Hipertensión portal no cirrótica por didanosina: Un caso infrecuente / Non-cirrhotic portal hypertension due to didanosina: A rare case

El compromiso hepático es usualmente visto en pacientes con infección por el virus de inmunodeficiencia humana (VIH), sobretodo en pacientes coinfectados con el virus de la hepatitis B o C, con el abuso de alcohol, etc. Sin embargo, existe un grupo de pacientes que desarrolla compromiso hepático e hipertensión portal de causa no específica. La hipertensión portal no cirrótica (HPNC) es un desorden hepático descrito recientemente, potencialmente grave, que ha sido reportado en pacientes infectados por el VIH con terapia antirretroviral de gran actividad (TARGA), específicamente didanosina (DDI). La fisiopatología involucra al agente infeccioso (VIH) y a su tratamiento (TARGA), pues ambas generan una venulopatía prehepática portal. Además, la infección por el VIH genera un estado protrombótico por deficiencia de proteína S conllevando a la obliteración de pequeñas vénulas hepáticas. Se ha postulado a la didanosina como un cofactor en la patogénesis del HPNC. Todo ello conlleva a que en muchas de las biopsias hepáticas se evidencie una hiperplasia nodular regenerativa. Se reporta el caso de una paciente con infección del VIH y en tratamiento con DDI de larga data que debuta con hemorragia digestiva alta (HDA) y ascitis como consecuencia de la HPNC, cuyo diagnóstico fue corroborado por biopsia. No existe reporte de casos del tema en nuestro país

Liver involvement is usually seen in patients infected with the human immunodeficiency virus (HIV), especially in patients coinfected with hepatitis B or C, in alcohol abuse, etc. However, there is a group of patients who develop liver involvement and portal hypertension of unspecified cause. Non-cirrhotic portal hypertension (NCPH) is a liver disorder recently described, but potentially serious. It has been reported in HIV-infected patients with highly active antiretroviral therapy (HAART), specifically didanosine (DDI). The pathophysiology involves the infectious agent (HIV) and its treatment (HAART), since both generate a pre-hepatic portal venulopathy. Similarly, HIV infection produces a prothrombotic state by protein S deficiency leading to the obliteration of small hepatic venules. It has been postulated that DDI as a cofactor in the pathogenesis of NCPH. All this leads that many of the liver biopsies show nodular regenerative hyperplasia. We present the case of a HIV-infected patient who was treated with a longstanding DDI. She developed upper gastrointestinal bleeding (UGB) and ascites due to NCPH, whose diagnosis was confirmed by biopsy. However, there is no similar study in our country

A Case of Portal Hypertension after the Treatment of Oxaliplatin Based Adjuvant-Chemotherapy for Rectal Cancer / 대한소화기학회지

We report herein a case of 35-years-old woman in whom portal hypertension (esophageal varix and splenomegaly) developed after 12 cycles of oxaliplatin based adjuvant chemotherapy for rectal cancer. She was transferred for the evaluation of etiology of new-onset portal hypertension. The esophageal varix and splenomegaly were absent before the oxaliplatin based adjuvant chemotherapy. Thorough history taking and serological exam revealed no evidence of chronic liver disease. Liver biopsy was done and there was no cirrhotic nodule formation. Instead, perivenular fibrosis was noted. Considering new development of esophageal varices and splenomegaly after 12 cycles of oxaliplatin-based adjuvant chemotherapy, we could conclude that portal hypertension in this patient were due to sinusoidal injury by oxaliplatin. Finally, we recommend regular follow-up with endoscopy and radiologic examination for checking the development of varices and for screening of varices and splenomegaly in patients with colo-rectal cancer who receive oxaliplatin-based chemotherapy.

