Diabetes mellitus does not increase the risk of knee stiffness after total knee arthroplasty: a meta-analysis of 7 studies including 246 053 cases

Abstract: Purpose: The association of diabetes mellitus with knee stiffness after total knee arthroplasty is still being debated. The aim of this study was to assess through meta-analysis the impact of diabetes mellitus on the prevalence of postoperative knee stiffness after total knee arthroplasty. Methods: We conducted a literature search for terms regarding postoperative knee stiffness and diabetes mellitus on Embase, CINAHL, and PubMed NCBI. Results: Of 1142 articles, seven were suitable for analysis. Meta-analysis showed that diabetes mellitus does not confer an increased risk of primary or revision total knee arthroplasty-induced postoperative knee stiffness when compared to nondiabetic patients (primary total knee arthroplasty, estimated odds ratio [OR] 1.474 and 95% confidence interval [CI] 0.97–2.23; primary and revision total knee arthroplasty, OR 1.340 and 95% CI 0.97–1.83). Conclusion: There is no strong evidence that diabetes mellitus increases the risk of knee stiffness after total knee arthroplasty. The decision to proceed with total knee arthroplasty, discussion as part of the consent process, and subsequent rehabilitation should not differ between patients with and without diabetes mellitus with regards to risk of stiffness. Level of evidence: Level III (meta-analysis

Novel insights on diagnosis, cause and treatment of diabetic neuropathy: Focus on painful diabetic neuropathy

Diabetic neuropathy is common, under or misdiagnosed, and causes substantial morbidity with increased mortality. Defining and developing sensitive diagnostic tests for diabetic neuropathy is not only key to implementing earlier interventions but also to ensure that the most appropriate endpoints are employed in clinical intervention trials. This is critical as many potentially effective therapies may never progress to the clinic, not due to a lack of therapeutic effect, but because the endpoints were not sufficiently sensitive or robust to identify benefit. Apart from improving glycaemic control, there is no licensed treatment for diabetic neuropathy, however, a number of pathogenetic pathways remain under active study. Painful diabetic neuropathy is a cause of considerable morbidity and whilst many pharmacological and nonpharmacological interventions are currently used, only two are approved by the US Food and Drug Administration. We address the important issue of the ‘placebo effect’ and also consider potential new pharmacological therapies as well as nonpharmacological interventions in the treatment of painful diabetic neuropathy

Ophthalmic and clinical factors that predict four-year development and worsening of diabetic retinopathy in type 1 diabetes

To investigate the role of ophthalmic imaging markers - namely retinal thickness measures and corneal nerve morphology - in predicting four-year development and worsening of diabetic retinopathy (DR) in type 1 diabetes (T1DM).126 eyes of 126 participants with T1DM were examined at baseline and after four years. Diabetic retinopathy (DR) was graded using the Early Treatment Diabetic Retinopathy Study scale. HbA1c, nephropathy, neuropathy, cardiovascular factors, and retinal thickness using optical coherence tomography (OCT) and corneal nerve fiber length (CNFL) using corneal confocal microscopy at baseline were assessed by univariate and step-wise multiple logistic regression, and their diagnostic capabilities for single and combined measures.Four-year development of DR was 19% (13 of 68 without DR at baseline). Worsening of DR was seen in 43% (25 of 58 with DR at baseline). When adjusted for potential confounders, a lower CNFL (AUC=0.637, p=0.040, 64% sensitivity and 64% specificity at 14.9mm/mm(2) cut-off), higher triglycerides (AUC=0.669, p=0.012, 64% sensitivity, 62% specificity at 0.85mmol/L) and an elevated vibration threshold (AUC=0.708, p=0.002, 96% sensitivity, 40% specificity at 3.55Hz) were significant predictors for four-year worsening of DR.Reduced CNFL, elevated vibration perception threshold and higher triglycerides can predict future worsening of DR

