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)

In order to determine the effects of repetitive compression-decompression cycles on hematologic and hemostatic factors in humans, 14 subjects were exposed to 150 ft sea water gauge (fswg) for 30 min with standard U.S. Navy decompression on each of 12 consecutive days. Red blood cell number, volume, and size distribution; hemoglobin concentration; hematocrit; white blood cell number and differential counts; platelet number and volume; prothrombin and partial thromboplastin times; and fibrinogen and fibrin/fibrinogen degradation products were measured in venous blood samples collected before the first and after alternate dives. Subjects in the study had no symptoms other than pruritus and occasional fatigue following the exposures. More than 60% had venous gas emboli detectable by precordial doppler monitoring which generally persisted for 3-5 h after surfacing. Results show a small decrease in red cell mass, with an increase in size distribution and no change in mean corpuscular volume. No change in total white cell number was noted, but the basophilic granulocytes and atypical lymphocytes were elevated at the end of the series. A biphasic change was noted in monocyte number, and immature neutrophilic granulocytes were reduced. No change in platelet number or volume, or in the prothrombin/partial thromboplastine time, was apparent. Although fibrinogen concentration significantly decreased during the exposures, fibrin/fibrinogen degradation products remained undetectable. All changes remained in a clinically acceptable range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematologic and hemostatic changes with repetitive air diving. 646 54

There have been a few reports of infants with severe neonatal cholestasis related to a defect in primary bile acid synthesis. To assess the importance of such deficiency among children with progressive intrahepatic cholestasis (Byler disease), screening for inborn errors in bile acid synthesis was performed by fast atom bombardment ionization-mass spectrometry of urine samples from 30 affected children. Bile acid analysis revealed a specific fast atom bombardment ionization-mass spectrometry profile for 3 beta-hydroxy-C27 steroid dehydrogenase/isomerase deficiency in five children who had jaundice, hepatosplenomegaly, and fatty stools beginning at ages ranging from 4 to 46 months. None of them had pruritus. Liver function tests showed persistently normal serum gamma-glutamyltransferase activity, low serum cholesterol and vitamin E levels, normal serum bile acid concentrations despite raised serum bilirubin levels, and decreased prothrombin time and clotting factor V. In four of the cases a similar disease was observed in siblings. Liver function returned to normal after oral ursodeoxycholic acid therapy. We conclude that 3 beta-hydroxy-C27-steroid dehydrogenase/isomerase deficiency should be considered when idiopathic cholestatic liver disease with clinical features akin to Byler disease is characterized by the association of normal serum gamma-glutamyltransferase activity, normal serum bile acid concentration, absence of pruritus, and a return to normal liver function during ursodeoxycholic acid therapy. Early identification of these children is essential because they benefit from bile acid therapy and might thus avoid the need for liver transplantation.
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PMID:A new cause of progressive intrahepatic cholestasis: 3 beta-hydroxy-C27-steroid dehydrogenase/isomerase deficiency. 791 5

The aim of this study was to define factors predictive of the onset of the terminal phase, defined by hyperbilirubinemia or the occurrence of a severe clinical complication, in patients with primary biliary cirrhosis treated with ursodeoxycholic acid. The 97 primary biliary cirrhosis patients in this study participated in a 2-yr clinical trial. Four of the 49 patients treated with ursodeoxycholic acid (13 to 15 mg/kg/day) entered the terminal phase of the disease, compared with 9 of the 48 patients assigned to placebo. In addition to clinical, conventional biological and histological parameters, we analyzed three serum markers of connective tissue components--type III procollagen aminoterminal peptide, hyaluronic acid and laminin. In the ursodeoxycholic acid-treated group, hyaluronic acid, type III procollagen aminoterminal peptide, bilirubin and splenomegaly were the factors most closely associated with entry into the terminal phase of the disease. In multivariate analysis, after adjustment for age, the hyaluronic acid level was the only predictive factor. In the placebo-treated group, the bilirubin level, total bile acid level, Mayo score, type III procollagen aminoterminal peptide, hyaluronic acid, splenomegaly and pruritus were associated with aggravation of disease. In multivariate analysis, high bilirubin level, high type III procollagen aminoterminal peptide or hyaluronic acid levels and low prothrombin time independently implied poor prognosis. In conclusion, when patients with primary biliary cirrhosis are treated with ursodeoxycholic acid, bilirubinemia loses, in part, its predictive value. It is replaced by hyaluronic acid and type III procollagen aminoterminal peptide. This suggests that models used in deciding on the need for liver transplantation require adaptation for patients receiving ursodeoxycholic acid.
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PMID:Predictive factors in ursodeoxycholic acid-treated patients with primary biliary cirrhosis: role of serum markers of connective tissue. 811 88

