Although Henoch-Schönlein purpura due to Mycobacterium tuberculosis has been reported previously, it is uncommon. And there were some reports of direct skin lesions due to Mycobacterium avium-intracellulare complex (MAC). However, to date there are no reports of Henoch-Schönlein purpura in MAC. This is the first report of Henoch-Schönlein purpura associated with MAC infection. We should consider MAC infection as a potential cause of Henoch-Schönlein purpura.

A 57-year-old woman, a housekeeper, had been treated for MAC with various antituberculous drugs for 11 years. Oxygen therapy was initiated in December 1998 and clarithromycin was added in November 2001. Chest radiograph showed bilateral destroyed lung with multiple cystic lesions (Fig. 1). The patient demonstrated right pneumothorax and received bullectomy in 1998.

She presented with bloody sputum and high grade fever on 11 March 2002. The temperature was 38.1ºC. Analysis of arterial blood gases with nasal prongs at 3l/min showed that the partial pressure oxygen was 89.9 mmHg, the partial pressure of carbon dioxide was 49.6 mmHg, and the pH was 7.39. The white blood cell count was 11,400/mm³, 80% neutrophils, 13% lymphocytes, 7% monocytes. The serum albumin level was 4.0 g/dl and the CRP level was 5.0 mg/dl. Platelets were 357,000/mm³. Sputum culture yielded Mycobacterium (M.) avium and M. intracellulare. Since high grade fever continued, panipenem and fosfomycin were used for two weeks. The high grade fever was slightly lowered and bloody sputum disappeared, but a low grade fever persisted. After 3 days of recurrence of bloody sputum, the patient suddenly complained of palpable pururitic lesions on the bilateral lower extremities with bilateral gonalgia on 16 April (Fig. 2). Mainly dot hemorrhage with erythema spread to the bilateral dorsum pedis, lower leg and thigh, and the erythema did not fade by pressing with glass. It was partially accompanied by pigmentation. Platelet count was 329,000/mm³. Prothrombin time and partial thromboplastin time were normal. Serum antistreptolysin-O (ASO) was normal. Urine showed microhematuria. Styptic drugs and vitamin C were administered and the skin lesions were slightly improved. However, purpura recurred and worsened with microhematuria after 9 days. Therefore, 10 mg prednisolone was added. The purpura improved and prednisolone was decreased to 5 mg after 5 days. Prednisolone persisted, and there was no recurrence of purpura or bloody sputum.

Henoch-Schönlein purpura is a leukocytoclastic vasculitis that usually affects children. Palpable pururitic lesions, abdominal pain, and arthritis of the knees and ankles are common findings, but other organs may be involved as well. Several precipitating factors have been implicated, including infections, environmental chemicals, toxins, insect bites, physical trauma, complement C₂ deficiency, and malignancies (1).

Infections are proposed to be a causative factor and leukocytoclastic vasculitis due to M. tuberculosis has been reported previously (2–5), but is uncommon (6). There are two types of skin lesions associated with tuberculosis (7):

①Direct lesions where the bacillus is present, produced by three different mechanisms (inoculation from an exogenous source; cutaneous mycobacteriosis from an endogenous source, either by contiguous spread or by autoinoculation and third, those arising from hematogenous spread, such as lupus vulgaris, acute hematogenous dissemination and nodules or abscess.

②Hypersensitivity vasculitis, where the microorganism has never been found and the proposed pathogenic mechanism is the deposit (in the walls of small vessels) of immune complexes formed by antibodies to M. tuberculosis proteins (8). Henoch-Schönlein purpura is thought to be an immune complex disease, with 50% of patients producing IgA rheumatoid factor (9).

There have been some reports of direct skin lesions due to MAC (10–12). However, there are no reports of hypersensitivity vasculitis, Henoch-Schönlein purpura, in MAC. In the present case, the involvement of drugs was thought to be negative as a cause of the skin lesions, because there has not been any change in the drugs over 1 year. Since her condition has been continuously poor due to MAC infection, some immune response to the MAC infection might have contributed to the skin lesions. The fact that the steroid was effective also proves this possibility. As there were some reports of pulmonary hemorrhage in Henoch-Schönlein purpura, there might be some relation to the bloody sputum in this case. Henoch-Schönlein purpura may promote serious renal disturbance, and it is important to have an early diagnosis and treatment. It is also necessary to consider MAC infection as a potential cause of Henoch-Schönlein purpura.