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PubMed2002

Use of prostaglandins and bromocriptine mesylate for pregnancy termination in bitches.

OBJECTIVE: To assess the efficacy and safety of 2 protocols using bromocriptine mesylate and prostaglandins to terminate unwanted pregnancy in bitches. DESIGN: Prospective randomized single-blind controlled study. ANIMALS: 34 crossbred and purebred bitches referred for possible pregnancy termination. Seven additional pregnant bitches were used as controls. PROCEDURE: Pregnancy was assessed by ultrasonographic examination from day 25 after mating in all bitches. Of the 34 bitches, 25 were pregnant and were randomly allocated to a treatment group. Group-1 dogs (n = 12) received a combination of increasing amounts of bromocriptine mesylate (15 to 30 microg/kg [6.8 to 13.6 microg/lb], p.o., q 12 h) and dinoprost tromethamine (0.1 to 0.2 mg/kg [0.045 to 0.09 mg/lb], s.c., q 24 h). Group-2 dogs (n =13) received a combination of increasing amounts of bromocriptine mesylate (the same schedule as group-1 dogs) and cloprostenol sodium (1 microg/kg [0.45 microg/lb], s.c., q 48 h). Both groups were treated until pregnancy termination. Results-Treatment success was 100% in both groups. Days of treatment required for pregnancy termination did not significantly differ between groups (5.0 +/- 0.6 vs 3.7 +/- 0.6 days, group-1 and group-2 dogs, respectively) although adverse effects only developed in group-1 dogs. At the end of the protocols, pseudopregnancy was observed in 3 of 12 and 6 of 13 group-1 and group-2 dogs, respectively. Pregnancy termination was followed by a mucoid sanguineous vulvar discharge for 3 to 10 days. CONCLUSIONS AND CLINICAL RELEVANCE: Results of this study indicate that protocols that combine the use of bromocriptine mesylate and prostaglandins for the termination of unwanted pregnancy in bitches are efficient and safe. The use of bromocriptine mesylate and cloprostenol had the best results and could be easily used on an outpatient basis.

Abortifacient Agents, Nonsteroidal↗
PubMed2004

[Clinical effectiveness of ropivacaine mesylate in epidural anesthesia and postoperative analgesia].

OBJECTIVE: To compare the clinical effectiveness of ropivacaine mesylate and ropivacaine hydrochloride in epidural anesthesia and postoperative analgesia. METHODS: Forty-four patients undergoing epidural anesthesia for intraperitoneal hysterectomy or hysteromyomectomy were randomly assigned to two equal groups. Group ropivacaine hydrochloride received 15 ml ropivacaine hydrochloride of 7.5 mg/ml in anesthetic and 2 mg/ml in postoperative analgesic subsequently while group ropivacaine mesylate correspondingly received ropivacaine mesylate of both 15 ml of 8.94 mg/ml and 2.374 mg/ml. RESULTS: No significant differences were found in the onset, extent, and duration of sensory and motor blockage, and also in the hemodynamic stability, when ropivacaine mesylate was comparable with ropivacaine hydrochloride. No severe adverse events were observed in this study. CONCLUSION: Ropivacaine mesylate is an effective and safe alternative to ropivacaine hydrochloride in epidural anesthesia and postoperative analgesia.

Adolescent↗
PubMed2005

Effect of fenoldopam mesylate in critically ill patients at risk for acute renal failure is dose dependent.

BACKGROUND: Acute renal failure (ARF) is common and difficult to prevent, especially in intensive care unit (ICU) patients with cancer. Therapeutic trials with various agents have generally been ineffective in preventing ARF. We describe the effects of two different doses of the dopamine DA-1 receptor agonist fenoldopam mesylate on renal function in a series of critically ill cancer patients at risk of developing ARF. METHODS: We performed a retrospective chart review of 100 consecutive patients who received fenoldopam mesylate for at least 72 h in the medical and surgical ICUs of The University of Texas M. D. Anderson Cancer Center who were at risk of developing ARF. Eighteen patients received low-dose fenoldopam mesylate (< or =0.05 microg/kg/min). The remaining 82 patients received high-dose fenoldopam mesylate (0.07-0.1 microg/kg/min). Data were collected relating to drug dosage, patient demographics, severity of illness, and indices of renal function. RESULTS: Patients were moderately ill, with a mean APACHE II score of 18+/-6 at initiation of fenoldopam infusion. Eighty-five percent of patients had at least two risk factors for the development of ARF, and 20% had four. For the group overall, the incidence of ARF was 13%, and the hospital mortality rate was 37%. When compared with the low-dose group, patients who received high-dose fenoldopam had a significantly shorter ICU length of stay despite a significantly higher APACHE II score (p=0.01). The high-dose group also had a highly significant decrease in serum creatinine levels at 72 h (p=0.005). CONCLUSIONS: These data support the hypothesis that fenoldopam mesylate may provide a degree of dose-dependent renal protection in cancer patients with early acute renal failure.