A Case of Portal Hypertension after the Treatment of Oxaliplatin Based Adjuvant-Chemotherapy for Rectal Cancer / 대한소화기학회지

We report herein a case of 35-years-old woman in whom portal hypertension (esophageal varix and splenomegaly) developed after 12 cycles of oxaliplatin based adjuvant chemotherapy for rectal cancer. She was transferred for the evaluation of etiology of new-onset portal hypertension. The esophageal varix and splenomegaly were absent before the oxaliplatin based adjuvant chemotherapy. Thorough history taking and serological exam revealed no evidence of chronic liver disease. Liver biopsy was done and there was no cirrhotic nodule formation. Instead, perivenular fibrosis was noted. Considering new development of esophageal varices and splenomegaly after 12 cycles of oxaliplatin-based adjuvant chemotherapy, we could conclude that portal hypertension in this patient were due to sinusoidal injury by oxaliplatin. Finally, we recommend regular follow-up with endoscopy and radiologic examination for checking the development of varices and for screening of varices and splenomegaly in patients with colo-rectal cancer who receive oxaliplatin-based chemotherapy.

Effects on growth after hypertension portal induced in young rats

RACIONAL: Atraso no crescimento foi observado em crianças com hipertensão portal independentemente da presença de esquistossomose. Sugeriu-se que o desvio de sangue pelas colaterais portossistêmicas justificaria os achados clínicos encontrados. OBJETIVO: Estudar os efeitos da hipertensão portal no crescimento de ratos jovens. MÉTODOS: O crescimento de 20 ratos divididos nos grupos hipertensão portal n = 10, 103 ± 3,7 g e grupo-controle, n = 10, 102,6 ± 3,4 g) foi avaliado durante 5 semanas. Foram considerados a qualidade da dieta oferecida, a ingestão da dieta, o ritmo de crescimento ganho de peso, a excreção de creatinina urinária, o hematócrito e as provas de função hepática. Ao final do experimento, a pressão portal foi medida por via transesplênica. RESULTADOS/CONCLUSAO: Ratos do grupo hipertensão portal apresentaram atraso de crescimento na 1ª semana após a cirurgia, recuperando o seu ritmo de crescimento nas semanas seguintes. Ao final das 5 semanas, não houve diferenças entre os animais. Não houve diferenças com relação às provas bioquímicas e hematológicas, nem com relação ao ganho de massa magra. Esses resultados são evidência contra a hipótese de que hipertensão portal induzida nas fases iniciais da vida desses animais possa provocar atraso de seu crescimento.

Hepatic manifestations in chronic arsenic toxicity.

OBJECTIVE: The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognized. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. We report the nature and degree of liver involvement on the basis of hospital-based and cohort follow-up studies in patients who consumed arsenic-contaminated drinking water for 1 to 15 years. METHODS: 248 patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examinations including liver function tests and HBsAg status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. A cohort follow up of 23 patients who took arsenic-free water for 2-12 years was also carried out. RESULTS: Hepatomegaly was present in 190 of 248 patients (76.6%). Noncirrhotic portal fibrosis (91.3%) was the predominant lesion in liver histology. The maximum arsenic content in liver was 6 mg/Kg (mean 1.46 [0.42], control value 0.16 [0.04]; p < 0.001); it was undetected in 6 of 29 samples studied. Cohort follow-up studies showed elevation of globulin in four cases and development of esophageal varices in one case. CONCLUSION: We report the largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic-contaminated water. Noncirrhotic portal fibrosis is the predominant lesion in this population.

Hipertensäo portal em cäes por injeçäo de sílica na veia porta: estudos manométricos e histológicos / Portal Hypertension in dogs after injection of silica in the portal vein: manometric and histologic studies

Injeçöes de sílica sob diferentes formas e por vias diversas tem sido utilizadas para a produçäo experimental de hipertensäo portal. Neste trabalho foi utilizada a sílica na forma de talco comercial e procurou-se padronizar uma dose capaz de produzir hipertensäo portal em cäes com níveis compatíveis com a sobrevida dos animais. Procurou-se ainda produzir hipertensäo portal crônica por injeçöes repetidas de sílica na veia porta. A dose de sílica, 50 mg/Kg de peso corpóreo resultou em aumento de cerca de duas vezes a pressäo normal e morte espontânea de 20% dos animais: a dose de 100 mg/Kg levou todos os animais a óbito em menos de 24 horas. Injeçöes repetidas de sílica com acompanhamento por 4 meses levaram a hipertensäo portal sem repercusäo para a circulaçöa colateral e o modelo näo foi considerado válido, para os fins desejados. Além desse resultado hemodinâmico näo satisfatório houve também problema técnico porque depois de várias laparotomias houve intensa fibrose periportal dificultando o isolamento da veia