Complete remission of chemo-refractory multiple-metastatic upper tract urothelial carcinoma by autologous formalin-fixed tumor vaccine.

A patient with chemo-refractory multiple-metastatic upper tract urothelial carcinoma (UTUC) treated by monotherapy with autologous formalin-fixed tumor vaccine (AFTV) resulted in complete remission of the lung and para-aortic lymph node metastases (ongoing >3 years after AFTV). The tumor was immunohistologically negative for PD-L1. AFTV will be an attractive treatment option.

A transient increase and subsequent sharp decrease of chemo-refractory liver-metastasized uterine cervical small cell carcinoma to autologous formalin-fixed tumor vaccine plus anti-PD-1 antibody.

Uterine cervical small cell carcinoma is rare and aggressive with no standardized therapy. A patient bearing the advanced chemo-refractory carcinoma, treated with a tumor vaccine combined with 1 mg/kg of pembrolizumab, showed a transient increase and subsequent sharp decrease of the liver-metastasized lesion to less than half its maximum diameter.

Helicobacter pylori eradication shifts monocyte Fcgamma receptor balance toward inhibitory FcgammaRIIB in immune thrombocytopenic purpura patients.

Immune thrombocytopenia purpura (ITP) is a bleeding disorder in which platelet-specific autoantibodies cause a loss of platelets. In a subset of patients with ITP and infected with Helicobacter pylori, the number of platelets recovers after eradication of H. pylori. To examine the role of H. pylori infection in the pathogenesis of ITP, the response of 34 ITP patients to treatment with a standard H. pylori eradication regimen, irrespective of whether they were infected with H. pylori, was evaluated. Eradication of H. pylori was achieved in all H. pylori-positive patients, and a significant increase in platelets was observed in 61% of these patients. By contrast, none of the H. pylori-negative patients showed increased platelets. At baseline, monocytes from the H. pylori-positive patients exhibited an enhanced phagocytic capacity and low levels of the inhibitory Fcgamma receptor IIB (FcgammaRIIB). One week after starting the H. pylori eradication regimen, this activated monocyte phenotype was suppressed and improvements in autoimmune and platelet kinetic parameters followed. Modulation of monocyte FcgammaR balance was also found in association with H. pylori infection in individuals who did not have ITP and in mice. Our findings strongly suggest that the recovery in platelet numbers observed in ITP patients after H. pylori eradication is mediated through a change in FcgammaR balance toward the inhibitory FcgammaRIIB.

Effects of a Helicobacter pylori eradication regimen on anti-platelet autoantibody response in infected and uninfected patients with idiopathic thrombocytopenic purpura.

Thirty-seven patients with idiopathic thrombocytopenic purpura (ITP) were treated with a standard Helicobacter pylori eradication regimen irrespective of H. pylori infection. Our results indicate that platelet recovery results from the disappearance of H. pylori itself, and is mediated, in part, through suppression of anti-platelet autoantibody production.

Initial laboratory findings useful for predicting the diagnosis of idiopathic thrombocytopenic purpura.

PURPOSE: To identify initial laboratory findings useful for the later diagnosis of idiopathic thrombocytopenic purpura (ITP) in adult patients with thrombocytopenia. SUBJECTS AND METHODS: We studied 62 consecutive adult patients who had thrombocytopenia and whose peripheral blood film was normal except for thrombocytopenia at presentation. Each patient underwent physical examination and routine laboratory tests and was prospectively followed for 22.5 +/- 9.8 months (range, 8 to 41 months). The frequency of antiglycoprotein (GP) IIb/IIIa antibody-producing B cells, the presence of platelet-associated and plasma anti-GPIIb/IIIa antibodies, the percentage of reticulated platelets, and the plasma thrombopoietin level were examined at the first visit. The final diagnosis was based on the clinical history, physical examination, complete blood test, bone marrow findings, and the clinical course at last observation. RESULTS: Forty-six patients were diagnosed as having ITP and 16 as having another disorder, including myelodysplastic syndrome, aplastic anemia, amegakaryocytic thrombocytopenia, and reduced platelet production, with or without other cytopenias, and without dysplasia or evidence for destruction. Six initial laboratory findings discriminated ITP from other diagnoses: the absence of anemia, absence of leukocytopenia, increased frequency of anti-GPIIb/IIIa antibody-producing B cells, increased platelet-associated anti-GPIIb/IIIa antibodies, elevated percentage of reticulated platelets, and a normal or slightly increased plasma thrombopoietin level. Three or more of these ITP-associated findings were found at presentation in 44 patients (96%) with thrombocytopenia later diagnosed as ITP, compared with only 1 patient (6%) whose disorder was non-ITP. CONCLUSION: Initial laboratory findings can well predict future diagnosis of ITP. Further studies prospectively evaluating these same diagnostic criteria on another, independent set of patients are necessary.