Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male epileptic patients frequently complain of sexual dysfunction, particularly impotence and loss of libido. Epilepsy itself, antiepileptic drugs (AEDs), and psychosocial factors are believed to contribute to impaired sexuality. We studied luteinizing hormone (LH) pulsatile secretion, gonadotropin, and prolactin (PRL) responses to LH-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) in 37 adult male epileptic patients receiving AED monotherapy who were seizure-free and had normal EEGs. Sexuality was assessed by psychological interview. Impotence was diagnosed in 8 patients (in 2 combined with loss of sexual desire). The occurrence of hyposexuality (approximately 20%) was independent of epilepsy syndrome or AED. No change in total testosterone (T) level was observed. Free T (fT) and dihydrotestosterone (DHT) levels were lower and sex hormone binding globulin (SHBG) levels were higher in epileptic subjects than in healthy controls, but a statistically significant difference was not observed between hypo- and normosexual patients. In impotent epileptic patients, estradiol (E2) levels were significantly increased as compared with those of patients with preserved sexuality and of healthy controls. The unbalanced relation between androgen and E2 levels was emphasized by decreased T/E2, fT/E2, and DHT/E2 ratios obtained in hyposexual epileptic patients. In this group, LHRH induced blunted LH peaks. No changes were noted in LH pulsatility features. These findings of higher E2 levels and of decreased LH response to LHRH administration in some epileptic patients with impaired sexuality, may suggest they have subclinical hypogonadotropic hypogonadism.
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PMID:Sex hormones and pituitary function in male epileptic patients with altered or normal sexuality. 760 14

Sex steroid peripheral pattern, pulsatile luteinizing hormone (LH) secretion, gonadotropin and prolactin responses to LH-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) were studied in 35 male epileptics treated with phenobarbital (PB), carbamazepine (CBZ), or phenytoin (PHT), and in age-matched healthy males. Idiopathic generalized epilepsy (IGE) was diagnosed in 12 cases and partial epilepsy (PE) in 23 cases. Patients were seizure-free and did not show EEG abnormalities at repeated controls in the last 5 years, so that interfering effects of seizures were possibly excluded. The aim of the study was to evaluate both the role of epileptic syndromes and of anti-epileptic drugs on the endocrine function. Changes in sex hormone binding globulin, total and free testosterone, dihydrotestosterone and delta 4-androstenedione were found to be independent of the epileptic syndrome type. The LH response to LHRH was lower in PB-treated PE than in IGE subjects on the same drug regimen. An impairment of LH pulsatility with respect to controls was found in PE but not in IGE patients taking PB. Among antiepileptic drugs, PHT is associated with higher sex hormone binding globulin and estradiol and lower free testosterone and dihydrotestosterone levels. PB and CBZ, but not PHT, blunt the LH response to exogenous LHRH in PE. Prolactin responses to TRH were consistently enhanced in PE subjects treated with CBZ or PHT.
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PMID:Sex hormones, gonadotropins and prolactin in male epileptic subjects in remission: role of the epileptic syndrome and of antiepileptic drugs. 796 56

