Sudden death in a patient with chronic lymphocytic leukemia

The authors describe a 51-year-old man with chronic lymphocytic leukemia who presented with respiratory distress and then died suddenly while in hospital. Autopsy revealed pulmonary leukostasis and a large intracardiac mass containing mostly mature lymphocytes and fibrin. Although leukostasis and lymphocyte thrombi have been described (albeit rarely) in chronic lymphocytic leukemia, an intracardiac "clot" has not. It seems plausible that this intracardiac mass caused the patient's death.     

Therapeutic approach to acute myeloid leukemia

The treatment of acute myeloid leukemia has evolved considerably over the past decade. While induction therapy appears to have been almost standardized, there continues to be an ongoing debate and controversy regarding the best form of post-remission therapy. Attempts are being made to identify patients at particular risk of relapse to enable appropriate selection of best induction and post-remission therapies. In these respects, cytogenetics are useful. New concepts include the use of growth factors, immunotherapy, MDR modulation and therapies evolving from a better knowledge of the anomalies of the genes that cause leukemia.     

Chemotherapy-induced myocardial necrosis in a patient with chronic lymphocytic leukemia

Cardiac toxicity following the administration of chemotherapeutic agents is well documented. Vinca alkaloids, as well as high-dose cyclophosphamide, have been associated with myocardial ischemia. The present report describes a case of acute myocardial infarction occurring in a patient with no antecedent cardiac history who received both vincristine and conventional chemotherapeutic doses of cyclophosphamide for the treatment of chronic lymphocytic leukemia. Physicians should possess a heightened awareness of this potentially serious complication.     

Chronic systemic aspergillosis in a patient with acute myeloid leukemia

Systemic aspergillosis is a well-recognized complication of chemotherapy-induced neutropenia. In this report a patient with acute myeloid leukemia is described in whom a chronic aspergillosis with systemic involvement developed after recovery from neutropenia following intensive chemotherapy and allogeneic bone marrow transplantation. The clinical features of a chronic course of systemic aspergillosis suggest a distinct clinical entity comparable to chronic systemic candidiasis.     

Double mutations of the N-ras gene in a patient with acute myelomonocytic leukemia

We report a patient with acute myelomonocytic leukemia (AMMoL) who showed two independent point mutations of the N-ras gene at codons 12 and 13. Longitudinal analysis revealed that one mutation at codon 13 was detectable throughout his disease course and the other at codon 12 emerged as a second mutation 14 months after the diagnosis was made, at the refractory stage. Cloning to vector and subsequent sequencing confirmed that these mutations occurred in different alleles. Chromosome findings showed a simple abnormal karyotype at presentation and further karyotypic aberrations during his disease course, concomitantly with the second mutation of the N-ras gene. These findings revealed a close relationship among the disease progression, karyotypic evolution and a newly-appearing N-ras mutation.     

Lymphopenic effect of carbamazepine in a patient with chronic lymphocytic leukemia

OBJECTIVE: To report a dramatic and reproducible suppressive effect of carbamazepine on circulating lymphocytes in an elderly woman with chronic lymphocytic leukemia. CASE SUMMARY: An elderly woman taking phenytoin for a stroke-associated seizure disorder had lymphocyte count of 28,800 x 10(6) cells/L. Speculating an unusual lymphadenopathic effect of the phenytoin therapy, carbamazepine therapy was substituted. After 15 weeks of carbamazepine treatment, the lymphocyte count declined to 3200 x 10(6) cells/L. Because of severe diarrhea, carbamazepine therapy was stopped and phenytoin therapy was reinstituted. At the end of 4 months of phenytoin treatment, the lymphocyte count had increased to 23,200 x 10(6) cells/L. Phenytoin therapy was discontinued and carbamazepine therapy was begun. The lymphocyte count decreased to 10,700 x 10(6) cells/L. Severe diarrhea recurred and phenytoin treatment was reinstituted. Over 12 days the lymphocyte count increased to 28,900 x 10(6) cells/L. Phenytoin therapy was stopped and valproic acid therapy was started. The lymphocyte count continued to increase during valproic acid therapy, reaching a peak of 114,300 x 10(6) cells/L. DISCUSSION: In this patient with chronic lymphocytic leukemia, carbamazepine therapy had a significant and reproducible lymphopenic effect that was readily reversible upon discontinuation of the drug. Unfortunately, this effect was associated with severe diarrhea, preventing further attempts at exploiting this potentially beneficial action. CONCLUSIONS: Carbamazepine had a reproducible suppressive effect on lymphocyte counts in an elderly patient with chronic lymphocytic leukemia. This unique observation raises the possibility that carbamazepine therapy may have a useful effect in patients with chronic lymphocytic leukemia.     

