1/39. pancreatic pseudocyst extending into the liver via the hepatoduodenal ligament: a case report.A case of pancreatic pseudocyst extending into the liver via the hepatoduodenal ligament is reported. This is the first report clearly demonstrating that the hepatoduodenal ligament is another route of hepatic extension of pancreatic pseudocysts as well as the hepatogastric ligament, which is the most common. The importance of the topological anatomy of the peritoneum is emphasized in understanding the extrapancreatic extension of pancreatic pseudocysts.- - - - - - - - - - ranking = 1keywords = ligament (Clic here for more details about this article) |
2/39. The pathology of acute hepatic disintegration in hereditary haemorrhagic telangiectasia.AIMS: Hereditary haemorrhagic telangiectasia is a rare inherited disease in which telangiectases affect skin, mucous membranes and the gastrointestinal tract. Hepatic involvement is common but usually asymptomatic. We report a case of acute hepatic disintegration in hereditary haemorrhagic telangiectasia, document the histopathological findings and present a hypothesis to explain them. methods AND RESULTS: The patient presented at the age of 34 years with abdominal pain, leading to the surgical removal of a severely inflamed gallbladder. Signs of liver damage became increasingly apparent over the next few weeks, with disruption of the intrahepatic biliary tree and marked vascular shunting, necessitating liver transplantation. Six months after the transplant a diagnosis of hepatic hereditary haemorrhagic telangiectasia was made. The principal features of hepatic hereditary haemorrhagic telangiectasia are periportal telangiectases and sinusoidal congestion and dilatation. Acute hepatic disintegration is characterized by disruption of liver structure, hepatocyte necrosis, haemorrhage and extravasation of bile. CONCLUSIONS: Periportal telangiectases in a liver biopsy are highly suggestive of hereditary haemorrhagic telangiectasia. Acute hepatic disintegration is likely to be a consequence of rupture of telangiectases and ischaemic necrosis of intrahepatic bile ducts. patients with hereditary haemorrhagic telangiectasia are at risk of acute hepatic disintegration following intra-abdominal sepsis.- - - - - - - - - - ranking = 0.006712863160861keywords = membrane (Clic here for more details about this article) |
3/39. Unusual manifestations of yersinia enterocolitica infections diagnosed using novel methods.We report the cases of two patients who had infections due to yersinia enterocolitica. The first patient exhibited chronic recurrent fever, hepatic and splenic granulomas, and bone marrow abnormalities, and the second patient presented with enterocolitis with leukocytoclastic vasculitis of the skin. Cultures and agglutination titers were negative. Indirect immunofluorescence techniques with use of serotype-specific antisera and antisera to Yersinia outer-membrane proteins (Yops) were applied to biopsy specimens, and immunoblotting techniques for determining class-specific circulating antibodies to Yops were used for demonstrating these unusual manifestations of Y. enterocolitica infections.- - - - - - - - - - ranking = 0.006712863160861keywords = membrane (Clic here for more details about this article) |
4/39. Cyst of the falciform ligament of the liver: a rare cause of right upper quadrant pain.cysts of the falciform ligament are rare. Only a dozen cases have been reported in the English literature, with the first reported case in 1909. The etiology of these cysts is diverse but can be classified into primary and secondary causes. No specific complex exists and their presentations vary among persons. physical examination may demonstrate a mass in the right upper abdomen. Although rare, they should be considered in the differential diagnosis of right upper quadrant abdominal pain. They are treated through excision.- - - - - - - - - - ranking = 0.71428571428571keywords = ligament (Clic here for more details about this article) |
5/39. Successful treatment of hepatocellular carcinoma with the tyrosine kinase inhibitor imatinib in a patient with liver cirrhosis.Several mechanisms of development of hepatocellular carcinoma (HCC) in patients with liver cirrhosis have been discussed. One hypothesis suggests that the somatic stem cells of the liver, the so-called oval cells, may undergo malignant transformation. Oval cells are derived from the biliary cells of the canal of Hering and are characterized by c-kit-positivity, the transmembrane receptor of stem cell factor. Constitutively activated tyrosine kinases have been identified as major pathogenetic mechanisms in the development of malignant diseases like gastrointestinal stromal tumors (c-kit) and chronic myelogenous leukemia (bcr-abl). The prognosis of these diseases improved enormously since the drug imatinib, a tyrosine kinase inhibitor of c-kit and bcr-abl, was introduced. Here we report the successful cure of a patient with liver cancer by this tyrosine kinase inhibitor.- - - - - - - - - - ranking = 0.006712863160861keywords = membrane (Clic here for more details about this article) |
6/39. critical illness with hyponatraemia and impaired cell membrane integrity--the "sick cell syndrome" revisited.OBJECTIVE: To determine whether impaired cell membrane permeability exists in critically ill patients with "sick cell" type hyponatraemia. DESIGN AND methods: A 36 year old male patient was identified in an intensive care unit (ICU) with liver disease and multi-organ failure. His initial serum sodium (Na) was 101 mmol/L and osmolar gap 35 mmol/L. A flow cytometric system was used to assess lymphocyte membrane integrity using fluorescein diacetate (FDA) and propidium iodide (PI). Following this, similar studies were carried out in 17 hyponatraemic (Na < 130 mmol/L) and 19 normonatraemic (Na > 136 mmol/L) ICU patients. RESULTS: flow cytometry in the index patient showed two clear populations of cells-one was normal (with identical characteristics to a healthy control) and the other had dysfunctional cell membrane integrity. The extended patient series, however, revealed only 2 other patients with similar flow cytometric patterns-one hyponatraemic and one normonatraemic. CONCLUSIONS: Cell membrane studies in the index patient demonstrated supportive evidence for the "sick cell syndrome" in critically ill patients. The extended series revealed that 3/37 (8%) had this abnormality, which was however not consistently associated with hyponatraemia.- - - - - - - - - - ranking = 0.053702905286888keywords = membrane (Clic here for more details about this article) |
