Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven young cats were injected with feline leukemia virus (FeLV); six of them became viremic. All of the viremic cats developed AIDS-related symptoms, i.e. lymphopenia, neutropenia, thymic atrophy, and wasting syndrome, along with an altered pituitary and adrenocortical function. These symptoms closely resemble human AIDS induced by HIV. It was discovered that, after 2 weeks of infection, the average amount of plasma adrenocorticotropic hormone (ACTH) detected in the infected cats was reduced by 29% in comparison with that before the infection. In contrast to the second week, the fifth week of infection showed a 94% increase of plasma ACTH which then dropped back down to 38% after the sixth and seventh weeks. This opposing biphasic pattern of change was also observed in the plasma cortisol content of the infected cats. The amount of change in plasma cortisol did not correlate with the detected increase in plasma ACTH, indicating a weak adrenal response to pituitary action.
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PMID:Induction of feline immunodeficiency syndrome by feline leukemia virus: pituitary and adrenocortical dysfunctions. 196 24

Platelet-activating factor (PAF; 100 ng i.v.) transiently modified the number of circulating neutrophils in the mouse, inducing a fast neutropenia (2 min) followed by a late onset neutrophilia (2 h). The potential involvement in PAF-induced neutrophilia of granulocytotic agents such as interleukin-1 and tumor necrosis factor-alpha could be excluded on the basis of the ineffectiveness of interleukin-1 receptor antagonist and of a specific monoclonal antibody anti-murine tumor necrosis factor-alpha. PAF granulocytosis was preceded by a significant rise in plasma corticosterone at 20 min. The involvement of endogenous corticosteroids was confirmed by the experiments with adrenalectomized mice and in animals pretreated with the steroid antagonist RU486 (11 beta-(4-dimethyl amino-phenyl) 17 beta-hydroxy, 17 alpha(prop-1-ynyl) estra 4,9-dien-3-one), where PAF-induced neutrophilia was greatly reduced (approximately 50%). Moreover, sustained increase in plasma corticosterone by administration of adrenocorticotropic hormone was paralleled by an intense neutrophilia. We show evidence that endogenous corticosterone acts through the glucocorticoid-inducible protein lipocortin 1.
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PMID:Endogenous corticosteroids mediate the neutrophilia caused by platelet-activating factor in the mouse. 749 25

A 21-year-old man with isolated adrenocorticotropic hormone (ACTH) deficiency complained of loss of consciousness in association with hypoglycemia. Both plasma ACTH and cortisol levels were low and failed to respond to corticotropin-releasing hormone (CRH) stimulation. The patient also showed abnormal findings in hematological examination, such as neutropenia and anemia with lymphocytosis, activity of coagulation factors, and electroencephalography (EEG). Furthermore, mitogen-induced lymphocyte proliferation was increased. After successful replacement therapy with hydrocortisone 15 mg/day, most of these abnormalities including the lymphocyte proliferation were fully restored.
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PMID:Reversibly increased lymphocyte response to mitogens in a young man with isolated adrenocorticotropic hormone deficiency. 914 12

The aim of the study was to evaluate the effect of adrenal stimulation by adrenocorticotropic hormone (ACTH) on blood cortisol concentration and on circulating total and differential leukocyte counts during and in the 16 days after ACTH administration. Swedish Landrace boars aged approximately 6-7 months were used. ACTH-treated animals (n = 7) were given ACTH intravenously at 10 microg/kg body mass for 3 days. A control group of animals (n = 7) received 1 ml of sterile 0.9% saline intramuscularly. ACTH induced a highly significant increase (p>0.0001) in serum cortisol in treated boars. On the day after the last ACTH dose, the cortisol concentration was significantly higher, but the level of significance was lower than during ACTH administration (p>0.05). During ACTH treatment, a significant increase was recorded in total leukocyte count and neutrophil percentage (p>0.05 to p>0.0001), along with the increase in blood cortisol concentration, whereas percentage lymphocyte count showed a significant decrease. Lymphopenia disappeared upon cessation of treatment, but neutropenia developed in the week after treatment. On all three days of ACTH challenge, the neutrophil-to-lymphocyte ratio was significantly increased. An increase in eosinophil percentage was recorded on treatment days 1 and 2, whereas ACTH treatment had no effect on basophil percentage. In conclusion, three-day administration of ACTH to young boars during restraint caused effects similar to acute stress situations, as suggested by disappearance of the effects on immune function after the last drug dosage.
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PMID:Cortisol and immune measures in boars exposed to three-day administration of exogenous adrenocorticotropic hormone. 1650 11