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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.
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PMID:On the inappropriate in hypertension research. 7 8

Seven patients with compensated liver cirrhosis and esophageal varices, all with a base line wedge hepatic vein pressure greater than 20 cm H2O, received 1-mg doses of vasopressin hormonogen (tGLVP) intravenously. There was a significant mean decrease in wedge pressure of 32%, which lasted for at least 20 min (the duration of measurement), with no change in cardiac output measured. The only cardiac response was a 10 to 20% bradycardia at the height of the moderate pressor response-otherwise the ECG was without change. In 5 patients who received the same tGLVP dose during surgery, direct measurements of portal venous pressure showed the same degree of decrease within 10 min of intravenous injection. Fifteen patients with liver cirrhosis and severe bleeding from esophageal varices were treated conservatively with blood transfusion and tGLVP as the only major drug aside from antibiotics. A nonrandomized control group of 13 patients with the same age distribution, stage of disease, number of previous bleeds, etc., was treated conservatively in the same manner, except that they received either no hemodynamically active drugs or short acting neurohypophysial peptide preparations such as Pitressin. In the control group there was a 61.5% total mortality, a 53.8% mortality directly related to uncontrollable bleeding, and a mean duration of the bleeding episode of 11 days. In the tGLVP-treated group total mortality was 20%, mortality directly related to uncontrollable bleeding was 13.3%, and mean duration of the bleeding episode was 2.9 days. These results appear to justify a large scale clinical trial of the vasopressin hormonogen in this disease.
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PMID:Action of the triglycyl hormonogen of vasopressin (glypressin) in patients with liver cirrhosis and bleeding esophageal varices. 30 62

Lower gastrointestinal bleeding from intestinal varices cannot readily be detected at operation; hence, preoperative identification is important. Our experience with six patients having sudden, massive bleeding per rectum from intestinal varices suggests a group of common findings. These patients had cirrhosis, no blood in the stomach or duodenum, characteristic mucosal imprints on barium enema, or direct visualization of varices on sigmoidscopy or colonoscopy. Only two had demonstrable esophageal varices. The diagnosis was confirmed and the site of the varices localized on the venous phase of selective mesenteric angiography in five patients. Varices were located in the duodenojejunum in two, in the cecum and ascending colon in two, and in the rectum and sigmoid colon in two patients. Three patients were treated nonoperatively with transfusion and intraarterial infusion of vasopressin into the superior mesenteric artery; one died. One patient with cecal varices had a right hemicolectomy that controlled the bleeding, but progressive hepatic failure resulted in postoperative death. The remaining two patients had successful decompression of left colonic varices by portasystemic shunt.
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PMID:Massive lower gastrointestinal bleeding from intestinal varices. 31 92

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.
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PMID:[The physiopathology of ascites]. 46 62

In eight patients with cirrhosis of the liver and portal hypertension an intravenous infusion of lysine vasopressin induced a rapid increase in the plasma level of the fibrinolytic proenzyme plasminogen activator. In contrast, triglycyl lysine vasopressin (glypressin; GVP), in a dose known to lower portal venous pressure, produced no fibrinolytic response. This lack of fibrinolytic response represents an advantage of GVP over lysine vasopressin in addition to its longer in vivo half-life and lower cardiotoxicity. Clinical trials of GVP in the treatment of bleeding oesophageal varices are needed.
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PMID:Effects of lysine vasopressin and glypressin on the fibrinolytic system in cirrhosis. 48 51

Two human neurophysins, nicotine stimulated neurophysin (NSN), and estrogen stimulated neurophysin (ESN) were assayed during physiologic maneuvers and pathologic states in man. NSN is thought to be associated with vasopressin and was elevated in some subjects by volume depletion, surgical stress, hypotension and hypertonic saline infusion. Overnight dehydration did not elevate NSN in spite of urinary concentration. NSN was elevated in some subjects with the syndrome of inappropriate secretion of antidiuretic hormone and when tested was unresponsive to administered water, alcohol or nicotine. ESN was elevated during estrogen administration, in pregnancy, in newborns and in patients with cirrhosis. NSN was also acutely increased at parturition. These data support the association of NSN with vasopressin although changes in NSN were found only with potent stimuli for vasopressin release. ESN may be associated with oxytocin but demonstration of this awaits knowledge of oxytocin physiology in humans.
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PMID:Physiologic control of two neurophysins in humans. 55 58

Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). This contrasts with the conspicuous tendency of patients with Laennec's cirrhosis to retain salt and water. In an attempt to clarify this clinical observation, renal handling of sodium was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone in five patients with PBC. These PBC patients were compared with two control populations: five edema-free patients with Laennec's cirrhosis and nine healthy volunteers. The natriuretic and diuretic response to ECVE was significantly greater in the patients with PBC as compared with the two control groups. CH2O for given rates of urine flow were similar in PBC patients as compared with normal subjects. The data suggest that a supranormal rejection of sodium at the proximal tubule in response to ECVE underlies the exaggerated natriuresis of PBC. The augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this variety of cirrhosis.
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PMID:Exaggerated natriuretic response to volume expansion in patients with primary biliary cirrhosis. 60 57

Administration of vasopressin (0.4 units/minute) via the superior mesenteric artery (SMA) resulted in a mean 25% reduction in corrected hepatic venous wedge pressure (CHWP) in 9 stable non-bleeding patients with cirrhosis and portal hypertension. There was wide variation of response in individual patients with two of nine showing no decrease in CHWP to vasopressin. Selective intra-arterial infusion did not protect against the systemic effects of vasopressin and resulted in significant elevations in blood pressure (21%) and systemic vascular resistance (39%). A slight decrease in cardiac output (11%) was also observed. In 6 of these patients, vasopressin (0.4 units/minute) was also given intravenously. The resultant decreases in CHWP were similar to those observed with SMA administration.
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PMID:Hemodynamic effects of superior mesenteric arterial and intravenous vasopressin infusions in patients with portal hypertension. 86 24

1) Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). In an attempt to clarify this clinical observation, renal handling of sodium, water and divalent ions was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone (ADH) secretion in 5 patients with PBC and 9 normal subjects. 2) Mean fractional excretion of sodium, water, phosphate and calculated fractional distal delivery of sodium were significantly greater in patients with PBC as compared with normal controls. Fractional CH20 for given fractional urine flow was similar in patients with PBC and normals. 3) The data suggest that patients with PBC have a greater diminution of proximal tubular reabsorption of sodium in response to ECVE than controls. This augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this type of cirrhosis.
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PMID:Renal handling of sodium, water and divalent ions in patients with primary biliary cirrhosis. 89 21

The renal regulation of sodium is intertwined with the extracellular fluid volume (ECFV). Most adjustments in sodium elimination in man are accomplished via alterations in tubular reabsorption. The latter is sensitive to change in ECFV. An expanded ECFV results in less reabsorption and more excretion of sodium, and a contracted ECFV has the converse effect. There are direct and indirect mechanisms whereby ECFV influences sodium reabsorption. Patients with nephrotic syndrome, heart failure, and cirrhosis "behave" physiologically as normal individuals with a contracted ECFV. Water balance is normally determined by intake and losses in sweat which is always hypoosmotic to plasma, by evaporation from skin and lungs, and through renal excretion. The major factors that determine the ability to concentrate the urine are (1) the establishment of a concentrated environment around the collecting ducts, and (2) the elaboration and effects on the kidney of antidiuretic hormone. The evaluation of a patient with abnormalities of sodium and water rests initially and largely on clinical information. The clinical setting provides clues to anticipating, preventing, and interpreting distortions of body sodium and water. The laboratory can detect an abnormality, confirm or refute clinical assessment, and assist in the quantitative aspects of treatment and its efficacy.
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PMID:Sodium and water: an overview. 96 14


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