Liver lipocalin 2 expression in severely obese women with non alcoholic fatty liver disease.

BACKGROUND: Lipocalin 2 (LCN2) has been related to obesity, insulin resistance and metabolic disturbance. However, its relation with non alcoholic fatty liver disease (NAFLD) has hardly been studied. METHODS: We examined LCN2 circulating levels and its protein and gene expression in liver from women with severe obesity and NAFLD. We analyzed the liver histology of 59 white severely obese women (BMI ≥40 Kg/m²): 15 subjects presented normal liver histology or non-significant liver disease (NL), 18 simple steatosis (SS) and 26 non alcoholic steatohepatitis (NASH). We determined the anthropometric and metabolic features of the women. LCN2 levels were determined by an ELISA and liver mRNA expression by real time RT-PCR. We also studied LCN2 expression in HepG2 liver cells under various inflammatory stimuli. RESULTS: Liver LCN2 protein and gene expression were higher in NAFLD than in obese with NL. Liver LCN2 gene expression correlated with SS (r=0.351, p=0.016), and its protein expression correlated with NASH (r=0.705, p=0.003). LCN2 expression was detected in HepG2 cells after the administration of TNFα, IL6, resistin or adiponectin. LCN2 expression was induced by TNFα, IL6 and resistin. CONCLUSIONS: Liver LCN2 is related to NAFLD in severely obese women. Up-regulation of LCN2 expression is detected in HepG2 cells after exposure to TNFα, IL6 and resistin. These results suggest that LCN2 expression is induced under liver harmful conditions.

Edema of the uvula: etiology, risk factors, diagnosis, and treatment.

Edema of the uvula (EU) is a rare occurrence sometimes associated with angioedema, urticaria, and anaphylaxis. We analyze the causes, predisposing factors, and characteristics of EU in a group of 58 patients with a mean (SD) age of 48.2 (15.2) years over the course of a year. Of the 58 patients studied, 49 (84.5%) were male and 44 (75.9%) presented isolated EU. Thirty-two patients (55.1%) with no clear etiology were classed as idiopathic. Snoring and a high body mass index were more prevalent in these patients. A variety of probable causes were identified in 26 patients (44.9%). In this group, EU was usually accompanied by urticaria, angioedema, and anaphylaxis and there was also a greater prevalence of atopy. We found that EU was idiopathic in just over half of the patients studied and that the predisposing factors were being overweight and having a tendency to snore. Patients with EU should be tested for allergies to drugs, airborne allergens, and food.

Hepatitis aguda grave por flutamida y CA 19.9 elevado / Severe acute hepatitis due to flutamide and elevated CA 19.9

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Synchronus renal cell carcinoma and Bellini duct carcinoma: a case report on a rare coincidence.

Bellini duct carcinoma or collecting duct carcinoma (CDC) is a rare but aggressive primary renal neoplasm. The coexistence of two synchronous neoplasms in the same kidney is highly infrequent. As a result, it is hardly surprising that there are no references to renal cell carcinoma (RCC) combined with CDC of the same kidney in the literature. Histology and immunohistochemistry are important tools for differentiating between the two types of tumors involved. We present the first case of a synchronous occurrence of RCC and CDC of the same kidney.

Recovery of minimal change nephrotic syndrome and acute renal failure in a patient withRenal cell carcinoma.

We describe a 78-year-old patient with nephrotic syndrome due to minimal-change glomerulopathy, associated with a renal adenocarcinoma. Oliguric acute renal failure requiring hemodialysis was also observed. Surgical removal of the tumor and corticosteroid therapy resulted in resolution of the nephrotic state and improvement of the renal function. Nephrotic syndrome is an unusual complication of renal cell carcinomas, and the association of minimal-change glomerulopathy (MCG) and solid tumors is particularly uncommon. In spite of this, MCG should be considered in the nephropathies causing nephrotic syndrome and acute renal failure in patients with renal malignancies.

[Fibrinolytic treatment in acute myocardial infarction: analysis of delay]. / Tratamiento fibrinolítico en el infarto agudo de miocardio: análisis de los tiempos de demora.