We report the case of a 28-year-old-prostitute from Thailand with HIV infection stage B2 associated with retroperitoneal lymph node tuberculosis. 6 days after the beginning of anti-tuberculous therapy (isoniazid, rifampicin, pyrazinamid and ethambutol) the temperature rose to 40.5 degrees C, diarrhea, vomiting, and tachycardia developed and systolic blood pressure fell to 80 mm Hg. Liver function tests revealed acute hepatic failure (ALT 800 IU/l rising to 1500; serum bilirubin 89 mumol/l rising to 238.0; alkaline phosphatase 199 IU/l; glucose 1.8 mmol/l; prothrombin time 20%). Isoniazid, rifampicin, and pyrazinamid were replaced by streptomycin and PAS. A few days after withdrawal the liver profile returned to normal. Hours after the reintroduction of rifampicin total body erythema, pruritus, vomiting and severe hypotension developed, requiring saline methylprednisolone and epinephrine administration. The next reexposure to intravenous rifampicin produced a rash and was rapidly discontinued. Liver function tests remained normal. Later mild adverse reactions to streptomycin and pyrazinamid occurred, two drugs which had been well tolerated before. Subsequently the diagnosis of adrenal insufficiency was established. After initiation of steroid replacement (50 mg prednisolone) the antituberculous therapy with isoniazid, pyrazinamid and ethambutol was well tolerated. We conclude that the shock in this HIV-infected patient was either due to severe anaphylaxis to rifampicin or acute adrenal insufficiency ensuing on this drug. The reversible fulminant acute hepatic failure represents either an adverse effect of antituberculous drugs, especially hepatotoxic interactions of drug combinations, or an ischemic liver injury during hypotension caused by anaphylaxis. The case illustrates the complex nature of side effects of antituberculous drugs in HIV patients and their aggravation by adrenal insufficiency.
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PMID:[Fulminant, rapidly reversible hepatitis and life-threatening anaphylaxis following rifampicin in an HIV-positive female patient with latent adrenal cortex insufficiency]. 864 39

One hundred and twenty scabietic patients attending the outpatient clinic of the Department of Dermatology, Mansoura University Hospital, voluntarily participated in this uncontrolled, open label study to evaluate ivermectin 20 microg/kg as a scabietic after they had given their consent. The scabietic subjects included in this study were otherwise healthy, mentally competent, aged more than 18 years, and used no topical antiscabietic treatment in the week before ivermectin treatment, or during the 4-week study period. Patients were also required to show clinical evidence of scabies, and the microscopically demonstrated presence of Sarcoptes scabiei, their eggs, or their fecal pellets (scybala). A thorough history was taken, and a physical examination was conducted that included measurement of the pulse, blood pressure, temperature, and weight. For each participant, the distribution of scabies lesions was plotted on a body diagram, and the severity of disease was recorded as mild (10 or fewer lesions), moderate (11-49 lesions), or severe (50 or more lesions). Skin scrapings were examined for mites, eggs, or scybala. Urinalysis, stool analysis, a complete blood count, prothrombin time, and serum chemistry studies (serum creatinine, alanine aminotransferase (ALT), and total bilirubin) were performed before treatment, and 2 and 4 weeks after the drug was given. Ivermectin was administered as scored 6-mg tablets with water, and the dose was designed to provide 200 micrograms/kg (ivermectin was provided by Delta Pharma, Tenth of Ramadan City, Egypt). The patients were instructed to have recently worn clothing, sheets, and towels washed in a hot cycle the day after treatment. The patients were interviewed 3 days after treatment about any symptoms or subjective evidence of adverse reactions. Follow-up examinations were carried out 2 and 4 weeks after intake of ivermectin, and all examination procedures and laboratory investigations were repeated. Cure criteria included absence of nocturnal itching as well as dermatologic evidence of scabies, and negative skin scraping. Patients showing evidence of active scabies or having new lesions during the follow-up visits were given a second dose of ivermectin. All members of the household and immediate family were treated with either topical 5% permethrin cream or 1% gamma benzene hexachloride to reduce the chance of reinfestation.
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PMID:Oral ivermectin in the treatment of scabies. 1063 75

