BackgroundSpecialist Lifestyle Management (SLiM) is a structured patient education and self-management group weight management programme. Each session is run monthly over a 6-month period providing a less intensive long-term approach. The groups are patient-centred incorporating educational, motivational, behavioural and cognitive elements. The theoretical background, programme structure and preliminary results of SLiM are presented.Subjects/methodsThe study was a pragmatic service evaluation of obese patients with a body mass index (BMI) ≥35 kg/m2 with comorbidity or ≥40 kg/m2 without comorbidity referred to a specialist weight management service in the West Midlands, UK. 828 patients were enrolled within SLiM over a 48-month period. Trained facilitators delivered the programme. Preliminary anonymised data were analysed using the intention-to-treat principle. The primary outcome measure was weight loss at 3 and 6 months with comparisons between completers and non-completers performed. The last observation carried forward was used for missing data.ResultsOf the 828 enrolled within SLiM, 464 completed the programme (56%). The mean baseline weight was 135 kg (BMI=49.1 kg/m2) with 87.2% of patients having a BMI≥40 kg/m2 and 12.4% with BMI≥60 kg/m2. The mean weight change of all patients enrolled was −4.1 kg (95% CI −3.6 to −4.6 kg, p=0.0001) at the end of SLiM, with completers (n=464) achieving −5.5 kg (95% CI −4.2 to −6.2 kg, p=0.0001) and non-completers achieving −2.3 kg (p=0.0001). The majority (78.6%) who attended the 6-month programme achieved weight loss with 32.3% achieving a ≥5% weight loss.ConclusionsThe SLiM programme is an effective group intervention for the management of severe and complex obesity.
OBJECTIVEImpairment of skin quality may contribute to diabetic foot ulceration (DFU). Our goal was to determine whether high-risk patients exhibited specific skin structural and metabolic deficits that could predispose to foot complications.RESEARCH DESIGN AND METHODSA total of 46 patients comprising 9 diabetic control subjects, 16 with diabetic peripheral neuropathy (DPN) alone, and 21 with recurrent DFUs (including 9 with Charcot neuroarthropathy [CNA]) were recruited and compared with 14 nondiabetic control (NDC) subjects. DPN was assessed using the Michigan Neuropathy Screening Instrument (MNSI). Skin punch biopsies (3 mm) were performed on upper and lower leg skin for measurements of intraepidermal nerve fiber density (IENFD), structural analysis, type 1 procollagen abundance, tissue degrading matrix metalloproteinases (MMPs), and poly(ADP-ribose) (PAR) immunoreactivity.RESULTSMNSI scores were comparable across DPN groups. IENFD was decreased by diabetes and DPN but did not differ between neuropathic groups. Skin structural deficit scores were elevated in all neuropathic subjects, particularly in the DFU group. Type 1 procollagen abundance was reduced in DFU subjects 387 ± 256 units (mean ± 1 SD) compared with NDC subjects (715 ± 100, P < 0.001). MMP-1 and MMP-2 were activated by diabetes. PAR immunoreactivity was increased in DFU (particularly in the CNA group; P < 0.01) compared with other DPN subjects.CONCLUSIONSIncreased PAR, reduced type 1 procollagen abundance, and impaired skin structure are associated with foot complications in diabetes. The potential of therapies that improve skin quality to reduce DFU needs to be investigated.
Background In diabetes foot ulceration may result from increased skin fragility. Retinoids can reverse some diabetes-induced deficits of skin structure and function but their clinical utility is limited by skin irritation. The effect of diabetes and MDI 301 a non-irritating synthetic retinoid and retinoic acid have been evaluated on matrix metalloproteinases (MMPs), procollagen expression and skin structure in skin biopsies from non-diabetic volunteers and diabetic subjects at risk of foot ulceration using organ culture techniques. Methods Zymography and ELISA were utilized for analysis of MMP-1,-2,-9 and tissue inhibitor of metalloproteinase-1 (TIMP-1) and immunohistochemisty for type I procollagen protein abundance. Collagen structure parameters were assessed in formalin-fixed, paraffin-embedded tissue sections. Results The % of active MMP-1 and -9 was higher and TIMP-1 abundance lower in subjects with diabetes. Type 1 procollagen abundance was reduced and skin structural deficits were increased in diabetes. Three μm MDI 301 reduced active MMP-1 and -9 abundance by 29% (p<0.05) and 40% (p<0.05), respectively and increased TIMP-1 by 45% (p=0.07). MDI 301 increased type 1 procollagen abundance by 40% (p<0.01) and completely corrected structural deficit scores. Two μm retinoic acid reduced MMP-1 but did not significantly affect skin structure. Conclusions These data indicate that diabetic patients at risk of foot ulceration have deficits of skin structure and function. MDI 301 offers potential for repairing this skin damage complicating diabetes.
Objective. To present an unusual but known cause of hypomagnesaemia induced-hypocalcaemia in a chronic GORD patient with severe symptoms with a review of the current literature. Methods. Analysis of the clinical and laboratory findings of the patient and discussion of the multi-factorial nature of his disease and the underlying mechanisms. Results. Our patient described features of magnesium deficiency such as weakness, muscle twitches, and fits with clinical signs of hypocalcaemia: a carpal pedal spasm and paraesthesia. Preadmission blood results revealed low calcium and magnesium levels. He was admitted to ITU, when he presented with seizures and developed encephalopathy. The total vitamin D level was 52.4 nmol/L (>49.9). His U&Es and LFTs were within the normal range with the exception of potassium. He was on Omeprazole for his GORD. With omission of the PPI 1 day after admission and replacement therapy, his ion levels normalised. Conclusion. Hypomagnesaemia is often undiagnosed and is associated with multiple biochemical abnormalities. Treatment focus should be aimed at stopping the PPI and replacing the magnesium. Over use of PPIs is a problem in practice, with the FDA issuing a warning over long-term use. Continued monitoring and decision making on dose reduction/withdrawal is essential to avoid complications.
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