High physical fitness and physical activity are associated with favourable lipid levels, especially a high level of high density lipoprotein cholesterol (HDL-C). A person's skeletal muscle properties, metabolism and percentage of different muscle fibres (ST-%), which may modify coronary heart disease (CHD) risk factors, such as serum insulin, obesity and serum sex hormones may also influence his fitness level and leisure-time physical activity. We studied the associations of physical fitness, physical activity and ST-% with serum lipids and lipoproteins in 72 healthy men. Their parameters were compared with those of 20 men with defined CHD. Significant interrelationships between ST-%, fitness and leisure-time physical activity index (LTPAI) were observed. Multiple regression analysis showed that ST-%, fitness and leisure-time physical activity explained about 32% of the variation in HDL-C in the healthy men. In healthy men ST-% correlated positively with fitness (r(s) = 0.62, P < 0.001) and with LTPAI (r(s) = 0.62, P < 0.001). Fitness level also correlated significantly with LTPAI (r(s) = 0.81, P < 0.001). Serum insulin showed negative associations with ST-% (r(s) = -0.63, P < 0.001) and fitness (r(s) = -0.54, P < 0.001) and LTPAI (r(s) = -0.62, P < 0.001). Free fraction of testosterone correlated negatively with serum HDL-C level (r(s) = -0.34, P < 0.01), with fitness (r(s) = -0.41, P < 0.001) and with LTPAI (r(s) = -0.54, P < 0.001). In sedentary men with the lowest fitness and physical activity the mean of ST-% (45%) was similar to that in CHD patients (44%). However, ST-% in men in the highest tertile of physical activity and fitness (68%) was significantly higher than in CHD patients and in men in the lowest tertile of physical activity and fitness. Skeletal muscle enzyme activity in lipid metabolism was significantly lower in both CHD patients and in sedentary and low-fit men than that in fitter and physically active men. The present data imply that skeletal muscle properties are important determinants of risk profiles, such as physical activity, fitness and serum lipid and lipoprotein patterns. Although fitness is a graded, independent predictor of mortality from CHD, a relatively high fitness level is not enough. This was clearly observed in the clustering analysis, in which the healthy men, according to their ST-%, fitness, leisure-time physical activity and serum sex hormone binding globulin (SHBG), fell into three natural groups: (i) Inactive men with lowest ST-% (mean 42%), lowest fitness (10.7 METs) and lowest HDL-C (1.36 mm/l); (ii) Fit men with high ST-% (66%), high fitness (14.5 METs) and moderately high HDL-C (1.54 mol/l); (iii) Active men with high ST-% (66%), highest fitness (14.9 METs) and highest serum HDL (1.83 mmol/l). The results support the idea that both fitness and physical activity give further protection against CHD by modifying risk factors. Our findings also suggest that skeletal muscle properties should be considered in the studies which assess CHD risk factors and their modifications especially in the field of health-related fitness.
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PMID:Associations between skeletal muscle properties, physical fitness, physical activity and coronary heart disease risk factors in men. 962 81

The paper contains a review of reports concerned with how for hormones, epileptic seizures and antiepileptic drugs can be influenced by one another. Hormones influence brain excitability but, on the other hand, both epileptic seizures and antiepileptic drugs may alter hormone secretion and metabolism. Effect of hormones on seizures--Experimental studies revealed the properties which inhibit or stimulate convulsive reactivity of different hormones. Progesterone, testosterone, adrenocorticotropin and desoxycorticosterone are responsible for an increase in seizure threshold, while estradiol, cortisol and thyroid hormones cause a reduction. Effect of seizures on hormones--Epileptic seizures, chiefly tonic-clonic, also complex partial and sometimes simple partial seizures, result in "the hormonal storm". Immediately after an epileptic seizure, an increase is found in serum concentrations of prolactin, cortisol, adrenocorticotropin, triidothyronine, thyroxin, thyrotropin, luteotropin, follicular stimulating hormone and growth hormone. These changes may persist for two hours, while prolactin concentration even for 24 hours after a seizure. Effect of antiepileptic drugs on hormones--Antiepileptic drugs may affect hypothalamus-pituitary function directly or indirectly through neurotransmitter system. By induction of hepatic microsomal enzymes, some antiepileptic drugs cause acceleration of hormone metabolism, reducing hormone serum concentrations. Moreover, antiepileptic drugs enhance sex hormone binding globulin SHBG/synthesis, increase binding of these hormones and reduce their active fraction concentration in serum. Recognition of the relationship between epilepsy and hormonal system is necessary to obtain better understanding of this disease.
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PMID:[Epilepsy and hormones]. 1076 43

