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Few studies regarding palliative sedation (PS) have been carried out in home care (HC) setting. A comparison of PS rate and practices between hospice (HS) and HC is also lacking.Comparing HC and HS settings for PS rate, patient clinical characteristics before and during PS, decision-making process, and clinical aspects of PS.About 38 HC/HS services in Italy participated in a multicenter observational longitudinal study. Consecutive adult cancer patients followed till death during a four-month period and undergoing PS were eligible. Symptom control and level of consciousness were registered every eight hours to death.About 4276 patients were screened, 2894 followed till death, and 531 (18%) underwent PS. PS rate was 15% in HC and 21% in HS (P 0.001). Principal refractory symptoms were delirium (54%) and dyspnea (45%), respectively, more common in HC (P 0.001) and HS (P = 0.03). Informed consent was not obtained in 72% of patients but achieved by 96% of families. Midazolam was the most used drug (94% HS vs. 75% HC; P 0.001) mainly by continuous infusion (74% HC vs. 89% HS; P 0.001). PS duration was less than 48 hours in 67% of patients. Hydration during PS was less frequent in HC (27% vs. 49%; P 0.001). In the eight hours before death, consciousness level was unrousable to mild physical stimulation in 81% and symptom control complete in 89% of cases.Our results show feasibility of PS in HC and HS and suggest setting differences in rates, indications, and practice of PS, possibly related to patients' selection or care organization.

Objective: To investigate the possible role and tolerability of high-dose (>160 mg/day) oxycodone controlled release (CR) for the treatment of cancer and non-cancer pain. Design: 227 patients with cancer or non-cancer pain were enrolled in an open-label, multi-center, Italian study in order to assess the adequacy of their existing pain management (using a numerical rating scale [NRS]) and the possible benefit high-dose oxycodone CR may offer patients experiencing uncontrolled pain. Results: Pain was poorly controlled at baseline, with only 18.1% of patients reporting adequate pain relief (NRS

Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) sensitise nerves to mechanical stimuli experimentally and may induce bone and muscle pain when used as supportive drugs. G-CSF and GM-CSF produced endogenously by tumour cells can cause paraneoplastic leucocytosis. Whether paraneoplastic leucocytosis is associated with changes in pain sensitivity is not yet clear. We report on a patient with advanced-stage thyroid cancer who developed extreme leucocytosis within a period of 4 weeks (103 000 white blood cells/mm(3)), composed mostly of neutrophils and eosinophils. Parallel to this leukemoid reaction, allodynia and hyperalgesia developed in the absence of tissue inflammation. The course of disease of an elderly male with advanced stage metastatic thyroid cancer with new onset neuropathic pain followed by the development of extreme leucocytosis in a leukemoid reaction suggests paraneoplastic release of myeloid CSFs. The coincidence of pain sensitisation and extreme leucocytosis suggests a causal contribution of G-CSF and GM-CSF.

Serum lipid, lipoprotein and apoprotein parameters were evaluated in 15 patients (7 males and 8 females) with Friedreich’s ataxia. Serum lipid levels in patients showed no significant differences compared to controls. Small reduction in serum phospholipid and in total HDL and HDL3 cholesterol levels were observed, and the female patients presented a slight reduced total cholesterol level; among the serum apoproteins, apo B was reduced only in the males. The most interesting findings concerned the lipoproteins, since both lipid and protein masses of the VLDL, LDL and HDL2 fractions were reduced. In reference to lipoprotein composition, however, HDL2 was the most modified fraction, showing an important protein reduction. From this point of view, this lipoprotein seems the most responsible for the changes observed in our patients. The meaning of this modified lipoprotein pattern in the pathophysiology of Friedreich’s ataxia is not clear.