A patient with aplastic anaemia developed Sweet's syndrome (a febrile neutrophilic dermatosis) during granulocyte colony-stimulating factor (G-CSF) therapy. Three repeated episodes of appearance and disappearance of erythematous nodules after administration and withdrawal of G-CSF confirmed that G-CSF induced Sweet's syndrome in the patient. Sweet's syndrome has been reported in patients with myelodysplastic syndrome and acute leukemia, but not in patients with aplastic anaemia. This is the first report of a patient with aplastic anaemia who developed G-CSF-induced Sweet's syndrome.

Celiac disease (CD) has one of the strongest class II HLA associations of any human illness. We used DNA-RFLP typing to study the class II HLA genotypes of celiac disease patients from the West of Ireland, the geographic area with the highest rate of celiac disease in the world. We confirmed the high frequency of HLA-DR3 in this population, and we were also able to demonstrate the additional risk of developing celiac disease imparted by HLA-DR7. This was done by clearly distinguishing DR7,DQ2 haplotypes from DR7,DQ9 haplotypes, and by "subtraction analysis" of haplotype frequencies. As reported in other populations, most of the patients without DR3 were heterozygous for DR7 and DR11 or 12 (DR5), or had DR4. We used PCR-RFLP and direct sequencing of amplified DNA to examine HLA-DR4 subtypes. The frequency of HLA-DR4 was markedly decreased in patients compared with controls (p = 0.000001) and there was a significant alteration of DR4 subtypes of the patients compared with controls (p = 0.0227). Moreover, all of the CD patients (5 of 5) with DR4 had a haplotype associated with the DQB1*0302 allele compared with only 11 of 23 control subjects with DR4. Our results in this population with exceptionally high risk of CD strongly support the DQ heterodimer hypothesis and suggest that the recently described sequence difference between the DQB1*02 alleles of DR3 and DR7 may contribute to a synergistic increased risk when these haplotypes are inherited together. In addition, our findings suggest a role for HLA-DQ in DR4-associated CD.

Iwo myeloma cell lines were established from a patient. One that originated from the bone marrow (ILIM) requires interleikin 6 (IL-6) for Its growth' and the other thlt originated from the pleral effuslom (D4 proliferates in the absence of IL-6 in the culture mediaL To emine LAS oogem activation in both cell lin, the partial sucleotide sequene of N-AS Sens was detemined by a direct sequeocing method using polyerase chain reaction products. rAnalysis in exon 1 of I-IM genes from both cell lines revealed that neither hadany mutatioms around codo 12 or 13 region Point mutation of N-RAS genes is occasionally found in both lynphoid and myeloid malignancies2-4. In lywhoid malignancy, mutation at codon 12 or 13 was exclusively found while the mutation at codon 61 was detected only in myeloid malignancy4. No point mutation of N-LAS genes has been reported 1i multiple myeloma Therefore, this is the first report stating that the codon 61 of N-MS genes is altered in multiple myeloma and also in lymphoid malignancy.

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