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Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Secretion of bile salts into the duodenum was studied in eight normal subjects, in 10 patients with
cirrhosis
, and in two cholecystectomized subjects. Duodenal juice was aspirated continuously through a double-lumen tube during an unstimulated period, after an intravenous injection of pancreozymin/cholecystokinin, and during a continuous intravenous infusion of secretin given at a rate of 3 units per kilogram body weight per hour. Precautions were taken to try to ensure quantitative recovery during the studies, and recovery of an infused nonabsorbable marker was greater than 80% in all subjects. Secretin induced a flow of a greater volume of juice in the cirrhotic patients than in the normal group (49 to 57 ml per 10 minutes compared with 28 to 49 ml per 10 minutes). This change may have resulted from a higher effective dose of secretin if it is assumed that the cirrhotic liver fails to catabolize secretin. The bile acid response to pancreozymin/cholecystokinin followed by secretin in the cirrhotic subjects resembled that seen in patients after cholecystectomy in whom pancreozymin/cholecystokinin induces only a slight increase in bile salt output but in whom the output of bile salts during rest and secretin stimulation is markedly greater than normal. This response in
cirrhosis
is probably best interpreted as due to impaired function of the gallbladder. The total amount of bile salt liberated over the two hours of the test in the cirrhotic patients was similar to normal The concentration of bile salt after pancreozymin/cholecystokinin was less than in normal subjects, but similar to that in cholecystectomized patients. It is unlikely therefore that deficient output or concentration of bile salt can be held responsible for steatorrhea in
cirrhosis
. THERE WAS A MARKED DECREASE IN
THE
DEOXYCHOLATE CONJUGATES AND A REDUCTION IN
THE
GLYCINE: taurine ratio in the bile of cirrhotic patients. The former change may reflect a change in bacterial flora and the latter a defect in hepatic conjugating mechanisms.
...
PMID:Bile salt secretion in cirrhosis of the liver. 544 81
A family is described in which there occurred two cases of the lupoid type of active chronic hepatitis with
cirrhosis
, one of chronic persistent hepatitis, and one of myasthenia gravis. The two cases of lupoid hepatitis were in the proposita, a schoolgirl aged 16 years, and her great-aunt aged 69 years whom she had never met. The case of myasthenia gravis was that of the father. The whole family, except the great-aunt, had been exposed to an epidemic of infectious hepatitis five years previously, and the girl and her brother had contracted this disease. The schoolgirl later developed active chronic hepatitis while her brother had chronic persistent hepatitis without immunological concomitants. APART FROM COINCIDENCE, SOME COMBINATION OF THREE PROCESSES WAS REQUIRED TO ACCOUNT FOR
THE
ILLNESSES IN THIS FAMILY: a genetic predisposition to chronic liver disease in particular, a genetic predisposition to autoimmune reactions in general, and a ;triggering' effect of infection with the hepatitis virus.
...
PMID:An interplay of genetic and environmental factors in familial hepatitis and myasthenia gravis. 548 30
The use of helical CT, infusing pump and non-ionic contrast media has enabled the evaluation of different hepatic circulatory phases during contrast injection. Starting the acquisition of scans 20 to 30 seconds after the injection at a rate of 3 to 4 ml/sec the arterial enhancing of the liver is depicted. THROMBOSIS OR COMPRESSION OF
THE
PORTAL VEIN: Hypervascular triangle-shaped was with peripheral base can be seen, secondary to the increased arterial flow to compensate for the diminished portal flow. ARTERIOPORTAL SHUNTS: This condition can be caused by tumors such hepatocellular adenocarcinomas and hemangiomas, trauma, interventional procedures,
cirrhosis
, AVMs and surgery. INFLAMMATORY LESIONS: Hypervascular areas can be seen during the arterial phase in abscesses or cholecystitis, returning to their normal condition in the arterial phase. ANATOMIC VARIANTS: Third veins coming from the periphery (capsular veins, accessory cystic vein and an aberrant gastric vein) supply enhanced blood earlier than the portal circulation. OTHER CAUSES: In
liver cirrhosis
diffuse hyperattenuated areas can be seen during the arterial circulation. In right-sided heart failure, pericardial disease and Budd-Chiari Syndrome, "mosaic areas" can also be noted. In other patients these perfusion disorders were considered unknown. TUMORS: The well-differentiated hepatocellular carcinoma is a lesion with a predominant arterial blood supply, thus appearing in general hyperdense in this phase. Hemangiomas may appear as highly hyperdense lesions in the arterial phase and can be misinterpreted as HCC if smaller than 2 cm. (30% of cases). Focal nodular hyperplasia is a benign lesion (vascular malformation associated with focal nodules of hepatocellular hyperplasia) with increased arterial blood supply. Hepatic adenomas show an important hypervascularity during the arterial phase and, if large, they may present a small central scar and or capsule. Low or high-grade dysplastic nodules can sometimes be seen as hypervascular areas during the arterial phase. Although most metastasis are depicted as hypodense lesions sometimes they can show arterial hypervascularity such as carcinoid and pancreatic islet cell metastasis.
