**Background:** HIV infection is associated with a 2- to 10-fold increased risk of venous thrombosis compared to the general population, with VTE incidence of 0.19–7.63%/year. Risk factors include low CD4 count, clinical AIDS, protein S/C deficiency, and opportunistic infections. Pulmonary TB is a common co-infection in HIV patients, particularly in high-burden settings like Indonesia. This report describes a rare case of DVT in a patient with concurrent HIV/AIDS and pulmonary TB.
**Methods:** This is a single case report following SCARE 2020 guidelines. The patient was a 30-year-old Indonesian male with known AIDS (on Tenofovir+Lamivudine+Efavirenz) and pulmonary TB (on first-line anti-TB drugs for 3 months). He presented with 1 month of pain, erythema, tenderness, and swelling in the left leg. Physical examination revealed pitting edema, erythema, tenderness, and a positive Homans sign. Laboratory findings included: WBC 6640/µl, hemoglobin 8.4 g/dl, platelets 362,000/µl, absolute CD4 77 cells/µl. Acid-fast bacilli test (+), GeneXpert MTB (+), Rifampicin sensitive. FNAB of right cervical nodes showed chronic suppurative inflammation suggestive of TB lymphadenitis. Left lower extremity Doppler ultrasound showed partial DVT in the common femoral vein, superficial femoral vein, and left popliteal vein. Chest radiography showed minimal left pleural effusion.
**Key Results:** The patient was diagnosed with left lower extremity DVT, AIDS, and pulmonary TB. He received fondaparinux 1×5 mg and warfarin 2 mg/day. On day 6: PPT 10.3 s, APTT 39.4 s, INR 1, D-dimer 2252 ng/ml. Warfarin was increased to 3 mg/day. On day 9: PPT 10 s, APTT 34.9 s, INR 1. Warfarin increased to 4 mg/day. On day 14: swelling and pain had resolved, no bleeding. PPT 10.5 s, APTT 33 s, INR 1, CD4 improved to 262 cells/µl. The patient was discharged to outpatient care on warfarin 1×4 mg.
**Clinical Implications:** This case illustrates that DVT can occur in HIV/TB co-infected patients, even while on appropriate antiretroviral and anti-TB therapy. The proposed mechanisms include low CD4 count (77 cells/µl) leading to a hypercoagulable state, and Mycobacterium tuberculosis inducing anticardiolipin antibodies and pro-inflammatory cytokines (TNF-α, IL-1, IL-6) that block the protein C anticoagulant pathway and promote tissue factor production. Management followed standard ACCP guidelines for DVT in non-HIV patients, using fondaparinux (LMWH alternative) bridged to warfarin with INR monitoring. The favorable outcome suggests that standard anticoagulation is effective in this population. Clinicians should maintain a high index of suspicion for DVT in HIV/TB patients presenting with unilateral leg symptoms.