What are the potential causes of purpura in a 36-year-old patient with a diagnosis of tuberculosis (TB)?

Purpura in a 36-Year-Old with Tuberculosis

Direct Answer

In a 36-year-old patient with tuberculosis and purpura, the most likely cause is immune thrombocytopenic purpura (ITP) directly triggered by active TB infection, which requires combined treatment with antituberculous therapy and corticosteroids. 1, 2

Primary Mechanism: TB-Associated Immune Thrombocytopenic Purpura

Tuberculosis can directly cause ITP as a presenting or concurrent manifestation, occurring in approximately 1% of active TB cases. 1 This represents an immune-mediated destruction of platelets triggered by the mycobacterial infection itself.

Key Clinical Features of TB-Associated ITP:

• Platelet counts typically range from 4,000-21,000/mm³ with visible purpura as the presenting sign 1, 3
• Bone marrow examination shows increased megakaryocytes, confirming peripheral platelet destruction rather than production failure 1
• Poor initial response to corticosteroids alone is characteristic—platelet recovery occurs only when antituberculous drugs are added to treatment 1, 2
• Platelet normalization occurs 2-6 weeks after initiating combined therapy with prednisone and antituberculous medications 1

Distribution of TB Types in ITP Cases:

• Disseminated miliary TB (33% of cases) 1
• Abdominal TB or lymphadenitis (33% of cases) 1
• Pulmonary TB (33% of cases) 1, 3
• Notably, splenomegaly is typically absent 1

Secondary Consideration: Thrombotic Thrombocytopenic Purpura (TTP)

TTP associated with TB is a rare but life-threatening alternative diagnosis characterized by the classic pentad of thrombocytopenia, microangiopathic hemolytic anemia, neurological symptoms, renal dysfunction, and fever. 4

Distinguishing TTP from ITP:

• TTP requires plasma exchange and fresh frozen plasma infusions as primary therapy, not just corticosteroids 4
• Pathogenesis involves IL-1-mediated increased procoagulant activity on endothelial cells 4
• Complete remission may take 3 months even with appropriate treatment 4
• Look for schistocytes on peripheral smear, elevated LDH, and decreased haptoglobin to confirm TTP

Tertiary Consideration: Henoch-Schönlein Purpura (HSP)

Disseminated TB can trigger HSP, an immune complex-mediated systemic vasculitis, though this is exceedingly rare. 5

HSP Diagnostic Features:

• Non-thrombocytopenic palpable purpura (platelet count remains normal) 5
• Renal involvement with proteinuria and hematuria 5
• Skin biopsy shows leukocytoclastic vasculitis 5
• Renal biopsy reveals IgA deposits in mesangium with granulomatous inflammation 5
• Responds to antituberculous medication alone without requiring additional immunosuppression 5

Diagnostic Algorithm

Step 1: Confirm Active TB

• Obtain three sputum specimens for AFB smear and culture 6
• Review chest radiograph for upper lobe infiltrates with cavitation 7
• Assess for systemic TB symptoms: weight loss, night sweats, fever >2-3 weeks 7

Step 2: Characterize the Purpura

• Check complete blood count with platelet count immediately
• If platelets <50,000/mm³: Consider ITP or TTP 1, 3
• If platelets normal with palpable purpura: Consider HSP 5

Step 3: Differentiate Thrombocytopenic Causes

• Peripheral blood smear: Schistocytes suggest TTP 4
• Bone marrow examination: Increased megakaryocytes confirm ITP 1
• LDH, haptoglobin, indirect bilirubin: Elevated in TTP hemolysis 4
• Renal function and urinalysis: Abnormal in TTP or HSP 4, 5

Step 4: Consider Skin/Renal Biopsy if Needed

• Skin biopsy for leukocytoclastic vasculitis if HSP suspected 5
• Renal biopsy for IgA deposits if proteinuria/hematuria present 5

Treatment Approach

For TB-Associated ITP (Most Likely):

• Initiate standard 4-drug antituberculous therapy immediately (isoniazid, rifampin, pyrazinamide, ethambutol) 8, 1
• Add prednisone 0.5-1 mg/kg/day concurrently 1, 3
• Avoid IVIg or high-dose corticosteroids alone—these fail without antituberculous treatment 2
• Monitor platelet count weekly—expect normalization in 2-6 weeks 1

For TB-Associated TTP:

• Initiate plasma exchange immediately as primary therapy 4
• Administer fresh frozen plasma infusions 4
• Start antituberculous therapy concurrently 4
• Add antiplatelet agents and corticosteroids as adjunctive therapy 4

For TB-Associated HSP:

• Antituberculous therapy alone is sufficient—no additional immunosuppression needed 5
• Monitor renal function closely for progressive glomerulonephritis 5

Critical Pitfalls to Avoid

• Do not delay antituberculous therapy while treating purpura—the purpura will not resolve without treating the underlying TB 1, 2
• Do not assume standard ITP treatment will work—corticosteroids or IVIg alone fail in TB-associated ITP 2
• Do not miss TTP—failure to initiate plasma exchange promptly can be fatal 4
• Do not overlook drug-induced thrombocytopenia from antituberculous medications once treatment starts—rifampin can cause immune-mediated thrombocytopenia 8
• Monitor liver function closely in patients receiving both corticosteroids and antituberculous drugs, as hepatotoxicity risk increases 8