Broad-Ranging Nutritional Deficiencies Predict Amputation in Diabetic Foot Ulcers.

Diabetic foot ulcers present across the spectrum of nonhealing wounds, be it acute or many months duration. There is developing literature highlighting that despite this group having high caloric intake, they often lack the micronutrients essential for wound healing. This study reports a retrospective cohort of patients' micro- and macro-nutritional state and its relationship to amputation. A retrospective cohort was observed over a 2-month period at one of Australia's largest tertiary referral centers for diabetic foot infection and vascular surgery. Patient information, duration of ulcer, various biochemical markers of nutrition and infection, and whether the patient required amputation were collected from scanned medical records. A cohort of 48 patients with a broad-spectrum of biochemical markers was established. Average hemoglobin A1c (HbA1c) was 8.6%. A total of 58.7% had vitamin C deficiency, including 30.4% with severe deficiency, average 22.6 L} 5.8 µmol/L; 61.5% had hypoalbuminemia, average albumin 28.7 L} 2.5 g/L. Average vitamin B12 was 294.6 L} 69.6 pmol/L; 57.9% had low vitamin D, average 46.3 L} 8.3 nmol/L. Basic screening scores for caloric intake failed to suggest this biochemical depletion. There was a 52.1% amputation rate; biochemical depletion was associated with risk of amputation with vitamin C (P < .01), albumin (P = .03), and hemoglobin (P = .01), markedly lower in patients managed with amputation than those managed conservatively. There was no relation between duration of ulceration and nutrient depletion. Patients with diabetic foot ulceration rely on multidisciplinary care to optimize their wound healing. An important but often overlooked aspect of this is nutritional state, with micronutrients being very important for the healing of complex wounds. General nutritional screening often fails to identify patients at risk of micronutrient deficiency. There is a high prevalence of vitamin deficiency in patients with diabetic foot ulcers. This presents an excellent avenue for future research to assess if aggressive nutrient replacement can improve outcomes in this cohort of patients.

African Australians living with HIV: a case series from Victoria.

BACKGROUND: This research aimed to describe the characteristics of African-born Victorians living with HIV, identify associations with delayed HIV diagnosis and describe their response to combination antiretroviral therapy (cART). METHODS: A case series of African-born adults living with HIV in Victoria was conducted. Data was collected in interviews and reviews of case notes. Associations with delayed HIV diagnosis (CD4 below 200 cells microL(-1) at diagnosis and/or AIDS within 3 months of HIV diagnosis) were explored using univariate regression. AIDS-defining illnesses and response to cART were described. RESULTS: Fourteen males and six females were included. Ten were born in the Horn of Africa (nine in Ethiopia). Sixteen had sexual exposure (12 heterosexual; four male-to-male sex). Seven reported acquiring HIV in Australia. Median CD4 count at diagnosis was 145 cells microL(-1). Ten had delayed HIV diagnosis, of whom eight were born in the Horn of Africa. Delayed HIV diagnosis was associated with birth in the Horn of Africa (odds ratio: 11.56). Nine had a diagnosis of AIDS, including three cases of tuberculosis, three of Pneumocystis jiroveci pneumonia and two of cerebral toxoplasmosis. Eighteen had received cART, of which 16 achieved virological suppression and 15 achieved a CD4 count above 200 cells microL(-1). Clinical failure and virological failure occurred in seven and five cases, respectively. CONCLUSIONS: HIV prevention strategies for Victoria's African communities should address HIV exposure in Australia. Ethiopian-born Victorians with HIV appear to be at particular risk of delayed diagnosis. Response to cART in this series was comparable to that observed in other industrialised countries.