PurposeMore than 1 million new occurrences of cancer are diagnosed in India annually. Among patients with cancer, pain is a common and persistent symptom of the disease and its treatment. However, few studies to date have evaluated the prevalence of pain and the adequacy of pain management in Indian hospitals. This cross-sectional study aimed to assess the prevalence and sociodemographic patterns of cancer pain and pain management among a sample of inpatients and newly registered outpatients at four large regional cancer centers in India.MethodsA sample of 1,600 patients with cancer who were current inpatients or newly registered outpatients were recruited and administered a questionnaire that was based on the Brief Pain Inventory. The survey tool included questions on demographics, medical history, and extent of clinical pain experienced. In addition, a pain management index score was created to link the severity of cancer pain with medication prescribed to treat it.ResultsA total of 88% of patients reported pain in the past 7 days, and approximately 60% reported that their worst pain was severe. Several demographic and medical characteristics of the study population predicted severe pain, including the following: lower educational level, outpatient status, and debt incurred as a result of illness. A total of 67% of patients were inadequately treated with analgesics. Inadequate pain management was associated with both treatment hospital and patient type, and patients who reported debt as a result of their illness were more likely to have inadequate pain management.ConclusionA majority of Indian patients with cancer experience significant pain and receive inadequate pain management. Improvement of pain management for Indian patients with cancer is needed urgently.

The induction of heat shock proteins (HSP) protects isolated islet cells against the cytotoxicity of inflammatory mediators in vitro. Very little information is available about the effect of HSP overexpression on function of preconditioned islet grafts. The present study investigated the function of heat-exposed pig islets after transplantation into immunocompetent mice in comparison with in vitro resistance against inflammatory mediators. Pig islets were preconditioned at 43°C or sham treated prior to subcapsular transplantation into diabetic C57/Bl6j mice. Nondiabetic mice simultaneously receiving preconditioned and control islets were subjected to bilateral nephrectomy for determination of pig insulin. Resistance against H 2 O 2 , NO, human Il-1β, IFN-γ, or TNF-α was assessed by trypan blue exclusion and insulin determination. Heat-induced protein expression was confirmed by Western blot analysis. Graft preconditioning increased resistance against H 2 O 2 , NO, or cytokines ( p < 0.05) but decreased survival in nondiabetic mice ( p < 0.05) and function in diabetic mice ( p < 0.01). Upregulation of caspase-3 activity as well as Bax, Fas, FasL, and DFF expression ( p < 0.05) indicated simultaneous induction of apoptosis. The coexpression of HSP and proapoptotic proteins reveals the dual character of the stress response simultaneously starting mechanisms for protection and apoptosis. In vitro assays seem to reflect only insufficiently the situation of islets after transplantation.

During the isolation procedure and after transplantation islets are subjected to numerous variables associated with the induction of apoptosis. The present study investigated the effect of transient pretreatment with caspase inhibitors on function and survival of transplanted pig islets. Isolated porcine islets (3000 IEQ) were incubated overnight in 200 µM of the caspase-3 inhibitor DEVD-CMK prior to transplantation into diabetic nude mice. Glucose-stimulated insulin release of pretreated islets was assessed during static incubation. DEVD-CMK successfully prevented the expression of capase-3 and DFF as demonstrated in heat-shocked pig islets. Nevertheless, transient pretreatment of freshly isolated pig islets with DEVD-CMK resulted in a significantly decreased final graft function of 50.0% (n = 16) compared to 85.7% (n = 14) in control islets (p < 0.05). Glucose-stimulated insulin release of porcine islets (n = 6) was not significantly effected by overnight culture with DEVD-CMK. Morphological assessment revealed that this caspase-3 inhibitor significantly increased the percentage of necrosis to a small, but nevertheless significant, extent in comparison to control islets (p < 0.05). The study demonstrates that short-time pretreatment with the caspase-3 inhibitor DEVD-CMK reduces the capacity of transplanted porcine islets to restore normoglycemia in diabetic nude mice.