Acute Kidney Injury↗
PubMed2002

Response of extraabdominal desmoid tumors to therapy with imatinib mesylate.

BACKGROUND: Desmoid tumor represents a rare monoclonal neoplasm arising from deep musculoaponeurotic structures and may occur sporadically or in association with the familial adenomatous polyposis and Gardner syndromes. Desmoid tumors do not appear to demonstrate metastatic potential; however, local infiltrative growth results in significant morbidity and potential mortality. Although the delineation of optimal therapy for desmoid tumors has been confounded by several factors, surgical resection with adjuvant radiotherapy for a positive surgical margin remains the standard approach. Responses have been demonstrated to nonsteroidal antiinflammatory agents, antiestrogen compounds, and a variety of other agents in small series. Imatinib mesylate appears to demonstrate inhibitory activity against multiple class 3 receptor tyrosine kinases, including platelet-derived growth factor receptor (PDGFR)-alpha and PDGFR-beta, as well as c-kit. METHODS: The authors performed immunohistochemical and qualitative real-time polymerase chain reaction analysis on nine desmoid tumor specimens that demonstrated consistent positivity for c-kit as well as PDGFR-alpha and PDGFR-beta. At the time of last follow-up, 2 patients had received therapy with imatinib mesylate at a dose of 400 mg twice daily. RESULTS: Both patients demonstrated ongoing radiographic and clinical responses with a duration of 9 months and 11 months, respectively. CONCLUSIONS: Imatinib mesylate has been reported to have activity against desmoid tumor, most likely because of c-kit and PDGFR receptor tyrosine kinase activity inhibition, and warrants further study. The relative novelty of this agent and the lack of long-term toxicity data should prompt its use only in the salvage setting in which established local and systemic approaches fail to control disease. In addition, the use of imatinib mesylate in the treatment of this neoplasm preferably should be in the context of a formal prospective clinical trial.

Adolescent↗
PubMed2003

Prediction of initial cytogenetic response for subsequent major and complete cytogenetic response to imatinib mesylate therapy in patients with Philadelphia chromosome-positive chronic myelogenous leukemia.

BACKGROUND: Obtaining a major (Philadelphia chromosome [Ph] of < 35%) or a complete cytogenetic response (Ph of 0%) has been associated with excellent long-term survival. Cytogenetic response may continue to improve with therapy. Because early allogeneic stem cell transplantation (SCT) may be associated with a better outcome, early parameters predicting for subsequent cytogenetic responses would optimize the treatment decision-making. METHODS: The current study was performed to analyze whether early cytogenetic responses may be predictive of later major or complete cytogenetic responses to imatinib mesylate therapy in patients with Ph-positive chronic myelogenous leukemia (CML). RESULTS: Two hundred sixty-one patients with Ph-positive, chronic-phase CML after failure with interferon therapy who were treated with imatinib mesylate therapy were analyzed. A persistence of 100% Ph-positive cells after > or = 6 months of imatinib mesylate therapy was associated with a major cytogenetic response rate of 9-13% and a complete cytogenetic response rate of 0-4%. However, a minor cytogenetic response after 3-12 months of therapy still was associated with high rates of major (68-83%) or complete (35-54%) cytogenetic response rates. CONCLUSIONS: Patients with Ph-positive, chronic-phase CML who have persistent 100% Ph-positive disease after > or = 6 months of imatinib mesylate therapy may be offered allogeneic SCT or considered for alternative investigational therapies.

