Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tiazofurin is a novel C-nucleoside with significant antitumor activity in murine tumor models. In a phase I clinical trial, patients received tiazofurin by bolus iv infusion daily for 5 days. Six doses ranging from 550 to 4100 mg/m2/day were evaluated. Thirty-one treatment courses were initiated in 21 patients. Tiazofurin induced multiple, transient toxic effects at all but the lowest dose level, and treatment interruption was a common result. Nine of 28 treatment courses initiated at doses greater than or equal to 1100 mg/m2/day were interrupted at less than 5 days; only five of eight courses initiated at 1100 mg/m2/day were completed. Symptoms leading to treatment interruption included headache, nausea and emesis, and lethargy and malaise. Other significant, transient toxic effects included skeletal muscle injury manifest as pain, weakness, or serum biochemical abnormalities; mucocutaneous effects; and mental or mood changes. One case each of transient pericarditis and fatal cardiomyopathy occurred at the highest dose. Myelosuppression was observed but was transient and not dose limiting. In addition to leukopenia and thrombocytopenia, unexpected declines in serum hemoglobin were observed, although these were of uncertain significance. Tiazofurin induced significant increases in uric acid production which could be reversed with coadministration of allopurinol. Pharmacokinetic analysis revealed tiazofurin plasma elimination to be at least biphasic, with a beta-half-time of 4.2 hours; most of an injected dose could be recovered from the urine as unaltered compound within 24 hours. From this study we conclude that an appropriate dose for phase II trials with this schedule is less than or equal to 1000 mg/m2/day. The schedule may be a difficult one for clinical evaluation of antitumor activity, however, because of the possibility of frequent treatment interruption due to multiple systemic toxic effects.
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PMID:Phase I trial of tiazofurin administered by i.v. bolus daily for 5 days, with pharmacokinetic evaluation. 380 11

A Phase II study of interferon alfa-2a was conducted in 64 patients with multiple myeloma (42 IgG, 16 IgA, 5 Bence-Jones type, and 1 IgD) in a multi-institutional cooperative trial. Partial remission was obtained in 10 (21.3%) of 47 evaluable patients, and minor responses in 5 (10.6%) of 47. Remission was reached at 22 to 89 days (median, 29 days) after the initiation of interferon alfa-2a and lasted 4 to 55 weeks (median, 8 weeks). Side effects were noted in more than two-thirds of patients, and included fever (58%), malaise (20%), anorexia (52%), nausea-vomiting (26%), lethargy (2%), and myelosuppression (56%). They were all reversible on discontinuation of interferon alfa-2a. Antibody to interferon alfa-2a was detected in 1 of 20 patients tested during the course of treatment. Thus, interferon alfa-2a was effective in multiple myeloma, producing unequivocal response in 21.3% of patients without unacceptable side effects.
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PMID:Treatment of multiple myeloma with recombinant interferon alfa-2a. 394 39

Methylene chloride is a chlorinated hydrocarbon used widely in home and industry. Its intentional abuse has not been reported previously. We describe the case of a 14-year-old boy who presented with lethargy, nausea, and chills six hours after the intentional inhalation of a household product containing methylene chloride. The patient's elevated carboxyhemoglobin level responded well to 100% oxygen therapy. The pathophysiology and treatment of methylene chloride are discussed.
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PMID:Methylene chloride inhalation: an unusual form of drug abuse. 402 92

A 49-year-old woman was admitted to Hacettepe Medical Faculty Hospital with the complaints of headache, nausea, vomiting, lethargy, and weakness on her right side. She revealed a history of pulmonary Cryptococcus infection 5 years before and she had been treated with amphotericin B. After clinical and laboratory investigation she was thought to have an intracranial mass, but her deteriorating situation did not allow any surgical intervention; she died within 7 days. On necropsy, hard, gray-white nodular pulmonary lesions, ranging 0.1-4 cm in diameter, basal meningitis, infarcts, and a nodular lesion 1.5 cm in diameter similar to those of the lung were present in the white matter of the right hemisphere of the brain. Microscopic examination revealed granulomatous inflammation caused by Cladosporium, which had brown pigment and septate hyphae.
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PMID:Cerebral cladosporiosis. 403 53

