64 Letters and Correspondence

REFERENCES TABLE I. Evolution of Endoaenous Cytokine Levels*

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

Kaden BR, Rosse WF, Hauch Tw: Immune thrombocytopenia in lymphoprolifera- tive diseases: Blood 53545, 1979. Clancy R, Jenkins E, Firkin B: Qualitative platelet abnormalities in idiopathic thrombocytopenic purpura: N Engl J Med 286:622, 1977. Hedge UM, Powell DK, Bowes A, Gordon-Smith EC: Enzyme linked immunoas- say for the detection of platelet associated IgG: Br J Haematol 48:39, 1981. Cines DB, Schreiber AD: Immune thrombocytopenia: Use of a Coomb‘s antiglob- ulin test to detect IgG and C3 on platelets: N Engl J Med 300:106, 1979. Sugiura K, Steiner M, Baldini MG, Pawtnckect RE: Platelet antibody in idiopathic thrombocytopenic purpura and other thrombocytopenias. A quantitative sensitive and rapid assay: J Lab Clin Med 96640, 1980. Von dem Borne AEG KR, Verheugt FWA, Oosterhof F, von Riesz E, de la Rivere .4B, Engelfriet C P A simple immunofluorescence test for the detection of platelet antibodies: Br J Haematol 39:195, 1978. Keltnn JG, Carter CJ, Rodger C, Behenek G, Gauldie J, Sheridan D, Kassam YB, Kean WF, Buchanan WW, Rooneley PJ, Beanchi F, Benburg J: The relation- ship among platelet associated IgG, platelet life span and reticuloendothelial cell function: Blood 63:1434, 1984. Sugiyama H, Yagita M, Takahashi T, Nakamura K, Iho S, Hoshino T, Imura H: Megakaryocytopoiesis in idiopathic thrombocytopenic purpura: Acta Haematol Jpn 50119, 1987. Branehog I, Kutti J, Weinfeld A: Platelet survival and platelet production on idiopathic thrombocytopenic purpura (ITP). Br J Haematol 27: 127, 1974. Ballem PJ, Segal GM, Stratton JR, Gernsheimer J, Adamson JW, Slichter SJ: Mechanisms of thrombocytopenia in chronic autoimmune thrombocytopenic pur- pura. Evidence of both impaired platelet production and increased platelet clear- ance: J Clin Invest 80705. 1987.

Sweet’s Syndrome During Acute Myeloid Leukaemia: Is There a Role for Hematopoietic Growth Factors?

To the Editor: The pathogenesis of Sweet’s syndrome (SS) remains un- known. However, recent data have focused attention on the potential role of G-CSF [I-31. We report herein the course of endogenous G-CSF, GM- CSF, and IL6 levels in a patient with SS and AML.

In October 1993, a 28-year-old man had been hospitalized with a 1 month history of fever, abdominal and articular pain, and skin lesions. Physical examination revealed tender erythematous lesions on the hands and legs consistent with SS. Laboratory data were as follows: leucocytes 6.6 X 109/L with 40% PMNs, 22% lymphocytes, 23% monocytes, and 15% myeiocytes and metamyelocytes; haemoglohin 13.8 g/dl; thrombocytes 58 X 109/L. The bone marrow examination showed the presence of 40% blast cells (AML4 according to FAB-classification). A biopsy from skin lesions revealed a dense dermal infiltrate of mature neutrophils without vasculitis or blastic infiltrate. The histologic condition was suggestive of SS. Induction chemotherapy lead to complete remission. Corticosteroid therapy was not given. Lesion of SS disappeared promptly after a few days of chemotherapy. Four months later, relapse in the bone marrow was diagnosed, without recurrence of SS. The patient died during the course of an unrelated allogeneic bone marrow transplantation.

During the course of SS and induction chemotherapy, GM-CSF, G-CSF, and 1L6 serum levels were monitored. Evolution of endogenous cytokine levels is summarized in Table 1. At diagnosis, GM-CSF and G-CSF were under the limits of detection. While lesions of SS disappeared, G-CSF serum levels rose to 290 and 3,430 pg/ml, even though GM-CSF levels remained unchanged. Initial IL6 level was 23 pg/ml and rose to 77 and 221 pg/ml during aplasia.

Recently, several observations have drawn attention to the possible role of several cytokines in the pathogenesis of SS. Some observations of SS occuring during G-CSF therapy [ 1,2] have given weight to this hypothesis. Moreover, Reuss-Borst et al. [3] showed that G-CSF and IL6 were elevated

Davs 0 5 10 14 ~~

Chemotherapy +

GM-CSF (pg/ml) 0 0 ND < 10

lL6 (pglml) 23 71 ND 221 P M N ~ (x 1 0 9 ~ ) 2,31 O S 0 0

G-CSF (pglml) 0 290 ND 3,430

ss + 2 - -

*ND: not done.

during a case of SS associated with myelodysplasia. These authors suggested that endogenous G-CSF production could explain the leucocytosis in the dermis, while I I -6 could induced the inflammatory process [3]. Our results are in disagreement with those. At diagnosis, when lesions of SS were present, G-CSF and GM-CSF levels were undetectable in the serum and IL6 was low. Secondary raising in G-CSF levels, while SS had completely resolved, may be explained by severe neutropenia following chemotherapy 141. Similar results were reported by Loraas et al. [5], who could not find any elevated systemic levels of G-CSF in a case of SS.

Finally, in our observation, SS could not be explained by systemic produc- tion of cytokines. Alternatively, we can not exclude that local tissue levels of G-CSF (or GM-CSF) might be different from serum levels and that high tissue levels may be present in SS.

PHILIPPE GENET MARC PULIK

FRANFOIS LIONNET CHARLO~E PETITDIDIER

ANTOINE PETIT

ALAIN GAULIER

Department of Hematology,

Department of Dermatology,

Department of Pathology, Service d‘Hematologie, Hdpital Victor-Dupouy, Argenteuil, France

REFERENCES

1. Park JW, Mehrotra B, Bamett BO, Baron AD, Venook A P The Sweet syndrome during therapy with granulocyte colony-stimulating factor. Ann Intern Med 116:996-998, 1992.

2. Paydas S, Sahin B, Seyrek E, Soylu M, Gonsulsen G, Acar A, Tuncer I: Sweet’s syndrome associated with G-CSF. Br J Haematol 85191-192, 1993.

3. Reuss-Borst MA, Pawelec G, Saal JG, Horny HP, Muller CA, Waller H D Sweet’s syndrome associated with myelodysplasia: possible role of cytokines in the patho- genesis of the disease. Br J Haematol 84356-358, 1993.

4. Cebon J, Layton JE, Maher D, Morstyn G Endogenous haematopoietic growth factors in neutropenia and infection. Br J Haematol 86265-274, 1994.

5. Loraas A, Waage A, Lanvik J: Cytokine response in Sweet’s syndrome associated with myelodysplasia. Br J Haematol 87:669.

Streptococcus lactis Septicemia in a Patient With Chronic Lymphocytic Leukemia

To the Editor: Streptococcus lactis is a gram-positive lactic acid bacteria widely used as a starter organism in the production of fermented dairy products [l]. Bovines are the natural host, and human infection is uncommon [l]. Here, a patient with chronic lymphocytic leukemia who developed Streptococcus lactis septicemia after yoghourt ingestion is described.

A 69-year-old man with Rai stage IV B-cell chronic lymphocytic leuke-