Benzamides↗
PubMed2004

Imatinib mesylate as treatment for adenoid cystic carcinoma of the salivary glands: report of two successfully treated cases.

BACKGROUND: Adenoid cystic carcinoma (ACC) is a malignant neoplasia of the salivary glands that is treated primarily by surgery. Local control and survival are usually compromised despite surgery. Expression of KIT tyrosine kinase is involved in the pathogenesis of ACC. Imatinib mesylate is a potent inhibitor of KIT tyrosine kinase, so we explored the possibility that ACC could be a potential target for this drug. METHODS: We report two cases of unresectable ACC treated with imatinib mesylate in the context of recurrent disease (case 1) and locally advanced tumor at its initial presentation (case 2). RESULTS: Both patients responded well to treatment with imatinib mesylate. Significant regression of recurrent disease (case 1) resulted in a successful salvage surgical resection; the locally advanced tumor (case 2) had an excellent response to treatment, but, unfortunately, the patient refused salvage resection. CONCLUSION: This is the first time ACC is reported to respond to imatinib mesylate. Studies in which more patients are enrolled in controlled clinical trials are needed to confirm this observation.

Antineoplastic Agents↗
PubMed2005

Differential tyrosine phosphorylation of leukemic cells during apoptosis as a result of treatment with imatinib mesylate.

Bcr-Abl fusion tyrosine kinase contributes to leukemic transformation. Imatinib mesylate inhibits Bcr-Abl tyrosine kinase, resulting in a blockage of tyrosine phosphorylation in its downstream pathways. We analyzed the alteration of tyrosine phosphorylation, on BCR/ABL+ chronic myelogenous leukemia cells, after treatment with imatinib mesylate. Data were collected using a two-dimensional gel electrophoresis followed by Western blot and mass spectrometry. The inhibition of Bcr-Abl tyrosine kinase by 2.5 microM imatinib mesylate caused both cell cycle arrest in the G0/G1 phase and increased the portion of apoptotic cells. As a result, the population of leukemic cells decreased by 30% and 70% compared to controls at 24 and 72 h, respectively. Furthermore, treatment with imatinib mesylate altered tyrosine phosphorylation of 24 protein spots as the incubation time proceeded from 0 to 24 and 72 h. Ten of the 24 protein spots are visible at all three times. Four are detectable at both the 0 and 24 h points in time. Eight were detectable only at time 0.

Antineoplastic Agents↗
PubMed2006

Imatinib mesylate inhibits proliferation and modulates cytokine expression of human cancer-associated stromal fibroblasts from colorectal metastases.

Recent data have expanded the concept that cancer-associated stromal fibroblasts (CAFs) play an important role in tumor invasion and angiogenesis. Here, we show that platelet-derived growth factor (PDGF) is a mitogen for human CAFs isolated from hepatic metastases of colorectal cancer. The tyrosine kinase inhibitor imatinib mesylate (1 microM) abrogated the PDGF-induced DNA synthesis, and furthermore counteracted an inhibitory effect of PDGF on the expression of alpha-smooth muscle actin (alpha-SMA). High-dose imatinib mesylate (10 microM) decreased the viability of CAFs in vitro independent from co-stimulation with PDGF. Interestingly, imatinib mesylate (10 microM) strikingly induced the expression of the pro-inflammatory and pro-angiogenic cytokines interleukin (IL)-6 and IL-8, and mildly stimulated the release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). Our results suggest that imatinib mesylate, due to its anti-proliferative activity, may be effective in combination with other substances for the treatment of colorectal metastasis progression.

Antineoplastic Agents↗
PubMed1996

Posttranslational changes in band 3 in adult and aging brain following treatment with ergoloid mesylates, comparison to changes observed in Alzheimer's disease.

