Hypereosinophilic syndrome (HES) is defined as (1) persistent marked eosinophilia of over 6 months duration, (2) of unknown origin (3) complicated by end organ damage. An association between hypereosinophilia of short duration and exposure to sawdust has yet not been reported.

We report a 75 years old white male who presented with a four day history of extreme fatigue, diarrhea and fever. A CBC on admission revealed WBC 18.0 x109/L, hemoglobin 17.5 g/dL and platelets 170 x109/L with 2% eosinophils along with slightly abnormal liver function tests and raised BUN (54 mg/dL) and creatinine (3.0 mg/dL). A CT of the abdomen and pelvis revealed mild mural thickening of the rectum, sigmoid and descending colon. The impression on admission was gastroenteritis with dehydration. The patient was given IV hydration and empirically started on intravenous metronidazole and levofloxacin; and cultures were obtained which turned out to be negative. The patient’s condition soon worsened. He developed respiratory distress and because of apparent sepsis he was transferred to the ICU. His antibiotics were changed to vancomycin, cefepime, flagyl and fluconazole with no apparent improvement. On the 6th day of his admission a CBC revealed WBC 27.7 x109/L, hemoglobin 13.5 g/dL and platelets 27 x109/L with 43% eosinophils and his kidney and liver function continued to deteriorate. A search for tissue invasive parasitic disease was negative and a bronchoalveolar lavage from the left lung demonstrated only 3% eosinophils and no eosinophils were seen in the bronchoalveolar lavage from the right lung.

At this point a hematology consult was requested. Because of his marked and progressive eosinophilia, no apparent cause and evidence of end organ damage a diagnosis of HES was made. The patient was immediately placed on high dose methyl prednisolone to which he responded well. After three weeks of hospitalization his blood counts were normalized and he was discharged. Following his recovery the patient gave a lucid history that he is a freelance wood carver and a few days prior to his falling ill he was massively exposed to sawdust while cleaning the vacuum apparatus of his wood cutting machine.

One of the criteria for the diagnosis of HES is unknown etiology but in this case it was most likely to be due to the exposure to sawdust. On one hand the patient showed evidence of HES in that his eosinophil counts were markedly elevated (Abs Eos 9.8 109/L, normal = < 0.7) and also showed evidence of end organ damage in the form of thrombocytopenia, abnormal liver function tests, and elevated BUN and creatinine levels. However, unlike classic HES the patient’s hypereosinophilia was of short duration (only weeks not months) and there was a definite probable cause of his hypereosinophilia (exposure to sawdust). Further, the patient also responded well to steroid therapy without any recurrence of the disease two years after his initial presentation. This case suggests that inhaled environmental antigens may be associated with some cases of HES.

Disclosures

No relevant conflicts of interest to declare.

Author notes

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Asterisk with author names denotes non-ASH members.

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