Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the period of two weeks a 19-year-old man developed gradually increasing painless jaundice with dark urine and light-coloured soft stools (6-7 times daily), as well as loss of appetite, nausea and nagging itch. Biochemical tests indicated marked cholestasis (alkaline phosphatase 800 U/l, gamma-GT 206 U/l). Abdominal ultrasound examination revealed high-grade stenosis of the distal choledochal duct caused by an enlargement of the head of the pancreas and computed tomography confirmed a tumour in this location. Endoscopic retrograde cholangiopancreatography demonstrated filiform stenosis of the major pancreatic duct and prepapillary stenosis of the choledochal duct. Several needle biopsies failed to establish a definitive diagnosis. A Whipple operation was performed: the stomach was preserved but about 40% of pancreatic tissue resected. Histologically there was chronic suppurative pancreatitis of the head of the pancreas. The patient was symptom-free 6 months after the operation. The case illustrates that it is not always possible in a painless pancreatic tumour to distinguish between pancreatitis and malignant tumour.
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PMID:[Chronic purulent, draining, indolent pancreatic head pancreatitis with extrahepatic cholestasis]. 193 34

Nine women with symptomatic precirrhotic primary biliary cirrhosis have been treated with oral pulse methotrexate, 15 mg/wk, for 12-34 months. Three women had pruritus, two fatigue, and four pruritus and fatigue. Itching disappeared and fatigue lessened or disappeared in all within 4-11 months after starting methotrexate. All who itched were able to discontinue cholestyramine (five) or antihistamines (two). Biochemical tests of liver function improved in all patients and then worsened in three when methotrexate was discontinued or the dose lowered. Mean serum alkaline phosphatase decreased from 471 to 171 U/L (P less than 0.01), serum bilirubin from 0.99 to 0.59 mg/dL (P less than 0.05), and serum alanine aminotransferase from 132 to 61 U/L (P = 0.02), and serum cholesterol fell from 265 to 213 mg/dL (NS). The decrease in serum cholesterol was significant, P = 0.05, if data were used just from the six women whose baseline serum cholesterol levels were elevated. Serum albumin remained normal in all. The serum bilirubin levels became normal in three of four patients with elevated levels. The serum alkaline phosphatase levels became normal in four patients and the alanine aminotransferase levels in three. Liver histology improved in five patients and was stable in the remaining four based on a quantitative evaluation of coded liver biopsy specimens. The improvement in histology was primarily due to decreased portal inflammation and bile duct injury. The titer of antimitochondrial antibody decreased in seven patients. The data suggest that methotrexate may be effective treatment for precirrhotic primary biliary cirrhosis. Controlled trials are needed to evaluate long-term efficacy and toxicity.
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PMID:Treatment of primary biliary cirrhosis with low-dose weekly methotrexate. 193 16

We investigated the effects of once-daily oral administration of 10 mg/kg ursodeoxycholic acid (generic name, ursodiol) on elevated serum enzyme activities, bilirubin, cholesterol, bile acids and symptoms in patients with primary sclerosing cholangitis. A 30-mo, open-label, pilot trial was designed to cover four periods: (a) 3 mo of pretreatment observation (period 1), (b) 6 mo on ursodiol (period 2), (c) 3 mo withdrawal of treatment (period 3) and (d) 18 mo of extended retreatment (period 4). Diagnosis was confirmed by cholangiography and liver biopsy specimens. We enrolled 12 patients with persistently elevated pretreatment alkaline phosphatase and gamma-glutamyltransferase levels (at least twice the upper limit of normal), and observed them for a median of 37 mo. Significant reductions in serum total cholesterol levels and in serum enzyme activities indicating cholestasis and hepatocellular injury occurred during ursodiol treatment in both treatment periods 2 and 4 and relapsed with treatment interruption in period 3. Elevated serum bilirubin and symptoms of disabling fatigue, pruritus and diarrhea were improved by ursodiol. Improvements have continued after 2 yr of treatment in 10 patients (1 patient had a transplantation after he relapsed on withdrawal of ursodiol therapy; another died of postoperative complications of colon resection for carcinoma). No other cases of clinical deterioration were observed in the retreatment period. The longer term reductions of alkaline phosphatase, transaminases, bilirubin and cholesterol after 2 yr of treatment were even greater than the initial reductions after 6 mo of treatment. These results justify initiation of larger, controlled clinical trials, with serial morphological evaluations of the liver and biliary tree.
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PMID:Ursodeoxycholic acid for the treatment of primary sclerosing cholangitis: a 30-month pilot study. 193 90

