Abstract
BACKGROUND: To systematically describe the clinical characteristics of tuberculosis (TB) complicated by hemophagocytic lymphohistiocytosis (HLH), with the aim of informing early diagnosis, precise classification, and therapeutic decision-making. METHODS: A total of 19 hospitalized patients diagnosed with TB-HLH between January 2020 and December 2025 were consecutively enrolled. Based on the presence of disseminated TB, patients were divided into a disseminated group (n = 10) and a non-disseminated group (n = 9). Demographic data, clinical symptoms, laboratory parameters, imaging findings, treatment regimens, and clinical outcomes were systematically collected and compared between the two groups. RESULTS: No statistically significant differences were observed in baseline characteristics such as age and gender between the two groups (P > 0.05). Common clinical symptoms included fever, fatigue, weight loss, and hepatosplenomegaly. Central nervous system symptoms (e.g., headache, impaired consciousness) were observed only in the disseminated group (4 cases vs. 0 case, P = 0.033). The disseminated group had significantly lower serum C-reactive protein (CRP) levels compared to the non-disseminated group (73.20 ± 42.38 mg/L vs. 125.41 ± 61.45 mg/L, P = 0.044). Eighteen patients received anti-tuberculosis therapy, one patient with AIDS discontinued treatment due to critical illness. Glucocorticoids were administered to 16 patients as adjunct therapy for HLH. Among the three patients who did not receive steroids, one had a short disease course and mild bone marrow suppression, one presented with concurrent acute hepatic and renal failure, and one exhibited hematologic and symptomatic improvement following after anti-TB treatment. The overall mortality rate was 21.1% (4/19). CONCLUSION: This study suggests that central nervous system symptoms serve as a critical indicator for disseminated TB complicated by HLH. The inflammatory profile in TB-HLH exhibits unique features, such as relatively lower CRP in disseminated cases. Clinical management requires a combination of effective anti-TB therapy and a stratified immunomodulatory strategy based on the severity of the hyperinflammatory state.