| Objective: To explore the clinical characteristics,treatment and prognosis of Talaromycosis marneffei complicated with Sweet Syndrome,improve clinicians’ understanding of this kind of disease and provide experience for clinical diagnosis and treatment.Methods: The clinical data of 1 hiv-negative patient with Talaromycosis marneffei complicated with Sweet Syndrome admitted to the First Affiliated Hospital of Guangxi Medical University were analyzed retrospectively,and the literature was reviewed.Results: 1.Middle-aged woman,43 years old,with a history of erythema nodosum,G-6-P-D enzyme deficiency,long-term oral glucocorticoid treatment,fever,lymph node swelling and pain,accompanied by cough,sputum,chest pain,misdiagnosed as tuberculosis for more than 1 month.Peripheral blood white blood cells were increased,albumin was low,ESR and CRP were increased,large patchy consolidation shadow of the left lung with pleural effusion,and bone lysis was destroyed.Finally,TM growth was cultured from alveolar lavage fluid and lymph node tissue,and voriconazole was administered for more than 2 months,and the condition was improved.1 month later,fever,rash and salmonella were found again.Skin biopsy pathology showed superficial and deep dermal neutrophils diffuse tissue cell infiltration.No suppurative or granulomatous changes were observed,which was consistent with the changes of Sweet Syndrome.Imipenem and Cilastatin Sodium treatment for 1 month and glucocorticoid therapy,the condition improved.Then voriconazole,glucocorticoid maintenance therapy.After 9 months,there was a systemic skin rash,swollen lymph nodes,and newly occurring osteolytic destruction,which was considered to be combined with NTM.Moxifloxacin,clarithromycin,ethambutol were added for treatment for 3 months,and the symptoms and osteolysis were improved.After switching to itraconazole,the rash appeared again.After discontinuation of itraconazole,the rash disappeared.The glucocorticoid was gradually reduced and discontinued.During the course of the disease,positive anti-gamma-interferon autoantibodies were repeatedly detected,which were significantly increased in different pathogen infection states.2.Review of the literature: 8 patients were hiv-negative,6 were positive for anti-gamma-interferon autoantibodies,6 were associated with nontuberculous mycobacterium infection,and 2 were associated with bacterial nontyphoid salmonella and pseudomonas Burkholderia,respectively.The skin rash with Sweet Syndrome is characterized by a variety of manifestations,including painful erythema,papules,nodules,pseudovesicular rash,and pustules.The skin rash may occur on the limbs,face,neck,and trunk.The skin rash may occur before or after TSM diagnosis,or with enlarged lymph nodes.All the patients were treated for TM and other pathogenic bacteria,and treated with glucocorticoid therapy.Conclusions: 1.In hiv-negative host TSM patients,different types of rashes occur during the course of the disease,including skin lesions specific to TM infection or associated with SS,as well as rashes from other causes,and timely skin biopsy pathology can help identify them.2.TM induced SS is more likely to occur in hiv-negative patients with anti-gamma-interferon autoantibodies positivity,with lymph node enlargement in addition to skin lesions.3.The patients with positive anti-gamma-interferon autoantibodies were susceptible to TM,Salmonella and NTM,accompanied by further increase of antibody and the appearance of SS syndrome,suggesting that the occurrence of SS may be related to the sharp increase of anti-gamma-interferon antibody after pathogen infection.4.The treatment of TSM patients with SS was mainly antifungal therapy to control TM infection.On this basis,rational use of glucocorticoid therapy,such as recurrence of rash,should be excluded with other new opportunistic infections or drug eruptions. |
PDF Full Text Request