The prevalence of peripheral neuropathy severe enough to cause a loss of protective sensation in a population-based sample of people with known and newly detected diabetes in Barbados: a cross-sectional study.

AIMS: To determine the prevalence and potential risk factors for diabetic peripheral neuropathy with a loss of protective sensation in Barbados. METHODS: A representative population sample aged > 25 years with previously diagnosed diabetes or a fasting blood glucose ≥ 7 mmol/l or HbA1c ≥ 48 mmol/mol (6.5%) was tested by 10 g monofilament at four plantar sites per foot and a 28 Hz tuning fork and neurothesiometer at the hallux. Data were adjusted to the age structure of people with diabetes in Barbados. Multivariable logistic regression assessed associations with peripheral neuropathy with a loss of protective sensation. RESULTS: Of 236 participants [74% response rate, 33% men, 91% black, median age 58.6 years, mean BMI 30.1 kg/m2 , mean HbA1c 54 mmol/mol (7.1%)], 51% had previously diagnosed diabetes. Foot examination demonstrated that 25.8% (95% CI 20.2 to 31.5) had at least one insensate site with monofilament testing, 14.8% (95% CI 10.2 to 19.4) had an abnormal tuning fork test and 10.9% (95% CI 6.9 to 14.9) had a vibration perception threshold > 25 V. Peripheral neuropathy with a loss of protective sensation prevalence was 28.5% (95% CI 22.7 to 34.4) as indicated by monofilament with ≥ 1 insensate site and/or vibration perception threshold > 25 V. With previously diagnosed diabetes the prevalence was 36.4% (95% CI 27.7 to 45.2) with 98.4% of cases identified by monofilament testing. Increasing age, previously diagnosed diabetes, male sex and abdominal obesity were independently associated with peripheral neuropathy with a loss of protective sensation. CONCLUSIONS: Over a third of people with previously diagnosed diabetes had evidence of peripheral neuropathy with a loss of protective sensation. Monofilament testing alone may be adequate to rule out peripheral neuropathy with a loss of protective sensation. Monofilament and neurothesiometer stimuli are reproducible but dependent on participant response.

Management of chronic venous disease by primary care.

OBJECTIVE: To assess the patterns of referral for chronic venous disease (CVD). METHOD: General practitioners (GPs) were invited by an email to complete a validated online survey evaluating the referral and community management of CVD. RESULTS: A total of 138 participants were recruited. Most GPs (85%) saw fewer than 50 patients with CVD a year. Thirty-one percent were aware of National Institute for Clinical Excellence referral guidelines for CVD and 36% were aware of and agreed with local referral guidelines. Eleven percent were aware of clinical venous scoring systems. Sixty-three percent believed mild CVD would progress and 84% believed treatment would improve the quality of life. Sixteen referred C3 disease, 43% C4, 37% C5 and 65% C6 disease. Forty-one percent would refer on request. Pain symptoms increased referral in C2 disease. Endothermal ablation was believed available to 33% and traditional stripping to 62% and 27% were unaware of the treatment options. Forty-five percent were happy to provide postoperative care. CONCLUSIONS: Despite national guidelines, the management of CVD in the UK is variable.

Medicare reimbursement for home infusion therapy: a contributor to the development of community acquired vancomycin-resistant enterococci?

Vancomycin is a bacteriocidal antibiotic widely used to treat gram-positive infections, including methicillin-resistant Staphylococcus aureus. During the past 5 years, there have been increasingly frequent reports of infections caused by enterococci species resistant to vancomycin. Until recently, this was a phenomenon limited almost exclusively to the hospital. Presently, there are reports of vancomycin-resistant enterococci developing in the outpatient and home care population. The intent of this article is to present one possible explanation for this trend in the hope that further research will be stimulated.

A model of the G1 phase of the cell cycle incorporating cyclin E/cdk2 complex and retinoblastoma protein.

A mathematical model of cyclin E, cdk2 and retinoblastoma protein control of the G1 phase of the human cell cycle is proposed. The model includes retinoblastoma (Rb) protein phosphorylation by a cyclin E/cdk2 complex and its subsequent dephosphorylation at the end of the cell cycle. The numerical solutions to this model demonstrates the cyclic behavior of the cyclin E/cdk2 complex, with and without Rb function, cell cycle. This model suggests an inhibition of cyclin E/cdk2 complex formation (or its activation) by hypophosphorylated retinoblastoma protein. The experimental results of cell cycle arrest upon injection of transforming growth factor-beta, alpha-interferon or D-erythro-sphingosine during G1 phase are reproduced. Cell cycle behavior predicted by this model for increasing the concentration of hypophosphorylated retinoblastoma protein during the G1 phase is discussed. Additional results are obtained by numerical simulation.