Band 3, the most heavily used anion transport system in vertebrates, ages as cells and tissues age. Posttranslational changes in band 3 in adult and aging brain were investigated following treatment with ergoloid mesylates and compared to changes observed in Alzheimer's disease (AD). The study was conducted in a double blind fashion and was decoded only after the study was completed. The following posttranslational changes in brain band 3 occur with age: increased breakdown of band 3; decreased phosphorylation; and decreased anion transport. Autoantibodies to senescent cell antigen (SCA) synthetic peptides residue 538-554 and 812-827 increase with age, but antibodies to the former peptide are significantly reduced in ergoloid mesylate treated old mice. This is a critical transport region of band 3. Results showed the aged/altered band 3 increased in Alzheimer's disease (AD) as determined by quantitative antibody binding. Ergoloid mesylates altered the age-related posttranslational changes as follows: the observed age-related decrease in brain band 3 was partially reversed and anion transport was increased. This is consistent with the data indicating decreased autoantibodies to a critical anion transport segment of band 3. Aging appears to result in damage to a critical transport region of the anion transporter which is reflected by decreased anion transport, increased breakdown, alteration of the molecule itself, and an increase in autoantibodies to the region. Ergoloid mesylates seem to protect against this damage.

Aging↗
PubMed2002

BCR/ABL amplification in chronic myelocytic leukemia blast crisis following imatinib mesylate administration.

The onset of accelerated phase or blast crisis of chronic myelocytic leukemia (CML) is usually associated with the acquisition of new chromosome abnormalities in addition to the t(9;22)(q34;q11) that is characteristic of the chronic phase CML. We describe the cytogenetic and molecular genetic findings in two cases of myelocytic blast crisis of CML, one occurring 6 months after commencing treatment with the ABL-specific tyrosine kinase inhibitor imatinib mesylate (STI571, Glivec, or Gleevec) and the second treated with imatinib mesylate for established blast crisis. In both cases, multiple secondary cytogenetic abnormalities were observed at transformation, with homogeneously staining regions that were shown to contain BCR/ABL amplification by fluorescence in situ hybridization appearing after imatinib mesylate administration. BCR/ABL amplification is emerging as an important mechanism of acquired resistance to imatinib mesylate.

Adult↗
PubMed2006

Imatinib mesylate is effective in children with chronic myelogenous leukemia in late chronic and advanced phase and in relapse after stem cell transplantation.

A multicentric phase 2 study was conducted to determine the efficiency and the tolerance of imatinib mesylate in children with chronic myelogenous leukemia (CML) in advanced phase of the disease, in relapse after stem cell transplantation, or in case of failure to an interferon alpha-based regimen. In all, 30 children from eight European countries were enrolled. In 18 children assessable for hematologic response, imatinib mesylate induced complete hematologic response in eight (80%) of the 10 patients included in chronic phase and in six (75%) of eight enrolled in advanced phase of the disease with acceptable toxicity. In 27 patients assessable for cytogenetic response, imatinib mesylate induced disappearance of Philadelphia chromosome-positive bone marrow cells in 12 (60%) of 20 children included in chronic phase and in two (29%) of seven included in advanced phase. A reduction of the bcr-abl/abl ratio to less than 10(-4) was achieved in 11 (50%) of the children included in chronic phase. Estimated 12-month overall survival rate was 95% (95% CI, 87-100%) for the patients included in chronic phase and 75% (95%CI, 45-100%) for those enrolled in advanced phase. Imatinib mesylate is well tolerated and molecular remission can be achieved in children with CML.

Adolescent↗
PubMed2003

Effective treatment of hypereosinophilic syndrome with imatinib mesylate.

Imatinib mesylate treatment is highly effective in chronic myeloid leukaemia and recent data have suggested that imatinib mesylate is also effective in the treatment of idiopathic hypereosinophilic syndrome (HES). Six patients with HES were treated daily with 100 mg imatinib mesylate. Five patients had normal karyotype and one showed trisomy 8. RT-PCR was negative for ETV6-PDGFRB and BCR-ABL fusion mRNAs. All patients rapidly achieved complete haematological remission. One patient remained in remission for more than 6 weeks after discontinuing treatment. No significant side effect was noted. Imatinib mesylate should be considered in the first-line therapy of idiopathic HES.

Adult↗
PubMed2003

Clinical and genetic studies of ETV6/ABL1-positive chronic myeloid leukaemia in blast crisis treated with imatinib mesylate.