Myositis caused by hydroxyurea in a patient with chronic myelogenous leukemia

A 59-year-old man with chronic myelogenous leukemia (CML) had a white-blood-cell (WBC) count of 55,400/microliter when admitted in July 1997, and was placed on oral hydroxyurea (HU) of 1,500 mg/day. Treatment with 600 MU/day of interferon alpha (IFN alpha) was started on August 5. HU was discontinued when the patient's WBC count dropped to 8,100/microliter on August 18. However, HU was resumed about a month later, after his WBC count increased to 10,100/microliter, but discontinued when the patient started to complain of chills, high fever, and bilateral femoral pain. HU treatment was initiated again one week later, after the patient's WBC count had begun rising but ceased again after he experienced chills, high fever, and bilateral femoral pain. The patient's myogenetic enzymes were found to be increasing the following day, and a lymphocyte stimulation test (LST) with HU showed a high stimulation index of 41.7%. The elevation of myogenetic enzymes and the results of the LST suggested that myositis due to HU was the cause of the patient's clinical manifestations. His myositis spontaneously disappeared after HU was discontinued. Although the patient is no longer receiving HU, IFN alpha has brought his CML under control. To our knowledge, this is the first reported case of myositis caused by HU.     

慢性粒细胞白血病患者血浆伊马替尼浓度检测与临床疗效分析

目的 探讨慢性粒细胞白血病(CML)患者服用伊马替尼治疗后,伊马替尼血浆浓度在个体间的差异以及与临床疗效的关系.方法 2005年7月至2008年2月开始服用伊马替尼治疗的CML患者共51例纳入研究,其中男34例,女17例,服用剂量300 mg/d 9例、400 mg/d 37例,600 mg/d5例;采用高效液相色谱法(HPLC)测定患者空腹伊马替尼血浆谷浓度;SPSS13.0软件进行统计分析.结果 伊马替尼血浆谷浓度与服用剂量有关,且个体之间差异较大,为(342～4688)ng/ml;300mg/d剂量组的伊马替尼血浆谷浓度为(1037±514)ng/ml,低于400mg/d剂量组的(2123±1016)ng/ml(t=2.34,P=0.032);300 mg/d剂量组的治疗有效率为66.67%(6/9),低于400 mg/d剂量组的89.19%(33/37)(χ2=7.14,P=0.008);在300、400mg/d剂量组中,39例治疗有效,伊马替尼血浆谷浓度高于治疗效果不理想患者,差异有统计学意义(t=2.25,P=0.037);受试者工作特征曲线(ROC曲线)结果提示伊马替尼血浆谷浓度低于1050 ng/ml者,其临床疗效可能较差,敏感度为84.6%,特异度为71.1%.结论 CML患者服用伊马替尼治疗后药物血浆浓度与服用剂量有关,不同个体间差异较大,血浆谷浓度低于1050 ng/ml提示其临床疗效可能较差.     

Therapeutic monitoring of teicoplanin in a severely burned patient

It is now well documented that E-cadherin expression correlates inversely with tumor grade in various carcinomas including prostate cancer. We also demonstrated a statistically significant correlation between decreased E-cadherin expression and progression-free period in early stage patients treated by radical prostatectomy and decreased survival in patients with advanced stage disease. We now study the relationship between E cadherin and alpha-catenin expression, because in prostate cancer cell lines, mutational inactivation of the alpha-catenin gene can be the cause of the impaired E-cadherin function. Twenty patients treated by radical prostatectomy and 32 advanced stage patients were evaluated immunohistochemically for E-cadherin and alpha-catenin expression. The results were related to tumor grade and disease progression. Four patients in the radical prostatectomy group had aberrant E-cadherin and alpha-catenin expression and showed disease progression. The other 16 patients were free of progression and had normal E-cadherin and alpha-catenin expression. In the advanced stage group, 4 of 13 patients with normal E-cadherin staining showed aberrant alpha-catenin expression and 2 patients (50%) progressed, compared with only 22% progression in patients with both normal E-cadherin and alpha-catenin expression. The other 19 patients with aberrant E-cadherin and alpha-catenin staining had the poorest prognosis. Our results suggest that loss of alpha-catenin expression could be one of the mechanisms responsible for the loss of E-cadherin-mediated cell-cell adhesion in human prostate cancer and might in some cases provide prognostic information.     

Pre-B acute lymphoblastic leukemia in a patient with partial lipodystrophy and acanthosis nigricans

In patients with lipodystrophies a post binding defect in insulin action has been described involving phosphorylation of the beta subunit of the insulin receptor, suggesting the presence of a genetically determined defect in insulin action; the receptor gene has been mapped to the distal short arm of chromosome 19 close to the break-point of a specific chromosome translocation frequently found in pre-B Acute Lymphoblastic Leukemia (ALL). We report on a 13 years old female patient with partial lipodystrophy, acanthosis nigricans and insulin resistance who developed a pre-B ALL. Since lipodystrophy and pre-B ALL are rare disorders, a possible causal relationship between the two diseases is suggested possibly mediated by a mutation in the insulin receptor gene.