Analysis Of Clinical Presentation And Skin Tissue Pathology In 30 Cases With Sweet's Syndrome

ObjectiveTo explore the relationship between the pathological features,pathological features and clinical manifestations and clinical prognosis of Sweet Syndrome.MethodsThe clinical manifestations,laboratory examinations and histopathological findings of 30 patients with Sweet syndrome in our hospital were retrospectively analyzed.The expression of MPO and CD34 in tissue cells was detected by immunohistochemistry.The data were analyzed using SPSS22.0 statistical software.Result1.30 patients from the study,aged 13 to 65 years old,with a male to female ratio of 1:1.7,11 males and 19 females.The affected parts were:upper limb(70%),lower limb(66.7%),face(63%),and trunk(50%).Three patients had a history of tumor,which were mediastinal tumor,rectal cancer,and uterine fibroids.2.There were 7 patients with Talaromyces marneffei infection or non-tuberculous mycobacterial infection,as follows:(1)The average CRP count of patients with Talaromyces marneffei infection or non-tuberculous mycobacterial infection was:(107.56±51.72)mg/L.The average CRP count of non-infective patients was:(68.42±36.39)mg/L.There was significant difference between the two(P<0.05).(2)The average white blood cell count in patientswithTalaromycesmarneffeiinfectionwithnon-tuberculous mycobacterial infection was(20.62±5.30)×10~9/L,and the average white blood cell count of non-infective patients was(18.91±6.28)×10~9/L.The results showed no statistics significance(P>0.05).(3)The average neutrophil count in patients with Talaromyces marneffei infection or non-tuberculous mycobacterial infection was(15.93±4.75)×10~9/L.The average neutrophil count in non-infective patients was(14.86±5.88)×10~9/L.The results showed no statistical significance(P>0.05).(4)The mean erythrocyte sedimentation rate of patients with Talaromyces marneffei infection or non-tuberculous mycobacterial infection for(86.42±34.86)mm.The mean erythrocyte sedimentation rate of non-infectious patients is(58.13±36.15)mm.The results showed no statistical significance(P>0.05).3.Histopathology:27 cases of lesions showed inflammatory cells involving sweat glands,inflammatory cells involving subcutaneous fat lobules in 15 cases,perivascular infiltration in 3 cases,vascular wall with cellulose deposition in 6 cases.Eosinophil infiltration was observed in6 cases of lesions combined with Talaromyces marneffei infection or non-tuberculous mycobacterial infection.Immunohistochemistry:MPO and CD34were not expressed in the infiltrating tissue of the lesions in 30 patients.Immunohistochemistry:MPO and CD34 were not expressed in the infiltrated tissue cells of the lesions of 30 patients.Conclusion(1)Inflammatory infiltration in the skin lesions of sweet syndrome can involve appendages,subcutaneous fat lobules,and even peripheral nerve fibers.(2)Inflammatory infiltrating tissue cells have no obvious myeloid markers.(3)The presence of eosinophils in the skin lesions of sweet syndrome may be induced by infection.