Noninvasive assessment of liver fibrosis. Serum markers and transient elastography (FibroScan).

Both the prognosis and potential treatment of chronic liver disease greatly depend on the progression of liver fibrosis, which is the ultimate outcome of chronic liver damage. Historically, liver biopsy has been instrumental in adequately assessing patients with chronic liver disease. Histological assessment allows clinicians both to obtain diagnostic information and initiate adequate therapy. However, the technique is not exempt of deleterious effects. Multiple diagnostic tests have been developed for the staging of fibrosis using noninvasive methods, most of them in the setting of chronic hepatitis C. The goal of this paper is to review available data on the staging and assessment of liver fibrosis with two methods: serum markers and transient elastography (FibroScan).

Noninvasive assessment of liver fibrosis. Serum markers and transient elastography (FibroScan)

Both the prognosis and potential treatment of chronic liver diseasegreatly depend on the progression of liver fibrosis, which isthe ultimate outcome of chronic liver damage. Historically, liverbiopsy has been instrumental in adequately assessing patients withchronic liver disease. Histological assessment allows cliniciansboth to obtain diagnostic information and initiate adequate therapy.However, the technique is not exempt of deleterious effects.Multiple diagnostic tests have been developed for the staging of fibrosisusing noninvasive methods, most of them in the setting ofchronic hepatitis C. The goal of this paper is to review availabledata on the staging and assessment of liver fibrosis with two methods:serum markers and transient elastography (FibroScan®)(AU)

The pathogenesis of primary biliary cirrhosis.

Primary biliary cirrhosis (PBC) would develop when the immune system comes across a microorganism with proteins similar to those in the piruvate dehydrogenase complex E2 (PDC-E2), or a neoantigen resulting from a xenobiotic-modified autoantigen. This would lead to an innate immune response where TLRs would play a pivotal mediating role, which would give rise to a local microenvironment favoring an adaptive immune response. Such response would be particularly strong in individuals with selected genetic characteristics. The genetic characteristics underlying this predisposition remain unknown, but they likely entail small numbers of scarcely-active regulatory T cells. The AE2 anion exchanger, which is deficient in patients with PBC, may reduce the number and activity of regulatory T cells. NK cells are also pivotal in the preparation of an adaptive response, as they release a number of cytokines and chemokines that favor and recruit antigen-presenting cells to activate B and T cells - CD4+ Th1 and CD8+. An activation of the former would increase the production of IgM and anti-mitochondrial IgG and IgA antibodies against PDC-E2. An activation of CD8+ cells, also sensitive to PDC-2 as aberrantly expressed on the surface of BECs and SECs, would result in apoptosis for these epithelial cells, and in small bile-duct destruction. Immune response is likely inadequately suppressed because of the small numbers of scarcely-active regulatory T cells, the latter resulting from low genetic expression and activity of the AE2 transporter.

Chronic intestinal pseudo-obstruction: a diagnosis to be considered.

Chronic intestinal pseudoobstruction (CIPO) is a rare entity characterized by recurrent clinical episodes of intestinal obstruction in which no mechanical cause is identified. There are multiple causes for this syndrome but two main groups can be distinguished: a) secondary to a systemic non-gastrointestinal disease; and b) primary or idiopathic originated from alterations in the components of the intestinal wall. The latter forms are the most uncommon and their diagnosis is generally difficult. In the present article, we describe nine patients with CIPO that were diagnosed in our center over the last six years. Four of them were diagnosed with primary or idiopathic form of CIPO and another four were clearly secondary to a systemic disease. The ninth case, which was initially diagnosed as secondary, is probably also a primary form of the disease. The number of patients diagnosed in our center, even thought small, makes us to hypothesize that the prevalence of CIPO is probably greater than is generally believed and that the reasons of its rarity are the incomplete understanding of its physiopathology and the difficulties to achieve a correct diagnosis.

