68 Ga-labelled prostate-specific membrane antigen (PSMA) is rapidly emerging as a significant step forward in the diagnosis of recurrent prostate cancer, based on the fact that PSMA is a type II transmembrane protein with high expression in prostate carcinoma cells [1,2]. Recently it has been demonstrated to accumulate in metastatic clear-cell renal cell carcinoma [3] and interestingly several studies have provided evidence that PSMA is also expressed in the tumour-associated vasculature of primary breast cancers and distant metastases [4,5].We report the case of a 33-year-old woman with metastatic breast carcinoma who underwent 68 Ga-PSMA and 18 F-FDG PET/CT imaging for restaging and evaluation of the most appropriate therapeutic option. Images demonstrated intense and extensive skeletal uptake in the axial and appendicular skeleton with liver metastases.Concordance of 68 Ga-PSMA and 18 F-FDG lesions suggests that 68 Ga-PSMA may provide helpful prognostic information. Furthermore, 68 Ga-PSMA-avid metastatic sites may in future aid in selecting tumours with high PSMA expression for PSMA-directed therapy.

Previous reports document transient improvements after daily zolpidem (CAS 82626-48-0) in patients with brain damage. This multi-patient study evaluates the response to zolpidem in neurologically disabled patients, using 99m TcHMPAO brain SPECT scans and clinical rating scales. Method: 23 of 41 consecutive adult patients, at least 6 months after brain damage were identified as neurologically disabled patients by scoring less than 100/100 on the Barthel Index. Causes of their brain damage included stroke (n = 12), traumatic brain injury (n = 7), anaphylaxis (n = 2), drugs overdose (n = 1) and birth injury (n = 1). The selected 23 patients had a baseline 99m TcHMPAO brain SPECT scan before starting daily zolpidem therapy and a second within two weeks of therapy, performed 1 h after 10 mg oral zolpidem. Scans were designated as improved when at least two of three assessors detected improvement after zolpidem. The rest were designated non improved. After four months daily zolpidem therapy, patients were rated on the Tinetti Falls Efficacy Scale (TFES) before and after zolpidem. The TFES ratings were compared using a Wilcoxon non parametric signed rank test. Scan improvers were compared with non improvers, using a two sample t test with unequal variance. Results: Mean overall improvement after zolpidem on TFES was 11.3%, from 73.4/100 to 62.1/100 (p = 0.0001). 10/23 (43%) patients improved on SPECT scan after zolpidem. Their mean TFES improvement was 19.4% (?16.75) compared with 5.08% (?5.17) in 13/23 non improvers (p = 0.0081). Conclusion: This prospective study adds further evidence to previous reports of zolpidem efficacy in patients with established brain damage.

There was no significant difference in F-FDG metabolic parameters, IPS, and other risk indicators between HIV-infected and HIV-uninfected patients with Hodgkin lymphoma.

HIV infection is not associated with a higher tumor burden in patients with Hodgkin lymphoma. HIV infection is, however, a strong predictor of poor therapy outcome in patients treated with standard regimen of ABVD.