Ursodeoxycholic acid (UDCA) was administered to 10 patients diagnosed as having primary biliary cirrhosis (PBC) after liver biopsy. Eight patients were anicteric, and two were icteric cases. One patient was in stage I, seven were in stage II, one in stage I-III, and one in stage III-IV of Scheuer's classification. Six hundred milligrams of UDCA were administered orally after meals three times daily to all of the patients for more than 1 yr. The period of UDCA administration ranged from 6 to 41 months. The major findings are as follows: 1) in six out of seven patients with pruritus, itching disappeared 1 month after administration of UDCA; 2) both serum alkaline phosphatase and gamma-glutamyltranspeptidase levels began decreasing significantly the first month after the onset of UDCA treatment, and continued decreasing throughout the treatment; 3) GOT and GPT levels also decreased significantly during the administration of UDCA, compared with before-treatment levels; 4) in one icteric patient with portal hypertension, although serum biliary enzyme levels improved after treatment, serum bilirubin level got worse, and the patient died of esophageal variceal hemorrhage. In another icteric case, biliary and bilirubin levels improved slightly after treatment; 5) antimitochondrial antibody titer decreased in four cases, but IgM levels and other immunological parameters were not changed; 6) serum UDCA increased significantly during UDCA treatment; in particular, glyco-UDCA occupied up to 40% of the total bile acid and CDC decreased to 25%; 7) portal inflammation activity decreased in all five patients who had undergone follow-up liver biopsy, more than 1 yr after UDCA administration--bridging fibrosis decreased in three cases; and 8) no side effects were observed in any of the cases. Although large-scale, randomized, controlled, double-blind tests are necessary, it is speculated that the long-term administration of UDCA is a safe and effective treatment for the improvement of biliary enzyme levels and pruritus in anicteric PBC.
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PMID:Improvement of biliary enzyme levels and itching as a result of long-term administration of ursodeoxycholic acid in primary biliary cirrhosis. 196 12

The effects of ursodeoxycholic acid (UDCA, 750-1250 mg/day) were evaluated prospectively in 15 patients with primary sclerosing cholangitis (PSC). Five patients had associated inflammatory bowel disease. After 6 months of treatment, the proportion of patients suffering from fatigue or pruritus decreased from 60% to 20% and from 33% to 20%, respectively. No exacerbation of associated disorders was observed. Serum alkaline phosphatase levels (normal less than 100 IU/l) decreased from 401 +/- 53 to 222 +/- 42 (mean +/- S.E.; p less than 0.001), those of gamma-glutamyl transpeptidase, (normal less than 40 IU/l) from 520 +/- 89 to 185 +/- 32 (p less than 0.001) and those of alanine aminotransferases, (normal less than 30 IU/l) from 79 +/- 12 to 42 +/- 6 (p less than 0.02). In three patients, the discontinuation of UDCA was associated with an aggravation of the liver test results. In conclusion, this study shows that 6 months of treatment with UDCA leads to clinical and biochemical improvements in patients with PSC. These results suggest that UDCA could be an effective treatment for PSC, and may justify a controlled therapeutic trial.
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PMID:Ursodeoxycholic acid for primary sclerosing cholangitis. 197 18

Based on uncontrolled observations, we have proposed ursodeoxycholic acid (UDCA) as a novel therapeutic approach in primary biliary cirrhosis (PBC). To confirm and extend our original findings, we have designed a double-blind multicentre randomized clinical trial. An interim analysis was planned at 6 months, involving all subjects included in the trial, with a final analysis at 2 years. The UDCA-PBC trial began in June 1987 and will be completed in March 1990. Seventy patients were randomized to receive UDCA and 68 a placebo. The two groups were well matched with respect to age, sex, duration and prevalence of symptoms and histologic severity (50% of the UDCA group had stage III-IV disease vs. 37% of the placebo group). During the first 6 months of follow-up, six patients withdrew from the trial. At 6 months, the proportion of patients with jaundice was significantly lower (p less than 0.01) in UDCA recipients than in the placebo group. There was a similar decrease in the proportion of patients with pruritus and fatigue in both groups. The following laboratory test values were significantly lower in UDCA recipients than in the placebo group after 6 months of therapy: serum bilirubin, alkaline phosphatase, alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), gamma-glutamyltranspeptidase activities (p less than 0.001), cholesterol (p less than 0.003) and IgM levels (p less than 0.03). The results of this interim analysis confirm and extend the biochemical data provided by our previous pilot study. However the final analysis of the trial is necessary for a definitive assessment of the safety and efficacy of UDCA therapy in PBC.
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PMID:Ursodeoxycholic acid for the treatment of primary biliary cirrhosis. Interim analysis of a double-blind multicentre randomized trial. The UDCA-PBC Study Group. 197 19