Most chronic myeloid leukaemia (CML) patients are genetically characterized by the t(9;22)(q34;q11), generating the BCR/ABL1 fusion gene. However, a few CML patients with rearrangements of 9q34 and 12p13, leading to ETV6/ABL1 chimaeras, have also been reported. Here we describe the clinical and genetic response to imatinib mesylate treatment of an ETV6/ABL1-positive CML patient diagnosed in blast crisis (BC). A chronic phase was achieved after acute myeloid leukaemia induction therapy. Then, treatment with imatinib mesylate (600 mg/d) was initiated and the effect was assessed clinically as well as genetically, including by repeated interphase fluorescence in situ hybridization studies. Until d 71 of imatinib mesylate therapy, stable improvements in the clinical and laboratory features were noted, and the frequency of ABL1-rearranged peripheral blood cells decreased from 56% to 11%. At d 92, an additional t(12;13)(p12;q13), with the 12p breakpoint proximal to ETV6, was found. The patient relapsed into BC 126 d after the start of the imatinib mesylate treatment and succumbed to the disease shortly afterwards. No mutations in the tyrosine kinase domain of ABL1 of the ETV6/ABL1 fusion were identified in the second BC. However, whereas the ETV6/ABL1 expression was seemingly the same at diagnosis and at second BC, the expression of ETV6 was markedly lower at the second BC. This decreased expression of wild-type ETV6 may have been a contributory factor for the relapse.

Adult↗
PubMed2003

Use of gabexate mesylate in Italian hospitals: a multicentre observational study.

INTRODUCTION: Gabexate mesylate has been proposed as a therapeutic or prophylactic agent in a variety of diseases (e.g. disseminated intravascular coagulation, prophylaxis of pancreatic damage and acute pancreatitis), but its clinical effectiveness is still unclear. As the drug is widely used in Italy, we conducted an observational study to determine the pattern of prescription of gabexate in Italian hospitals and to assess the outcome of patients with acute pancreatitis when this treatment is given. An updated meta-analysis of the use of the drug is also presented. MATERIALS AND METHODS: From 20 May to 20 July 2001, all consecutive patients admitted to 13 Italian hospitals were enrolled. The following information was recorded from each patient: indication for the use of gabexate, total dose and duration of gabexate administration, need for surgical treatment and outcome of hospitalization (alive or dead). In the patient subgroup with acute pancreatitis, the outcome data of our observational study were compared with those reported by the randomized trials (RCTs) previously published. For this purpose, the survival data of the RCTs were summarized in an updated meta-analysis. RESULTS: A total of 170 patients were enrolled in the study. The main clinical indications were acute pancreatitis in 88 cases (52%) and prophylaxis of pancreatic damage in 62 cases (36%). At the end of the study, 80 of the 88 patients treated for acute pancreatitis (91%) were alive and eight (9%) had died. In the subgroup of patients with necrotic-haemorrhagic pancreatitis (n = 10), six died during the observation period. Our meta-analysis showed that gabexate mesylate did not improve survival in comparison with placebo. The meta-analytic odds ratio was 0.70 (95% CI: 0.45-1.09). DISCUSSION: The study described the pattern of use of gabexate mesylate in Italian hospitals and provided information on the outcome of the subgroup treated for acute pancreatitis. A meta-analysis of current data from RCTs, together with our findings, indicates that gabexate mesylate does not significantly improve survival in acute pancreatitis.

Acute Disease↗
PubMed2003

Marked regression of metastatic pilocytic astrocytoma during treatment with imatinib mesylate (STI-571, Gleevec): a case report and laboratory investigation.

Pilocytic astrocytomas are the most common childhood glioma. Most children with pilocytic astrocytomas survive many years with their tumor, but alternative treatment approaches are needed for those with refractory or metastatic disease. Signaling by the platelet-derived growth factor tyrosine kinase receptor pathways have been postulated to contribute to the development of gliomas. The authors treated a single patient with refractory, metastatic pilocytic astrocytoma with the tyrosine kinase inhibitor imatinib mesylate and observed marked, transient regression of tumor during treatment. Immunohistochemistry was used to assess expression of reported target genes of imatinib mesylate in this patient's tumor tissue and of the PDGFR in pilocytic astrocytomas from 19 other patients. Immunohistochemistry showed that the patient's tumor cells did not express any of the reported target molecules inhibited by imatinib mesylate. PDGFR expression was detected in tumor vasculative in the panel of 20 tumors, and not in the tumor cells. The authors suggest that the PDGFR-signaling pathway postulated to contribute to the development of gliomas in adults might not contribute to pilocytic astrocytomas in children, and that treatment with imatinib mesylate should be considered in patients with refractory pilocytic astrocytoma.

