Percutaneous microwave ablation of renal masses in a UK cohort.

OBJECTIVES: To report a tertiary referral centre's experience of microwave ablation (MWA) for suspected renal cell carcinoma (RCC), describing complications and oncological outcomes. PATIENTS AND METHODS: Consecutive MWA procedures (n = 113) for renal masses (October 2016 to September 2019) were maintained on a prospective database. Data describing patient, disease, procedure, complications, and oncological outcomes were analysed. RESULTS: The median (range) age was 68 (33-85) years, 73% were male, and the median Charlson Comorbidity Index was 0. The median (interquartile range [IQR]) tumour diameter was 25 (20-32) mm. In all, 95% had renal mass biopsy, with histologically confirmed cancer in 75%. The median (IQR) R.E.N.A.L. (Radius, Exophytic/Endophytic, Nearness, Anterior/Posterior, Location) nephrometry score was 7 (6-8). The median ablation time was 6 min and length of stay was 1 day for 95% of the patients. Clavien-Dindo complication Grades I, II, IIIb and IV occurred in 18%, 1.8%, 0.9% and 0.9%, respectively. The median follow-up was 12 months and the median (IQR) renal function change was -4 (-18 to 0)%. One patient (0.9%) had local recurrence, treated with re-ablation; two developed metastatic progression; and two (1.8%) had indeterminate findings on follow-up (one lung nodule and one possible local recurrence), managed with ongoing protocolised computed tomography surveillance. Post-procedure complications were associated with total ablation time (odds ratio [OR] 1.152/min, 95% confidence interval [CI] 1.040-1.277) and total ablation energy (OR 1.017/kJ, 95% CI 1.001-1.033). CONCLUSIONS: We describe the largest UK series of MWA treatment for T1a/small T1b renal masses to date. MWA was well tolerated, with 95% discharged the following day and low complication/re-admission rates. Current follow-up demonstrates favourable disease control. MWA appears to be safe and effective and should be considered in future prospective comparisons of treatments for T1a/small T1b renal masses.

Clinical Features and Genetic Risk of Demyelination Following Anti-TNF Treatment.

BACKGROUND: Anti-TNF exposure has been linked to demyelination events. We sought to describe the clinical features of demyelination events following anti-TNF treatment and to test whether affected patients were genetically predisposed to multiple sclerosis [MS]. METHODS: We conducted a case-control study to describe the clinical features of demyelination events following anti-TNF exposure. We compared genetic risk scores [GRS], calculated using carriage of 43 susceptibility loci for MS, in 48 cases with 1219 patients exposed to anti-TNF who did not develop demyelination. RESULTS: Overall, 39 [74%] cases were female. The median age [range] of patients at time of demyelination was 41.5 years [20.7-63.2]. The median duration of anti-TNF treatment was 21.3 months [0.5-99.4] and 19 [36%] patients were receiving concomitant immunomodulators. Most patients had central demyelination affecting the brain, spinal cord, or both. Complete recovery was reported in 12 [23%] patients after a median time of 6.8 months [0.1-28.7]. After 33.0 months of follow-up, partial recovery was observed in 29 [55%] patients, relapsing and remitting episodes in nine [17%], progressive symptoms in three [6%]: two [4%] patients were diagnosed with MS. There was no significant difference between MS GRS scores in cases (mean -3.5 × 10-4, standard deviation [SD] 0.0039) and controls [mean -1.1 × 10-3, SD 0.0042] [p = 0.23]. CONCLUSIONS: Patients who experienced demyelination events following anti-TNF exposure were more likely female, less frequently treated with an immunomodulator, and had a similar genetic risk to anti-TNF exposed controls who did not experience demyelination events. Large prospective studies with pre-treatment neuroimaging are required to identify genetic susceptibility loci.

Management of the chronic leukemias: special considerations in the elderly patient. Part III rarer chronic myeloid leukemias.

The manifestations, diagnosis and management of the rarer chronic myeloid leukemias are reviewed, with special attention to problems that affect elderly patients. The spectrum of disorders includes atypical myeloproliferative syndrome, so-called Ph-negative CGL, chronic myelomonocytic leukemia, and leukemias characterized by chronic proliferation of neutrophil, eosinophil, or basophil leukocytes. These latter are sometimes difficult to differentiate from chronic nonleukemic proliferations of the index cells. Termination in an acute myeloid leukaemia that is usually refractory to treatment may occur in any of the above disorders but is not a constant event.

Pentostatin (2prime prime or minute-Deoxycoformycin): Clinical Pharmacology, Role In Cancer Chemotherapy, and Future Prospects.

Pentostatin (2prime prime or minute-deoxycoformycin, dCF) is a product of the fermentation of Streptomyces antibioticus. It is a tight-binding inhibitor of adenosine deaminase (ADA), an enzyme essential in cellular metabolism of purines. Children with congenital absence of ADA suffer from atrophy of lymphoid tissues and severe combined immune deficiency (SCID) syndrome. It was speculated that pentostatin would be lymphocytotoxic, and this proved to be the case, promoting its investigation in lymphoid neoplasms. It was anticipated that pentostatin would be most active in neoplasms with high intracellular concentrations of ADA---e.g., acute lymphocytic leukemia (ALL), particularly its T cell variety. Although pentostatin proved to be active in ALL, large doses were required and toxic effects outweighted therapeutic benefits. By contrast, pentostatin proved to be exceptionally active in hairy cell leukemia (HCL), a B cell neoplasm with low intracellular concentrations of ADA. Pentostatin has since been shown to possess activity in chronic lymphocytic leukemia, prolymphocytic leukemia, cutaneous T cell lymphomas, adult T cell lymphoma-leukemia, and low-grade non-Hodgkin's lymphomas. It potentiates the activity of vidarabine against viruses and against the cells of acute myeloid leukemia. Pentostatin is inactive in melanoma and renal carcinoma, but has not been adequately evaluated in other solid tumors. The toxic effects of pentostatin include renal failure, central nervous system (CNS) depression, immunosuppression, keratoconjunctivitis, and opportunistic infections. In the absence of pre-existing bone marrow compromise, pentostatin produces only mild myelosuppression. Aside from its use as an antineoplastic agent, pentostatin has potential applications as an immunosuppresive drug, as an antiviral agent, as an antimalarial compound, and in the protection of cells of the CNS from damage induced by ischemia and anoxia.