Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ketoconazole has only recently been recognized as a cause of hepatic injury, with most reports coming from outside the United States. In order to characterize more fully the U.S. experience, we undertook an analysis of 54 reports of alleged ketoconazole-induced liver injury submitted to the Food and Drug Administration from the time of initial marketing in 1980. Thirty-three reports were considered likely instances of ketoconazole-induced hepatitis. The majority of these cases occurred in women more than 40 yr of age. Jaundice was recorded in 27 individuals after therapy of 11-168 days with an average daily dose of 200 mg. Anorexia, malaise, nausea, and vomiting accompanied liver injury in one-third of cases. No instances of rash or eosinophilia were recorded. Serum transaminase and alkaline phosphatase values were consistent with acute hepatocellular injury in 18 patients, with primarily cholestatic injury in 5 patients, and with a mixed pattern in 9 individuals. Only one death seemed attributable to ketoconazole. In that patient, the drug was continued after the appearance of clinical and biochemical evidence of hepatic injury and massive hepatocellular necrosis was present at autopsy. The incidence of symptomatic, potentially serious hepatic injury appears to be very low, perhaps 1 in 15,000 exposed individuals. The presumed mechanism of injury is metabolic idiosyncrasy, although hypersensitivity has not been completely dismissed in some cases reported in the literature. The incidence of mild, asymptomatic, reversible elevations in serum transaminases occurring in ketoconazole recipients has been estimated to be 5%-10%. Periodic biochemical testing and monitoring for symptoms of hepatitis during ketoconazole therapy is recommended to help prevent the development of serious or fatal hepatic injury.
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PMID:Hepatic injury associated with ketoconazole therapy. Analysis of 33 cases. 631 20

III infants and children need zinc replacement in total parenteral nutrition solutions, but assessment of these needs and total body zinc status is difficult. Seven infants with severe diarrhea initially given 80 to 100 micrograms/kg/day of elemental zinc developed systemic zinc deficiency as indicated by an acrodermatitis-like skin rash and low serum alkaline phosphatase. Serum zinc levels were borderline low only in conjunction with hypoalbuminemia. Daily urinary zinc excretion was normal. With increased zinc supplementation of 200 to 300 micrograms/kg/day, the rash healed and serum alkaline phosphatase rose to normal levels for age. The activity of the metalloenzyme alkaline phosphatase accurately reflects total body zinc status in infants. With diarrheal illness, infants, need high doses zinc supplementation to replace considerable stool losses.
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PMID:Serum alkaline phosphatase and zinc undernutrition in infants with chronic diarrhea. 680 64

Ninety-four cases of pyelonephritis including 20 who had concurrent bacteremia were treated with cefamandole alone or in combination with either gentamicin or tobramycin. Doses of cefamandole ranged from 1--2 g by intermittent intravenous (VI) infusion every 4 to 8 h; gentamicin and tobramycin doses ranged from 1--1.7 mg/kg every 8 h also by intermittent IV infusion. Duration of therapy ranged from 5 to 23 days (mean 7.3 days). Both single and combination therapy successfully treated acute pyelonephritis and bacteremia in all patients. Seven strains of E. coli and one of Klebsiella pneumoniae responsible for initial infection were resistant to cephalothin but sensitive to cefamandole. Relapse with cefamandole sensitive bacteria occurred in 27% of patients receiving only cefamandole and 8% of those patients receiving combination therapy. Reinfection with cefamandole resistant organisms, predominantly Pseudomonas aeruginosa occurred in five patients. One patient had an intrarenal abscess due to E. coli which was successfully treated with 23 days of cefamandole. One patient died. However, death was due to acute pulmonary embolism, not infection. None of the patients receiving cefamandole plus gentamicin or tobramycin experienced a significant decrease in creatinine clearance during or after therapy. Skin rash, mild thrombophlebitis at the IV site and transient elevation of alkaline phosphatase and SGOT were the only side effects noted.
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PMID:Cefamandole alone and combined with gentamicin or tobramycin in the treatment of acute pyelonephritis. 701 May 44