A multi-center double-blind controlled trial of ursodeoxycholic acid (UDCA) for treatment of primary biliary cirrhosis (PBC) was carried out. Twenty two and 23 patients were treated with 600 mg/day UDCA and placebo, respectively, for 24 weeks. In UDCA-treated patients, fall of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyltranspeptidase activities started within 4 weeks after start of the trial and continued throughout the trial period. The serum IgM level fell in 7 UDCA-treated patients examined but not in 10 placebo-treated patients examined. Serum bilirubin concentration showed no significant change at the end of the study in either of UDCA- and placebo-treated group of patients. There was no significant difference between these two groups with respect to the frequency of improvement of pruritus. In UDCA-treated patients, serum bile acid composition changed markedly, though its concentration showed no significant change. The percentage of total bile acid which ursodeoxycholic acid took up increased, whereas those which cholic acid, chenodeoxycholic acid and deoxycholic acid took up were decreased.
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PMID:A multi-center double-blind controlled trial of ursodeoxycholic acid for primary biliary cirrhosis. 198 Jun 54

We describe the clinical features, liver histology, and ultrastructure in reversible diclofenac-induced hepatitis and review previous reports of this entity. Although rarely reported, diclofenac hepatitis may be severe, and even fatal. Symptoms, which develop from 1 week to 11 months after starting the drug, include jaundice, pruritus, fever, abdominal pain, nausea, vomiting, and rash. Bilirubin and alkaline phosphatase are mildly elevated, transaminases often markedly so. The nature of the idiosyncratic injury appears variable, some cases having features of a hypersensitivity reaction, most being more suggestive of a toxic metabolic effect. Light microscopy shows a nonspecific hepatitis with portal and lobular activity, and focal hepatocellular injury that may progress to zonal or massive necrosis. The ultrastructural features in our case are typical of drug or toxin injury. This may be of value in distinguishing this entity from other forms of hepatitis, which is important in view of the frequent reversibility of this potentially lethal form of injury.
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PMID:Reversible hepatitis associated with diclofenac. 203 30

In this randomised study subtotal parathyroidectomy (PTX) is being compared with total parathyroidectomy including autotransplantation (PTX + AT) in 40 patients with secondary hyperparathyroidism. Both groups were followed up twice, first 19 +/- 6 months (PTX + AT) respectively 19 +/- 7 months (subtotal PTX) and secondly 43 +/- 9 respectively 40 +/- 7 months after surgery. In each group there were 17 patients alive at the time of the second postoperative follow-up. In the meantime 2 patients with subtotal PTX required reoperation because of recurrences originating from the remaining parathyroid tissue, another 2 patients of this group were hypercalcaemic. After PTX + AT serum-calcium normalized significantly more often (p less than 0.03), a corresponding result was seen in alkaline phosphatase. Reoperation was not required in this group. Also radiological alterations reformed significantly more often after PTX + AT, so did clinical signs like pruritus (p less than 0.005) and muscular weakness (p less than 0.04). Considering these results and the fact that in case of recidive a reoperation of the autograft in the forearm is much easier to perform than a reoperation in the neck, PTX + AT is recommended as method of choice in surgical treatment of sHPT.
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PMID:[Subtotal parathyroidectomy versus total parathyroidectomy with autotransplantation in secondary hyperparathyroidism. A randomized study]. 203 94

We examined the predictive value of urea kinetics for patient outcomes in CAPD by measuring dialysis index (DI; a means of quantifying CAPD dose using urea kinetics), KT/V and normalized protein catabolic rate (PCRN) on 222 occasions in 76 new patients at the time of starting CAPD and at subsequent six month intervals. We investigated how these indices altered with time and in relation to each other, and how they correlated with a wide range of subsequent patient outcomes. DI, KT/V and PCRN all tended to decrease with time on CAPD (P less than 0.0004, less than 0.0001 and 0.0005, respectively). DI and KT/V were highly correlated with each other (r = 0.89, P less than 0.0001) and both correlated with PCRN (r = 0.57, P less than 0.0001 and r = 0.60, P less than 0.0001, respectively). DI and KT/V both correlated inversely with subsequent values for serum creatinine (P less than 0.0001), urea (P less than 0.0002), potassium (P less than 0.02) and phosphate (P less than 0.002), and directly with bicarbonate (P less than 0.0001). PCRN correlated inversely with serum creatinine (P less than 0.0002) and directly with urea (P less than 0.0001) and with the number of blood transfusions received (P less than 0.03). None of these indices correlated with levels of hemoglobin, PTH, alkaline phosphatase or albumin, or with nerve conduction velocity or any other subsequent clinical outcomes including death, technique failure, hospital days, peritonitis rate and subjective indices of fatigue, pruritus and insomnia. We conclude that the urea kinetic model is predictive of some biochemical outcomes but not of clinical outcomes in CAPD patients.
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PMID:Lack of correlation between urea kinetic indices and clinical outcomes in CAPD patients. 205 26


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