Bone-marrow relapse in acute lymphoblastic leukaemia in childhood.

The outcome after bone-marrow relapse was assessed in 53 children with acute lymphoblastic leukaemia (ALL). Twenty-five out of 37 children (67%) whose first remission ended in relapse during treatment (group A) achieved a second remission, as did 15 out of 16 (94%) who relapsed after treatment had been stopped (group B). Nevertheless, the median duration of second remission was only 12 weeks in group A and 35 weeks in group B. The median survival from time of relapse was 32 weeks in group A and 75 weeks in group B. It is concluded that marrow relapse is equally serious whether it occurs during treatment or after treatment has been stopped, and that most children with ALL have a single chance of cure at the time of diagnosis.     

Methotrexate-induced malabsorption in children with acute lymphoblastic leukaemia.

A one-hour D-xylose absorption test was performed on 18 children with acute lymphoblastic leukaemia. Xylose absorption was normal in children who had not received methotrexate, but there was a significant degree of malabsorption in those who had taken methotrexate within the previous seven days. There was a progressive and significant increase in malabsorption related to the cumulative dose of methotrexate. These findings provide further evidence that regular methotrexate treatment every seven days is more toxic than if it is more widely spaced. The spacing of treatment is currently under investigation.     

Combination chemotherapy for acute lymphoblastic leukaemia in adults.

Fifty-one adults with acute lymphoblastic leukaemia were entered into a trial of intense initial chemotherapy and early "prophylaxis" of the central nervous system (CNS). Initial treatment with OPAL (Oncovin (vincristine), prednisolone, adriamycin (doxorubicin), and L-asparaginase (colaspase)) followed by craniospinal or cranial irradiation and intrathecal methotrexate produced remission in 36 patients (71%). Seventeen of these patients relapsed three to 18 months after the start of remission; the remainder had been in remission for 12 to 52 months by the end of the study. The predicted median duration of complete remission was 18.5 months. None of the four patients who initially had clinical evidence of CNS disease, three of whom also had leukaemic cells identical to those found in Burkitt's lymphoma, achieved remission. Those patients who initially had hepatomegaly or splenomegaly had a shorter remission than those without. The predicted median survival was 27 months in those who achieved complete remission, one month in those who did not, and 21 months overall. The addition of colaspase and doxorubicin to vincristine and prednisolone and the use of early CNS treatment clearly improved the remission rate among adults with acute lymphoblastic leukaemia, though the presence and length of remission was affected by the extent of disease at presentation. Burkitt-like leukaemia, which had a poor prognosis, is probably a separate disease and may benefit from a different therapeutic approach.     

血淀粉酶持续升高时间对急性胰腺炎合并代谢综合征预后的预测价值

目的 探讨血淀粉酶持续时间对急性胰腺炎合并代谢综合征预后的预测价值。方法 选择急性胰腺炎患者150例,其中单纯胰腺炎患者50例,合并代谢综合征患者100例。合并代谢综合征患者中,血淀粉酶恢复正常时间超过5 d患者50例,5 d内恢复正常患者50例。150例急性胰腺炎患者出院后均随访1个月,对是否合并代谢综合征,其血淀粉酶及升高持续天数进行比较,同时统计合并代谢综合征患者,血淀粉酶恢复时间与血脂血糖水平变化情况以及发生并发症情况。结果 合并代谢综合征患者血淀粉酶水平高于未合并代谢综合征患者(P<0.05),且血淀粉酶升高持续天数长于未合并代谢综合征患者(P<0.05)。血淀粉酶恢复时间超过5 d患者的总胆固醇、甘油三酯、空腹及餐后2 h血糖水平均高于5 d内恢复正常患者(P<0.05)。血淀粉酶恢复时间超过5 d患者,发生低蛋白血症、血糖异常、低钾血症、低钙血症及低镁血症的比例显著高于5 d内恢复正常患者(P<0.05)。结论 急性胰腺炎合并代谢综合征患者的血淀粉酶持续升高时间越长,其越容易发生血脂、血糖代谢异常,治疗中应注意调节患者电解质。     

Clofarabine in the treatment of acute myeloid leukaemia and acute lymphoblastic leukaemia: a review

