Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pentamidine, recently released for clinical use, is effective in therapy for the hemolymphatic stage of Gambian trypanosomiasis, antimony-resistant leishmaniasis, and Pneumocystis carinii pneumonia. The mechanism of action is unclear and may differ for different organisms. Trypanosomes actively transport pentamidine intracellularly, and the drug may then interfere with DNA biosynthetics. However, pentamidine appears to kill nonreplicating P. carinii. The mechanism of killing is unexplained. The pharmacokinetics of pentamidine has been incompletely studied in humans. The estimated volume of distribution is 3 liters/kg. Levels in plasma of pentamidine range from 0.3-1.4 microgram/ml after standard 4 mg/kg dosing, with no appreciable increase in drug levels on successive dosing and no correlation between levels and creatinine clearance or adverse reactions. The drug appears to be concentrated in the kidney and excreted in the urine, with levels detectable six to eight weeks after cessation of therapy. Immediate adverse reactions have included hypotension, nausea, and vomiting. Local pain or abscess formation at an injection site, mild azotemia, leukopenia, abnormal findings from liver function tests, and hypoglycemia may also occur.
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PMID:Pentamidine: a review. 390 42

In the rat compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The pain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotrophic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and G2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na+ and K+ by the nephron.
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PMID:[Influence of nutritional factors on the enhancement of renal compensatory hypertrophy by hyperadrenocorticism in the rat (author's transl)]. 627 45

The data presented confirm in human volunteers our previous observations in animal models. The DNA free HSV 2 subunit vaccine used elicited an antibody and a cell-mediated immune response in 15 subjects without past evidence of HSV 1 or HSV 2 infections and increased the immunity level in 28 subjects suffering from HSV 1 or HSV 2 infections. Although we did not follow a double-blind, placebo controlled protocol our results suggest that the vaccine may reduce the frequency and severity of HSV infections. The time between the recurrences, the pain and the time to complete healing decreased significantly after the vaccination.
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PMID:Immune responses to DNA free herpes simplex proteins in man. 629 43

Acyclovir (acycloguanosine) is a new antiviral compound with activity against certain herpes viruses. Acyclovir is phosphorylated preferentially in virus-infected cells into its active form, acyclovir triphosphate, an inhibitor of viral-induced DNA polymerase. Acyclovir, which possesses an acyclic carbohydrate moiety, also causes premature DNA chain termination. Acyclovir has shown clinical activity against herpes simplex virus (HSV) types 1 and 2 and varicella zoster virus (VZV), but its usefulness in cytomegalovirus, Epstein-Barr virus, and chronic hepatitis B infections requires further study. In randomized clinical trials of infections caused by HSV and VZV, intravenous acyclovir has been shown to shorten the duration of viral shedding and lesion pain and hasten the resolution of skin lesions, with minimal toxicity.
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PMID:The clinical use of intravenous acyclovir. 631 3

Acyclovir (aciclovir) is a nucleoside analogue antiviral drug related to cytarabine, idoxuridine, trifluridine and vidarabine. In common with these earlier antivirals, acyclovir is active against some members of the herpesvirus group of DNA viruses. The efficacy of topical acyclovir has been convincingly demonstrated in ocular herpetic keratitis, and in initial and primary initial genital herpes infection, but little or no clinical benefit was seen when non-primary initial genital infections were assessed separately. Acyclovir ointment demonstrated little benefit in recurrent genital herpes but topical acyclovir cream decreased the course of the infection by 1 to 2 days. Orally and intravenously administered acyclovir were beneficial in initial genital herpes infections, and oral therapy shortened the duration of recurrent infections by 1 to 2 days but did not ameliorate pain. In non-immunocompromised patients with recurrent herpes simplex labialis, generally little clinical benefit was seen with the use of topical acyclovir ointment even when therapy was initiated during the prodromal phase, while topical acyclovir cream effected small but significant improvements in the clinical but not the symptomological course of the disease. However, in immunocompromised patients, both intravenous and topical acyclovir shortened the clinical course of herpes simplex virus infections occurring mainly on the lips, oral mucosa and face, and prophylaxis with either oral or intravenous acyclovir suppressed the appearance of recurrent lesions from latent virus for the period of drug administration, but acyclovir did not eradicate latent herpesviruses. In non-immunocompromised patients, intravenous acyclovir was shown to decrease the acute pain of zoster, especially in the elderly, but postherpetic neuralgia was not ameliorated. When immunocompromised patients were studied, intravenous acyclovir inhibited the progression of zoster infections and shortened the healing time and duration of viral shedding in patients with cutaneous disseminated zoster. However, acute and post-herpetic pain were not significantly affected. Well designed controlled studies are underway to establish the efficacy of acyclovir in herpes simplex encephalitis and cytomegalovirus infections in immunocompromised patients, infections due to Epstein-Barr virus, and neonatal herpesvirus infections. Despite some aspects of the drug's use which require further clarification, acyclovir will make a major impact on the treatment of herpesviral infections. Barring unexpected findings with wider clinical use, it will become the agent of choice in several conditions.
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PMID:Acyclovir. A review of its pharmacodynamic properties and therapeutic efficacy. 631 32