...
PMID:[Liver hyperdensity during arterial phase on CT exams]. 1147 23
AVP receptors represent a logical target for drug development. As a new class of therapeutic agents, orally active AVP analogs could be used to treat several human pathophysiological conditions including neurogenic diabetes insipidus, the syndrome of inappropriate secretion of AVP (SIADH), congestive heart failure, arterial hypertension,
liver cirrhosis
, nephrotic syndrome, dysmenorrhea, and ocular hypertension. By immunoprecipitation and immunoblotting, we elucidated the phosphorylation pattern of green fluorescent protein-tagged AVP receptors and showed interactions with the specific kinases PKC and GRK5 that are agonist-, time- and receptor subtype-dependent. The tyrosine residue of the NPWIY motif present in the 7th helix of AVP receptors is rapidly and transiently phosphorylated after agonist stimulation. This phosphorylation is instrumental in the genesis of the mitogenic cascade linked to the activation of this receptor, presumably by establishing key intramolecular contacts and by participating in the creation of a scaffold of proteins that produce the activation of downstream kinases. The random screening of chemical entities and optimization of lead compounds recently resulted in the development of orally active non-peptide AVP receptor agonists and antagonists. Furthermore, the identification of the molecular determinants of receptor-ligand interactions should facilitate the development of more potent and very selective orally active compounds via the approach of structure-based drug design. We developed three-dimensional molecular docking models of peptide and non-peptide ligands to the human V1 vascular, V2 renal and V3 pituitary AVP receptors. Docking of the peptide hormone AVP to the receptor ligand binding pockets reflects its dual polar and non-polar structure, but is receptor subtype-specific. The characteristics of non-peptide AVP analogs docking to the receptors are clearly distinct from those of peptide analogs docking. Molecular modeling of the results of site-directed mutagenesis experiments performed in CHO cells stably transfected with the human AVP receptor subtypes revealed that non-peptide antagonists establish key contacts with a few amino acid residues of the receptor subtypes that are different from those involved in agonist binding. Moreover, these interactions are species-specific. These findings provide further understanding of the signal transduction pathways of AVP receptors and new leads for elucidation of drug-receptor interactions and optimization of drug design. NOTE TO
THE
READER: The recent cloning and molecular characterization of AVP/OT receptor subtypes call for the revision of their nomenclature. For the sake of clarity and reference to their main site of expression, we call the V1a receptor the V1 vascular receptor, the V2 receptor the V2 renal receptor and the V1b or V3 receptor the V3 pituitary receptor in the present review.
...
PMID:Molecular pharmacology and modeling of vasopressin receptors. 1243 35
A POTENTIALLY SEVERE EVENT: Upper gastrointestinal haemorrhage in a cirrhotic patient is always extremely serious, particularly in the case of rupture of the oesophageal varices, which is the most frequent cause.
THE
TWO POLES OF TREATMENT: Early vasoactive treatment permits elastic ligature in optimal conditions using an endoscope. The prevention of other complications of
cirrhosis
is an essential element in the management of these patients.
...
PMID:[The place of endoscopic treatment in portal hypertension]. 1261 Apr 67
MANAGING
THE
RESPONSIBLE AGENT: Hepatic fibrosis with its end-point,
cirrhosis
, are the principle complications responsible for morbidity and mortality in chronic liver diseases. It is therefore important to address the question of whether these lesions can disappear, once installed in the liver. Regression can only occur when the agent responsible for the fibrosis (virus, alcohol, poison, iron, autoantibodies, etc) is eradicated or controlled.
THE
FORMS OF REGRESSION: Once the agent controlled, regression of fibrosis can either be spontaneous, a rare situation, although some bona fide cases of fibrosis or even
cirrhosis
reversion have been reported in the literature, or assisted by specific therapy. It is therefore necessary to take into consideration the development of new treatments based on enhanced knowledge of the mechanisms of fibrosis.
