Trends in the presentation and surgical management of the acute diabetic foot.

BACKGROUND: This study examines trends in the presentation and surgical management of acute diabetic foot problems in a single institution. METHOD: Prospective audit of all diabetic patients who had a primary procedure for critical lower limb ischaemia (CLI) and/or foot sepsis between 1st January 1990 and 31st December 2002. Primary and secondary intervention, mortality and limb salvage rate within 6 weeks of the index procedure were recorded. RESULTS: There were 661 patients (417 men and 244 women of median age 69, range 31-99, years) with 799 affected limbs. CLI alone was present in 625 (78%) limbs, combined CLI and foot sepsis in 53 (7%) and foot sepsis alone in 121 (15%). The primary intervention was minor amputation in 323 (40%) limbs, revascularisation in 288 (36%), major amputation in 185 (23%) and sympathectomy in three limbs. Within 6 weeks, 125 (16%) limbs required secondary intervention, the peri-procedural mortality rate was 38 of 924 (4%), and the limb salvage rates for patients with CLI, combined CLI and sepsis and sepsis alone were 66, 66 and 80%, respectively. There was a significant decline in the proportion of patients presenting with CLI alone and a significant increase in the proportion presenting with combined CLI and sepsis and sepsis alone. In patients with CLI alone, there was a significant increase in the primary major amputation rate and a significant decline in the minor amputation rate with no significant change in the revascularisation rate. CONCLUSION: There has been a progressive decline in the proportion of patients presenting with CLI alone and a greater proportion of patients presenting with an element of foot sepsis. In patients with CLI alone, the primary major amputation rate has increased at the expense of a decline in minor amputation rate.     

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Experimental animal models of pancreatic carcinogenesis and metastasis

Pancreatic cancer is a lethal disease characterized by early metastasis, local invasion, and resistance to conventional therapies. To understand its etiology and eventually make prevention of it possible and effective, appropriate carcinogenesis models will certainly help us understand the effects of environmental and genetic elements on pancreatic carcinogenesis. The development of new treatment strategies to control cancer metastasis is of immediate urgency. Fulfillment of this task relies on our knowledge of the cellular and molecular biology of pancreatic cancer metastasis and the availability of biologically and clinically relevant model systems. Many of the existing pancreatic cancer carcinogenesis and metastasis animal models are described in this review. The advantages and disadvantages of each model and their clinical implications are discussed, and special attention is focused on experimental therapeutic strategies targeting pancreatic cancer metastasis.     

Interdisciplinary approach to abdominal Burkitt’s lymphoma

Burkitt’s lymphoma is a high-grade, rapidly growing B-cell neoplasm. It is recognized by its aggressive course, brief median survival, and low rates of long-term survival. The authors discuss the case of a patient who acutely presented with intraabdominal complications from a new onset of Burkitt’s lymphoma. The clinical and pathological features, staging, treatment options, and survival data are reviewed. In addition, the role of surgical intervention is carefully analyzed.     

Polymorphisms in glutathione-S-transferase genes (GST-M1, GST-T1 and GST-P1) and susceptibility to prostate cancer among male smokers of the ATBC cancer prevention study.

Glutathione-S-transferase (GST) genes encode a family of detoxification enzymes that offer protection against endogenous and exogenous sources of reactive oxygen species (ROS). Germline variations in GST genes may alter the catalytic efficiency of GST isoenzymes leading to a potential increase in susceptibility to the genotoxic effects of ROS and electrophilic substances. A nested case-control study design was used to examine the association between the polymorphic GST genes and prostate cancer risk among Finnish male smokers of the ATBC Cancer Prevention Study. A case-case analysis was used to determine the association between these genetic polymorphisms and prostate cancer progression. Germline DNA was obtained from 206 prostate cancer cases and 194 controls frequency matched on age, intervention group and study clinic. Cases and controls were genotyped for three GST genes using MALDI-TOF mass spectrometry or multiplex polymerase chain reaction (PCR). Relative to the wild-type genotype, we observed a 36% reduction in prostate cancer risk associated with the GST-M1-null genotype (odds ratio (OR) 0.64, 95% confidence interval (CI) 0.43, 0.95). Unlike GST-M1, GST-T1-null (OR 0.74, 95% CI 0.42, 1.33) and GST-P1*B (OR 1.10, 95% CI 0.72, 1.69) were not strongly associated with prostate cancer risk. We did not observe any significant associations between the selected polymorphic GST genes and tumour grade or stage. In conclusion, we did not observe a direct association between polymorphic GST-T1 or GST-P1 and prostate cancer risk. Our observation of a relatively strong inverse association between the GST-M1-null genotype and prostate cancer risk needs to be confirmed in larger association studies.