Clinical problem-solving: costly errors.
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Biomedical subjects
Publications and source records attributed to D Daliani.
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Light chain deposition disease (LCDD) and light and heavy chain deposition disease (LHCDD) are rare clinical entities that have been associated with multiple myeloma, with monoclonal gammopathy of unknown significance (MGUS), or without any detectable protein abnormality. Renal failure is common, the diagnosis is difficult and prolonged survival is rare. The first patient with LHCDD and MGUS who progressed to multiple myeloma after 11 years is presented. A rising level of monoclonal IgA immunoglobulin, bone marrow plasmacytosis, and the presence of multiple bone marrow lesions on magnetic resonance imaging provided the first evidence of disease evolution. When management of serious complications permits a long survival, some patients with LCDD or LHCDD will develop multiple myeloma.
The combination of 5-fluorouracil (5-FU) and folinic acid (FA) has demonstrated activity in colorectal cancer (CC). Cisplatin is reported to have synergistic activity with 5-FU. We examined the combination FA + 5-FU + cisplatin in patients who had previously received chemotherapy with FA + 5-FU and relapsed. Two months after the last dose of FA + 5-FU and documentation of relapse, patients continued with the regimen consisting of cisplatin 20 mg/m2 in 15 min i.v. infusion followed by FA 500 mg/m2 in 1 h i.v. infusion, in the middle of which 5-FU 500 mg/m2 i.v. bolus was administered, with adequate post-hydration. This was repeated weekly for 4 weeks followed by a 2 week rest, for a maximum of six cycles. A total of 30 patients with CC that had relapsed to the combination of FA + 5-FU were treated; 23 had previous surgery and none had radiotherapy. Local recurrence was found in eight patients, metastases in the liver in 21, in lymph nodes in six, lung six and peritoneal metastases in seven. Seven patients responded partially. Toxicity requiring dose reduction or discontinuation of treatment included neutropenia 42% (grade 3:7%), mucositis 28% (grade 1:2), diarrhea 63% (Grade 3:10%), nausea-vomiting 55% (Grade 3:10%), increased creatinine value in three patients and peripheral neuropathy in two patients. We conclude that evaluation of this regimen shows substantial toxicity, with satisfactory response as a second line chemotherapy in these heavily pretreated patients.
The purpose of this study was to determine whether preloading administration of ondansetron given 12.5 h before cisplatin therapy, every 6 h, is better in controlling acute cisplatin-induced emesis than a standard dose every 8 h. All patients had previously received three cycles of CDDP-based chemotherapy in a dose of 100 mg/m2. Ondansetron was given according to two schedules: in group A (40 patients) at a dose of 8 mg in 100 ml normal saline over 10 min by intravenous infusion before the infusion of CDDP continued with 1 tablet of 8 mg after 8 and 16 h; in group B (40 patients) it was administered in six intravenous doses (every 6 h) starting 12.5 h before cisplatin administration. During the following 3 days, patients from both groups continued with tablets of 8 mg orally, every 8 h in group A and every 6 h in group B. The only difference in terms of the antiemetic response noticed between the two groups was in the number of patients that presented with nausea, which was increased in group A (32) in comparison to group B (25; p < 0.022). No difference was found in the number of vomiting episodes, retches or control of emesis, during the 3-day evaluation period after cisplatin infusion, and in secondary side effects. In conclusion the total dose of 24 mg ondansetron during the acute phase of emesis is as effective as preloading and increasing the total dose to 32 mg.