Clinical Appreciation of LHRH Analogue Formulations

Lemay, André

doi:10.1159/000181319

Cited by 17 publications

(3 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Esse mecanismo de ação da elcometrina permite uma supressão da ovulação tão eficiente quanto aquela induzida pelos análogos do LHRH, porém, ao contrário dos análogos, o uso, mesmo prolongado do esteróide, não provoca a sintomatologia de menopausa que geralmente se apresenta nas usuárias dos análogos 13,14 . Enquanto a gestrinona e o danazol se ligam à CBG (globulina fixadora de corticosteróides) e SHBG (globulina fixadora de hormônios sexuais), o ST-1435 não é capaz de deslocar testosterona A ocorrência de amenorréia foi predominante em 76,6% das pacientes.…”

Section: Discussionunclassified

Tratamento de endometriomas ovarianos com implantes subcutâneos de ST-1435 (Elcometrina)

Bastos¹,

Carreira²,

Gonçalves³

et al. 1999

Rev. Bras. Ginecol. Obstet.

View full text Add to dashboard Cite

IntroduçãoA endometriose é uma das doenças mais difíceis de tratar em Ginecologia. O tratamento médico consiste essencialmente na inibição da ovulação e conseqüente supressão da dismenorréia, que constitui a principal fonte de sofrimento para a paciente. Os anticoncepcionais orais contendo etinilestradiol são eficientes inibidores da ovulação mas não são indicados no tratamento da endometriose, porque a doença é estrogênio-dependente e se agrava com a administração dos estrogênios, que tendem a aumentar o volume das lesões.O tratamento da endometriose com progestínicos baseia-se no fato de que os implantes endometrióticos se assemelham ao endométrio normal e têm receptores para estrógenos e progestínicos. Os progestínicos reduzem o número de receptores estrogênicos e reduzem o efeito dos estrógenos disponíveis por meio do aumento da

show abstract

Section: Discussionunclassified

Tratamento de endometriomas ovarianos com implantes subcutâneos de ST-1435 (Elcometrina)

Bastos¹,

Carreira²,

Gonçalves³

et al. 1999

Rev. Bras. Ginecol. Obstet.

View full text Add to dashboard Cite

show abstract

“…A loss of bone mineral density, with trabecular bone being most affected, has been observed during chronic gonadotropin-releasing hormone (GnRH) treatment, related to the hypoestrogenic state [192][193][194][195]. The effect has been observed in both sexes, but female patients have a lower initial bone mass than males, and their fracture risk is therefore higher.…”

Section: Miscellaneous Drugsmentioning

confidence: 99%

Musculoskeletal Adverse Drug Reactions: A Review of Literature and Data from ADR Spontaneous Reporting Databases

Conforti

Chiamulera²,

Moretti³

et al. 2007

CDS

View full text Add to dashboard Cite

The musculoskeletal system can be a target organ for adverse drug reactions (ADRs). Drug-induced muscle, bone or connective tissue injuries may be due to, i), primary direct drug action, or, ii), undirected consequence of generalized drug-induced disease. Musculoskeletal ADRs may be only temporarily disabling, such as muscle cramps, as well as in other cases may be serious and life-threatening, such as rhabdomyolysis. In the last few years there has been an increasing awareness of musculoskeletal ADRs. Some recent drug safety issues dealt with serious or uncommon musculoskeletal reactions like rhabdomyolysis associated to statins and tendon rupture associated to fluoroquinolones. In this review, we firstly selected those drug classes having a significantly high percentage of musculoskeletal disorder reports in the WHO adverse drug reaction database, maintained by the Uppsala Monitoring Centre. Secondly, the different musculoskeletal ADRs were closely analyzed through the data obtained from an Italian interregional ADRs spontaneous reporting database. The findings on drugs associated to different musculoskeletal disorders, have been integrated with a review of the epidemiological data available in the literature. For the most involved drugs (HMG-CoA reductase inhibitors, fluoroquinolones, corticosteroids, bisphosphonates, retinoids) the underlying musculoskeletal ADR mechanisms were also reviewed and discussed.

show abstract

“…Figure 9. Aminoacid sequence of natural LHRH vs modified LHRH agonist derivatives used in intranasal formulations an almost complete and constant inhibition of the pituitary-ovarian axis, they are mainly useful for the treatment of sex steroid-dependent pathologies [2]. Because of their clinical side-effects (hot flushes, vaginal dryness) and their potential detrimental biological effect -mainly bone demineralization -the application of these treatments is usually limited to 6 to 9 months.…”

Section: Nafarelinmentioning

confidence: 99%

Intranasal LHRH agonist combined periodically with a progestogen for contraception

Lemay

1989

Adv Contracept

Self Cite

View full text Add to dashboard Cite

Mechanism of action and clinical uses of LHRH agonist formulationsIt is now well known that repetitive or continuous exposure of the gonadotroph to pharmacological amounts of natural LHRH or superactive LHRH agonists leads to a down-regulation of LH and FSH secretion and to subsequent inhibition of ovarian function ( Figure 1). The initial effect of an LHRH agonist administration is a maximal and prolonged release of LH and FSH, replacing the usual pulsations by a massive discharge of hormones. Following a single administration of a LHRH agonist, serum gonadotrophin levels remain elevated for several hours and usually return to baseline levels within 24 h. During such a supraphysiological stimulation, the gonadotroph cell becomes refractory to a subsequent dose for several hours after the initial dosing. Repetitive administration produces a progressive inhibition of gonadotrophins and the more frequent the administration, the greater the inhibition of circulating levels of LH and FSH and the decrease in ovarian steroidogenesis.LHRH agonists cannot be administered by the oral route since these small peptides are rapidly destroyed by digestive enzymes before they can be absorbed in the gastrointestinal tract. Besides the administration by s.c. injection, the first alternative mode of administration to be developed was the intranasal spray. Although the absorption through the nasal mucosa is limited, inhibition of ovarian function can be achieved following intranasal insufflation (Figure 2).Several years ago, the first clinical trials using the intranasal LHRH agonist buserelin once daily tested the potential use of this new analog as a new antiovulatory contraceptive approach. Over the subsequent years, multiple intranasal doses and larger s.c. doses of several LHRH agonists have been used, mainly to suppress ovarian steroidogenesis for the treatment of several steroid-dependent gynecological conditions such as endometriosis, leiomyoma uteri and polycystic ovarian disease [1]. In the last few years, slow-release formulations where an LHRH agonist is embedded in biodegradable polylactide-glycolide copolymer, have been developed, such as microcapsules suspension for i.m. injection and a cylindrical implant for s.c. injection. These new formulations can be administered on a monthly basis. Since they produce

show abstract

Clinical Appreciation of LHRH Analogue Formulations

Cited by 17 publications

References 7 publications

Tratamento de endometriomas ovarianos com implantes subcutâneos de ST-1435 (Elcometrina)

Tratamento de endometriomas ovarianos com implantes subcutâneos de ST-1435 (Elcometrina)

Musculoskeletal Adverse Drug Reactions: A Review of Literature and Data from ADR Spontaneous Reporting Databases

Intranasal LHRH agonist combined periodically with a progestogen for contraception

Contact Info

Product

Resources

About