No abstract

Albumin is the predominant product of hepatic protein synthesis and one of the more abundant plasma proteins. Among its multiple physiologic roles, it plays an essential part in the generation of colloid-oncotic pressure. In the United States, the indications for which albumin therapy are considered include hypovolemia or shock, burns, hypoalbuminemia, surgery or trauma, cardiopulmonary bypass, acute respiratory distress syndrome, hemodialysis, and sequestration of protein-rich fluids. The use of this relatively expensive therapy accounts for up to 30% of the total pharmacy budget in certain hospitals. The use of albumin therapy in different clinical situations and its influence in morbidity and mortality have been reviewed in multiple randomized controlled trials and meta-analyses. Despite frequent reviews, the use of albumin remains controversial in several clinical situations. At the same time, these valuable reviews seem to have documented the advantages of albumin therapy in the management of ascites and clarified the use of albumin in volume resuscitation. More studies have been recommended to investigate the use of albumin in different doses and its role in hypoalbuminemia. This article will provide an overview of albumin metabolism, use of albumin for volume expansion, the potential therapeutic role of albumin in liver disease, and the role of albumin therapy in nutrition.

Alcoholic liver disease (ALD) remains a leading cause of death from liver disease in the United States. In studies from the Veterans Administration, patients with cirrhosis and superimposed alcoholic hepatitis had greater than 60% mortality over a 4-year period, with most of those deaths occurring in the first month. Thus, the prognosis for this disease is more ominous than for many common types of cancer (eg, breast, prostate, and colon). Moreover, ALD imposes a significant economic burden from lost wages, health care costs, and lost productivity. Unfortunately, there is still no Food and Drug Administration-approved or widely accepted drug therapy for any stage of ALD. Thus, a pressing need exists for a more detailed understanding of mechanisms of liver injury. This article reviews recent advances in mechanisms and therapy related to five major areas of direct relevance to ALD: oxidative stress; gut-liver axis and cytokine signaling; malnutrition; fibrin/clotting; and stellate cell activation/fibrosis. We also review why therapies related to these mechanisms have performed well in experimental animals and in vitro systems, but have not necessarily translated into effective therapy for humans with ALD.

The objective of this study was to analyse the survival rate and cause of death in children with systemic lupus erythematosus (SLE) during the past 30 years in Chile. A retrospective analysis was performed between 1969 and 2000 on patients attending pediatric rheumatology centres in Santiago, Chile. Survival and causes of death in 31 children followed from 1969 to 1980 fulfilling the 1982 American College of Rheumatology criteria for SLE and treated with oral steroids were compared with 50 other patients who were treated with oral steroids and an aggressive treatment of IV bolus of cyclophosphamide (38 patients) and azathioprine (12 patients). Global survival at five and 10 years follow-up for the patients studied from 1969 to 1980 was 68 and 40%, respectively. During the second study period these values were significantly improved and global survival reached 95% at five years and 90% at 10 years follow-up (P < 0.05). Survival at 10 years follow-up for patients with lupus nephropathy increased from 28% (study period 1964-1980) to 86% (study period 1984-2000). Twelve children died (38%) during the 1964-1980 study period. The causes of death were six due to kidney failure, three due to infectious conditions and another three of unknown causes. During the 1980-2000 study period mortality reached 6% (three cases), two cases died of a lupus flare-up and one case due to infection. In the last three decades, we have seen an important increase in the survival of children with SLE, especially in those patients with renal involvement. Management with immunosuppressive drugs, such as IV cyclophosphamide or azathioprine has changed the prognosis in these children. These results demonstrate that our children with SLE increased their life expectancy but are now faced with new types of morbidity because of the sequelae related to the disease itself.

It was uncommon for an EGD to alter antireflux therapy. The management was improved in approximately one-third of the patients by dilating esophageal stricture, finding BE to initiate surveillance, or finding severe esophagitis. EGD should be performed when alarm symptoms are present, especially in males.

Barrett's esophagus is the transformation of normal esophageal squamous epithelium to specialized intestinal metaplasia (SIM). Among the Barrett's specialized cells, those that can develop protective mechanisms against apoptosis may have potential to become malignant. Studies have shown that overexpression of metallothionein (MT), low molecular protein that protects cells from apoptotic stimuli, appears to be associated with more advanced, highly malignant tumors. We thus investigated the relationship between MT expression and apoptosis in different stages of Barrett's carcinogenesis. Terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling and immunohistochemical dual-staining assay were performed in human biopsy samples of normal, SIM, dysplasia, and adenocarcinoma. Apoptotic index and MT expression were quantified by using an image system to analyze the converted digital data. A negative correlation between MT expression and apoptotic index was found. MT expression was significantly increased along with the histologic progression towards adenocarcinoma. This study thus suggests that MT may contribute to cytoprotection, thereby inhibiting apoptosis and leading to carcinogenesis of Barrett's esophageal cells.

No abstract

Antithyroid medications can cause antineutrophil cytoplasmic antibody (ANCA) vasculitis. However, no literature in English describes the coexistence of granulomatosis with polyangiitis (GPA) and untreated Graves' disease. We present a 19-year-old female with thyroid storm and additional complaints of cough, hemoptysis, nasal discharges, polyarthralgia, and skin lesions. Imaging showed peri-hilar cavities and acute-on-chronic sinusitis. Elevated cytoplasmic pattern antineutrophil cytoplasmic antibody (C-ANCA) and anti-proteinase-3 antibody levels plus histopathology of the nasal and skin biopsies suggested GPA. Propranolol, methimazole, and potassium-iodide resolved the thyroid storm. Induction therapy (steroids, rituximab) for GPA provided relief of chronic symptoms stressing the importance of early recognition and swift initiation of treatment Categories: Endocrinology/Diabetes/Metabolism, Allergy/Immunology, Rheumatology