7/39. Homozygosity for a gross partial gene deletion of the C-terminal end of ATP7B in a Wilson patient with hepatic and no neurological manifestations.We identified a partial gene deletion of ATP7B in a patient with Wilson disease with hepatic onset. The deletion covered exon 20 including major parts of the flanking introns. The breakpoints were identified and the size of the deletion determined to be 2144 bp. The deletion is predicted to lead to a mutated protein product containing 45 aberrant amino acids after transmembrane domain 7, and lacking the transmembrane domain 8 as well as the entire C-terminal cytoplasmic tail. This is the first time a partial gene deletion has been demonstrated in ATP7B. The patient presented at age 10 with hepatic manifestations, including severe jaundice, hepato-splenomegaly, ascites, and spider naevi. The liver biopsy showed fibrosis and early signs of cirrhosis. There was a Kayser-Fleischer ring but no neurological manifestations. All symptoms disappeared with penicillamine therapy. This suggests that the C-terminal cytoplasmatic tail of ATP7B, is not essential for its neurological function. Large deletions in ATP7B may be an overlooked cause of Wilson disease. patients that are homozygotes for deletions may be valuable for the understanding of the function of various regions of the ATP7B protein.- - - - - - - - - - ranking = 0.013425726321722keywords = membrane (Clic here for more details about this article) |
8/39. Pelvic insufficiency fracture related to autosomal dominant polycystic kidney disease.We report the case of a patient with autosomal dominant polycystic kidney disease (ADPKD) and an insufficiency-type fracture of the pelvis. A 60-year-old Japanese woman was admitted because of pain in the right ischium and pubis that began suddenly with no precipitating cause. Computed tomography showed the bony pelvis to be compressed by enlarged dependent kidneys and an enlarged liver. We relieved compression on the pelvic bones by means of transarterial embolization (TAE) to the kidneys and liver after initiation of hemodialysis therapy. The fracture healed gradually after TAE, and the patient could walk 4 months later. In an iliac bone specimen obtained before TAE, cancellous bone was intact, but periosteal and endosteal surfaces of cortical bone showed marked resorption and were irregular. Normally, many ligaments are connected tightly to the periosteal surface, supporting the cortical bone. However, because of extensive surface resorption associated with pressure from enlarged kidneys, connections between ligaments and the periosteal surface presumably became fragile, promoting an insufficiency fracture from unapparent external forces. Thus, ADPKD is a potential cause of insufficiency fracture owing to abnormalities of cortical bone.- - - - - - - - - - ranking = 0.28571428571429keywords = ligament (Clic here for more details about this article) |
9/39. Reactive lymphoid hyperplasia of the liver in a patient with multiple carcinomas: a case report and brief review.A rare case of reactive lymphoid hyperplasia (RLH) of the liver in a 75-year-old woman admitted to hospital for surgical treatment of gastric, caecal and colon carcinomas is described here. Two nodular lesions in the left and right lobes of the liver were clinically diagnosed as metastatic tumours by computed tomography of the abdomen. A demarcating grey-white mass of size 1.4 cm was observed in a partially resected liver specimen. On examining the lesion microscopically, it was found to be composed of hyperplastic lymphoid follicles, lymphocytes, plasma cells, other inflammatory cells and interlaced hyalinised fibrous tissues. In the portal tracts around the lesion, chronic inflammatory cell infiltrates were seen, but no interface hepatitis or lymphoid follicle was observed. No evidence of monoclonality was observed by immunohistochemistry for B and T cell markers, in situ hybridisation for kappa and lambda light chains, and polymerase chain reaction analysis of immunoglobulin heavy chains or T cell receptor beta and gamma gene rearrangements. Bcl-2 immunoreactivity was not observed in the germinal centre. Epstein-Barr virus (EBV) antigen (latent membrane protein-1) and EBV-encoded small RNAs were not detected. A proliferation neither of myofibroblasts nor of cells positive for follicular dendritic cell markers was observed. RLH, formerly known as pseudolymphoma, has been reported of the liver in only 14 cases and is considered to be a differential diagnosis of small nodular lesions of the liver. That RLH has an inflammatory reactive nature, not a neoplastic disposition, and that EBV does not participate in the pathogenesis of RLH is supported by this case.- - - - - - - - - - ranking = 0.006712863160861keywords = membrane (Clic here for more details about this article) |
10/39. Increased serum alkaline phosphatase activity: a possible indicator of renal damage.Increased levels of serum alkaline phosphatase (ALP) (E.C.3.1.3.1.) were observed in 25 patients with various urological conditions involving the kidneys: malignancy, complicated nephrolithiasis, and surgical and percutaneous manipulations. Other possible sources for increased ALP level, mainly hepatic and osseous, were excluded by history, laboratory tests, and liver and bone imaging. Studies of isoenzymes of ALP did not show a distinctive pattern. ALP levels returned to the normal range by treating the underlying lesions involving the kidney: nephrectomy, complete removal of stones, or removal of nephrostomy. The increase in serum ALP activity may be derived from the injury to the brush border membrane of the renal tubular cells. Renal function impairment and contrast media induced nephrotoxicity may also be responsible for the increased serum ALP. serum ALP may be a marker for involvement of the kidneys in pathological processes and an indicator of complete treatment. This clinical observation is worthy of further study.- - - - - - - - - - ranking = 0.006712863160861keywords = membrane (Clic here for more details about this article) |
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