New Concepts in the Management of Charcot Neuroarthropathy in Diabetes.

Charcot Neuroarthropathy (CN) is an uncommon, debilitating and often underdiagnosed complication of chronic diabetes mellitus though, it can also occur in other medical conditions resulting from nerve injury. Till date, the etiology of CN remains unknown, but enhanced osteoclastogenesis is believed to play a central role in the pathogenesis of CN, in the presence of neuropathy. CN compromises the overall health and quality of life. Delayed diagnosis can result in a severe deformity that can act as a gateway to ulceration, infection and in the worst case, can lead to limb loss. In an early stage of CN, immobilization with offloading plays a key role to a successful treatment. Medical therapies seem to have limited role in the treatment of CN.In case of severe deformity, proper footwear or bracing may help prevent further deterioration and development of an ulcer. In individuals with a concomitant ulcer with osteomyelitis, soft tissue infection and severe deformity, where conservative measures fall short, surgical intervention becomes the only choice of treatment. Early diagnosis and proper management at an early stage can help prevent the occurrence of CN and amputation.

Living donor and deceased donor liver transplantation for autoimmune and cholestatic liver diseases--an analysis of the UNOS database.

INTRODUCTION: Autoimmune hepatitis and cholestatic liver diseases have more favorable outcomes after liver transplantation as compared to viral hepatitis and alcoholic liver diseases. However, there are only few reports comparing outcomes of both living donor liver transplants (LDLT) and deceased donor liver transplants (DDLT) for these conditions. AIM: We aim to study the survival outcomes of patients undergoing LT for autoimmune and cholestatic diseases and to identify possible risk factors influencing survival. Survival outcomes for LDLT vs. DDLT are also to be compared for these diseases. PATIENTS AND METHODS: A retrospective analysis of the UNOS database for patients transplanted between February 2002 until October 2006 for AIH, PSC, and PBC was performed. Survival outcomes for LDLT and DDLT patients were analyzed and factors influencing survival were identified. RESULTS: Among all recipients the estimated patient survival at 1, 3, and 5 years for LDLT was 95.5%, 93.6%,and 92.5% and for DDLT was 90.9%, 86.5%, and 84.9%, respectively (p = 0.002). The estimated graft survival at 1, 3, and 5 years for LDLT was 87.9%, 85.4%, and 84.3% and for DDLT 85.9%, 80.3%, and 78.6%, respectively (p = 0.123). On multivariate proportional hazard regression analysis after adjusting for age and MELD score, the effect of donor type was not found to be significant. CONCLUSION: The overall survival outcomes of LDLT were similar to DDLT in our patients with autoimmune and cholestatic liver diseases. It appears from our study that after adjusting for age and MELD score donor type does not significantly affect the outcome.

Effect of liver transplant on pulmonary functions in adult patients with alpha 1 antitrypsin deficiency: 7 cases.

OBJECTIVES: Alpha 1 antitrypsin (A1A) is a 52 kD glycoprotein that is mainly synthesized in the liver. As a major protease inhibitor, it binds to and neutralizes neutrophil elastase, thereby limiting the damage to the normal tissues after an inflammatory response. A deficiency in A1A leads to end-stage liver disease, both in children and in adults. In addition, the deficiency also has a detrimental effect in the lungs of the adult population. Alpha 1 antitrypsin deficiency is corrected with hepatic replacement; however, the changes in pulmonary functions have not been studied before and after liver transplant. The purpose of this study was to observe the changes in the pulmonary functions of patients who underwent liver transplant for the treatment of A1A deficiency. MATERIALS AND METHODS: Nine patients underwent liver transplant for A1A deficiency. Seven patients (5 men, 2 women; mean age, 49.95 -/+ 7.09 years) had their pulmonary function tests available before the liver transplant (mean, 5.6 -/+ 3.4; range, 0.9-10.1 months) and after the liver transplant (mean, 30.3 -/+ 18.4, range 7.8-48.1 months) for analysis. RESULTS: The mean, preliver, transplant, FEV1 was 2.69 -/+ 0.9 L, which was nearly unchanged after the liver transplant to a mean of 2.7 -/+ 1.2 L. During the mean total interval of nearly 3 years, an estimated decline of 250 mL in FEV1 was expected. CONCLUSIONS: It appears from the results of our study that liver transplant probably prevented the progression of pulmonary disease in A1A-deficient patients. Further study and close, postliver, transplant follow-up is warranted to support our initial findings.