Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034069 (pulmonary fibrosis)
7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty-five patients with nonmetastatic (Stages I, II, and III) esophageal cancer (EC) were treated with radiotherapy (RT) alone (56.00 to 61.00 Gy in 6 to 7 weeks) or synchronous combinations of radiotherapy and chemotherapy (RT-CT). RT-CT consisted of 41.40 to 50.40 Gy in 4.5 to 8 weeks with continuous infusion 5-fluorouracil 5-FU (1000 mg/m2/d for 4 days in weeks 1, 4, and 8), mitomycin C (10 mg/m2 intravenously [IV] in weeks 1 and 8), cisplatin (75 mg/m2 IV in week 4). Maintenance CT consisted of methotrexate (200 mg/m2 IV), leucovorin (10 mg/m2 orally every 6 hours for 5 doses), and 5-FU (600 mg/m2 IV) in weeks 10, 12, and 14. Thirty-five patients treated by RT alone (Group A) were comparable in terms of age, sex, AJC staging, histologic condition, and location of primary with 30 patients treated by RT-CT (Group B). In Group A (range, 2- to 144+ months), two patients (42 and 144 months) are alive and well. In Group B (range, 2- to 59+ months), 12 patients (7 to 59 months) are alive and well. Median survival in Group A is 8 months, compared with 15 months for patients achieving a complete response (CR) in Group B. Patients in Group B achieved a 77% CR rate by endoscopy-biopsy, whereas 30% of the patients in Group A achieved a CR (P = 0.0001). The recurrence rates at the primary site/regional nodes were 77% and 27% in Groups A and B, respectively (P = 0.0001). The incidences of distant metastases were 29% and 20%, respectively (P = 0.423). In Group A, the 1-year and 2-year cumulative survival rates were 27% and 13%, respectively. In Group B, the cumulative survival rates were 53% at 1 year and 29% at 2 years (P = 0.023). Aside from reversible myelotoxicity, the incidences of pulmonary fibrosis, esophagitis, and fistulae formation were less frequent in the combined technique treatment group. A compilation of reported chemoradiation protocols for EC indicates consistently improved 1-year and 2-year survival rates, compared with surgical and RT series. The key to further improvement in the treatment of EC appears to lie in increasing the biologic response (RT fractionation and endocavitary RT) and optimal use of multiple effective CT agents with nonadditive toxicities.
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PMID:Radiotherapy alone and chemoradiation for nonmetastatic esophageal carcinoma. A critical review of chemoradiation. 272 May 85

The rational treatment of systemic sclerosis can be based on a model of its pathogenesis. This model posits a genetic background upon which external stimulae act, resulting in immune activation, vascular injury, fibroblast proliferation, and collagen deposition. The collagen, in turn, increases immune activation, thus resulting in perpetuation of the activation/injury cycle. If this pathogenetic model holds true, intervention can occur at the level of vascular damage, prevention of fibrosis or immunosuppression. Prevention of vascular damage and improvement of oxygenation has been attempted with prostacyclin derivatives, with mixed results. Prevention of fibrosis with interferon-gamma shows some hopeful results in pulmonary fibrosis. Relaxin, too, seems to hold hope for efficacy, whereas the results of therapy with D-penicillamine have been disappointing. Immunosuppression with chlorambucil has not been effective, but the study design was flawed in that trial. Methotrexate may work, but results are mixed. 5-Fluorouracil seems effective, but may be toxic. Cyclophosphamide is effective in open trials, and well-controlled trials are just starting. Finally, stem cell transplantation, a very aggressive form of immunosuppression, is showing some apparent efficacy, but its use is only in the pilot stages.
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PMID:Rational therapy in the treatment of systemic sclerosis. 1109 5

The pathogenesis of pulmonary fibrosis (PF) induced by bleomycin and its derivative, peplomycin (PEP), is insufficiently understood. To prevent PF and to administer PEP safely, we examined the influence of PEP on pulmonary function in 135 patients who underwent concomitant chemo (PEP + 5-FU)-radio (60Co) therapy and pulmonary function tests. In the inductive therapy, 5 mg of PEP was intramuscularly injected three times a week and a total of 41.6 +/- 14.3 mg was administered. Of the patients, 98 received oral azelastine hydrochloride (AZH, 4 mg/day) during the inductive therapy with the aim of prophylaxis of PF. The oxygen partial pressure in arterial blood (PaO2) only slightly decreased from 84.2 +/- 12.1 mmHg before treatment to 82.8 +/- 12.5 mmHg after treatment, while, carbon oxide diffusion (%DLco) decreased after treatment in most patients (p < 0.001, by paired t test) with mean values before treatment of 106.3 +/- 24.5% and after treatment 99.5 +/- 24.9%. The decrease of %DLco was associated with the dose of PEP until about 40 mg but further decreases of %DLco were not prominent. In the patients who underwent oral AZH, the decrease of %DLco weaker than that in patients without AZH: the decrease rates of %DLco in the former and latter were 4.3 +/- 9.4% and 14.1 +/- 15.9%, respectively. From the chest X-ray examination, mild PF was suspected in three patients but no advancement of PF or clinical symptoms were observed. From these results, it was concluded first that %DLco is more useful than PaO2 as the predisposing risk factor for PF, second that the decrease of %DLco depends on the dose of PEP until about 40 mg, third that AZH is expected to inhibit PEP-induced PF, and fourth that a small dose (20-40 mg) of PEP can be administered without inducing PF if care is exercised as to the patient's age, general condition and the value of %DLco in the use of PEP.
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PMID:[Influence of peplomycin on pulmonary function (PaO2, %DLco) in patients with oral carcinoma]. 1157 35