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F Colina

Publications and source records attributed to F Colina.

At least 37 records · Page 2Linked to original sources
PubMed1999

Hepatitis C virus-related fibrosing cholestatic hepatitis after cardiac transplantation: is azathioprine a contributory factor?

We report a patient who acquired hepatitis C virus (HCV) infection at cardiac transplantation, developing fibrosing cholestatic hepatitis (FCH) with early liver failure and a fatal outcome. FCH is a recently described clinicopathological entity characterized by a cholestatic pattern of serum liver enzyme abnormalities, a progressive course leading to liver failure, and a pathological picture defined by periportal fibrosis, neutrophilic infiltrates and signs of histological cholestasis. Although it was initially described secondary to hepatitis B virus infection, it has also been recently related to HCV infection. Some histopathological features consistent with azathioprine hepatotoxicity like cholestasis, perisinusoidal fibrosis, veno-subocclusive lesions and nodular regenerative hyperplasia were also observed in this case. Therefore, a direct cytopathic effect of HCV and the concurrent pathogenic role of azathioprine hepatotoxicity may be involved in the development of this complication of transplantation.

Azathioprine↗
PubMed1999

Collagenous gastrobulbitis and collagenous colitis. Case report and review of the literature.

A case is reported of collagenous gastrobulbitis on collagenous colitis in a 57-year-old woman with a 6-month history of watery diarrhea. Low serum levels of total proteins and albumin and increased fecal elimination of alpha1-antitrypsin were the only abnormal laboratory test results. Biopsy specimens from the colon, rectum, antrum, fundus, and duodenal bulb showed a thick subepithelial band composed of ultrastructurally normal collagen immunohistochemically negative for collagen IV and laminin. The diarrhea resolved with prednisone and responded to this treatment after a relapse 6 months later. One year later the patient developed severe alimentary intolerance and secondary weight loss. This symptom also responded to the same treatment. However, the collagen deposition did not disappear in the second biopsy samples of colonic and gastric mucosa. Only six cases have been previously reported with gastric and/or duodenal subepithelial collagenous deposition. Four were associated with collagenous colitis. One of these presented a subepithelial collagenous band in the terminal ileum. All these features suggest that this collagen deposition may affect the entire digestive tract with variable intensity, extension, and symptoms.

Colitis↗
PubMed1998

[Invasive fungal infections in liver transplant recipients: analysis of 21 cases].

BACKGROUND: Invasive fungal infections (IFI) are one of the most important causes of mortality in liver transplant (LT) recipients. The aim of this study was to describe the characteristics of IFI in the LT program of our institution with an special emphasis in the differences between Candida infections (CI) and that caused by other fungi (NCI). PATIENTS AND METHODS: Retrospective analysis of the hospital charts of 21 patients who underwent a LT from February 1987 to December 1995. The diagnosis of IFI required the histological evidence of tissue invasion or a positive culture in a tissue sample or in an usually sterile fluid. Esophageal candidiasis was not considered as IFI. Antifungal prophylaxis was performed either with nystatin or fluconazole. RESULTS: Twenty-one of 356 patients (6%) developed a total of 23 episodes of IFI. Pathogens were Candida spp. (n = 10), Aspergillus (n = 8), Zygomicetes (n = 4) and Cryptococcus (n = 1). Fifty-seven percent of the episodes of IFI (80% of those caused by Candida and 38% of those produced by other fungi; p < 0.05) developed in the first 3 months after transplantation and only 5 episodes appeared after the sixth month. The diagnosis of IFI was done at autopsy in 6 patients (29%). Overall, NCI (13 episodes) predominated over CI (10 episodes), being the later the cause of the 54% of the episodes in the first 178 recipients but only the 30% in the last 178 patients (p = 0.09). No differences were found in the distribution of the risk factors amongst those patients with CI or NCI. Seventeen of the 21 patients (71%) died and 15 of these deaths (72%) were attributable to fungi; 15 patients who died either did not receive amphotericin (n = 6) or received a cumulative dose lower than 500 mg. Six patients received a cumulative dose of more than 1.5 g (mean, 3.2 g) and four of them were cured. Mortality in the nonfungal infection group was 26% (p < 0.001). CONCLUSIONS: IFI was a rare but severe complication in our LT recipients. The relative frequency of CI was progressively decreasing during the study period, being NCI the predominant infections. Amphotericin therapy was effective only when a high cumulative dose could be administered.

