The patient was a 56-year-old woman with a history of hypertension and hyperlipidemia from one year ago. About two years ago, papule and pustular lesions emerged in the extensor area of both elbows; the lesions were accompanied by purulent discharge and brief itching, gradually turning into erythematous perforated indurated plaques and nodules within a month. These skin lesions then spread to the extensor surfaces of the knees, fingertips (painful lesions), scalp, and neck (Figures 1-3). The skin lesions appeared periodically and persisted for one month, with a two-three-month interval between each period. The patient complained of dyspnea on exertion but had no symptoms of cough, hemoptysis, weight loss, fever and chills, and night sweats. A PPD skin test was performed and returned positive; tuberculosis was also reported on a CT scan of the lungs. Furthermore, evidence in favor of tuberculosis was reported in a sample of the right axillary lymph nodes. After treatment, the lesions healed entirely, and only the elbow and knee scars remained.
What is your diagnosis?
Cutaneous leukocytoclastic vasculitis associated with tuberculosis.
Leukocytoclastic vasculitis with dermal necrosis and ill-defined granulomas
Microscopic examination showed large subcorneal abscess, ulceration, nearly full-thickness dermal necrosis, fibrinoid necrosis of small vessels, leukocytoclasis, and fibrin thrombi partially surrounded by palisaded histiocytes. There were scattered ill-defined granulomas, lymphoplasma cell infiltration, and few eosinophils in the deep dermis (Figures 4 & 5).
Vasculitis refers to blood vessel wall inflammation. Leukocytoclastic (neutrophil fragmentation) vasculitis is a small vessel vasculitis that can be idiopathic or secondary to infections, neoplasms, collagenosis, or the use of drugs 1 ; infections and drugs are the most common causes 2 .
For the first time in 1967, Parish et al. showed that Mycobacterium tuberculosis could cause vasculitis 3 . Tubercle bacilli aggression, immune complex deposition in the vessel wall, delayed hypersensitivity response, or rifampicin-dependent antibodies are possible reasons for cutaneous vasculitis associated with tuberculosis 4 . Unlike cutaneous tuberculosis, the tubercle bacilli itself is not present in the vessel wall in leukocytoclastic vasculitis 5 , 6 . Instead, the deposit of immune complexes in small vessels of the lower extremities is the primary mechanism of this type of vasculitis 5 . To treat these skin lesions, immunosuppression is not necessary, and treatment of tuberculosis is sufficient 7 .
Conflic of Interest
- Carlson JA, Ng BT, Chen K-R. Cutaneous vasculitis update: Diagnostic criteria, classification, epidemiology, etiology, pathogenesis, evaluation and prognosis. AM J Dermatopath. 2005; 27(6):504-28.
- Baigrie D, Crane JS. Leukocytoclastic vasculitis (hypersensitivity vasculitis). Treasure Island: StatPearls Publishing; 2018.
- Parish WE, Rhodes EL. Bacterial antigens and aggregated gamma globulin in the lesions of nodular vasculitis. Br J Dermatol. 1967; 79(3):131-47.
- Chan C, Chong Y, Sum A, et al. Cutaneous vasculitis associated with tuberculosis and its treatment. Tubercle. 1990; 71(4):297-300.
- Mínguez P, Pintor E, Burón R, et al. Pulmonary tuberculosis presenting with cutaneous leukocytoclastic vasculitis. Infection. 2000; 28(1):55-7.
- Carvalho M, Dominoni RL, Senchechen D, et al. Cutaneous leukocytoclastic vasculitis accompanied by pulmonary tuberculosis. Jornal Brasileiro de Pneumologia. 2008; 34:745-8.
- Martinez V, Zeller V, Caumes E, et al. Cutaneous vasculitis disclosing pulmonary tuberculosis. Annales de Medecine Interne. 2000; 151(8):664-666.