Unilateral bullous retinal detachment in a child with acute lymphoblastic leukaemia,and hypopyon as the first sign of leukaemic relapse

Dear Editor,I report a case of bullous retinal detachment in a child with acute lymphoblastic leukaemia （ALL） at diagnosis of systemic disease and the recurrence of detachment, hypopyon and secondary glaucoma as signs of relapse of leukaemia after chemotherapy remission of systemic disease. All the principles outlined in the Declaration of Helsinki （2008） were followed and an informed consent was taken by father of the child whenever the child was admitted in the ward. A brief review of literature of this disease is also included.

Expression of SODD and P65 in ALL of Children and Its Relationship with Chemotherapeutic Drugs

The expression of silience of death domains (SODD) and its clinical significance and relationship with phospho-NF-κB-p65 proteins in bone marrow cells of childhood acute lymphoblas- tic leukaemia (ALL) were explored, and the expression of SODD and phospho-NF-κB-p65 in Jurkat cells treated with chemotherapeutic drugs was detected in order to find a new chemotherapeutic target. The expression of SODD and phospho-NF-κB-p65 proteins in bone marrow cells was detected by immunohistochemistry in 25 children with ALL. The apoptosis rate was measured by An- nexin-V-Fluorescence/PI double-labeling flow cytometry and the expression of SODD and phos- pho-NF-κB-p65 proteins determined by Western blotting in the Jurkat cells. It was found that the ex- pression of SODD and active P65 in ALL was significantly higher than that in normal control group (P<0.05). The expression of the SODD and phospho-NF-κB-p65 proteins in the high-risk (HR) group was significantly higher than that in the standard-risk (SR) group (P<0.05). The Pearson rank correla- tion analysis revealed that there was a positive correlation between SODD and phospho-NF-κB-p65 expression (P<0.01, r=0.69). VCR could effectively induce the apoptosis of Jurkat cells, and down-regulate the expression of SODD and phospho-NF-κB-p65 proteins in a time-dependent man- ner, but DNR could not down-regulate the expression of SODD effectively. It was concluded that SODD may be closely related to the clinical classification and prognosis of ALL in children. The ex- pression of SODD and phospho-NF-κB-p65 had a definite synergistic relationship with the onset and development of ALL. VCR could down-regulate the expression of SODD and inhibit the NF-κB ac- tivation, which could recover the sensibility of apoptosis in leukemic cells.

The Effect of the Fas/FasL Pathway during Chemotherapeutic Drug-induced Apoptosis of Leukameic Cells

The mechanism of chemotherapeutic drug-induced apoptosis in leukaemic cells was studied to further investigate whether Fas/FasL system was involved in apoptosis induced by chemotherapeutic drugs and assess their effects when used in combination with soluble FasL (sFasL). The expression of Fas on human leukaemic cell lines K562, HL-60 and U937 treated with daunorubicin (DNR) or cytosine arabinoside (Ara-C) was detected by using flow cytometry. The activities of sFasL, DNR and Ara-C inducing apoptosis of leukaemic cells, in the absence or presence of neutralizing anti-Fas IgG antibody, were detected by using flow cytometry and TUNEL. The results showed that flow cytometric profiles of K562, HL-60 and U937 cells treated with DNR or Ara-C failed to show any significant increase in Fas expression over 18 h (P>0.05). Anti-Fas monoclonal antibody (IgG) could not block the apoptosis in leukaemic cells induced by DNR or Ara-C, but could block the apoptosis induced by sFasL. A role of sFasL in a cytotoxic synergistic effect when used in combination with chemotherapeutic drugs was revealed. It was concluded that chemotherapeutic drug-induced apoptosis in human leukaemic cells (UG37, HL-60) is independent of the Fas/FasL system, but combination of sFasL and drug treatment produces a synergistic cytotoxic effect on human luekaemic cells.

Secondary pulmonary alveolar proteinosis associated with myelodysplastic syndrome

Pulmonary alveolar proteinosis （PAP） IS an uncommon disease first reported by Rosen et al^1 in 1958, and characterized by the accumulation of surtactant proteins and phospholipids within the alveolar spaces. Acquired PAP is divided into two forms based on clinical features： idiopathic PAP and secondary PAE Secondary PAP is reported to be associated with haematological malignancies, Pneumocystis carinii pneumonia and inhalation of silica or titanium, and the most frequent underlying disease of secondary PAP is haematological malignancy. The exact incidence of PAP in haematological malignancies is still obscure, since there have been only sporadic reports of secondary PAP.^ 2, 3