THE
ACTIVITY AND EFFICACY OF TREATMENTS: These treatments target one of the three following mechanisms: the blockade of hepatic stellate cell activation, enzymatic digestion of fibrous tissue and stimulation of liver cell regeneration. Although these treatments have shown efficacy on experimental models of fibrosis, to date, there are no published results formally confirming the efficacy and safety of these treatments in man.
...
PMID:[Regression of hepatic fibrosis physiopathological aspects and clinical reality]. 1275 52
CURRENTLY,
THE
PORPHYRIAS ARE CLASSIFIED IN FOUR MAIN GROUPS: congenital porphyria, acute intermittent porphyria, porphyria cutanea tarda hereditaria, and porphyria cutanea tarda symptomatica. The acquired form of porphyria (porphyria cutanea tarda symptomatica) occurs in older males and is nearly always associated with chronic alcoholism and
hepatic cirrhosis
. The main clinical changes are dermatological, with excessive skin fragility and photosensitivity resulting in erosions and bullae. Biochemically, high levels of uroporphyrin are found in the urine and stools. Treatment to date has been symptomatic and usually unsuccessful.A case of porphyria cutanea tarda symptomatica is presented showing dramatic improvement of both the skin lesions and porphyrin levels in urine and blood following repeated phlebotomy.Possible mechanisms of action of phlebotomy on porphyria cutanea tarda symptomatica are discussed.
...
PMID:ACQUIRED PORPHYRIA CUTANEA TARDA: REPORT OF A CASE SUCCESSFULLY TREATED BY PHLEBOTOMY. 1434 52
Needle biopsy of the liver provides concrete diagnostic information that cannot be as readily obtained in any other way. This report reviews 401 liver biopsies in 312 patients.
THE
MAJOR INDICATIONS FOR USE OF THIS PROCEDURE ARE: To determine the cause of an obscure liver enlargement; to establish the cause of jaundice; to distinguish between malignant disease and
cirrhosis of the liver
; to determine when hepatitis has subsided; and to evaluate the results of treatment. At times, systemic disease that has not been recognized by other means may be diagnosed by this technique. There is risk in performing this test, and the 0.25 per cent mortality in this series compares favorably with that reported from other clinics. Where the diagnosis by biopsy could be compared with observations at operation or autopsy, the correct diagnosis was made by biopsy in 85 per cent of cases. Greater accuracy was obtained by two or more biopsic examinations in one case then by single biopsy. In several cases in which surgical operation was considered, biopsic information made it unnecessary, and vice versa.
...
PMID:Needle biopsy of the liver; general considerations. 1488 54
FROM
THE
ABOVE STUDIES
THE
FOLLOWING CONCLUSIONS HAVE BEEN REACHED: 1. That copper or its compounds used does not cause the deposition of pigment in the livers of rabbits, guinea pigs or rats. Neither does it produce a
cirrhosis
in these animals. 2. That spontaneous deposition of pigment occurs frequently in the livers of normal rabbits on the usual laboratory diet. 3. That the feeding of a diet of carrots exclusively will produce pigment deposition in the livers of rabbits, in every way identical with that ascribed to copper. 4. That the pigment deposited in the livers of rabbits is probably of exogenous origin.
...
PMID:A CHEMICAL AND PATHOLOGIC STUDY OF THE EFFECTS OF COPPER ON THE LIVER. 1986 36
IDIOPATHIC PORTAL HYPERTENSION (IPH) COMPRISES DISORDERS DEVELOPING INCREASED PORTAL PRESSURE IN
THE
ABSENCE OF
CIRRHOSIS
: the clear mechanisms to explain this disease are still not well recognized. IPH usually suggests a benign prognosis, but sometimes is complicated with severe hemorrhage due to ruptured esophageal varices, or massive splenomegaly. Conventional treatments for those complications for patients with
cirrhosis
usually works when diverted to patients with IPH, although some of those patients might require liver transplantation if the treatment fails. However, there are few consistent treatment strategies for IPH itself, its complications or the indications for liver transplantation. In this mini review, we summarize the clinical manifestations and several potential theories to explain the etiology, as well as the current treatment options for IPH.
...
PMID:The current clinical aspects of idiopathic portal hypertension. 2534 10
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