The pathogenesis of primary biliary cirrhosis

Primary biliary cirrhosis (PBC) would develop when the immunesystem comes across a microorganism with proteins similarto those in the piruvate dehydrogenase complex E2 (PDC-E2), ora neoantigen resulting from a xenobiotic-modified autoantigen.This would lead to an innate immune response where TLRswould play a pivotal mediating role, which would give rise to a localmicroenvironment favoring an adaptive immune response.Such response would be particularly strong in individuals with selectedgenetic characteristics. The genetic characteristics underlyingthis predisposition remain unknown, but they likely entailsmall numbers of scarcely-active regulatory T cells. The AE2 anionexchanger, which is deficient in patients with PBC, may reducethe number and activity of regulatory T cells. NK cells arealso pivotal in the preparation of an adaptive response, as they releasea number of cytokines and chemokines that favor and recruitantigen-presenting cells to activate B and T cells – CD4+ Th1 andCD8+. An activation of the former would increase the productionof IgM and anti-mitochondrial IgG and IgA antibodies againstPDC-E2. An activation of CD8+ cells, also sensitive to PDC-2 asaberrantly expressed on the surface of BECs and SECs, would resultin apoptosis for these epithelial cells, and in small bile-duct destruction.Immune response is likely inadequately suppressed becauseof the small numbers of scarcely-active regulatory T cells,the latter resulting from low genetic expression and activity of theAE2 transporter(AU)

Chronic intestinal pseudo-obstruction: a diagnosis to be considered

Chronic intestinal pseudoobstruction (CIPO) is a rare entitycharacterized by recurrent clinical episodes of intestinal obstructionin which no mechanical cause is identified. There are multiplecauses for this syndrome but two main groups can be distinguished:a) secondary to a systemic non-gastrointestinal disease;and b) primary or idiopathic originated from alterations in thecomponents of the intestinal wall. The latter forms are the mostuncommon and their diagnosis is generally difficult. In the presentarticle, we describe nine patients with CIPO that were diagnosedin our center over the last six years. Four of them were diagnosedwith primary or idiopathic form of CIPO and another four wereclearly secondary to a systemic disease. The ninth case, whichwas initially diagnosed as secondary, is probably also a primaryform of the disease. The number of patients diagnosed in our center,even thought small, makes us to hypothesize that the prevalenceof CIPO is probably greater than is generally believed andthat the reasons of its rarity are the incomplete understanding ofits physiopathology and the difficulties to achieve a correct diagnosis(AU)

Predicción de fibrosis hepática con pruebas no invasivas. Una apuesta de futuro / No disponible

No disponible

Anisakiasis múltiple / No disponible

No disponible

[Tolerability, safety, and efficacy of sodium phosphate preparation for colonoscopy: the role of age]. / Tolerancia, seguridad y eficacia de la preparación para colonoscopia con fosfato de sodio: el papel de la edad.

OBJECTIVES: To compare subjective tolerance and secondary adverse events to bowel cleansing prior to colonoscopy with polyethylene glycol (PEG) and sodium phosphate (NaP) in adult patients and in those 65 or more years old. MATERIAL AND METHODS: Retrospective matched study, choosing 140 patients among all of those who underwent colonoscopy from March 2004 to May 2005. We investigated the presence of the next adverse events during bowel preparation: Fever, low digestive bleeding, abdominal pain, perianal pain, nausea, vomiting, thirst, somnolence, agitation, tremor and convulsions. We considered bad objective tolerance if the patient presented any one of these events. We also asked patients about subjective tolerance to preparation. RESULTS: Seventy patients prepared with PEG and seventy with NaP were included (69 women and 71 men, mean age 60.6 +/- 14.8 years). There was no relationship between subjective tolerance or the presence of adverse events and bowel cleansing with any of the products in general population or in elderly patients (p = 0.09 and p = 0.45 in the elderly). However, patients prepared with NaP showed more nausea than those who employed PEG (p < 0.009), overall women of 65 or more years old. There were no severe adverse events in patients prepared with NaP. Elderly showed better tolerance than younger patients, and women worst tolerance than men, irrespective of the lavage preparation employed. Patients prepared with PEG unfinished bowel cleansing more frequently than those with NaP. Cleanliness achieved with NaP was significantly better than that obtained with PEG. CONCLUSIONS: Bowel cleansing prior to colonoscopy with NaP is as well tolerated, safe and effective as with PEG, even in elderly healthy patients, although it causes more nausea. Cleanliness with NaP is better than that achieved with PEG.