We investigated the impact of temporal lobe epilepsy surgery on sex hormones and menstrual cycles. Sixteen female patients with temporal lobe epilepsy were investigated prior to surgery and 3, 6, and 12 months after surgery. The patients received carbamazepine (CBZ) as monotherapy (10 patients) or in combination with other antiepileptic drugs (six patients). Antiepileptic drugs were maintained after surgery. During the 1-year follow-up after surgery eight patients (50%) remained completely free of seizures. In another four patients (25%) only rare disabling seizures occurred. There were no significant differences between pre-surgical and post-surgical serum concentrations of testosterone, free testosterone, prolactin, dehydroepiandrosterone sulfate, growth hormone, cortisol and sex hormone binding globulin. There was, however, a significant increase in serum androstenedione concentration 6 months post-surgically (P < 0.02). Documentation of menstrual cycles in addition to laboratory parameters revealed individual post-surgical changes of the menstrual cycle in eight patients. Four patients had a change in menstrual periodicity: two patients with complete seizure control had regular cycles instead of oligomenorrhoea and two patients with incomplete seizure control had oligomenorrhoea instead of regular cycles. These data indicate that at least in some patients with temporal lobe epilepsy surgical treatment influences menstrual periodicity.
Seizure 2000 Sep
PMID:The impact of epilepsy surgery on sex hormones and the menstrual cycle in female patients. 1098 94

The purpose of this study was to compare the serum levels of androgens between hyposexual and non-hyposexual patients with epilepsy. Adult male patients with epilepsy were investigated. Serum levels of testosterone (T) and free-T, estradiol, and sex hormone binding globulin (SHBG) were measured and the free androgen index (FAI) was calculated. While there were no differences between hyposexual and non-hyposexual patients in the serum levels of T, free-T, and estradiol, or to the FAI, the serum levels of SHBG were significantly higher in hyposexual patients than in non-hyposexual patients. Thus, the effects of increased SHBG upon serum levels of testosterone biologically active in patients with epilepsy and hyposexuality were not detected by the methods used in this study. Four (44%) of nine hyposexual patients who were re-evaluated after two years follow-up improved sexual performance. Thus, clinical treatment that results in good seizure control may improve sexual performance in some patients with epilepsy.
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PMID:Interictal hyposexuality in male patients with epilepsy. 1129 26

Sexual disorders (both hyposexuality and sexual dysfunction) are common in people with epilepsy, occurring in up to two-thirds of patients. However, characteristically, patients do not spontaneously report these problems. Nocturnal penile tumescence testing suggests that the erectile dysfunction has a neurophysiological component. The aetiology remains uncertain but is likely to be multifactorial, involving neurological, endocrine, iatrogenic, cognitive, psychiatric and psychosocial factors. Epilepsy-related factors include the age of onset/duration of epilepsy along with the seizure type and focus. In addition, seizure frequency might be relevant as successful epilepsy surgery can result in an improvement in sexual functioning despite remaining on anticonvulsant medication. Endocrine changes (raised sex hormone binding globulin and reduced free testosterone) have been reported in men with epilepsy, especially when treated with hepatic-enzyme inducing antiepileptic drugs. Studies have not been performed evaluating anticonvulsants that do not induce hepatic enzymes such as lamotrigine. The association between these endocrine changes and hyposexuality is not known. The relationship between seizures, hormones and anticonvulsant medication in women is explored, focusing on issues such as catamenial epilepsy, the menopause, hormone replacement therapy and the polycystic ovarian syndrome. Suggestions for future research and treatment issues are discussed.
Seizure 2001 Jul
PMID:Seizures, hormones and sexuality. 1148 44