Astrocytoma↗
PubMed2006

Imatinib mesylate in a patient with metastatic disease originating from a dermatofibrosarcoma protuberans of the scalp.

Dermatofibrosarcoma protuberans is a soft-tissue tumor that may recur locally and rarely causes metastases to vital organs. Dermatofibrosarcoma protuberans has specific chromosomal abnormalities involving the platelet-derived growth factor beta-chain locus that may render these tumors responsive to targeted therapy with the tyrosine kinase inhibitor imatinib mesylate. A patient with locally recurrent and metastatic dermatofibrosarcoma protuberans who had already undergone surgery 22 times was initially treated with imatinib mesylate 400 mg/day. The treatment dose was increased after 7 days to 400 mg twice daily. The patient was followed up for response and toxicity by physical examination and imaging studies, comprising computed tomography and fluorodeoxyglucose positron emission tomography. Clinical response could be demonstrated after the first month of treatment, and subsequent computed tomography and positron emission tomography documented a response to imatinib mesylate therapy. Our patient is now in sustained remission with minimal toxicity. We conclude that antitumor activity of metastatic dermatofibrosarcoma protuberans can be obtained with imatinib mesylate treatment with minimal side-effects.

Antineoplastic Agents↗
PubMed2006

Imatinib mesylate inhibits proliferation of rheumatoid synovial fibroblast-like cells and phosphorylation of Gab adapter proteins activated by platelet-derived growth factor.

Receptors for platelet-derived growth factor (PDGF) are abundantly expressed on synovial fibroblast-like (SFL) cells from patients with rheumatoid arthritis (RA), and stimulation with PDGF enhances both the anchorage-dependent and -independent growth of RA-SFL cells. To elucidate the molecular mechanisms responsible for the excessive growth of RA-SFL cells and to seek a novel molecular-targeting therapy for RA, we examined the expression of adapter proteins and the effect of the specific inhibition of PDGF receptor activation by imatinib mesylate. Cultured SFL cells were used in the present study after 2-5 passages. The anchorage-dependent and -independent growth patterns of the SFL cells were evaluated using a tetrazolium-based assay and colony formation in 0.3% agar, respectively. Adapter proteins Gab1 and Gab2 were expressed in RA-SFL cells, and both proteins were rapidly (< 1 min) tyrosine-phosphorylated after the stimulation of RA-SFL cells with 10 ng/ml of PDGF and, to a lesser extent, after stimulation with 100 ng/ml of epidermal growth factor (EGF). The inhibition of PDGF receptor tyrosine kinase activation by 1 microM or less of imatinib mesylate specifically suppressed the PDGF-dependent, but not EGF-dependent, tyrosine phosphorylation of various proteins. Moreover, imatinib mesylate abolished both the anchorage-dependent and -independent proliferation of RA-SFL cells induced by PDGF stimulation. These results suggest that Gab adapter proteins are expressed and likely to be involved in the growth signalling of rheumatoid synovial cells and that imatinib mesylate, a key drug in the treatment of chronic myeloid leukaemia, may also be effective for the treatment of RA.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

Vitiligo-like lesions and diffuse lightening of the skin in a pediatric patient treated with imatinib mesylate: a noninvasive colorimetric assessment.

Imatinib mesylate is a drug that has been recently approved for the treatment for chronic myeloid leukemia. It acts as a potent and selective inhibitor of BCR-ABL tyrosine kinase. It also inhibits both c-kit and platelet-derived growth factor receptor tyrosine kinases. Hypopigmentation of the skin in patients receiving this drug has been recently reported. We report a 17-year-old Caucasian patient affected by chronic myeloid leukemia in therapy with imatinib mesylate who developed hypopigmented vitiligo-like patches and generalized lightening of the skin. In order to evaluate the lightening observed clinically, we measured the progressive skin color hypopigmentation by using a colorimeter over several months. The colorimetric evaluation confirmed the generalized and gradual lightening of patient's skin over treatment with imatinib mesylate. We believe that this is the first reported instance of vitiligo-like lesions in a pediatric patient treated with imatinib mesylate, and the second in a Caucasian patient.

Adolescent↗