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A 7-year-old boy with prolonged and marked leukopenia diagnosed at 6 months of age is described. The polymorphonuclear cells presented no hypersegmented nuclei or concentrated nuclear chromatin, although vacuolated myeloid cells appeared in bone marrow smears. Neutrophils reversed in response to administration of G-CSF. His leukocyte counts were 400-1000/microL during afebrile periods and increased to 2000-3000/microL in response to infections. The increased leukocyte was usually neutrophils, but lymphocytes also increased at EB-virus infection. The serum IgG decreased gradually and was 364 mg/dL at 7 years of age. Antibody responses were normal and recurrent otitis media has been the patient's only problem. Granulocytopenia with hypogammaglobulinemia of this patient mimics myelokathexis with hypogammaglobulinemia, and lymphocytes also increased at viral infections.

baicalein (a lipoxygenases inhibitor) (1.2 µmol/animal) had no effect.4. Furegrelate (an inhibitor of thromboxane A 2 synthase) (1.8 µmol/animal) and (+)S-145 (a thromboxane A 2 receptor antagonist) (625 nmol/animal) attenuated the GLP-1-induced elevation of plasma adrenaline, but these reagents had no effect on the elevation of plasma noradrenaline. The GLP-1-induced elevation of plasma adrenaline was abolished by acute bilateral adrenalectomy, but the procedure had no effect on the elevation of plasma noradrenaline.5. These results suggest that centrally administered GLP-1 induces the secretion of adrenaline from the adrenal medulla by brain thromboxane A 2 -mediated mechanisms, while the peptide evokes the release of noradrenaline from sympathetic nerves by brain prostanoid other than thromboxane A 2 -mediated mechanisms in rats.

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