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F Colina

Publications and source records attributed to F Colina.

103 records · Page 6Linked to original sources
PubMed1982

Nodular regenerative hyperplasia of the liver. Report of two cases associated with autoimmune disease.

Nodular regenerative hyperplasia of the liver (N.R.H.) is an uncommon clinicopathological entity characterized by diffuse regenerative hepatocytic nodules without fibrosis. Grossly the lesion is often mistaken for cirrhosis. The etiology and pathogenesis are unknown. We report two new cases of N.R.H. diagnosed by liver biopsy. Peritoneoscopically the liver showed a nodular surface resembling micronodular cirrhosis. Both patients showed some clinical and immunological features of autoimmune disease, and in both cases N.R.H. was associated with chronic active hepatitis. We discuss the pathological differential diagnosis of N.R.H., its relation to other associated diseases and review the hypotheses for the pathogenesis of this condition.

Aged↗
PubMedDate not supplied

Hepatic injury in the toxic epidemic syndrome caused by ingestion of adulterated cooking oil (Spain, 1981).

We describe the clinico-pathological characteristics of hepatic injury associated with the toxic-epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic-epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life. No statistical significance was found in relation to alcohol consumption, treatment with potentially hepatotoxic antibiotics, or adult respiratory distress syndrome. Most (91.6%) patients with hepatic injury were asymptomatic; jaundice or abdominal pain was rarely noted. One patient died of acute liver failure following Budd-Chiari syndrome. Serum gamma-glutamyl transpeptidase activity was raised in all cases, alkaline phosphatase in 94.6%, and less frequently lactate dehydrogenase (80%), SGPT (84.7%), and SGOT (76%). Serum total bilirubin was usually normal (89.2%). The histologic lesion was similar to drug-induced cholestatic hepatitis. Lamellar inclusions, canalicular injury, giant mitochondria, and hyperplasia of the smooth endoplasmic reticulum were seen by electron microscopy. Ultrastructural signs of cholestasis were common (78.9%). The pathogenesis of this lesion is unknown; however, because of similarities with chlorpromazine-induced cholestatic hepatitis, we suggest that a combination of hypersensitivity and intrinsic hepatoxicity is a possible mechanism.

Adult↗
PubMedDate not supplied

Nodular regenerative hyperplasia of the liver associated with the toxic oil syndrome: report of five cases.

Nodular regenerative hyperplasia of the liver developed in five patients who had the toxic oil syndrome caused by ingestion of adulterated cooking oil. This hepatic complication was detected from 19 to 37 months (mean-2.5 years) after the onset of the toxic oil syndrome. Nodular regenerative hyperplasia was asymptomatic, although all patients had persistently abnormal liver function. Hepatomegaly was present in four cases, mild jaundice in three and signs of portal hypertension in two. Pathogenesis of nodular regenerative hyperplasia in toxic oil syndrome is unknown, but probably microcirculatory disturbances within the liver might have played a role. Fibrosis in Zone 3, sinusoidal dilatation and occasionally intralobular hemorrhage were seen in three cases; in one of them, characteristic lesions of veno-occlusive disease were also present. In another case, endarteritis changes of hepatic arterioles were evident.

Adolescent↗
PubMedDate not supplied

Twelve-month interferon-alpha therapy induces a similar sustained response in anti-HBe-positive and HBeAg-positive chronic hepatitis B patients.

