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Biomedical subjects

J Aranda-Michel

Publications and source records attributed to J Aranda-Michel.

10 recordsLinked to original sources
PubMed2006

Case report of lamivudine-resistant hepatitis B virus infection post liver transplantation from a hepatitis B core antibody donor.

The use of allografts from donors with hepatitis B core antibody in liver transplantation (LT) is associated with the risk of de novo hepatitis B virus (HBV) infection. Prophylaxis using hepatitis B Immune globulin (HBIg) and lamivudine alone or in combination has been reported. Yet, there are no standardized regimens and long-term efficacy is not known. We report a case of a patient who underwent LT for alcoholic liver disease who received an allograft from a donor with Hepatitis B core antibody. The patient had no previous exposure to HBV, was vaccinated against HBV, and had demonstrated Hepatitis B surface antibody present in serum before and 6 months after transplantation. Prophylaxis with short-term HBIg (1 week) and indefinite lamivudine was given. De novo HBV infection developed more than 3 years after LT with a lamivudine-resistant polymerase mutant containing the rtM204I and rtl180L/M mutations. We reviewed the risk of de novo post-LT HBV infection in recipients of livers from hepatitis B core antibody positive donors. High risk were HBV naïve recipients, moderate risk recipients had isolated hepatitis B surface antibody (anti-HBs) or hepatitis B core antibody (anti-HBc), while low-risk recipients had both anti-HBs and anti-HBc. We reviewed prophylaxis protocols reported in the literature and made recommendations for management.

Antiviral Agents↗
PubMed2001

Nutrition in hepatic failure and liver transplantation.

Protein-energy malnutrition (PEM) is a common problem in patients with end-stage liver disease, and it is universally present in patients undergoing orthotopic liver transplantation. Although PEM is an independent risk factor for morbidity and mortality, it need not be considered an absolute contraindication for liver transplantation. The etiology of PEM in liver disease is multifactorial and includes decreased nutrient and calorie intake, alterations in intestinal malabsorption and/or maldigestion, and diverse abnormalities of carbohydrate, fat, and protein metabolism. This article reviews the prevalence of malnutrition, its pathophysiology, different modalities for assessment of body composition, and general guidelines for nutritional support in patients with liver disease and liver transplantation.

Humans↗
PubMed2000

Histochemical and immunohistochemical characterization of foamy histiocytes (muciphages and xanthelasma) of the rectum.

Despite being relatively common in the rectum, foamy histiocytes have received scant attention as to the antecedent lesion that causes them to form or their histologic characterization on the types of muco-substances they accumulate. One-hundred consecutive tissue sections of the rectum from an equal number of patients were reviewed for the presence of foamy histiocytes, evaluated for their associated histologic features, and examined histochemically for five types of mucin. Immunohistochemical and electron microscopic studies were performed. Forty (40%) of the rectal biopsy tissues contained foamy histiocytes. Patients presented with diarrhea, hematochezia, intestinal habit change, constipation, hemorrhoids, and abdominal pain. Endoscopically, 19 patients were thought to have rectal nodules or polyps. Histologically, 25 of the patients had regenerative changes in the adjacent mucosa and 14 had hyperplastic changes. In 36 patients (90%), the foamy histiocytes were located superficially in the lamina propria. Associated changes indicated that they are found in areas that are subject to an injury that is in a healing phase. These changes included mild fibrosis and chronic inflammation of lamina propria with mild architectural distortion. Thirty-five (88%) cases showed staining for D-PAS, Alcian blue stain pH 2.5, and the cocktail Alcian blue stain/PAS. Mucicarmine was positive in 25 (63%) cases. The Alcian blue stain pH 1.0 was positive in 19 (59%) of 32 cases. Ultrastructural studies showed electron-dense globules. Two cases were histologically identical to the other 38 but they did not stain for any mucin. Ultrastructural features disclosed clear vacuoles and thus represent a xanthelasma of the rectum. The foamy cells in all cases were confirmed to be histiocytes by immunohistochemistry and electron microscopy. Although muciphages and xanthelasma of the rectum may mimic polyps endoscopically, they are not related to any specific symptom or clinical finding, despite the fact that they probably represent remnants of a previous injury. Muciphages contain neutral, weakly acidic or strongly acidic mucin. The main type of acidic mucin is sialomucin with a smaller component of sulfated mucin.

Adult↗
PubMed1999

Nefazodone-induced liver failure: report of three cases.

