scholarly journals SAT-LB1 Detection of Serum Macro-Luteinizing Hormone

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kanako Ogura-Ochi ◽  
Koichi Itoshima ◽  
Yasuhiko Kamada ◽  
Fumio Otsuka
Keyword(s):  
Luteinizing Hormone ◽  
Polycystic Ovary ◽  
Protein A ◽  
Gel Filtration ◽  
Clinical Signs ◽  
Serum Levels ◽  
High Concentration ◽  
Normal Ranges ◽  
Serum Lh ◽  
Lh Releasing Hormone

Abstract Macromolecules of prolactin (PRL) and thyrotropin (TSH), so called macro-PRL and macro-TSH, respectively, are rarely detected in the patients’ serum containing high concentrations of these hormones. The macromolecules are involved in increasing the serum concentrations due to aggregation with the autoantibodies in serum. Here we show a case having macromolecules of luteinizing hormone (LH), possibly due to the complex to immunoglobulin-G (IgG). A 35-year-old Japanese female who has complained menstrual irregularity and had a past surgical history of thyroid cancer was referred to our hospital. Laboratory examination showed an extremely high concentration of serum LH (>200 mIU/ml), while serum levels of follicle-stimulating hormone, estradiol, thyroid hormones, human chorionic gonadotropin, testosterone, and prolactin were all within the normal ranges. MRI study showed a normal pituitary shape without any tumorous lesion. Responses of gonadotropins to LH-releasing hormone (LHRH) stimulation were marginally blunted but showed an LH-dominant pattern such as polycystic ovary syndrome. We suspected the presence of macro-LH because of the divergence between the clinical features and the LH level. Of note, the recovery rate of LH levels after precipitation with polyethylene glycol (PEG) was less than 5%, and the gel-filtration analysis further demonstrated an LH peak slightly earlier fraction than IgG. One case report documented the presence of macro-LH in the serum from a young female patient complicated with autoimmune thyroiditis, suggesting the formation of macro-LH related to some latent autoimmune diseases. To assume macro-LH and to re-examine LH levels after serum precipitation by PEG or protein A/G and fractionation are important to avoid unnecessary treatment to increased LH conditions. In clinical practice, we should suspect the presence of macro-LH, if serum LH levels are unexpectedly high compared to the clinical signs.

RESTORATION OF OESTROGEN POSITIVE FEEDBACK EFFECT ON LH RELEASE BY BROMOCRIPTINE IN HYPERPROLACTINAEMIC PATIENTS WITH GALACTORRHOEA-AMENORRHOEA

1979 ◽  
Vol 91 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Toshihiro Aono ◽  
Akira Miyake ◽  
Takenori Shioji Motoi Yasuda ◽  
Koji Koike ◽  
Keiichi Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Prolactin ◽  
Serum Luteinizing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
The Mean ◽  
Lh Rh ◽  
Lh Releasing Hormone ◽  
Positive Feedback Effect

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

CHANGES IN SERUM LEVELS OF FOLLICLE STIMULATING HORMONE AND LUTEINIZING HORMONE SHORTLY BEFORE AND AFTER PARTURITION IN RATS

1974 ◽  
Vol 75 (3) ◽  
pp. 491-496 ◽  
Author(s):  
Junichi Mori ◽  
Hiroshi Nagasawa ◽  
Reiko Yanai ◽  
Junji Masaki
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Levels ◽  
Sprague Dawley ◽  
Appreciable Change ◽  
Serum Lh ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Average Serum ◽  
Stimulating Hormone

ABSTRACT The sequence of changes in the serum levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) from 2 days before to 24 h after parturition of primiparous Sprague-Dawley rats was investigated by radioimmunoassay. No appreciable change in average serum FSH levels was observed during 2 days before and 1 h after parturition. After this the levels increased gradually to show a peak at 7 h after parturition and then declined gradually until 24 h after parturition. However, the level at 24 h after parturition was still twice as high as that at parturition (0 h). The average serum LH levels which were low between 2 days before and 1 h after parturition, showed a peak at 7 h and decreased toward 13 h after parturition. The same levels as at parturition were maintained between 13 and 24 h after parturition. The time of surge of either FSH or LH was closely related to the time after parturition. There were some differences between FSH and LH in the patterns of sequence of changes in the serum levels near parturition.