A patient with refractory acute myelogenous leukemia was treated with high-dose cytosine arabinoside (3.0 g/m2 every 12 hours). Following ten doses over five days the patient developed excessive tearing, photophobia, burning ocular pain, and blurred vision. Ophthalmologic examination revealed conjunctival injection, central punctate corneal opacities with subepithelial granular deposits, and decreased visual acuity. Symptoms gradually resolved over the following four days; however, impaired visual acuity persisted for two weeks and corneal opacification did not disappear until four weeks following therapy. Prior and subsequent administration of cytosine arabinoside according to the same dose schedule for only four doses over two days and eight doses over four days were well tolerated and did not produce ocular toxicity. It is suggested that ocular toxicity results from inhibition of corneal epithelial DNA synthesis and is related to both drug dosage and duration of drug exposure. Strategies should be explored to eliminate this treatment-limiting adverse effect of potentially effective therapy.
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PMID:Ocular toxicity from high-dose cytosine arabinoside. 657 99

Three patients with leukemia developed corneal toxicity while receiving high doses (3 g/m2) of systemic cytarabine. Symptoms began five to seven days after initiation of treatment with high doses of systemic cytarabine and consisted of ocular pain, tearing, foreign-body sensation, photophobia, and blurred vision. All three patients developed bilateral conjunctival hyperemia and fine corneal epithelial opacities and refractile microcysts that were more numerous in the central than in the peripheral cornea. The symptoms disappeared without treatment in approximately one week. The corneal changes we observed with high doses of systemic cytarabine resembled descriptions of corneal toxicity from topical cytarabine and were probably secondary to inhibition of DNA synthesis in the corneal epithelium.
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PMID:Corneal toxicity with systemic cytarabine. 693 30

Twenty patients with active systemic lupus erythematosus (SLE) were treated with methyl prednisolone pulse therapy (MPPT) and followed up for up to 24 weeks (mean 18 weeks). Beneficial effects of MPPT were observed principally on arthralgia, pleuritic pain, vasculitic skin rash, pyrexia, and lymphadenopathy. The serological tests showing the most improvement were ds DNA binding and the serum C3 level. MPPT was found to be both safe and easy to administer. It may be of value in treating patients with SLE whose disease is not controlled by moderate doses of corticosteroids and may also enable the dose of maintenance corticosteroids to be reduced appreciably.
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PMID:Methyl prednisolone pulse therapy in the treatment of systemic lupus erythematosus. 711 16

Embelin, a plant-based benzoquinone derivative, has been found to exhibit significant antitumor activity in methylcholanthrene-induced fibrosarcoma in albino rats besides enhancing their survival time. The drug also has an appreciable action on pain and inflammation. The changes in DNA, RNA and protein levels in various organs in the tumor-bearing control and the drug-treated animals were also studied.
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PMID:Antitumor, anti-inflammatory and analgesic property of embelin, a plant product. 751 Jun 5

A 15-year-old girl (case 1) was admitted to our hospital because of progressive muscle weakness of the lower limbs and numbness of the upper limbs. She noted these symptoms beginning at 13 years of age. Neurological examination revealed that deep tendon reflexes were absent and hypesthesia of touch and pain sensation were distributed in a glove-and-stocking pattern. Muscle weakness and atrophy were predominantly present in the distal portions of the extremities. There were obvious pes cavus and champagne-bottle shape deformities. The motor conduction velocity of the median nerve was markedly delayed and sensory potentials were not evoked in any nerves examined. Lumbar MRI showed thickening of the nerve radices. Cranial MRI showed thickening of the acoustic nerves, as well. Histological studies of a biopsied sural nerve revealed a marked decrease in the number of myelinated and unmyelinated fibers and remarkable onion bulb formation. The patient's clinical manifestations and histological findings were more severe than that seen in the usual case of CMT1A. Her mother (case 2, 39 years old) had similar neurological and electrophysiological findings. DNA duplication encoding peripheral myelin protein 22, was not detected in either case 1 or 2. Sequencing of DNA from these patients revealed the presence of a mutant allele containing an A- to G-substitution of nucleotide 245, which replaced tyrosine with cysteine in the extracellular Ig-domain of the P0 protein.
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PMID:[A familial Charcot-Marie-Tooth disease type 1B (CMTD1B) manifesting a new mutation of myelin P0 gene]. 753 89


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