Clofarabine, a synthesised adenosine nucleoside, has recently demonstrated single-agent activity in the acute leukaemias. Originally developed to capture the best qualities of cladribine and fludarabine, clofarabine contains halogenated carbons, rendering it resistant to inactivating enzymes and maintaining its stability in acidic environments. Like other adenosine nucleosides, clofarabine acts by inhibiting ribonucleotide reductase and DNA polymerase, thereby depleting the amount of intracellular deoxynucleoside triphosphates available for DNA replication and also resulting in premature DNA chain termination. Clofarabine has also been shown to induce apoptosis in transformed cell lines, indicating that clofarabine results in cell death in both cycling and non-cycling cells. Interest in the development of clofarabine was initially hampered by the availability of other active nucleoside analogues for the treatment of haematological malignancies. However, the results of several early-phase trials evaluating the use of clofarabine in acute leukaemias in adults and children have rekindled enthusiasm for further investigation into its use. This article describes the development, pharmacology, toxicity and clinical activity of clofarabine, as well as discuss its potential role in the treatment of acute leukaemia.     

Clofarabine in the treatment of acute myeloid leukaemia and acute lymphoblastic leukaemia: a review

Clofarabine, a synthesised adenosine nucleoside, has recently demonstrated single-agent activity in the acute leukaemias. Originally developed to capture the best qualities of cladribine and fludarabine, clofarabine contains halogenated carbons, rendering it resistant to inactivating enzymes and maintaining its stability in acidic environments. Like other adenosine nucleosides, clofarabine acts by inhibiting ribonucleotide reductase and DNA polymerase, thereby depleting the amount of intracellular deoxynucleoside triphosphates available for DNA replication and also resulting in premature DNA chain termination. Clofarabine has also been shown to induce apoptosis in transformed cell lines, indicating that clofarabine results in cell death in both cycling and non-cycling cells. Interest in the development of clofarabine was initially hampered by the availability of other active nucleoside analogues for the treatment of haematological malignancies. However, the results of several early-phase trials evaluating the use of clofarabine in acute leukaemias in adults and children have rekindled enthusiasm for further investigation into its use. This article describes the development, pharmacology, toxicity and clinical activity of clofarabine, as well as discuss its potential role in the treatment of acute leukaemia.     

急性淋巴细胞白血病患者血清乳酸脱氢酶水平与VDLP 方案临床疗效的关系

目的探讨在急性淋巴细胞白血病患者（ALL）中血清乳酸脱氢酶水平与VDLP方案临床疗效的关系。方法选取70例初治儿童急性淋巴细胞白血病患者,并选取同时期40例健康儿童作为对照组。检测治疗前后及复发患者S-LDH水平,并与对照组LDH水平比较,分析LDH水平变化的临床意义。结果ALL患者LDH水平明显高于健康对照组（P〈0．01）,而通过治疗（完全缓解／部分缓解）患者S-LDH明显下降（P〈0．01）,NR患者虽出现下降,但与治疗前比较无统计学差异（P〉0．05）;CR／PR治疗前s-LDH水平亦低于NR治疗前（P〈0．05）;获得CR／PR患者复发后,S-LDH又明显升高,复发患者治疗前S-LDH水平高于未复发患者（治疗前）（P〈0．05）。结论S-LDH可能可以作为成人急性淋巴细胞白血病预后的评估指标。     

Changing patterns of acute lymphoblastic leukaemia in Nigeria

An increase in the number of Nigerian patients with acute lymphoblastic leukaemia (ALL), relative to those having acute myelogenous leukaemia, was predicted some years ago. This was expected to result from an enhanced socio-economic status of most members of the general population and improved nutrition. A review of the features of ALL patients seen in University College Hospital, Ibadan, during different periods over the past three decades revealed not only the predicted changes but also an increasing proportion of pediatric and female patients. Except for an unusual number of patients with the rare L3 morphological variant seen within the last 2 years, little else changed in the clinical and laboratory features of the disease. Atrophy of the thymus resulting from malnutrition is thought to inhibit the occurrence of common-ALL in the first decade of life. This inhibition is removed by improved nutrition, thus allowing more cases of common-ALL to develop in children. The trend in Nigeria has been observed earlier among Arabs in the Gaza Strip in the Sinai Peninsula. If the hypothesis is correct, undernutrition occurring for a long enough time in a previously well-nourished population should lead to changes opposite to those observed. The increasing percentage of patients who are either young, female or of high socio-economic class imply better prognosis for more Nigerian ALL patients.     