Adult↗
PubMed1998

Hilar biliary cysts in hepatic transplantation. Report of three symptomatic cases and occurrence in resected liver grafts.

Hilar cysts are infrequent post-transplant biliary tract complications. Thirteen cases were discovered among 493 consecutive liver transplants (2.6%). Three (0.60%) were symptomatic (obstructive jaundice) while the other ten were found by systematically searching in the hilum in a series of 129 consecutive, resected grafts at retransplantation or autopsy (n = 54). Two types of cysts were detected: in eight grafts (1.6%), these were blind unilocular cavities with viscid mucous content, located adjacent to the biliary tract anastomoses. These had been inadvertently created as a result of the sequestered remnant cystic duct after cholecystectomies and biliary tract reconstructions, where a double-barreled common duct and long cystic duct had been present in the donor liver. These mucoceles ranged from 0.5 to 5.5 cm in diameter (median 1.7 cm). The three symptomatic cases were diagnosed by imaging techniques 3.5 years after transplantation; however, this type of cyst was found as early as the 2nd month post-transplantation when detected in lost liver grafts. Five livers (1%), lost between 5 months and 2.8 years post-transplantation, showed cystically dilated peribiliary glands, sometimes with multilocular, and occasionally multiple, cavities ranging from 0.5 to 2 cm in diameter (median 0.8 cm). This type of cyst was asymptomatic and located adjacent to the left, right, or common hepatic ducts. Threads were found near four cysts, suggesting that surgical injury may have been responsible for obstructing the neck of the glands. With the increasing number of long-term survivors of liver transplantation, unless preventive surgical methods are implemented, the number of symptomatic cysts of these origins can be expected to grow. Transplantation teams should, therefore, be aware of these potential causes of biliary tract complications.

Adolescent↗
PubMed1998

Steroid withdrawal is safe and beneficial in stable cyclosporine-treated liver transplant patients.

BACKGROUND: In the immunosuppression of orthotopic liver transplant recipients, steroids are used despite their unspecific action and long-term side effects. Few studies have been carried out on steroid withdrawal and many aspects remain to be elucidated. METHODS: A prospective study was performed to analyse the effect of steroid withdrawal on 86 patients with stable graft function, more than 1 year after orthotopic liver transplant. Thirty patients had chronic hepatitis in the graft. Seventy-two continued with cyclosporine (CsA) and 14 with CsA-azathioprine (AZA) therapy. The follow-up was 23.2 +/- 8.1 months (range 12-52 months). A paired t-test was used for statistical analysis. RESULTS: No acute or chronic rejection occurred, and steroids were not reinstituted. There were no changes in serum transaminase levels, but bilirubin levels decreased (p < 0.01). At the end of the follow-up, we found improvements in blood pressure in hypertensive patients (systolic 156.1 +/- 8.4 mmHg vs. 139.4 +/- 8.7 mmHg, p < 0.001); body weight (72 +/- 13.5 kg vs. 70.8 +/- 13 kg, p < 0.05); serum cholesterol (211.3 +/- 42 mg/dl vs. 191.6 +/- 43.5 mg/dl, p < 0.001) and bone mineral density in lumbar spine (0.823 +/- 0.13 g/cm2 vs. 0.893 +/- 0.135 g/cm2, p < 0.001). Four of ten diabetic patients were no longer insulin-dependent and insulin requirements decreased in the remaining six. No significant biochemical changes were found in patients with hepatitis in the graft, and we found an improvement in inflammatory activity in the nine biopsied patients. CONCLUSIONS: Steroid withdrawal with CsA monotherapy is feasible, safe and beneficial in patients who have stable liver graft function 1 year after orthotopic liver transplant. We consider that AZA therapy is not necessary unless drastic reduction of CsA levels is required because of renal dysfunction.