BACKGROUND/AIMS: We compared the response to interferon-alpha 2a in 35 patients with antibody to HBeAg (anti-HBe) and 20 patients with HBeAg in serum, and histological features of chronic hepatitis B. METHODOLOGY: Patients were treated with 4.5-6 MU of interferon-alpha 2a, three times a week for 12 months, and followed for 30.8 +/- 13.5 additional months. RESULTS: All of them had elevated serum levels of aminotransferases and positive test for hepatitis B virus-DNA in serum. Patients with anti-HBe-positive chronic hepatitis were older and had higher serum aminotransferase levels than HBeAg-positive patients, but no differences were seen between both groups with respect to sex, history of acute hepatitis, mode of transmission of the infection or histological appearance before interferon therapy. Serum levels of alanine transaminase became normal and hepatitis B virus-DNA undetectable by PCR at the end of therapy in 25 (71%) of anti-HBe-positive patients and in 10 (50%) of HBeAg-positive patients (P > 0.05). Although 10 (29%) of the anti-HBe-positive and none of the HBeAg-positive patients relapsed, no significant difference was seen in the rate of sustained response (43% vs. 50%, respectively). The histological improvement was similar in both groups. CONCLUSIONS: The results of this study indicated that biochemical, virological and histological response to 12-month interferon-alpha 2a therapy was similar in patients with anti-HBe antibody than in patients with the classical HBeAg-positive of chronic hepatitis B.

Adolescent↗
PubMedDate not supplied

Liver transplantation and hepatitis C virus. Results in a Spanish center since 1989.

BACKGROUND/AIMS: Hepatitis C-related liver disease is the main indication for liver transplantation in many centers. Viral RNA remains after transplantation in almost 100% of the patients, and more recent reports show a graft hepatitis rate of about 90%. The progression of this hepatitis seems to be quicker than in the nontransplant setting. METHODOLOGY: From June 1989 to October 2000, 197 adult patients had 213 for HCV-related liver disease at our institution. Basal immunosuppression consisted of a triple therapy with cyclosporine, azathioprine and steroids, or dual therapy with tacrolimus and steroids. None of the patients was treated with antivirals after liver transplantation. RESULTS: Pure HCV-related cirrhosis was the indication for liver transplantation in 114 patients, another 14 with hepatocellular carcinoma, 8 associated metabolic diseases, 43 high alcohol intake, 4 hepatitis B, 5 cholestatic diseases, and 3 other diseases. Six patients out of the 197 transplanted in this period were already grafted before this time, and had their first retransplantation of the liver after 1989 (their first liver transplantation was done when HCV was not known). Sixteen additional retransplantation procedures were done in the period considered. Hepatitis was diagnosed in 84.3% of the grafts biopsied later than 90 days after liver transplantation (118/140), and in 92.9% if it was done after one year (92/99). Cirrhosis was diagnosed in 21 grafts at a mean time of 1004.7 days, 21.2% of the grafts biopsied after 1 year and 28.6% after 2 years. Nine grafts in 8 patients were diagnosed as fibrosing cholestatic hepatitis. Patient actuarial survival was 80.9%, 69.7%, 67.5% and 50.6% at 1, 3, 5 and 10 years. Liver failure and hepatoma recurrence were the cause of death in 42.4% of the patients. Actuarial graft survival was 75.2%, 64.9%, 63.5% and 48.6% at 1, 3, 5 and 10 years, and was significantly affected by Child stage (B vs. C, P = 0.004). When compared to 228 non-HCV- infected patients with chronic parenchymatous disease, these had an almost significantly better patient survival (P = 0.0577), but a nonsignificant difference in graft survival. Graft loss related to liver causes was 17.6% in HCV+ patients 14.6% in HCV- patients. Liver causes of death were 14.0% in HCV+ patients and 4.8% in HCV-patients (P = 0.002). CONCLUSIONS: HCV infected liver transplantation recipients present very often graft hepatitis, which may progress to advanced stages in a quite short interval. Mid-term patient and graft survival is comparable to those of non-HCV recipients, but causes of death related directly to liver disease are more common in HCV+. This makes one think that long-term prognosis (more than 10 or 15 years) will be worse in HCV patients.

Actuarial Analysis↗
PubMedDate not supplied

Pseudomyxoma peritonei: a clinicopathologic analysis and follow-up of 21 patients.

