A 64-year-old White man (non-smoker), with rheumatoid arthritis, recently diagnosed with plasma cell dyscrasias (i.e., light chain disease) with humoral abnormalities, was admitted to our hospital. Previously (~ half a year earlier) noticed ulcers appearing on the skin of the leg were initially diagnosed as a result of rheumatoid nodules. The patient did not use hot tubs, whirlpools, and swimming. According to the patient's account, the changes were initially non-specific, an unremarkable reddish papulonodular and painless lesion forms, which rapidly enlarged and erode within 1-2 months (Figure 1A). Despite treatment with topical glucocorticosteroids (3 months), then systemic [plus cyclophosphamide (100 mg/day)], the confluent lesions enlarged into big necrotizing ulcers. Subcutaneous nodules (symptoms of P. aeruginosa sepsis) were not observed. No purulent exudate, green color, or other signs of pseudomonas folliculitis were observed (Figure 1). Finally, enlarged non-healing demarcated ulceration (with an indurated base and edges) was initially red and then dark blue and finally turned black (Figure 1B) possibly due to hemolysis. Deep ulcers cause scarring of muscles and tendons, finally leading to permanent disability (Figure 1B). Unlike, in scrofuloderma, enlarged lymph nodes were not observed in this case. Although asthenia and weight loss have been observed, crusts and plaques were not seen. General swelling and a sensation of creeping on the skin were observed; next, renal and neurovascular (e.g., TIA) symptoms such as asthenia, bleeding, ocular, and cardiovascular manifestations appeared; loss of weight by 5 kg followed by pulmonary symptoms with multiple organ failure during admission to our hospital. There was no evidence of acute deep vein thrombosis of the lower limbs and saphenous venous thrombosis. Because of vasculopathy and the risk of hemorrhage (a constitutional symptom of hyperviscosity is bleeding and cardiovascular manifestations), surgical intervention and skin biopsy have not been performed. Contrary to the advancement of paraproteinemia, vascular process, and complications, respiratory symptoms did not dominate. Chest CT scan showed small thick-walled cavities that correspond with normal blood pressure, pH = 7.48, partial pressure of oxygen (pO2 51.4 mmHg), as well as lack of pulmonary symptoms, including dyspnea and cough. Noteworthy, other extrapulmonary lesions or miliary TB were excluded. A bronchoscopic examination was performed with BAL and sputum/skin sampling. After his TB diagnosis (see Section 2.1), he received a therapeutic regimen with conventional oral therapy. The patient was treated with a combination of four chemotherapy drugs: rifampicin, ethambutol, pyrazinamide, and isoniazid (streptomycin was not considered due to nephrotoxicity). Due to the patient's condition (WHO4) and tuberculous complications, he was disqualified from further hemato-oncological treatment of plasma cell dyscrasia. Although the TB therapeutic regimen was introduced and the big skin ulcer and pulmonary symptoms were stable (no further enlargement of the necrotic ulcer was observed by 2 months), his health condition worsened day by day. The bacterial culture from blood (Mycobacterium spp. as well as aerobic and anaerobic bacteria) was negative. He died within 3 months after admission due to hypoalbuminemia, exudates, microcirculatory abnormalities, anuria (secondary membranous nephropathy), and finally brain edema and multiple organ insufficiency (there was no consent to the autopsy).