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Neutrophilia with subclinical Cushing's disease: A case report and literature review

Journal

OPEN LIFE SCIENCES
Volume 18, Issue 1, Pages -

Publisher

DE GRUYTER POLAND SP Z O O
DOI: 10.1515/biol-2022-0540

Keywords

subclinical Cushing's disease; silent corticotropin adenomas; leukocytosis; pituitary adenoma; case report

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The increase in the level of neutrophils following subclinical Cushing's disease is a rare phenomenon without significant biochemical or clinical evidence of hypercortisolism. This case study presents a 37-year-old female patient who exhibited increased neutrophils that were unresponsive to anti-infection therapy. The patient was initially suspected to have a urinary tract infection, but further examination ruled out this possibility and revealed the presence of silent corticotropin adenomas.
The increase in the level of neutrophils following subclinical Cushing's disease is an uncommon clinical phenomenon that is characterized by insignificant biochemical or clinical evidence of hypercortisolism. In this study, we reported a 37-year-old female patient who presented with palpitations and fatigue, and showed increased neutrophils that were unaffected by anti-infection therapy. The patient was suspected of having a urinary tract infection because of occasionally with urinary frequency, urgency, increased procalcitonin, leukocytosis, and an increased proportion of neutrophils. The ineffectiveness of anti-infection therapy ruled out the possibility of urinary tract infection. Further examination of the bone marrow excluded the possibility of blood disease. However, the levels of blood cortisol and adrenocorticotropic hormone (ACTH) increased, and a magnetic resonance imaging examination revealed lesions in the sphenoidal sinus and sella area of the sphenoidal bone, which confirmed the relationship between increased glucocorticoids and increased neutrophils. This was further confirmed by follow-up surgery and pathological examination, which revealed silent corticotropin adenomas, which are characterized by the lack of biochemical or clinical evidence of hypercortisolism with positive immunostaining for ACTH.

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