BACKGROUND: The delay time from the onset of symptoms to the initiation of intravenous fibrinolytic treatment in patients with acute myocardial infarction (AMI) is herein described. METHODS: A study was carried out of the consecutive AMI diagnosed in the Medical Area of the Emergency Department of the Hospital del Mar in Barcelona, Spain, with a 24-hour follow up from 15 May 1993 to 14 January, 1994. All the patients under the age of 80 years with transmural AMI of any localization and evolution of under 6 hours were considered to receive fibrinolytic treatment. The following delay times were analyzed: total delay time, extrahospitalary delay time and intrahospitalary delay time, which included assistance delay time, delay in fibrinolytic treatment indication and delay time in performance of the same. RESULTS: During the study period 18,316 patients were attended in the Emergency Medical Area, of which 80 corresponded to AMI. Fibrinolytic treatment was initiated with intravenous streptokinase in 33 patients (41.3%). The total delay time was 287.2 +/- 202.6 (mean +/- SD) minutes; the extrahospitalary and intrahospitalary delays were 159.8 +/- 151.7 and 126.8 +/- 161.7 minutes, respectively. The delay time for assistance was 8.5 +/- 12.7 minutes, the delay time in treatment indication was 78.8 +/- 101.8 minutes and in performance it was 39.5 +/- 52.6 minutes. This latter time was analyzed on the basis of the administration site, with statistically significant differences (p < 0.005) if the fibrinolytic treatment was performed in the Emergency Medical Area (12.5 +/- 0.7 minutes), in the observation room (41.4 +/- 50.7 minutes) or in the Intensive Care Unit (61.4 +/- 75.8 minutes). CONCLUSIONS: Most of the intrahospitalary delay in the administration of fibrinolytic treatment is due to decision delay in regards to carrying out this therapy.

Apolipoprotein(a) genetic polymorphism and serum lipoprotein(a) concentration in patients with peripheral vascular disease.

Serum lipoprotein(a) (Lp(a)) levels were measured in 89 men with peripheral vascular disease (PVD) and 129 (100 male and 29 woman) healthy controls. Apolipoprotein(a) genetic polymorphism was determined by immunoblotting in all subjects. Patients with PVD had significantly higher serum Lp(a) levels than controls. Apolipoprotein(a) phenotype frequencies in patients with PVD did not differ from those of the control group. Both patients and controls with phenotype S2 had higher serum Lp(a) levels than those with phenotype S4. It should be emphasized that serum Lp(a) levels were significantly higher in PVD patients than controls for those with phenotype S2, S3/S4 and S4. Raised serum Lp(a) levels together with other lipoprotein abnormalities in patients with PVD imply a high cardiovascular risk. Genetic polymorphism clearly influences serum Lp(a) levels both in patients and controls. In patients with PVD, environmental and/or other genetic factors must play a role in raising Lp(a) levels.

Tuberculous pericarditis as the first manifestation of AIDS.

Although it is known that extrapulmonary tuberculosis in patients with AIDS has a broad spectrum of clinical manifestations, pericardial involvement has rarely been described. We report a case of this condition as the first manifestation of AIDS with good response to antituberculous therapy. Although unusual, the diagnosis of tuberculous pericarditis in symptomatic HIV-infected patients should be aggressively pursued because of the beneficial clinical response to treatment.

Serum lipoprotein(a) concentration in patients with chronic renal failure receiving haemodialysis: influence of apolipoprotein (a) genetic polymorphism.

Serum lipoprotein(a) (Lp(a)) was measured in 101 men with end-stage chronic renal failure (CRF) receiving haemodialysis and in 101 age-matched male controls. Apolipoprotein(a) genetic polymorphism was determined by immunoblotting in 100 patients and in 92 controls. Patients with CRF on haemodialysis had significantly greater serum Lp(a) than controls. Apolipoprotein(a) phenotype frequencies in patients with CRF did not differ from those of the control group. Both patients and controls with phenotype S2 had greater serum Lp(a) than those with phenotype S4. It should be emphasized that serum Lp(a) was significantly greater in patients on haemodialysis than controls, both for those with phenotype S2 and those with S4. Increased serum Lp(a) together with other lipoprotein abnormalities in patients with CRF on haemodialysis imply an increased cardiovascular risk. Genetic polymorphism clearly influences serum Lp(a) both in controls and patients. In the latter group CRF itself, dialysis, or both, also play a role in increasing Lp(a).

Arthritis in Mediterranean spotted fever.

Although arthralgia is a common complaint in Mediterranean spotted fever, frank arthritis is very unusual. We report two cases of this condition during the course of Mediterranean spotted fever. Synovial fluid was inflammatory in both patients and the disease resolved after doxycycline therapy. Immunofluorescence test for Rickettsia conorii in synovial fluid was negative, suggesting a reactive arthritis.