[Portal and mesenteric thrombosis associated with protein S deficiency]. / Trombosis portal y mesentérica asociada al déficit de la proteína S.

INTRODUCTION: liver cirrhosis is the main cause of portal thrombosis (PT), while hypercoagulability syndromes are rarely found as the etiology of PT. We report a case of portal and mesenteric thrombosis secondary to protein S deficiency. CASE REPORT: a 74-year-old woman was admitted with melena secondary to upper gastrointestinal bleeding. She reported mild, diffuse abdominal pain in the last 2 weeks. Endoscopy revealed ruptured esophageal varices. Doppler ultrasonography and CT demonstrated a heterogeneous liver, splenomegaly and ascites, and complete non-occlusive PT involving the hilum and portal branches, as well as the superior mesenteric vein, with portosystemic collaterals. At this point a complete study for cirrhosis etiologies was negative, including a liver biopsy that showed nonspecific architectural changes secondary to diminished blood flow, which suggested non-cirrhotic portal hypertension. The search for hypercoagulability states determined a deficiency of S protein, with total pS = 107% and free pS = 56%. The patient was started on anticoagulant treatment and no other thrombotic events occurred. DISCUSSION: PT usually manifests without specific symptoms. The most common presentation is upper gastrointestinal bleeding, as occurred in our patient. Liver cirrhosis is one of the most frequent cause of PT. Up to 65% of these patients present an associated prothrombotic state, including protein S deficiency. Our case reminds us of the importance of a systematic search for hipercoagulability syndromes in patients with TP, even when the etiology can be conferred to liver cirrhosis.

A pilot trial of fenofibrate for the treatment of non-alcoholic fatty liver disease.

BACKGROUND: Dyslipidaemia and insulin resistance are two important risk factors for non-alcoholic fatty liver disease. Both factors can improve with fenofibrate. AIMS: To evaluate the effect of fenofibrate on the clinical, analytical and histological evolution of patients with non-alcoholic fatty liver disease. SUBJECTS AND METHODS: Sixteen consecutive patients with biopsy-confirmed non-alcoholic fatty liver disease were treated with 200mg/day of fenofibrate for 48 weeks. A clinical and biochemical follow-up was done every 3 months. A new liver biopsy was performed in all patients at the end of therapy. RESULTS: All patients completed 48 weeks of therapy with fenofibrate, without adverse events. At the end of the study, a significant decrease in triglyceride, glucose, alkaline phosphatase and gamma-glutamyl transpeptidase and an increase of apolipoprotein A1 levels were found. Insulin levels and insulin resistance showed a trend to decrease. Moreover, a reduction in the proportion of patients with abnormal aminotransferase levels (>45IU/L) was observed (alanine aminotransferase: 93.7% vs. 62.5%, p=0.02; aspartate aminotransferase: 50% vs. 18.7%, p=0.02). The body mass index did not show any significant change, but the proportion of patients with metabolic syndrome decreased significantly (43.7% vs. 18.7%, p=0.04). A control biopsy after treatment revealed a decrease in the grade of hepatocellular ballooning degeneration (p=0.03), but the grade of steatosis, lobular inflammation, fibrosis or non-alcoholic fatty liver disease activity score did not change significantly. CONCLUSIONS: In patients with non-alcoholic fatty liver disease, treatment with fenofibrate is safe and improves metabolic syndrome, glucose and liver tests. However, its effects on liver histology are minimal.