A 41-year-old man developed severe hepatic dysfunction following a 3.5-week course of terbinafine (250 mg/day). He suffered marked pruritus, jaundice, malaise, anorexia and loin pain. Serum bilirubin rose to a peak value of 718 micromol/l with alkaline phosphatase at 569 U/l, alanine aminotransferase at 90 U/l, aspartate aminotransferase at 63 U/l and a prolonged prothrombin time of 21 s, unresponsive to vitamin K. Transjugular liver biopsy showed canalicular cholestasis consistent with a drug reaction. Symptoms resolved 11 months after drug cessation, with liver function tests returning to normal values after 15 months. This case represents the most severe cholestatic reaction reported to date, resulting in patient recovery without liver transplantation. A comprehensive literature review is provided.
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PMID:Terbinafine-induced hepatic dysfunction. 1156 66

Possible hepatic effects of oral contraceptives (OCs) include tumors, intrahepatic cholestasis, and less well known vascular lesions such as Budd-Chiari syndrome and peliosis, a disseminated pseudocystic dilatation of the sinusoid capillaries of the liver. A 29-year-old woman with a history of 4 pregnancies, hypertension and diabetes both requiring daily medication, and use since April 1983 of an oral contraceptive (OC) containing .15 mg levonorgestrel and .03 mg of ethinyl estradiol complained in March 1984 of epigastric pain and increased abdominal volume. Ascitis was diagnosed and the patient was hospitalized. She had experienced a generalized pruritus for several months and had lost weight. The bilirubin, alcaline phosphatase, and Gamma GT levels were slightly elevated. Sonography showed a hypertrophied liver. Incipient esophageal varices were seen with gastric fibroscopy. The small subhepatic venous branches had a cloudy aspect. The peliosis hepatis was diagnosed by a transjugular puncture biopsy of the liver. With discontinuation of the OCs, the ascites did not reappear after puncture and the perturbations of the liver functioning normalized. On follow-up in April 1985, slight hepatomagaly persisted but the patient reported no further symptoms. She continued her medication for hypertension and diabetes. Peliosis hepatis was 1st described in 1964 and several cases related to OC use have been reported since 1972. Peliosis has the aspect of multiple small congestive cavities of 1-3 mm in diameter in the parenchyma. The lesions consist of areas of hepatocellular necrosis secondarily filled with blood. The cysts may be voluminous and subcortical, creating a risk of hemoperitoneum. The lesions may also be associated with a benign or malignant liver tumor. Regression of the lesions is possible with termination of the etiologic agent. Clinically, hepatomegaly, painful or not, sometimes associated with splenomegaly, is often found with peliosis. Moderate jaundice is very frequent. Ascites or edema of the legs are observed. Hyperbilirubinemia and augmentation of phosphatases and Gamma GT are the main laboratory findings. Transaminases may be slightly elevated, and the rate of prothrombin may be diminished. The condition is sometimes diagnosed with laparoscopy, celiomesenteric arteriography, or phlebography, but hepatic puncture biopsy usually establishes the diagnosis. The contition may improve if the etiologic agent is removed or it may worsen because of liver failure or a complication such as hemoperitoneum or an associated tumor.
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PMID:[Peliosis hepatis and oral contraceptives: a case report]. 1228 Oct 5