Alstrom syndrome (OMIM 203800): a case report and literature review

<p>Abstract</p> <p>Background</p> <p>Alstrom syndrome (AS) is a rare autosomal recessive disease characterized by multiorgan dysfunction. The key features are childhood obesity, blindness due to congenital retinal dystrophy, and sensorineural hearing loss. Associated endocrinologic features include hyperinsulinemia, early-onset type 2 diabetes, and hypertriglyceridemia. Thus, AS shares several features with the common metabolic syndrome, namely obesity, hyperinsulinemia, and hypertriglyceridemia. Mutations in the <it>ALMS1 </it>gene have been found to be causative for AS with a total of 79 disease-causing mutations having been described.</p> <p>Case presentation</p> <p>We describe the case of a 27-year old female from an English (Caucasian) kindred. She had been initially referred for hypertriglyceridemia, but demonstrated other features suggestive of AS, including blindness, obesity, type 2 diabetes, renal dysfunction, and hypertension. DNA analysis revealed that she is a compound heterozygote with two novel mutations in the <it>ALMS1 </it>gene – H3882Y and V424I. Examination of her family revealed that her phenotypically unaffected mother and younger sister also had heterozygous mutations in the <it>ALMS1 </it>gene. In addition to presenting these novel molecular findings for AS, we review the clinical and genetic features of AS in the context of our case.</p> <p>Conclusion</p> <p>Two novel mutations in the <it>ALMS1 </it>gene causative for AS have been reported here, thereby increasing the number of reported mutations to 81 and providing a wider basis for mutational screening among affected individuals.</p

Longitudinal changes in corneal cell and nerve fiber morphology 2 in young patients with type 1 diabetes with and without diabetic 3 retinopathy: a 2-year follow-up study

LBL

Increased Intraepidermal Nerve Fiber Degeneration and Impaired Regeneration Relate to Symptoms and Deficits in Parkinson's Disease

Background: Previous studies have shown cutaneous small fiber pathology in patients with Parkinson's disease (PD). These studies have focused on nerve degeneration, but recent reports suggest that nerve regeneration may also be important in PD pathology.Objective: To establish the extent of intraepidermal nerve fiber (IENF) degeneration and regeneration and its relationship to clinical and neurological deficits in Parkinson's disease (PD).Methods: Twenty-three PD patients and 10 age-matched controls underwent skin biopsy and assessment of somatic and autonomic symptoms and deficits. We have assessed Intraepidermal Nerve Fiber Density (IENFD) using standard PGP9.5 staining and GAP-43 to assess Mean Axonal Length (MAL) and Intraepidermal Total Nerve Fiber Length (IETNFL).Results: IENFD (p &lt; 0.0001), MAL (p &lt; 0.0001), IETNFL/Area (p = 0.009), and IETNFL/Length (p = 0.04) were significantly reduced in patients with PD compared to controls. IENFD correlated significantly with disease duration (p = 0.03), cumulative levodopa dose (p = 0.02), Unified Parkinson's Disease Rating Scale, Part III (UPDRS-III) (p = 0.01), Schwab and England Activities of Daily Living (ADL) (p = 0.03), NSP (p = 0.03), and 30:15 ratio (p = 0.03). IETNFL/Area correlated with the Autonomic Scale for Outcomes in Parkinson's Disease (SCOPA-AUT) (p = 0.03) and Diabetic Neuropathy Symptom score (DNS) (p = 0.04) and IETNFL/Length correlated with DNS (p = 0.03). MAL correlated with SCOPA-AUT (p = 0.01), DNS (p = 0.02), and DB-HRV (p = 0.02).Conclusion: Increased IENF degeneration and impaired regeneration correlates with somatic and autonomic symptoms and deficits in patients with PD

Corneal nerve fractal dimension: a novel corneal nerve metric for the diagnosis of diabetic sensorimotor polyneuropathy

Objective: Corneal confocal microscopy (CCM), an in vivo ophthalmic imaging modality, is a noninvasive and objective imaging biomarker for identifying small nerve fiber damage. We have evaluated the diagnostic performance of previously established CCM parameters to a novel automated measure of corneal nerve complexity called the corneal nerve fiber fractal dimension (ACNFrD). Methods: A total of 176 subjects (84 controls and 92 patients with type 1 diabetes) with and without diabetic sensorimotor polyneuropathy (DSPN) underwent CCM. Fractal dimension analysis was performed on CCM images using purpose-built corneal nerve analysis software, and compared with previously established manual and automated corneal nerve fiber measurements. Results: Manual and automated subbasal corneal nerve fiber density (CNFD) (P < 0.0001), length (CNFL) (P < 0.0001), branch density (CNBD) (P < 0.05), and ACNFrD (P < 0.0001) were significantly reduced in patients with DSPN compared to patients without DSPN. The areas under the receiver operating characteristic curves for identifying DSPN were comparable: 0.77 for automated CNFD, 0.74 for automated CNFL, 0.69 for automated CNBD, and 0.74 for automated ACNFrD. Conclusions: ACNFrD shows comparable diagnostic efficiency to identify diabetic patients with and without DSPN