L-asparaginase-induced coagulopathy in children with acute lymphoblastic leukaemia

Haemostatic changes induced with vincristine (VCR), prednisone (PDN) and L-asparaginase (L-ase) in 53 children with ALL were prospectively evaluated. Relative to pretreatment values, mean FG concentration diminished significantly in the first week with a minimal level in the third week and PT was prolonged during the first weeks of induction. APTT decreased significantly in the last week and after cessation of L-ase therapy. Mean concentration of factor VIII remained elevated during the entire period of L-ase therapy. Three children (5.6%) developed a cerebral thrombo/haemorrhagic complication. These data demonstrate that the tendency for thrombosis is the predominant clinical manifestation of L-ase-induced coagulopathy, when the drug is associated with VCR and PDN.     

血清C-反应蛋白对急性心肌梗死患者预后的价值

目的　通过检测急性心肌梗死 (acutemyocardialinfarction ,AMI)患者血清C 反应蛋白 (C re activeprotein ,CRP) ,探讨其峰值水平对评价患者预后的价值。方法　采用免疫散射比浊法测定 72例AMI患者血清CRP的系列变化值 ,得出其峰值。结果　AMI患者心功能按Killip分级 ,Ⅲ、Ⅳ级组血清CRP峰值水平显著高于Ⅰ、Ⅱ级组 (P <0 .0 1) ;心脏事件组 (包括出院后随访 6个月内的心衰、再发心梗、严重心律失常、住院期间及随访期内的死亡 )与出院后随访 6个月内无心脏事件组相比血清CRP峰值差异非常显著 (P <0 .0 1)。结论　检测AMI患者血清CRP峰值水平有助于AMI患者预后判断     

Clinical and prognostic value of serum procollagen levels in chronic alcoholic liver disease

Liver fibrogenesis involves the synthesis of collagen fibrils and proteoglycans by various types of liver cells, including Ito cells, transitional cells, myofibroblasts and hepatocytes. Synthesis of collagen fibrils follows a complex metabolic pathway with intermediate products such as type III procollagen (III-PC). Serum levels of III-PC may reflect the activity of the fibrogenetic process. We analysed the relationship between the serum levels of III-PC (N-terminal peptide) and diverse clinical, biochemical and histological parameters of 77 alcoholic patients (27 cirrhotics), comparing them with those of 15 age- and sex-matched controls. A highly significant difference was obtained between controls and patients (P less than 0.0001), but no differences were observed between cirrhotics and non-cirrhotics. Serum III-PC significantly correlated with clinical and biochemical data of liver function derangement (prothrombin activity, serum albumin, bilirubin, gynecomastia, ascites, encephalopathy, edema, splenomegaly); with the duration of ethanol addiction and with MCV. Sixty patients were followed up for a period ranging between 3 and 1056 days (mean = 356 days); 9 of them died. Patients with III-PC levels above 38 ng/ml had a significantly higher mortality (P = 0.006) than those with levels under 38 (log rank test). Thus, serum III-PC may be a useful tool in the clinical evaluation and prognostic assessment of patients with chronic alcoholic liver disease.     

Prognostic implications of chromosomal findings in acute lymphoblastic leukaemia at diagnosis.

Chromosomes were studied on diagnostic bone-marrow samples from 39 children with acute lymphoblastic leukaemia (ALL). The patients were classified, according to the chromosomal characteristics of the major proportion of their leukaemia cells, into five categories; hyperdiploid, pseudodiploid, diploid, hypodiploid, and mixed. Patients in the hyperdiploid category had significantly longer first remissions than those in all other categories, and those in the pseudodiploid category had the shortest. Neither the absence of any normal cells nor the presence of detectable clones appeared to be an adverse feature. We suggest that the proportion of hyperdiploid cells, determined by conventional chromosomal staining techniques, may be used as an additional prognostic feature in childhood ALL.