In the United States, the drugs most commonly used to treat peptic ulcer disease are antacids and the H2-receptor antagonists cimetidine and ranitidine. Other available agents include anticholinergics and the coating agent sucralfate. Investigational drugs such as colloidal bismuth, carbenoxolone, prostaglandins, the tricyclic compound pirenzepine, and substituted benzimidazoles are not available for use in the United States. Most of the commercially available and investigational compounds have similar efficacy; therefore the optimal drug may be the one associated with the fewest adverse effects and the most convenient dosing regimen. Cimetidine causes a small number of adverse effects, including neuropsychiatric disorders, gynecomastia, impotence, loss of libido, elevation of serum creatinine and serum transaminases concentrations, and drug interactions. Some of these reactions have been of clinical significance. Presently, there are rare reports of gynecomastia, bradycardia, inhibition of acetylcholinesterase, headache, lethargy, diarrhea, and rash in patients receiving ranitidine. Antacids can produce either diarrhea or constipation and have been associated with low serum phosphorus concentrations, and metabolic alkalosis. Anticholinergics, especially in elderly or debilitated patients, can cause central nervous system disorders, intestinal atony, or urinary retention. Sucralfate may cause constipation, diarrhea, nausea, and headache. The investigational agents have their own side effect profiles. The adverse effects of anticholinergics make them unattractive therapeutic choices, and antacids and sucralfate have inconvenient dosing requirements compared with some equally efficacious alternatives. In addition, clinical experience with sucralfate in the United States is limited. The safety record of cimetidine is admirable. As clinical experience with ranitidine increases, currently unrecognized adverse effects may be reported. However, based on current data, ranitidine is as effective as cimetidine and is associated with a lower incidence of side effects.
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PMID:Problems associated with medical treatment of peptic ulcer disease. 609 62

The ability of polyriboinosionic acid [poly(rI)].polyribocytidylic acid [poly(rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) complexed with poly L-lysine and carboxymethylcellulose [poly(ICLc)] to induce interferon and the comparative toxicity of each in cats were evaluated. Each induced high levels of circulating interferon, although poly(ICLC) injected intravenously at 1 to 4 mg/kg induced up to 10 times more interferon than the other compounds. Each compound was pyrogenic and caused a transient decrease in leukocyte numbers. Poly(rI).poly(rC) and the mismatched analog caused severe diarrhea and nausea at the highest drug concentrations (1 to 4 mg/kg), but poly (ICLC) did not. Each compound also caused depression and lethargy and impaired coordination.
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PMID:Interferon induction by and toxicity of polyriboinosinic acid [poly(rI)].polyribocytidylic acid [poly (rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) L-lysine complexed with carboxymethylcellulose. 615 63

Thirty-six psoriatic patients resistant to or intolerant to PUVA, methotrexate and/or etretinate were treated with razoxane (ICRF 159) and EDTA derivative with antimitotic effects. The drug is highly effective in cutaneous and arthropathic psoriasis. Razoxane is well tolerated and appears to be free of hepatotoxicity. Besides some nausea and lethargy, 60% of the patients showed neutropenia, which can be easily controlled.
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PMID:Razoxane in the treatment of psoriatic patients resistant to or intolerant of PUVA, methotrexate and etretinate. 618 78

The premenstrual syndrome (PMS) is a complex of symptoms that usually occurs seven to ten days before menses in large numbers of women. These symptoms typically cease during the 24 hours after the onset of menses. PMS affects many areas of the body, with each afflicted woman having her personal set of symptoms. Frequently encountered signs and symptoms include breast tenderness and swelling, weight gain, headache, abdominal cramping and bloating, food cravings, thirst, nausea, joint pain, acne, dizziness, hyperalgesia and one or more psychologic symptoms: irritability, lethargy and fatigue, depression, anxiety, hostility and aggression. Theories relating PMS to hormonal imbalance, vitamin deficiency or psychosomatic aberration have failed to explain this condition fully. Treatments using hormones, vitamins, oral contraceptives or diuretics have failed to relieve all the symptoms of PMS. The prostaglandin (PG) theory proposes that these nearly ubiquitous substances, produced in pathophysiologic amounts in brain, breast, gastrointestinal tract, kidney and reproductive tract, can trigger many of the PMS symptoms. If that is true, then a PG inhibitor could counteract excessive PG production and successfully control those PMS symptoms related to prostaglandin excess or imbalance. Therapy based upon this theory can proceed to the use of PG inhibitors in conservative steps. First, permanent deletion of xanthine-containing beverages (coffee, tea, cola and chocolate) from the diet can reduce nervousness, irritability and breast tenderness. Luteal phase salt restriction, with a mild diuretic used if necessary the last week before menses, adds to this effect. For the 20-25% of women who need more help, either a PG inhibitor or natural progesterone (to oppose the action of PGs), given when PMS begins, brings relief. In women with depressive PMS complaints, small daily doses of an antidepressant may prove helpful.
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PMID:The use of prostaglandin inhibitors for the premenstrual syndrome. 635 May 80

Ten women with advanced locally recurrent breast cancer who had failed to respond to radiation and hormonal and cytotoxic agents were given up to 12 weeks of recombinant leucocyte interferon 20 X 10(6) U/m2 daily or 50 X 10(6) U/m2 three times a week. Within one hour of administration influenza-like symptoms began, which one week later were superseded by lethargy, anorexia, and nausea, with a consequent loss of weight in most patients. Other side effects included profound somnolence, confusion, paraesthesia, and (in one patient) signs of an upper motor neurone lesion in the legs. All these effects together with increased slow wave activity in electroencephalograms from all patients during treatment disappeared when interferon was withdrawn and did not recur on reintroducing the drug at a lower dosage. Studies are continuing to determine the mechanisms of these effects.
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PMID:Neurological effects of recombinant human interferon. 640 63

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
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PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49


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