Coagulopathy is a life-threatening complication of liver cirrhosis. We describe the effect of molecular adsorbent recirculating system (MARS), a cell-free dialysis technique, on the blood coagulation of cirrhotic patients. From February 2002 to July 2002, nine patients--five males (55.5%) and four females (44.4%), age 47-70 yr (median 56)--underwent 12 courses (4-7 sessions each) of MARS. Patients were treated for the following indications: six (66.6%) acute-on-chronic hepatic failure, three (33.3%) intractable pruritus. Platelet count, prothrombin time (PT), international standardized ratio and thromboelastography were measured before and after each MARS session. Coagulation factors II, V, VII, VIII, IX, X, XI, XII, XIII, von Willebrand, lupus anticoagulant, protein C, protein S, antithrombin III, plasminogen, alpha 2 antiplasmin, D-dimer, fibrin monomers, complement, and C(1) inactivator were measured before and at the end of each MARS treatment. We found a statistically significant difference (p < 0.05) in the platelet count, PT, all the thromboelastograph variables (reaction and constant time, alpha angle, and maximal amplitude), factor VIII, von Willebrand, and D-dimer, when measured before and after MARS. Previous reports have shown amelioration of blood coagulation following MARS treatments. However, we document that MARS induces coagulopathy through a platelet-mediated mechanism, whereby platelet may be mechanically destroyed during the passage of blood through the filters and lines. An alternative postulated mechanism is an immune-mediated platelet disruption - coagulopathy.
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PMID:Thromboelastography used to assess coagulation during treatment with molecular adsorbent recirculating system. 1523 11

The molecular adsorbent recirculating system (MARS) method removes from the blood catabolites either free in the plasma water such as uremic toxins and ammonia, taking advantage of dialysis or free albumin bound ones, like hepatic toxins, transferring them from the albumin in the blood to the albumin circulating in a closed loop where toxins are removed by adsorbtion on resins (charcoal and ion exchange resin). The efficacy of the method in removing the hepatic toxins either in the acute or in the acute on chronic liver failure is demonstrated in numerous studies. Based on these findings, 10 patients affected by acute on chronic liver failure were treated. The results demonstrated that the method, powerfully removing ammonia, bilirubin and bile acids (taken as method efficacy markers), reduced the blood concentrations of these molecules remarkably; allowing the elimination of the refractory pruritus (due to the lowering of plasma bile acid levels), an almost constant symptom in chronic liver diseases, especially with cholestasis, and improves other parameters (cholinesterase, alkaline phosphatase and prothrombin activity). These results agree with those reported in the literature concerning the efficacy of MARS in the replacement of the liver detoxifying function.
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PMID:[Molecular Adsorbent Recirculating System in liver function replacement therapy]. 1578 94

We report a case of acute hepatotoxicity in a 42-year-old woman after administration of clindamycin for a dental infection. After 6 d of treatment, she had fatigue, nausea, vomiting, anorexia, pruritus and jaundice. Her laboratory analysis showed alanine aminotransferase (ALT), 1795 IU/L (normal range 0-40); aspartate aminotransferase (AST), 1337 IU/L (normal range 5-34); alkaline phosphatase (ALP), 339 IU/L (normal range 40-150); gamma-glutamyl transpeptidase (GGT), 148 IU/L (normal range 9-64 IU/L); total bilirubin, 4.1 mg/dL; direct bilirubin, 2.9 mg/dL and prothrombin time (PT), 13.5 s, with international normalized ratio (INR), 1.04. She was hospitalized, with immediate drug discontinuation. Her liver biopsy specimen showed mixed-type (both hepatocellular and cholestatic) hepatic injury, compatible with a diagnosis of drug-induced hepatitis. An objective causality assessment using the Naranjo probability scale suggested that clindamycin was the probable cause of the acute hepatitis. In susceptible individuals, clindamycin use may lead to acute mixed-type liver toxicity. Complete recovery may be possible if the drug is discontinued before severe liver injury is established.
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PMID:Clindamycin-induced acute cholestatic hepatitis. 1787 18


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