BACKGROUND/AIMS: Pseudomyxoma peritonei is an uncommon disease characterized by the presence of mucinous peritoneal implants associated with an abdominal neoplasm. Our objective is to consider the characteristics of this entity in our western Mediterranean urban population. METHODOLOGY: All cases diagnosed with pseudomyxoma peritonei by our hospital during a period of 16 years were reviewed. Data from their clinical records and the biopsy samples were analyzed. RESULTS: We found 21 cases of pseudomyxoma peritonei with a male/female ratio of 10/11 and a mean age of 59 years. The predominant presentation symptom was abdominal pain (17 cases, 6 of them with acute abdomen). The most frequent primary site of origin of the pseudomyxoma was the appendix (10 cases). The histologic diagnosis was malignant (associated with carcinoma) in 17 cases and indeterminate behavior in 4. The follow-up was available for 15 patients (mean follow-up of 41 months), while six patients have been lost. Nine patients have died during the follow-up and the other 6 patients are still alive after follow-up. CONCLUSIONS: Laparotomy is the main tool for diagnosing pseudomyxoma peritonei. The appendix is the most frequent primary site of origin of pseudomyxoma peritonei, followed by bowel; the latter being more important than previously described. In most cases the histology is malignant. The prognosis is bad with a mortality greater than 60% at 5 years.

Adult↗
PubMedDate not supplied

Severe graft versus host disease following liver transplantation confirmed by PCR-HLA-B sequencing: report of a case and literature review.

A case of severe graft versus host disease in a liver transplant recipient is presented. Due to HLA similarity between donor and recipient, the demonstration of cellular chimerism had to be made by PCR-HLA-B sequencing. In addition, we review the literature on this entity emphasizing its poor outcome, the difficulty of the differential diagnosis, and the need for the development of new prophylactic and therapeutic strategies in its management.

Adult↗
PubMedDate not supplied

[Systemic amyloidosis associated with common variable hypogammaglobulinemia and intestinal lymphoid nodular hyperplasia].

Common variable hypogammaglobulinemia syndrome with lymphoid nodular hyperplasia of the intestine forms part of the so-called hypogammaglobulinemic enteropathies. It is characterized by decreased serum immunoglobulins, recurrent respiratory tract infections and chronic diarrhea. The development of systemic amyloidosis is infrequent, but it can be explained by the multiple infections in this setting. The case of a 47-years old woman with hypogammaglobulinemic enteropathy, who developed systemic amyloidosis is presented. It was manifested as a nephrotic syndrome. The previously published reports include 12 cases of common variable hypogammaglobulinemia with systemic amyloidosis. Half of them presented nephrotic syndrome as a manifestation of their amyloidosis. It is important to keep in mind this complication in these patients' follow-up in order to increase the doses of gammaglobulin. That is the way to compensate their additional losses because of the nephrotic syndrome that they usually develop.

Agammaglobulinemia↗
PubMedDate not supplied

Orthotopic liver transplantation in 4 patients with portal hypertension and non-cirrhotic nodular liver.

BACKGROUND/AIMS: Non-cirrhotic nodular liver may occasionally be associated with portal hypertension, with complications such as ascites, bleeding esophageal varices and sometimes hepatic encephalopathy. Four patients treated with transplantation are hereby described. METHODOLOGY: All 4 patients had orthotopic transplantation. Cyclosporine based immunosuppression was used in all patients. RESULTS: The first patient had nodular regenerative hyperplasia in the resected native liver and in the graft seven years after the transplant, what could be considered as recurrence of the disease. There were two more cases of nodular regenerative hyperplasia; one of them was diagnosed 9 years before transplantation, but he developed progressive liver failure. The fourth patient had chronic renal failure and a nodular liver. His general condition and fear of untreatable ascites after a portosystemic shunt, prompted us to perform a liver-kidney transplantation. CONCLUSIONS: Portal hypertension associated with non-cirrhotic nodular liver disease can be, in general, successfully treated with medical and endoscopic measures, or in certain more serious cases with portosystemic shunting. Nevertheless, there are certain cases where liver insufficiency, associated diseases or the unawareness of the pathological diagnosis determines a liver transplantation.

Adult↗