A 75 year-old man developed fever after one month of quinidine administration 800 mg/day. Significant enlargement of the liver and spleen became evident, associated with marked rise in serum GOT, GPT and alkaline phosphatase. Arthritis also developed, but there was no skin rash nor any changes in the haemoglobin, leucocytes or platelets. The signs and biochemical findings regressed within a few days of stopping quinidine and the temperature became normal. Rechallenge with four doses of the drug produced a rise in the GOT, GPT and alkaline phosphatase. It is thought that this hypersensitivity response is consistent with the description of granulomatous hepatitis, and represents a much less common manifestation of quinidine hypersensitivity than the well known skin, gastro-intestinal and haematological side-effects.
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PMID:Hepatosplenomegaly as a manifestation of quinidine hypersensitivity. 721 71

The safety of AmBisome was evaluated in 187 transplant recipients treated for 197 episodes. Patients included 89 bone marrow transplant recipients, 64 liver transplant recipients, 20 renal transplant recipients and 14 recipients of combined organs. AmBisome was instituted for verified invasive fungal infection in 34 cases, suspected invasive fungal infections in 80 cases and as prophylaxis in 83 cases. AmBisome was given for a median of 11 days (range 1-112 days) with a maximum daily dose of 1.49 +/- 0.70 mg/kg/day (mean +/- SD). The total cumulative dose of AmBisome was 1.11 +/- 1.78 g (mean +/- SD). Side-effects definitely attributed to AmBisome therapy included low potassium (n = 3), low back pain (n = 3), dyspnoea (n = 2), allergic rash (n = 1), nausea and vomiting (n = 1), confusion (n = 1), rise in alkaline phosphatase (n = 1) and cholecystitis (n = 1) with an overall incidence of 13 of 197 (7%). AmBisome was discontinued due to side-effects in 6 (3%) of the cases. During AmBisome treatment the mean cyclosporin dose was 9.6 +/- 28.8 mg/kg/day. Compared to pre- and post-AmBisome therapy there was a significantly increased cyclosporin concentration in blood during AmBisome therapy. Side-effects with possible association to AmBisome therapy included low serum potassium (36%), increase in serum creatinine (31%), rise in alkaline phosphatases (26%) and fever (3%). The overall mean increase in serum creatinine was 20%. Other possible side-effects like headache, abdominal pain, rash, rise in bilirubin, cramps and pancreatitis was seen in single patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of liposomal amphotericin B (AmBisome) in 187 transplant recipients treated with cyclosporin. 770 25

Trimetrexate is a folinic acid analogue structurally related to methotrexate, whose primary mechanism of action is believed to be inhibition of dihydrofolate reductase. This reduces the production of DNA and RNA precursors and leads to cell death. Trimetrexate is lipophilic and can passively diffuse across cell membranes including those of Pneumocystis carinii and its mammalian host. To minimise toxicity, trimetrexate must be coadministered with calcium folinate (leucovorin calcium), a reduced folate coenzyme, which is transported into, and protects, mammalian host cells but not P. carinii cells. In noncomparative trials trimetrexate was effective in the treatment of P. carinii pneumonia (PCP) in patients with AIDS who were intolerant of or refractory to cotrimoxazole (trimethoprim/sulfamethoxazole) and pentamidine treatment. In these patients, 2- to 4-week survival rates of 48 to 69% were reported. In a comparative trial in the initial therapy of PCP, trimetrexate was less effective than cotrimoxazole in moderate to severe disease as evidenced by a significantly higher failure rate. Trimetrexate was better tolerated than cotrimoxazole when used in this setting, however. Significantly fewer patients receiving trimetrexate plus calcium folinate discontinued treatment because of adverse events than did patients receiving cotrimoxazole. The most common adverse effect associated with trimetrexate is myelosuppression (neutropenia and thrombocytopenia); this is mitigated by coadministration of calcium folinate and is generally reversible upon dosage reduction or discontinuation. Other adverse effects include increases in serum aminotransferase levels, anaemia, fever, rash/pruritus, and increased alkaline phosphatase or serum creatinine levels. Further research into the use of trimetrexate, including its efficacy as prophylaxis, in combination with other agents and as an oral formulation, is needed to clearly define its role in the treatment of PCP and to identify patients most likely to benefit. Currently, trimetrexate should be considered as an alternative treatment option in immunocompromised patients with moderate to severe PCP who have not responded to or are intolerant of first-line therapy.
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PMID:Trimetrexate. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the treatment of Pneumocystis carinii pneumonia. 778 90

