 30 to 60 mg/m2/day. Severe stomatitis and dermatitis occurred at doses effective in reducing the leukocyte count (45 mg/m2). Reduction of the dose to 30 mg/m2 resulted in less toxicity and less chemotherapeutic effect. These results indicate that at tolerable doses given as described, pyrazofurin had little antileukemic activity in acute myeologenous leukemia.
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PMID:Phase I study of pyrazofurin in refractory acute myelogenous leukemia. 15 46

The glucagonoma syndrome is characterized by dermatitis, stomatitis, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia--all in association with a glucagon-secreting alpha-cell tumor of the pancreas. A review of 21 cases showed strikingly similar features. A generalized, symmetrical dermatitis initially appeared to be asteatotic or eczematous over the perineum, buttocks, and lower extremities. Gradually, a more characteristic migratory necrolytic erythema with transient bulla formation and erosions developed in intertriginous and dependent areas. Histologically, the most specific features included necrolysis of the upper epidermis, with liquefaction necrosis of the granular cell layer and subcorneal clefting or blister formation. The dermatologist is often first to examine such patients; early recognition of this syndrome with prompt surgical removal of the primary pancreatic lesion may afford cure of the neoplasm.
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PMID:Glucagonoma syndrome. Report of two cases and literature review. 19 36

A 34-year-old man presented with classic glucagonoma syndrome manifested by weight loss, dermatitis, stomatitis, anemia, and mild diabetes mellitus. The diagnosis of glucagonoma was made by light and electron microscopic demonstration of a metastatic alpha cell carcinoma in a liver biopsy specimen. Plasma glucagon concentration was abnormally high. The patient also had symptoms and signs of involvement of the central nervous system. Radionuclide and CAT scans of the brain, negative CSF cytology and myelography excluded the possibility of metastases or other space-occupying lesions. Glucagon was demonstrated in the CSF. We postulate that the neurologic symptoms were due to direct or indirect effect of this hormone on the brain. Following therapy with streptozotocin and 5-fluorouracil, the patient had a subjective and objective clinical and hormonal remission of his disease including amelioration of his neurological impairment.
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PMID:Neurologic involvement in glucagonoma syndrome: response to combination chemotherapy with 5-fluorouracil and streptozotocin. 22 32

The occurrence of overall toxicity was analyzed for 43 patients with osteosarcoma who received 349 high-dosage courses of methotrexate (HD-MTX) with citrovorum factor (Leukovorin) "rescue" (CF). The dosages of HD-MTX ranged from 50 to 350 mg/kg. Overall toxicity was assessed on the basis of five manifestations of toxicity: stomatitis, dermatitis, myelosuppression, liver dysfunction, and kidney function abnormalities. The great majority (91.4%) of the infusions were well tolerated, but 8.6% were associated with moderate or severe toxicity. Stomatitis and serum glutamic-oxaloacetic transaminase (SGOT) changes were the most frequent postinfusion findings. Three patients died from causes related to MTX toxicity. Dose, age, sex, and number of prior infusions were investigated by logistic regression analysis for prognostic effect on frequency of moderate to severe overall toxicity. Age and number of prior infusions had significant (P less than 0.06) effects on overall toxicity. Patients older than 15 years with greater than 10 prior infusions constituted the "high risk" group with a risk of moderate to severe toxicity 6.3 times that of the younger patients with fewer than 10 infusions.
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PMID:Evaluation of overall toxicity of high-dosage methotrexate regimens. 31 42

Plasma methotrexate (MTX) concentrations at 48 hours were determined for 40 patients with osteosarcoma who received 256 infusions of high-dose methotrexate-citrovorum rescue (HD-MTX-CF) regimen. Five manifestations of toxicity (dermatitis, stomatitis, myelosuppression, liver dysfunction, and kidney dysfunction) were considered in the assessment of the overall toxicity. Logistic regression analysis was applied to study the effect of number of prior infusions, age, and 48-hour MTX plasma level on the risk of moderate or severe overall toxicity. Each factor had a significant effect with P less than 0.08. The predicted incidence of moderate-severe overall toxicity in the high-risk group (48-hour MTX level greater than 1.00 x 10(-6) mol/l., prior infusions greater than 10, age greater than or equal to 15 years) was 33.2% compared to only 2.4% in the "low-risk" group (48-hour MTX level less than or equal to 1.00 x 10(-6) mol/l., prior infusions less than or equal to 10, age less than 15 years). The plasma MTX determination at 48 hours postinfusion was found to be independent of both dose infused and patient's age.
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PMID:Significance of the 48-hour plasma level in high-dose methotrexate regimens. 31 68

"BAR" therapy is a combined therapy with BUdR (Radiosensitizer), Antimetabolites (5-FU, FT-207 etc.) and Radiation for malignant tumours. How radiation can be reduced as far as possible and how the effects of treatment can be increased as much as possible are the objectives of this study of combining radiation and BUdR therapy. The authors attempted to irradiate 3-5 days after the BUdR and antimetabolite had been infused via the superficial temporal artery, in 12 malignant oral tumours (11 squamous cell carcinomas and 1 reticulum-cell sarcoma). BUdR 50-250 mg/day, antimetabolites (5-FU) 10-250 mg/day and a total irradiation dose of 6000 rads by 6 MeV Linac X-ray or Co-60 gamma ray, 200 rads/day were given. 9 marked responses, 2 moderate responses and 1 no response (2 cases were operated on by local resection) were obtained by the authors. Side effects of treatment were observed during the course of "BAR" therapy. Stomatitis was found in all patients and it occurred on the mucosa of the tumour-affected site especially. Dermatitis of the skin of the face was noted in 6 cases, resembling irradiation dermatitis. Fever was observed in 4 cases and it always occurred after irradiation. Diarrhoea was noted in 3 cases and occurred before irradiation, 2 out of 3 were given BUdR 0.1 g and the remaining one was given BUdR 1 g, and 5-FU lg. In addition, there were: 1 loss of appetite, 1 nausea and 1 exfoliation of nails.
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PMID:The effects of "BAR" therapy on oral malignant tumors. 35 11

Adult cotton top marmosets made niacin deficient by long-term dietary deprivation, developed a syndrome characterized by anorexia, weight loss, weakness, diarrhea, dermatitis, enterocolitis and stomatitis. The stomatitis was highlighted by a necrotizing gingivitis and periodontitis and by an ulcerative and atrophic glossitis.
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PMID:Studies on the biology of the periodontium of marmosets. XIII. Histopathology of niacin deficiency stomatitis in the marmoset. 40 31


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