Epilepsy, antiepileptic drugs (AEDs), and the reproductive system have complex interactions. Fertility is lower in both men and women with epilepsy than in the general population. Moreover, reproductive endocrine disorders are more common among patients with epilepsy than among the population in general. These disorders have been attributed both to epilepsy itself and to AEDs. The use of the liver enzyme inducing AEDs phenobarbital, phenytoin and carbamazepine increases serum sex hormone binding globulin (SHBG) concentrations in both men and women with epilepsy. Over time the increase in serum SHBG levels leads to diminished bioactivity of testosterone and estradiol, which may result in diminished potency in men and menstrual disorders in some women, and, thus, to reduced fertility. Valproate (VPA) medication may have effects on serum androgen concentrations and it reduces serum follicle stimulating hormone levels in men with epilepsy. However, the clinical significance of the VPA related reproductive endocrine changes in men is unknown. On the other hand, in women the use of VPA is associated with a frequent occurrence of reproductive endocrine disorders characterized by polycystic changes in the ovaries, high serum testosterone concentrations (hyperandrogenism) and menstrual disorders. Young women with epilepsy seem to be especially vulnerable to the effects of VPA on serum androgen levels. The endocrine effects of the new AEDs have not been widely studied. However, it seems they may offer an alternative if reproductive endocrine problems emerge during treatment with the older antiepileptic drugs. On the other hand, it seems that in many cases the reproductive endocrine effects of the AEDs are reversible, if the medication is discontinued.
Seizure 2008 Mar
PMID:Disorders of reproduction in patients with epilepsy: antiepileptic drug related mechanisms. 1816 16

Contraceptive counseling is a critical component of the management of the female patient with epilepsy because of the increased risk of pregnancy associated with epilepsy and the multitude of interactions between antiepileptic drugs (AEDs) and hormonal contraception. Steroid hormones and many of the AEDs are substrates for the cytochrome P450 enzyme system, in particular, the 3A4 isoenzyme. As a result, concomitant use of hormonal contraceptives and AEDs may pose a risk for unexpected pregnancy, seizures, and drug-related adverse effects. The risk of combined oral contraceptive (COC) failure is slightly increased in the presence of cytochrome P450 3A4 enzyme-inducing AEDs. Several AEDs induce the production of sex hormone binding globulin (SHBG) to which the progestins are tightly bound, resulting in lower concentrations of free progestin that may also lead to COC failure. There is no increase in the risk of COC failure in women taking nonenzyme-inducing AEDs. Oral contraceptives significantly increase the metabolism of lamotrigine, posing a risk of seizures when hormonal agents are initiated and/or toxicity during pill-free weeks. There is no evidence that COCs increase seizures in women with epilepsy. While higher dose COCs are one contraceptive option for women on enzyme-inducing AEDs, a variety of other options are available. Injectable contraception (depot medroxyprogesterone acetate) appears effective with AED use, but the potential for bone mineral density loss is a concern. Intrauterine devices (IUDs) and barrier methods do not rely on hormonal components for contraceptive efficacy, and are therefore appropriate to recommend for use in women using enzyme-inducing medications. This chapter reviews the evidence regarding the pharmacokinetic interaction between AEDs and oral contraceptive hormones, the known or potential interactions with alternative contraceptive methods, and provides practical advice for management of contraceptive needs in reproductive-age women.
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PMID:Contraception in women with epilepsy: pharmacokinetic interactions, contraceptive options, and management. 1892 78

Antiepileptic drugs (AEDs) are known to have endocrine side effects in both men and women. These can affect fertility, sexuality, thyroid function, and bone health, all functions of major importance for well-being and quality of life. The liver enzyme inducing antiepileptic drugs (EIAEDs), like phenobarbital, phenytoin, and carbamazepine, and also valproate (VPA), a non-EIAED, are most likely to cause such side effects. AED treatment can alter the levels of different sex hormones. EIAEDs increase sex hormone binding globulin (SHBG) concentrations in both men and women. Over time, this elevation can lead to lower levels of bioactive testosterone and estradiol, which may cause menstrual disturbances, sexual problems, and eventually reduced fertility. VPA can cause weight gain in both men and women. In women, VPA can also lead to androgenization with increased serum testosterone concentrations, menstrual disturbances, and polycystic ovaries. Lamotrigine has not been shown to result in endocrine side effects. The newer AEDs have not yet been thoroughly studied, but case reports indicate that some of these drugs could also be suspected to cause such effects if endocrine changes commence after treatment initiation. It is important to be aware of possible endocrine side effects of AEDs as they can have a major impact on quality of life, and are, at least partly, reversible after AED discontinuation.
Seizure 2015 May
PMID:Interactions between antiepileptic drugs and hormones. 2579 88


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