A study of the clinical profile of 59 patients who presented with hepatitis A virus infection showed that dark urine, fatigue, gastrointestinal complaints, and fever were the most common presenting symptoms. The most frequent physical findings were hepatomegaly and jaundice. The mean presenting laboratory tests included total bilirubin of 5 mg/dL, alkaline phosphatase of 269 units/L, and serum aspartate aminotransferase and alanine aminotransferase levels of 1442 mIU/mL and 1952 mIU/mL, respectively. Atypical manifestations included relapse, cholestasis, rash, and arthralgia. Two patients presented with hepatitis A and concomitant type I autoimmune chronic hepatitis, and both required immunosuppressive therapy. Five patients who presented with hepatitis A were pregnant, and during follow-up, none of their infants developed elevated serum transaminase values or had detectable IgM anti-HAV antibody. All 59 patients experienced complete clinical and biochemical recovery within 6 months after onset of illness.
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PMID:Clinical manifestations of hepatitis A: recent experience in a community teaching hospital. 787 41

We characterized urinary excretion of C3 fragments among patients with systemic lupus erythematosus (SLE) as a possible indicator of renal involvement. 28 patients, representing a broad range of disease activity were admitted to our study. Urinary proteins were separated on 4-20% gradient SDS-PAGE gels, under reducing conditions, and transblotted to nitrocellulose. Western blots were developed with a polyvalent goat-anti-human C3d antiserum, and an alkaline phosphatase-conjugated rabbit anti-goat IgG. Three patterns were obtained: 1) no bands detected; 2) bands suggesting the presence of intact C3; and 3) samples with additional low molecular (< 4 x 10(4)) bands. The 12 patients with no C3 bands had minimal disease activity (e.g. fatigue, arthralgia, arthritis, rash, oral ulcers). The seven patients with intact C3 patterns also had minimally active disease. Their primary clinical findings included fatigue, pleurisy, renal disease which had been treated, hemolytic anemia, and arthritis. Patients with low molecular weight C3 fragments in their urine formed two sub-sets, based upon their presenting features. The first group had severe disease and contained all patients with active lupus nephritis (n = 4), while the second consisted of non-renal patients with primary clinical findings of moderate disease activity (e.g. thrombocytopenia, pneumonitis, arthritis). Our results suggest urinary excretion of low molecular weight C3 fragments correlates with active renal disease, but is a variable finding among SLE patients with non-renal manifestations of disease activity.
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PMID:Complement C3 fragments in urine: detection in systemic lupus erythematosus patients by western blotting. 819 18

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

Antineoplastons, which were firstly described by Burzynski, are naturally occurring peptides and amino acid derivatives which control neoplastic growth. We conducted a toxicological study of the Antineoplastons A-10 and AS2-1 in combination with other anticancer agents or radiation in 42 patients, 46 tumors with terminal stage cancer. Antineoplaston A-10 oral formulation and A-10 injectable formulation was administered in 14 and 25 patients respectively. The maximum daily dose was 10 g and 40 g, respectively and the longest term of administration was 610 days and 67 days, respectively. Antineoplaston AS2-1 oral formulation and AS2-1 injectable formulation was administered in 33 and 10 patients, respectively, the maximum daily dose was 12 g and 30 g, respectively, and the longest term was 1070 days and 25 days, respectively. The major adverse effects that may have been related to these agents as used in combination with other conventional chemotherapeutic agents or radiation were general weakness, myelosuppression, and liver dysfunction, but these effects were not seen when either Antineoplaston was administered alone. The minor adverse effects observed in single use of either Antineoplaston A-10 or AS2-1 were excess gas, maculopapullar rash, fingers rigidity, reduced cholesterol, reduced albumin, increased amylase, eosinophilia, increased alkaline phosphatase, headache, hypertension, palpitation, peripheral edema but these adverse effects did not limit to continuation of either agent. The evaluation of the usefulness of the Antineoplastons in combination therapy based on the imaging findings during the course of treatment revealed disappearance or measurable shrinkage of the tumor lasting more than one months as visualized by magnetic resonance imaging or computed tomography was seen in 15 tumors (32.6%). No increase in size of tumor for more than 3 months was observed in 8 (17.4%). The mean survival time of these patients was significantly longer than that in patients with tumors showing progressive increasing (17.52 + 3.31 months vs 4.80 + 0.65 months, p < 0.005). Antineoplaston A-10 and AS2-1 are less toxic than conventional chemotherapeutics and they were useful in maintenance therapy for cancer patients.
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PMID:Toxicological study on antineoplastons A-10 and AS2-1 in cancer patients. 866 95


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