Adult↗
PubMed1998

Intrahepatic enhanced expression of beta2-microglobulin conformational epitope in acute liver allograft rejection: evidence of modulation by glucocorticoids.

The mechanisms by which glucocorticoids are effective in acute liver rejection therapy are not entirely clear. The aims of this study were to characterize the intrahepatic immunological phenotype in acute liver rejection, as well as the effect of glucocorticoids on cytokine-stimulated hepatocyte cell lines. Biopsy sections from these patients were studied by immunohistochemistry. Cytokine-stimulated hepatocyte cell lines treated with glucocorticoids were evaluated by flow cytometry. The intrahepatic expression of both beta2-microglobulin conformational epitope and intercellular adhesion molecule-1 was higher in acute rejection than in resolving rejection. Interestingly, glucocorticoids were able to modulate in vitro the cytokine-induced expression of these molecules on hepatocyte cell lines. Beneficial effects of the glucocorticoid treatment appear to be associated with a modulation of a beta2-microglobulin conformational epitope and the intercellular adhesion molecule-1 on intrahepatic cellular targets in the acute rejection process.

Acute Disease↗
PubMed1998

Clinical, virological, and histologic evolution of hepatitis C virus infection in liver transplant recipients.

We designed a prospective study to assess the time course and evolution of hepatitis C virus (HCV) infection in 152 patients who underwent a liver transplantation (LT) in our institution. Forty-four recipients (29%) were infected by HCV after transplantation: 40 who developed recurrent infection after LT and four who acquired infection during or after LT. No differences were found in survival actuarial rates at 1, 2, and 4 years after transplantation for patients infected by HCV vs. noninfected ones. Graft hepatitis occurred in 66% of HCV-infected recipients: 18 developed chronic active hepatitis (10 of them with intense fibrosis) and 2 developed cirrhosis during the follow-up. Infection by the HCV-1b genotype was found in 79% of the infected recipients and in 100% of those in whom histologic evolution was worst. Fourteen grafts were lost in 44 HCV-infected recipients, in comparison with 12 in 108 HCV-negative patients (P = .007), mostly because of chronic rejection. HCV infection did not affect life expectancy in the midterm follow-up for LT patients. However, it was often associated with the occurrence of early and severe graft hepatitis and with a higher incidence of graft loss due to chronic rejection.

Adult↗
PubMed1998

Esophagitis dissecans superficialis (esophageal cast) complicating esophageal sclerotherapy.

Esophagitis dissecans superficialis is a rare and benign condition that involves the formation of an esophageal cast. This disorder has been described in association with a variety of etiologic factors. We report a case of an esophageal cast in a patient included in a program of sclerotherapy of varices. We discuss the possible relationship existing between sclerotherapy and the development of esophagitis dissecans superficialis.

Aged↗
PubMed1998

Fibrosing cholestatic hepatitis in hepatitis C virus-infected renal transplant recipients.

Severe hepatitis C virus (HCV)-related fibrosing cholestatic hepatitis leading to early liver failure has been reported only exceptionally. Of 259 HCV-infected renal transplant (RT) patients in one hospital unit, four (1.5%) are described, representing the first series of this particular post-RT disease. Patient mean age was 55.7 yr. Three were men. All had pretransplant, hepatitis B surface antigen-negative and were anti-HCV antibodies positive. Three of them showed pretransplant mild liver enzyme abnormalities, and all received kidneys from HCV-negative donors. All were on steroids, cyclosporine, and azathioprine (AZA). The clinical pattern appeared early after RT (mean, 11.5 mo). In three patients, hyperbilirubinemia (6.5 to 20 mg/dl) and high alkaline phosphatase levels (428 to 859 IU/L) were observed. Also, in all subjects, high gamma glutamyl transpeptidase levels (639 to 4270 IU/L), mild aspartate aminotransferase and alanine aminotransferase abnormalities, and serum HCV RNA were observed. Liver biopsy revealed diffuse fibrosis, leukocyte infiltrates, and different degrees of cholestasis, with typical signs of HCV hepatitis in only one patient. Two patients developed subfulminant liver failure and died 2 and 3 mo after biopsy, respectively. One patient also suffered hepatic failure, receiving a liver transplant. The fourth is alive on dialysis awaiting a combined kidney and liver transplant. It is concluded that fibrosing cholestatic hepatitis is a new, early, and severe complication after RT in HCV(+) patients, which appears in patients with ongoing HCV infection under AZA therapy, despite a nonaggressive immunosuppressive protocol. Both HCV and AZA could play a concurrent role in the pathogenesis of this severe complication after RT.