BACKGROUND: Liver failure is a rare but devastating result of drug toxicity. OBJECTIVE: To describe three cases of subfulminant liver failure that were probably caused by nefazodone, a new antidepressant that is a synthetically derived phenylpiperazine. DESIGN: Case series. SETTING: Two university medical centers and a children's hospital. PATIENTS: Three women 16 to 57 years of age. INTERVENTION: Two patients underwent liver transplantation; the third was listed for transplantation but subsequently improved. MEASUREMENT: Liver biopsy. RESULTS: Nefazodone was administered for 14 to 28 weeks before the onset of symptoms. The duration of jaundice before onset of encephalopathy ranged from 4 to 6 weeks. All cases of liver failure had similar histologic appearance, with prominent necrosis in the centrolobular areas (zone 3). One patient had successful liver transplantation, one underwent transplantation but died, and one improved without transplantation. The temporal onset of disease after the start of nefazodone therapy suggested severe hepatocellular injury caused by the drug. CONCLUSIONS: Because nefazodone seems to cause severe hepatocellular injury in an idiosyncratic manner, routine liver chemistries should be performed before starting nefazodone therapy and patients should be monitored regularly. Therapy should be discontinued if liver enzyme concentrations become abnormal.

Adolescent↗
PubMed1999

Rimantadine for treatment of hepatitis C infection in liver transplant recipients.

Hepatitis C recurrence after liver transplantation is a serious problem, leading to increased graft loss and morbidity in some individuals. Treatment with interferon and other agents is controversial and not highly efficacious. The use of an effective antiviral agent to reduce or eliminate viral burden is desirable. To this end, we performed an open-label pilot trial to determine if rimantadine would show antiviral activity against hepatitis C virus (HCV) in the posttransplantation setting. Eleven patients with recurrent post-liver transplantation disease, characterized by transaminase level abnormality and HCV RNA in serum and liver biopsy specimens consistent with HCV infection were offered enrollment onto the study. Patients were treated for 12 weeks with rimantadine, 100 mg orally twice daily, and followed up after treatment for up to 8 additional weeks. Serum was collected at 2-week intervals to assess transaminase and HCV RNA levels. Nine patients completed the planned course of therapy. There was no significant change in serum alanine aminotransferase levels during treatment. No patients cleared HCV RNA from the serum, and fluctuations in the viral titer were not clearly associated with the initiation and completion of the active-treatment phase. Rimantadine was well tolerated, with only one patient who stopped therapy for perceived side effects. We conclude that rimantadine monotherapy has no role in the management of recurrent hepatitis C after liver transplantation.

Adult↗
PubMed1999

Acute diarrhea: a practical review.

This review provides a practical, simple, and logical approach to the diagnosis and management of patients with acute infectious diarrhea, one of the most common diagnoses in clinical practice. Diarrhea in the immunocompromised host, traveler's diarrhea, and diarrhea in the hospitalized patient are also discussed. Most episodes of acute diarrhea are self-limited, and investigations should be performed only if the results will influence management and outcome. After an adequate history and physical examination, the clinician should be able to classify the acute diarrheal illness, assess the severity, and determine whether investigations are needed. Most patients do not require specific therapy. Therapy should mainly be directed at preventing dehydration. Various home remedies frequently suffice in mild, self-limited diarrhea. However, in large-volume, dehydrating diarrhea, oral rehydration solutions should be used, as they are formulated to stimulate sodium and water absorption. Antidiarrheal agents can be useful in reducing the number of bowel movements and diminishing the magnitude of fluid loss. The most useful agents are opiate derivatives and bismuth subsalicylate. Antibiotic therapy is not required in most patients with acute diarrheal disorders. Guidelines for their use are presented.

AIDS-Related Opportunistic Infections↗
PubMed1998

Tests of the liver: use and misuse.

Physicians frequently order batteries of tests that are used to assess liver injury or function. These tests are frequently ordered to screen for disease. However, a lack of understanding of the nature of the assays and the laboratory assignment of normal versus abnormal often leads to unnecessary workup or missed disease. We attempt to describe the nature of the most commonly used laboratory tests for liver disease, including alanine and aspartate aminotransferases, alkaline phosphatase, bilirubin, and gamma glutamyl transpeptidase. In addition, the role of functional tests of the liver, including prothrombin time, and metabolite clearance tests, such as aminopyrine and monoethylglycinexylidine, are examined.

Albumins↗
PubMed1995

Helicobacter pylori.

Helicobacter pylori is an important cause of chronic active gastritis and is strongly associated with peptic ulcer disease and gastric cancer. H. pylori colonizes the surface of the gastric epithelium with production of a number of factors, resulting in inflammation and an altered mucosa. H. pylori infection occurs world-wide and the mode of transmission most likely is from human to human via the fecal-oral and/or the oral-oral route. Treatment and, in the future, prevention of this infection may result in a marked diminution of upper gastrointestinal tract disease.

Animals↗