Caso 3/19: “O 18º espaço porta”

Caso relatado na Reunião de Discussão de Casos Clínicos do Hospital Universitário Prof. Polydoro Ernani de São Thiago, iniciada pelos Profs. Jorge Dias de Matos, Marisa Helena César Coral e Rosemeri Maurici da Silva, em julho de 2017. No dia 12 de agosto de 2019, no bloco do curso de medicina, realizou-se a apresentação e discussão do caso cujo registro é apresentado a seguir: um paciente masculino de 25 anos é encaminhado ao serviço de gastroenterologia com esplenomegalia e hipertensão portal. Qual é o diagnóstico

Analise morfologica dos rins de pacientes portadores de lupus erimatoso sistemico: correlacao anatomoclinica dos tipos histologicos e dos indices de atividade e cronicidade

BV UNIFESP: Teses e dissertaçõe

Acute Tubulointerstitial Nephritis due to Phenytoin: Case Report

Introduction: Acute tubulointerstitial nephritis (ATIN) is an acute kidney injury (AKI) resulting from damage to the tubulointerstitial tissue due to infection, trauma, or use of medication. It is clinically non-specific. Case: A teenager with multiple trauma, hospitalised after lowering of level of conscience, and convulsion fits. While in the emergency ward, he received: midazolam, fentanyl and phenytoin. The cranial and abdominal CT scans were normal. He was stable with no signs of shock, trauma or infection; he developed oliguria and serum creatinine (Scr) 1.7mg/dL), 12 hours after the admission. After 36 hours, Scr levels were at 3.4mg/dL and urea at 55mg/dL. He had AKI according to pRIFLE (66.2% reduction in clearance). After other causes of AKI had been ruled out, the possibility of ATIN was raised; the phenytoin was suspended and pulse therapy, with methylprednisolone, was promptly initiated. After the first pulse, there was already a decline in the creatinine and urea readings; 48 hours later: Scr at 2.2mg/dL and urea at 86mg/dL. Thirty days after being discharged from hospital, the patient was in good health and had full restoration of kidney function. Discussion: The singularity of this report relies on the rarity of ATIN secondary to the use of phenytoin and also in the importance of recognizing this aetiology as being one of the origins of AKI. Conclusion: Early diagnosis allows the reversal of AKI through suppression of treatment with phenytoin and introduction of corticosteroid therapy, when necessary

Autoantibody profile in individuals with chronic hepatitis C

Introduction Autoantibodies are often produced during infection with chronic hepatitis C virus (HCV), but it remains controversial whether they influence the biochemical profile and histological features of this disease. Therefore, this current study sought to describe these autoantibodies and evaluate their impact on the clinical and histological presentation of hepatitis C. Methods This cross-sectional analytical study assessed patients with HCV (RNA+) from October 2011 to July 2012. Results This study included 66 patients, with a mean age of 53.2±10.5 years. Of these patients, 60.6% were male, and 54.3% presented with genotype 1. Non-organ-specific autoantibodies (NOSA) were detected in 24% of the patients; of these, 7.6% were anti-mitochondrial antibodies (AMA+), 26.7% were anti-smooth muscle antibodies (SMA+) and 6.8% were liver kidney microsomal type 1 antibodies (LKM1+). With respect to the thyroid autoantibodies, 7.4% were anti-peroxidase (ATPO+) antibodies, and none were anti-thyroglobulin (ATG+) antibodies. Regarding celiac disease autoantibodies, 5.8% were endomysial antibodies (EMA+), and no transglutaminase (TTG+) antibodies were detected. Cryoglobulins were found in 2.1% of patients. When NOSA+ individuals were compared to patients without the presence of NOSAs, they exhibited higher median alkaline phosphatase (0.7 vs. 0.6 xULN; p=0.041), lower median platelet counts (141,500.0 vs. 180,500.0/mm 3 ; p=0.036), lower mean prothrombin activity (72.6±11.5% vs. 82.2±16.0%; p=0.012) and an increased prevalence of significant fibrosis (E≥2) (45.5% vs. 18.2%; p=0.012). There was also a tendency for a greater proportion of NOSA+ cases to have marked periportal activity (APP≥3) (44.5% vs. 15.6%; p=0.087). Conclusions In addition to the high prevalence of autoantibodies associated with HCV infection, it was observed that NOSA positivity was associated with a more severe histological and biochemical profile of hepatitis C infection

Clinical and laboratory characteristics associated with dyslipidemia and liver steatosis in chronic HBV carriers

Introduction Chronic hepatitis B virus (HBV) infection and liver steatosis (LS) are the most common causes of chronic liver disease, and their coexistence is frequently observed in clinical practice. Although metabolic syndrome is the main cause of LS, it has not been associated with HBV infection. The aims of this study were to describe the lipid profile and prevalence of LS among HBV carriers and to identify the characteristics associated with LS in this group. Methods This retrospective cross-sectional study included hepatitis B surface antigen (HBsAg)-positive patients evaluated during 2011 and 2012. Results Of the 83 patients included, the mean age was 46.4±12.5 years, 53% were men, and 9.1% were hepatitis B e antigen (HBeAg) -positive. These patients exhibited the following lipid profile: total cholesterol = 175.4±38.8mg/dL, low-density lipoprotein (LDL) = 113.0±32.7mg/dL, and triglycerides = 91.1±45.2mg/dL. Their fasting glucose was 95.3±14.5g/dL, and fasting insulin was 6.1±5.9µIU/mL. Liver steatosis was observed on abdominal ultrasound in 11.3% of individuals. Factors associated with the presence of LS included higher levels of total cholesterol, prothrombin activity, fasting insulin, and body mass index (BMI) as well as lower levels of aspartate aminotransferase (AST). Conclusions These findings suggest that LS in patients with chronic HBV appears to be a consequence of metabolic alterations and insulin action rather than of viral factors

Prevalence and clinical features of celiac disease in patients with hepatitis B virus infection in Southern Brazil

Introduction Celiac disease is an autoimmune disorder that involves gluten intolerance and can be triggered by environmental factors including hepatitis B virus (HBV) infection. This study aimed to describe the prevalence of celiac disease in individuals with HBV infection and to describe the clinical and laboratory characteristics of celiac disease associated with HBV. Methods This cross-sectional study included 50 hepatitis B patients tested for IgA anti-endomysial antibodies (EMAs) and tissue anti-transglutaminase (TTG) between August 2011 and September 2012. Results Fifty patients were included with a mean age of 46.0 ± 12.6 (46.0) years; 46% were female and 13% were HBeAg+. Six patients had positive serology for celiac disease, four were EMA+, and five were TTG+. When individuals with positive serology for celiac disease were compared to those with negative serology, they demonstrated a higher prevalence of abdominal pain (100% vs. 33.3%, p = 0.008), lower median creatinine (0.7mg/dL vs. 0.9mg/dL, p = 0.007) and lower mean albumin (3.6 ± 0.4g/L vs. 3.9 ± 0.3g/L, p = 0.022). All individuals with positive serology for celiac disease underwent upper digestive endoscopy, and three of the patients exhibited a macroscopic pattern suggestive of celiac disease. Histologically, five patients demonstrated an intra-epithelial lymphocytic infiltrate level > 30%, and four patients showed villous atrophy associated with crypt hyperplasia on duodenal biopsy. Conclusions An increased prevalence of celiac disease was observed among hepatitis B patients. These patients were symptomatic and had significant laboratory abnormalities. These results indicate that active screening for celiac disease among HBV-infected adults is warranted