Adult↗
PubMed1998

[Idiopathic ductopenia in adults as a cause of cryptogenic cirrhosis and complications of portal hypertension].

We describe a 56 years old male patient with long-term chronic liver disease of unknown etiology presenting with esophageal varices rupture. Prophylaxis of re-bleeding with propranolol and endoscopic sclerotherapy failed to prevent further haemorrhagic events and the placement of a transjugular intrahepatic portosystemic shunt (TIPS) was needed. The portal hemodynamic data revealed sinusoidal portal hypertension and the liver biopsy displayed ductopenic cholestasis. The patient met all criteria of idiopathic ductopenia. Subsequently, the jaundice worsened and the patient required liver transplantation.

Bile Ducts, Intrahepatic↗
PubMed1998

[Gaucher's disease suspected by abdominal echography findings].

Abdominal ultrasonographic findings of Gaucher's disease had been reported, but a specific pattern has not been described. We report here a patient with an abdominal sonographic pattern which was concluded to be strongly suggestive of Gaucher's disease: solid focal splenic lesions with different patterns (hypoechoic, hiperechoic and mixed nodules associated with hypoechoic irregular areas) and bright liver and spleen echo pattern with posterior beam attenuation. Gaucher's disease was subsequently confirmed by determination of leukocyte beta-glucosidase activity and mutations of glucocerebrosidase gene.

Abdomen↗
PubMed1997

Diffuse fatty liver in familial heterozygous hypobetalipoproteinemia.

A 34-year-old man had asymptomatic hepatomegaly, slightly increased serum alanine aminotransferase and gamma-glutamyl transpeptidase levels, and a sonographic pattern suggesting diffuse hepatic steatosis. Liver biopsy revealed fatty change in 25% to 50% of hepatocytes. The patient also had low serum levels of cholesterol and triglycerides and met clinical, biochemical, and familial diagnostic criteria of heterozygous hypobetalipoproteinemia. We could not relate his hepatic steatosis to any already known cause of fatty liver and could only attribute it to heterozygous hypobetalipoproteinemia. Familial heterozygous hypobetalipoproteinemia should be ruled out in patients with unexplained hepatic steatosis.

Adult↗
PubMed1997

Influence of viral genotype and level of viremia on the severity of liver injury and the response to interferon therapy in Spanish patients with chronic C infection.

BACKGROUND: We wanted to investigate the influence of viral genotype on the severity of liver injury and response to interferon and whether the level of viremia differs in accordance with genotype, severity of liver disease, and response to interferon in patients with hepatitis C virus (HCV) infection. METHODS: We studied 118 patients with HCV-related liver disease. HCV genotypes were determined with a line probe assay, and serum HCV RNA levels with a competitive reverse transcription polymerase chain reaction assay. RESULTS: HCV type 1b was the most prevalent genotype (88%). It was present in 100% of cirrhotic patients, with or without hepatocellular carcinoma (HCC), but only in 78% of patients with chronic hepatitis (P < 0.001). The response to interferon was better in patients infected with non-1b HCV genotypes (P = 0.002). In a multivariate analysis non-1b HCV genotypes and a low hepatic fibrosis correlated with a favorable response to interferon. Among patients with chronic hepatitis those infected with HCV type 1b were older (P < 0.001), and age was the only independent factor associated with HCV type 1b. Viremia levels differed neither between genotypes nor in response to interferon and was significantly lower in patients with cirrhosis and HCC. CONCLUSIONS: HCV 1b was associated with more severe liver disease and a worse response to interferon therapy. Non-1b genotypes and a lower liver fibrosis were the only independent predictors of a favorable response to interferon. Levels of HCV viremia differed neither among different genotypes nor in response to interferon and decreased with advanced liver disease.

Aged↗