Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An overview of the use of kallikrein to treat male sterility is presented. Kallikrein was shown to increase sperm motility in both in vivo and in vitro studies. The vitality and longevity of the sperm are also enhanced. These effects are due to the stimulation of the intracellular concentration of cyclical adenosonemonophosphates in the sperm. Quinine receptors on the sperm surface are assumed to be the mechanism responsible for the kallikrein effect. Kallikrein stimulates spermal penetration of cervical mucus by about 80% and causes a significant increase in total sperm output 3 months from the beginning of treatment. After 2 months of use, kallikrein leads to an increase in the number of normally formed spermatozoa in the ejaculate. Kallikrein is indicated in cases of asthenospermia and oligozoospermia, in some cases of teratozoospermia, in cases of the vegetative-functional congestion syndrome desecribed by Hoffmann, and is recommended in cases of testicular parenchyme damage involving tubulus function. Parenteral administration involves 40 KE (1KE=8mcg) thrice weekly, oral administration 300-600 KE daily. Kallikrein is added directly to the ejaculate in instrumental insemination in cases of therapy-resistant decrease in motility associated with asthenospermia or oligozoospermia. Concentrations of 5 KE per ml ejaculate are used in such cases. Chronic infection, especially in the genital area, and the incidence of dizziness during therapy are contraindications to kellikrein use.
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PMID:[Therapy of male fertility disorders with kallikrein]. 79 6

CNS adverse drug events are dramatic, and case reports have influenced clinical opinion on the use of antimalarials. Malaria also causes CNS symptoms, thus establishing causality is difficult. CNS events are associated with the quinoline and artemisinin derivatives. Chloroquine, once considered too toxic for humans, has been the antimalarial of choice for 40 years. While a range of serious CNS effects have been documented during chloroquine therapy, the incidence is unclear (extrapyramidal symptoms occur with an incidence of 1 in 5000). Amodiaquine has a higher incidence of mild CNS effects than chloroquine. Mefloquine therapy causes dose-related transient dizziness. Serious CNS events during mefloquine therapy occur in 1:1200 Asians and 1:200 Caucasians/Africans. Risk factors include dosage, concomitant drug use/interactions, previous history of a CNS event and disease severity. Retreatment (within a month) increases the risk in Asians 7-fold. Studies indicate that the frequency of serious CNS events with mefloquine prophylaxis (1:10,000) is similar to that with chloroquine (1:13,600). Quinine causes cinchonism at standard therapeutic doses. High-tone hearing loss occurs, but irreversible auditory or ocular effects are very rare. The artemisinin derivatives are associated with dose-dependent brain lesions in rodent, canine and nonhuman primates. At low doses, histological injury has been demonstrated, without clinical neurological signs. No significant toxicity has been reported in humans. Other antimalarial drugs are seldom associated with CNS adverse events. Data do not suggest a need to diminish the correct use of the quinoline derivatives. Irreversible effects are extremely rare and usually associated with overdosing or prior history of a serious CNS event. Concomitant therapeutic use of 2 drugs from the same family, or retreatment with the same drug, should be avoided. Onset of drug-associated serious CNS events requires drug discontinuation and future avoidance of the drug.
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PMID:CNS adverse events associated with antimalarial agents. Fact or fiction? 852 12