Choosing a biologic in psoriasis with latent TB and past hepatitis B
A 58-year-old man with plaque psoriasis since age 30 returns after a 3-month trial of narrowband UVB three times weekly (BSA 18%, PASI 16, DLQI 19) and an earlier 6-month methotrexate course stopped for transaminase elevation to twice the upper limit of normal. He has never taken cyclosporine or acitretin. Comorbidities: BMI 34, type 2 diabetes with HbA1c 7.8%, hypertension, and 20 pack-years of smoking (quit 4 years ago). Pre-treatment screening shows a positive interferon-gamma release assay with a normal chest radiograph and no symptoms; HBsAg negative, anti-HBc positive, anti-HBs positive, HBV DNA undetectable, and ALT 28 U/L. He has no history of inflammatory bowel disease, no demyelinating disease, and no recent infections. He asks about the injections that clear the skin and wants the fewest laboratory visits possible because of shift work.
1. Select a biologic class and state exactly what must happen regarding his latent tuberculosis and hepatitis B serologies before, and after, the first dose.
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Both positive screens drive the decision. Latent TB (positive IGRA, normal radiograph, no symptoms) must be treated with a standard regimen - 9 months isoniazid plus pyridoxine, 4 months rifampin, or weekly isoniazid/rifapentine for 3 months. TNF inhibitors carry the highest reactivation risk (odds ratios roughly 4-20), while IL-23 and IL-17 inhibitors carry markedly lower risk. Most guidance allows a non-TNF biologic to start once latent TB therapy is under way, often after 1-2 months, whereas TNF inhibitors typically wait until at least 1 month of therapy.
His hepatitis pattern (anti-HBc positive, anti-HBs positive, HBsAg negative, DNA undetectable) is resolved past infection - the lowest-risk serologic category, but not zero risk. TNF inhibitors carry the strongest reactivation signal. Because anti-HBs is positive and DNA undetectable, antiviral prophylaxis is not mandatory, but HBV DNA and ALT should be checked every 3 months and any rise acted on within days.
Given latent TB, obesity, diabetes, and no IBD, I would start an IL-23 inhibitor (risankizumab or guselkumab): minimal TB reactivation, no renal or hepatic monitoring burden, and maintenance dosing every 8-12 weeks, which matches his shift-work complaint. An IL-17 inhibitor would also be defensible but needs more frequent dosing and Candida surveillance.
2. Ten months later, still on the biologic, his HBV DNA is 12,000 IU/mL and ALT 95 U/L. He feels well. Outline your management, including whether the biologic must stop.
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This meets the definition of hepatitis B reactivation (HBV DNA above 2,000 IU/mL or a 100-fold rise from baseline, with or without ALT elevation). The urgent action is antiviral therapy, not biologic withdrawal. Start entecavir 0.5 mg daily or tenofovir alafenamide 25 mg daily the same day and obtain hepatology input within the week; antiviral suppression is what prevents hepatic decompensation.
Continue the IL-23 inhibitor in the interim. Stopping it abruptly produces a psoriasis flare without changing HBV biology, and continuing it under antiviral cover is standard practice. Check HBeAg, anti-HBe, hepatitis D, and a baseline hepatic ultrasound with AFP. Recheck HBV DNA and ALT at 1, 3, and 6 months, then every 6 months while on therapy, and stop antivirals only on hepatology advice with a defined off-treatment monitoring plan.
This episode points to the true error: anti-HBc positivity at baseline called for scheduled every-3-month DNA monitoring from the start, which he did not have. Also ask whether he received any systemic steroids or other immunosuppressants in the interval. Escalate immediately for encephalopathy, ascites, coagulopathy, or a rising bilirubin.