Ictericia obstructiva secundaria a migración de fragmentos de hepatocarcinoma a la vía biliar / Obstructive jaundice secondary to hepatocellular carcinoma fragments migrated to common bile duct

Obstructive j aundice is a rare presentation of hepatocellular carcinoma (HC), and when it occurs, usually is due to progressive damage from cirrhosis, or extensive tumor infiltration. Tumor growth through the bile duct is being described with increasing frequency as a cause of obstructive j aundice. Rarely, it may be hepatocarcinoma fragments that migrate to the bile duct, obstructing it. We present a case of obstructive jaundice due to migration of fragments of hepatocellular carcinoma to the bile duct in a patient treated 7 years before, for an HC with a curative resection.

La ictericia obstructiva es una presentación poco común en un hepatocarcinoma (HC). Cuando en estos casos existe ictericia, habitualmente se debe a daño progresivo por cirrosis, o a infiltración tumoral extensa. El crecimiento o vaciamiento tumoral hacia la vía biliar se ha descrito ocasionalmente como causa de ictericia obstructiva. En raras ocasiones, puede tratarse de fragmentos de hepatocarcinoma que migran hacia la vía biliar, obstruyéndola. Presentamos un caso de ictericia obstructiva por migración de fragmentos de hepatocarcinoma a la vía biliar, en un paciente tratado 7 años antes por un HC, con resección curativa.

Relación de la genotipificación de Helicobacter pylori con la forma e intensidad de la gastritis en población adulta portadora de patología gástrica benigna / Association between helicobacter pylori genotype and the severity of gastritis in infected adults

Background: The damaging capacity of Helicobacter pylori is variable and depends, in part, on its genetic polymorphism. Aim: To study H pylori genes vacA, cagA and iceA and the relationship of these genotypes with the features of acute damage in chronic gastritis. Material and methods: Gastric endoscopic biopsies were obtained in 75 adults for pathological study and genetic typification of H pylori by specific PCR. Results: In only 64 cases, complete information was available. In 53 of these, there was H pylori infection demonstrated by PCR. Twenty one percent had infection by two or more H pylori strains, vacA gene had genotypes s2/m2, s1/m1 and s1/m2 in 36, 25 and 8% of cases respectively, cagA gene was present in 49% of infected patients. iceA gene had genotypes iceA 1 ad iceA 2 in 15 and 60% of patients respectively. The presence of cagA or alleles s1/m1 and s1/m2 of vacA gene was directly correlated with polymorphonuclear infiltration and the severity of epithelial damage. The genotype s2/m2 of vacA gene was significantly associated with a milder or absent mucosal damage. No association was found between iceA alleles and the pathological features of gastritis. Conclusions: Alleles of vacA and cagA genes of H pilory are associated with the severity of gastric mucosal damage.

Alteraciones genéticas en gastritis crónica: Estudio de inestabilidad microsatelital y pérdida de la heterocigocidad / Genetic changes in chronic gastritis: study of microsatellite instability and loss of heterozygosity

Background: Multifocal chronic gastritis, associated to intestinal metaplasia, is considered a preneoplastic lesion, closely associated to intestinal type gastric cancer. Aim: To study the frequency of microsatellite instability (MSI) and loss of heterozygosity (LOH) in areas of chronic gastritis and intestinal metaplasia in gastric biopsies of patients without cancer. Material and methods: Gastric biopsy samples from 34 patients without cancer (22 with multifocal atrophic gastritis and 12 with diffuse antral gastritis), were studied. Glands from areas of chonic gastritis and intestinal metaplasia and lymphocytes, were collected using laser microdissection of paraffin embedded samples. The analysis of 15 mono and dinucleotide microsatellites was used to assess LOH and MSI. Results: LOH and MSI were found in some of the markers in 55% (12/22) and 59% (13/22) of cases with intestinal metaplasia, respectively. Only one of 12 areas with diffuse atrophic gastritis had MSI and a different area had LOH (p <0.05 or less, when compared with areas of multifocal atrophic gastritis). Three areas of normal epithelium in patients with multifocal atrophic gastritis, also had alterations. Most of these alterations were concordant with adjacent areas with intestinal metaplasia. Conclusions: LOH and MSI was found in areas of intestinal metaplasia in more than half of the studied cases and in few areas of atrophic gastritis without intestinal metaplasia. These findings suggest that genotypic alterations may precede phenotypic modifications and that intestinal metaplasia is a preneoplastic lesion (Rev Méd Chile 2003; 131: 1365-74).