Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the efficacy and toxicity of interferon alpha-2b (IFN-alpha2b) and levamisole treatment regimen in patients with metastatic renal cell carcinoma (RCC). Seventeen patients with metastatic RCC were treated using recombinant IFN-alpha2b at a dose of 10 MU/m2 body surface subcutaneously three times in a week, for 3 months, with levamisole 50 mg t.d.s orally on days 1-3 on alternate weeks. The mean follow-up period was 10.7 (range 2-23) months. We achieved 1 complete response (lasting for 12+ months) and 1 partial response (lasting for 15 months), for an objective response rate of 11.7%. A further 7 patients (41%) had a stabilization of disease. The overall toxicity was moderate, with mainly grade I or II side effects. Grade III toxicities reported among 3 patients including vomiting (2 patients) and anorexia (1 patient). There was no treatment related death. Although additions of levamisole to IFN-alpha do not result in any significant increase in treatment toxicity, the response rate appears to be no better than IFN-alpha monotherapy reported in the literature.
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PMID:Combined interferon alpha with levamisole in patients with metastatic renal cell carcinoma. 1223 Feb 71

Arterial chemoembolization with subsequent systemic chemotherapy was assessed prospectively. Of 94 consecutive patients with HCC, 31 patients were considered to have inoperable disease and were selected for chemoembolization. Twenty-two of the 31 patients underwent chemoembolization. In eight patients, technical problems with catheterization prevented the application of therapy, and one patient rejected further treatment. Regimen: Three monthly cycles of chemoembolization with cisplatin 20 mg/m(2) mixed with lipiodol delivered intraarterially with Gelfoam or collagen on day 1, followed by intravenous chemotherapy with cisplatin 60 mg/m(2) on day 2; interferon alpha-2c 30 microg (10 M IU) subcutaneously on days 2, 5, 9, and 12. Three percent of the patients (1/31) (CI 95% 0.08; 16.7) experienced a partial clinical response, in 53% alpha-fetoprotein levels decreased by more than 50%. On univariate analysis, performance status, Child score, Okuda stage, albumin levels, and lactate dehydrogenase were found to have an effect on survival. Postchemoembolization syndrome occurred in 68% of the patients, nausea/vomiting grades 3/4 (according to the World Health Organization WHO) in six patients, anemia grade 3 in three patients, leukopenia grade 3 in one patient and thrombocytopenia grade 3 in one patient. This treatment regimen is a very selective procedure. Because of the low response rate it is not recommended for routine clinical use.
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PMID:Chemoembolization with cisplatin, lipiodol and Gelfoam and subsequent systemic chemotherapy with cisplatin and interferon in patients with hepatocellular carcinoma: a non-randomized prospective study. 1288 22

We have reported that increasing the length of infusion from 5 min to 1 h appeared to substantially reduce the toxicity associated with fluorouracil (5-FU) modulated by leucovorin (LV) and interferon alpha-2a (IFN-alpha). This phase II study assessed the antitumor efficacy of this regimen. Patients (n=38) with colorectal cancer received IFN-alpha 5 MU/m(2) SC on days 1-6; on days 2-6, LV 200 mg/m(2) IV was given with 5-FU at initial doses of 370-425 mg/m(2)/h. The regimen was well-tolerated with no grade 4 toxicity. At 425 mg/m(2) 5-FU, grade 3 toxicities included diarrhea (8.6%), anorexia, fever and fatigue (5.7% each), neutropenia and nausea/vomiting (2.9% each). Individuals tolerated 5-FU doses up to 644 mg/m(2). Objective responses occurred in 27% of 37 patients; median time to progression and survival were 6.1 and 12.9 months. Only 1 of 25 informative tumor samples had high-frequency microsatellite instability (MSI), while 7 of 23 assessable patients (30%) with MSI-negative tumors had an objective response. With 425 mg/m(2), the average 5-FU Cp and AUC(0-1 h) were 37.4 microM and 1161 microM/h. Some 6 patients had extended sampling, and the half-lives of 5-FU and FBAL (apparent) were 8.6 and 100.0 min, respectively. A 1-h infusion of 5-FU is well tolerated; individual dose escalation of 5-FU allows each patient to receive the maximum tolerable dose.
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PMID:A phase II and pharmacologic study of fluorouracil given by a 1-hour infusion daily for 5 days with leucovorin and interferon alpha-2a in adenocarcinoma of the large bowel. 1587 Sep 35

We report the case of a 42-year-old woman with chronic hepatitis C (genotype 1), who in June 2004 started therapy with pegylated interferon alpha (PEG-IFNalpha) plus ribavirin. Two months later, she discontinued treatment because of polydipsia, polyuria and vomiting leading to a marked dehydration. Biochemical data showed type 1 diabetes mellitus with ketoacidosis, and insulin therapy was started. The patient, who before starting PEG-IFN alpha plus ribavirin therapy tested negative for glutamic acid decarboxylase antibodies (GADAb) and islet cell (ICAb) antibodies, became strongly positive for both autoimmune markers. This case confirms that patients with chronic hepatitis C who do not have baseline markers of pancreatic autoimmunity may develop severe ketoacidosis during treatment with PEG-IFNalpha, as well as with standard IFNalpha. In order to avoid this complication, as no guidelines are available and the pancreatic autoimmunity markers are not routinely analysed, we suggest frequent monitoring (e.g., every one to two weeks) of glycaemic values: e.g., every one to two weeks during the first 3 months (when this complication occurs most frequently) and monthly thereafter so as to identify diabetes at an early stage and before the onset of the appearance of severe ketoacidosis, which is life-threatening.
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PMID:A case of pegylated interferon alpha-related diabetic ketoacidosis: can this complication be avoided? 1772 57

Mastocytosis denotes a wide range of disorders characterized by having abnormal growth and accumulation of mast cells. Mast cells contain histamine and other inflammatory mediators, which have diverse actions within the body, and play crucial roles in acquired and innate immunity. The diverse actions of these inflammatory mediators can lead to puzzling symptoms in individuals with mastocytosis. These symptoms can include flushing, pruritus, nausea, vomiting, abdominal pain, diarrhea, vascular instability, and headache. These clinical features generally divide into cutaneous and systemic manifestations, giving rise to the two divisions of mastocytosis: cutaneous mastocytosis (CM) and systemic mastocytosis. CM has a highly favorable clinical prognosis. Systemic mastocytosis has a range of severity, with the milder forms often remaining chronic conditions, while the severe forms have rapid complex courses with poor prognoses. Generally, treatment is aimed at avoiding mast cell degranulation, inhibiting the actions of the constitutive mediators released by mast cells and, in severe cases, cytoreductive and polychemotherapeutic agents. Behavioral intervention includes avoidance of triggers, such as heat, cold, pressure, exercise, sunlight, and strong emotions. Treatment for released histamine and other inflammatory mediators includes H1 antihistamines, H2 antihistamines, proton pump inhibitors, anti-leukotriene agents, and injectible epinephrine (for possible anaphylaxis). For severe cases, treatment includes cytoreductive agents (interferon alpha, glucocorticoids, and cladribine) and polychemotherapeutic agents (daunomycin, etoposide, and 6-mercaptopurine). For very specific and severe cases, tyrosine kinase inhibitors, imatinib and midostaurine, have shown promise.
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PMID:Contemporary challenges in mastocytosis. 1963 28


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