scholarly journals Premenstrual Exacerbation of Life-Threatening Asthma: Effect of Gonadotrophin Releasing Hormone Analogue Therapy

1996 ◽  
Vol 3 (3) ◽  
pp. 203-206 ◽  
Author(s):  
Alun L Edwards ◽  
M Sarah Rose ◽  
Lois E Donovan ◽  
Gordon T Ford
Keyword(s):  
Menstrual Cycle ◽  
Gnrh Analogue ◽  
Hormonal Changes ◽  
Gnrh Analogues ◽  
Releasing Hormone ◽  
Life Threatening ◽  
Gonadotrophin Releasing Hormone ◽  
Premenstrual Exacerbation ◽  
Insight Into

Variability in the severity of asthma during various phases of the menstrual cycle has been frequently suspected. However, the hormonal changes that might affect mediators of bronchospasm have yet to be elucidated. The case of a 41-year-old woman suffering from longstanding asthma with life-threatening exacerbations is reported. The patient was treated with buserelin, a gonadotropin releasing hormone (GnRH) analogue, which created a temporary chemical menopause and thus permitted diagnosis of a premenstrual exacerbation of asthma and offered insight into potential therapy. GnRH analogues may therefore be of value in assessing women with severe asthma suspected to vary with the menstrual cycle. The addition of estrogens and progestins at the same time as treatment with GnRH analogue may be of value in determining the role of these hormones in the pathogenesis of menstrually related exacerbations of asthma.

Role of gonadotrophin releasing hormone secretory dynamics in the control of the human menstrual cycle

1993 ◽  
Vol 8 (suppl 2) ◽  
pp. 62-65 ◽  
Author(s):  
M. Filicori ◽  
G. Cognigni ◽  
P. Dellai ◽  
R. Arnone ◽  
M. Sambataro ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone ◽  
Human Menstrual Cycle

Characterization of the gonadotrophin-releasing hormone receptor in αT3-1 pituitary gonadotroph cells

1993 ◽  
Vol 136 (1) ◽  
pp. 51-NP ◽  
Author(s):  
L. Anderson ◽  
G. Milligan ◽  
K. A. Eidne
Keyword(s):  
G Protein ◽  
Inositol Phosphate ◽  
Rank Order ◽  
Second Messenger ◽  
Time Dependent ◽  
Binding Studies ◽  
Gnrh Analogues ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

ABSTRACT The present study has characterized the gonadotrophin-releasing hormone (GnRH) receptor in immortalized αT3-1 pituitary gonadotroph cells. GnRH and GnRH analogues produced both a dose- and time-dependent increase in total inositol phosphate (IP) accumulation. The rank order of potency of these analogues was the same as that obtained in parallel receptor-binding studies in αT3-1 cells. These responses were abolished following pretreatment with a GnRH antagonist. The use of a specific inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) assay demonstrated a rapid but short-lived rise in Ins(1,4,5)P3 production. Intracellular calcium ([Ca2+]i) was subsequently measured in αT3-1 cells using dual wavelength fluorescence microscopy combined with dynamic video imaging. GnRH produced a biphasic rise in [Ca2+]i. The initial calcium transient was complete within seconds while the smaller secondary plateau phase lasted several minutes. G-protein involvement in the IP response to GnRH in αT3-1 cells was investigated using sodium fluoride (NaF) and pertussis toxin (PTx) which activate and inactivate G-proteins respectively. Like GnRH, NaF produced a dose- and time-dependent increase in IP accumulation. Activation of phospholipase C in these cells by either GnRH or NaF was PTx-insensitive, suggesting that the G-protein involved was neither Gi nor Go but more probably Gq. Immunoblot analysis of αT3-1 cell membranes using antisera raised against the predicted C-terminal decapeptide of the α subunit of Gq demonstrated the presence of Gq in αT3-1 cells. Collectively these results show that the GnRH receptors expressed in αT3-1 cells are coupled to the phosphatidylinositol second messenger pathway via a specific G-protein. αT3-1 therefore represents a convenient model in which to study GnRH-related second messenger pathways. Journal of Endocrinology (1993) 136, 51–58

Headache

2017 ◽  
Author(s):  
Regina Krel ◽  
Paul G. Mathew
Keyword(s):  
Menstrual Cycle ◽  
Chief Complaint ◽  
Menstrual Migraine ◽  
Clinical Implications ◽  
Menstrually Related Migraine ◽  
Neurology Clinic ◽  
Gender Specific ◽  
Insight Into ◽  
Pure Menstrual Migraine

Migraine is a common disorder that affects women of menstruating age, and it is frequently the chief complaint of women presenting in the neurology clinic. The prevalence of menstrually related migraine can range from 20–60%, while pure menstrual migraine occurs in less than 10% of women. In addition to utilizing non–gender-specific abortive and preventative strategies, understanding migraine and its relationship to hormones, particularly estrogen, can have clinical implications for optimal treatment. This chapter seeks to provide insight into diagnosing menstrually related migraine, the role of decreased estrogen just prior to menstrual cycle onset and migraine, as well as the therapeutic options that are available to treat and possibly prevent menstrual migraine attacks.

Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus

1995 ◽  
Vol 132 (1) ◽  
pp. 91-96 ◽  
Author(s):  
John AM Mattheij ◽  
Hans JM Swarts
Keyword(s):  
Luteinizing Hormone ◽  
The Netherlands ◽  
Small Dose ◽  
Great Majority ◽  
Gnrh Analogue ◽  
Releasing Hormone ◽  
Animal Physiology ◽  
Cause Of Formation ◽  
Gonadotrophin Releasing Hormone ◽  
Lh Secretion

Mattheij JAM, Swarts HJM. Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus. Eur J Endocrinol 1995;132:91–6. ISSN 0804–4643 The cause of formation of luteinized unruptured follicles (LUF) is unknown. Formation of LUF was studied after injection of a varying small dose of luteinizing hormone (LH) with or without subsequent injection of gonadotrophin-releasing hormone (GnRH); in addition, the effect of suppression of prolactin on LUF formation was studied. Luteinization without ovulation occurred in virtually all graafian follicles, if 0.5–1.0 μg of LH was injected some hours before the presumed endogenous LH surge (suppressed by Nembutal); with increasing doses of LH progressively increasing numbers of ovulations were observed. If in early pro-oestrus 1 μg of GnRH was given 4 h after 1 μg of LH, formation of LUF was partly prevented; if the interval between LH and GnRH was 8 h or more, the great majority of graafian follicles developed into LUF. If early in pro-oestrus 1 μg of LH was given and 8 h later 0.1 μg of a potent GnRH analogue, about 50% of the follicles became LUF; in similarly treated rats, suppression of prolactin by ergocryptine reduced but did not prevent LUF formation. The data support the idea that deficient LH secretion in the period before ovulation may be involved in the formation of LUF. John AM Mattheij, Department of Human and Animal Physiology, Haarweg 10, 6709 PJ Wageningen, The Netherlands

The role of hormone replacement therapy in women with a current or past history of endometriosis

2000 ◽  
Vol 6 (1) ◽  
pp. 19-22
Author(s):  
Andrew Prentice
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Past History ◽  
Hormone Replacement ◽  
Premenopausal Women ◽  
Bilateral Oophorectomy ◽  
Releasing Hormone ◽  
History Of ◽  
Gonadotrophin Releasing Hormone

Endometriosis is an oestrogen sensitive condition, leading to reluctance to prescribe hormone replacement therapy. Treatment of endometriosis either medically with gonadotrophin releasing hormone analogues or with surgery involving bilateral oophorectomy leads to oestrogen deficiency. While this may lead to vasomotor symptoms, the consequence which has been of most concern is a reduction in bone mass. Repeated courses of gonadotrophin releasing hormone analogues may mean that women with endometriosis enter the menopause with a below average bone density. Thus, there is a place for hormone replacement therapy both as add-back therapy in premenopausal women receiving gonadotrophin releasing hormone analogues, and in postmenopausal women with a past history of endometriosis. Addback therapy with continuous combined regimes and tibolone do not prevent disease resolution in the hypogonadal patient. The evidence regarding the use of hormone replacement therapy in patients with a history of endometriosis is poor, but suggests that we could be less conservative than we have been.

Effect of gonadotrophin-releasing hormone analogue (GnRH-A) administration on serum gonadotrophin and steroid levels in patients with polycystic ovarian disease

1986 ◽  
Vol 111 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Alessandro Mongioi ◽  
Grazia Maugeri ◽  
Maria Macchi ◽  
Aldo Calogero ◽  
Enzo Vicari ◽  
...  
Keyword(s):  
Marked Decrease ◽  
Close Correlation ◽  
Gnrh Analogue ◽  
Hormone Analogue ◽  
Polycystic Ovarian Disease ◽  
Releasing Hormone ◽  
Ovarian Disease ◽  
Serum Lh ◽  
End Of Treatment ◽  
Gonadotrophin Releasing Hormone

Abstract. A gonadotrophin-releasing hormone (GnRH) analogue, D-Ser[TBU]LRH-EA10, (GnRH-A), at a dose of 200 μg was given daily for 2 months to 6 women with polycystic ovarian disease (PCO). Prior to therapy the patients presented elevated LH, testosterone (T), oestrone (E1) and dihydrotestosterone (DHT) in the circulation. In response to GnRH-A, these subjects exhibited a marked decrease in circulating T, DHT and androstenedione (A) levels as measured 24 h after GnRH-A injection, by 4 weeks and onwards (P < 0.05). After 2 weeks of daily administration, the serum LH profile, evaluated by sampling at 2, 4. 7 and 24 h after injection of GnRH-A, was not different from baseline, whereas after 4, 6 and 8 weeks the levels were significantly lower (*P < 0.01). The profile of serum T levels was unmodified at the second week, but significantly decreased thereafter (*P <0.01). At the end of treatment, the E1 concentrations, elevated in pre-injection condition, were markedly decreased. These data demonstrate that in PCO subjects, GnRH-A significantly lowered the elevated levels of androgens commonly found in these patients. The close correlation observed between reduced serum LH and androgen concentrations suggests that pituitary desensitization could be responsible for the reduction in androgen levels, and may be evidence for a gonadotrophin dependence of the elevated concentrations of T in these patients.

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