Laryngo- rhino- otologie · 1996
[Chronic myeloid leukemia--a rare cause of labyrinth apoplexy].
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Woldag K, Schwarzer A
Аннотация
BACKGROUND: Cochleovestibular lesions in patients with acute myeloid leukemia or the blastic phase of chronic myeloid leukemia are usually due to leukemic infiltration, infection or hemorrhage. In contrast, the most likely cause of cochleovestibular lesions in the chronic phase of the chronic myeloid leukemia seems to be disturbed microvascular perfusion and vascular occlusion.
CASE REPORT: A 45-year old patient with a chronic myeloid leukemia presented with the sudden onset of profound deafness in his right ear combined with a total loss of vestibular function on the same side. The hemoglobin count was 10.5 g/dl; the white blood cell count 448 x 10(9)/I; the platelet count 71 x 10(9)/I. All of the plasmatic coagulation factors were in the normal range. The patient was treated with cytostatic drugs and responded well (rapid cytoreduction), but the deafness persisted.
DISCUSSION: Cochleovestibular lesions in the chronic phase of the chronic myeloid leukemia are very rare. The most likely cause in the case described above seems to be increased blood viscosity due to the high white cell count and alterations in the leukocyte rheology (leukostasis syndrome).
CONCLUSION: In patients with leukemia and acute cochleovestibular lesions in contrast to other patients with sudden deafness and/or sudden loss of peripheral vestibular function, a combination of chemotherapy and leukopheresis capable of rapid cytoreduction is necessary, whereas a conventional hemorrheologic therapy seems to be insufficient.
CASE REPORT: A 45-year old patient with a chronic myeloid leukemia presented with the sudden onset of profound deafness in his right ear combined with a total loss of vestibular function on the same side. The hemoglobin count was 10.5 g/dl; the white blood cell count 448 x 10(9)/I; the platelet count 71 x 10(9)/I. All of the plasmatic coagulation factors were in the normal range. The patient was treated with cytostatic drugs and responded well (rapid cytoreduction), but the deafness persisted.
DISCUSSION: Cochleovestibular lesions in the chronic phase of the chronic myeloid leukemia are very rare. The most likely cause in the case described above seems to be increased blood viscosity due to the high white cell count and alterations in the leukocyte rheology (leukostasis syndrome).
CONCLUSION: In patients with leukemia and acute cochleovestibular lesions in contrast to other patients with sudden deafness and/or sudden loss of peripheral vestibular function, a combination of chemotherapy and leukopheresis capable of rapid cytoreduction is necessary, whereas a conventional hemorrheologic therapy seems to be insufficient.