EFFECTS OF MATING AND INJECTION OF LUTEINIZING HORMONE RELEASING HORMONE ON SERUM LUTEINIZING HORMONE AND TESTOSTERONE CONCENTRATIONS IN RABBITS

1978 ◽  
Vol 76 (3) ◽  
pp. 417-425 ◽  
Author(s):  
C. A. BLAKE ◽  
PATRICIA K. BLAKE ◽  
NANCY K. THORNEYCROFT ◽  
I. H. THORNEYCROFT
Keyword(s):  
Luteinizing Hormone ◽  
Serum Testosterone ◽  
Serum Levels ◽  
Transient Increase ◽  
Marked Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Before And After ◽  
Lh Rh

The effects of coitus and injection of luteinizing hormone releasing hormone (LH-RH) on serum concentrations of LH, testosterone and dihydrotestosterone (17β-hydroxy-5α-androstan-3-one; DHT) were tested in male rabbits. Before experimentation, male and female rabbits were housed in individual cages in the same room. Male rabbits were then bled by cardiac puncture before and after placement with female rabbits or intravenous injection of LH-RH. Serum LH, testosterone and DHT were measured by radioimmunoassay. Sexual excitement (sniffing, chasing and mounting), with or without intromission, caused a marked rise in serum testosterone and DHT concentrations in only some of the bucks. These increases were accompanied or preceded by a small, transient increase in serum LH. In the rest of the bucks, sexual excitement with or without intromission had either no effect on serum levels of all three hormones, or only serum testosterone and DHT decreased during the collection period. Similar responses were measured in bucks which were housed in a room without does for 2–4 weeks before experimentation. Injection of 10, 30 or 100 ng or 50 μg LH-RH caused serum LH, testosterone and DHT to rise in all bucks tested, but the magnitude of the rises in serum testosterone and DHT were not related to the magnitude of the LH rise. In both mated and LH-RH-injected bucks, the rises in serum testosterone and DHT were greatest in animals with low initial testosterone and DHT values. Under the conditions of this study, the data suggest that: (1) serum testosterone and DHT rise in only some male rabbits after sexual excitement (with or without intromission), (2) the rises in serum testosterone and DHT are dependent on a small transient increase in serum LH and (3) sexual excitement is less likely to cause release of LH-RH in bucks with raised serum testosterone and DHT concentrations.

LUTEINIZING HORMONE RELEASING HORMONE-INDUCED RELEASE OF LUTEINIZING HORMONE FROM PITUITARY EXPLANTS OF COWS KILLED BEFORE OR AFTER OESTRADIOL TREATMENT

1981 ◽  
Vol 88 (1) ◽  
pp. 17-25 ◽  
Author(s):  
E. M. CONVEY ◽  
J. S. KESNER ◽  
V. PADMANABHAN ◽  
T. D. CARRUTHERS ◽  
T. W. BECK
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Oestradiol Treatment ◽  
Readily Releasable Pool ◽  
Serum Lh ◽  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Releasing Hormone

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.

THE EFFECT OF INTRAVENOUS L-DOPA ON GROWTH HORMONE AND LUTEINIZING HORMONE LEVELS IN MAN

1973 ◽  
Vol 73 (2) ◽  
pp. 259-265 ◽  
Author(s):  
Athanasius Souvatzoglou ◽  
Klaus von Werder ◽  
Peter Bottermann
Keyword(s):  
Growth Hormone ◽  
Luteinizing Hormone ◽  
Normal Subjects ◽  
Serum Levels ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Serum Growth Hormone ◽  
Provocative Test ◽  
Hormone Levels ◽  
Serum Lh

ABSTRACT The effect of various intravenous doses of L-dopa on growth hormone and LH-serum levels in 25 normal subjects was investigated. Growth hormone increased 30–40 minutes following the injection of 25 mg and 100 mg L-dopa whereas doses of less than 25 mg had no significant effect on the serum growth hormone levels. The serum LH-level was not significantly altered by the intravenous administration of various doses (1 to 100 mg) of L-dopa. These findings, which are in agreement with the results obtained with L-dopa given orally, suggest that the intravenous injection of 25 mg L-dopa may be useful as a short provocative test for growth hormone release in man.

Effects of chronic treatment with oestrogen, an oestrogen antagonist and a potent luteinizing hormone releasing hormone agonist analogue on pituitary responsiveness to luteinizing hormone releasing hormone in the rat

1983 ◽  
Vol 98 (3) ◽  
pp. 313-321 ◽  
Author(s):  
J. M. Hall ◽  
S. A. Whitehead
Keyword(s):  
Luteinizing Hormone ◽  
Chronic Treatment ◽  
Ex Vivo ◽  
Significant Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
Lh Releasing Hormone

The rise in gonadotrophin release which occurs after ovariectomy is caused by steroid withdrawal resulting in an enhanced pituitary responsiveness to LH releasing hormone (LHRH) associated with increased LHRH release and pituitary LHRH binding. The effects of oestrogen replacement after ovariectomy and chronic treatment of intact rats with an oestrogen antagonist, tamoxifen, on LH release and in-vitro pituitary responses to LHRH have been investigated. Capsules containing crystalline oestradiol, implanted at the time of ovariectomy, completely inhibited the rise in LH release although pituitary responsiveness was greater after 10 days in the oestrogen-treated rats than in untreated ovariectomized controls. On day 4 after ovariectomy pituitary responses to LHRH were comparable in both treated and untreated groups although in both groups the responses were greater than those measured in intact dioestrous rats. Treatment with tamoxifen over a 4-day period also augmented pituitary responsiveness but only at the lowest dose (0·5 mg/kg); no effect on serum LH concentrations was observed. Higher doses of the antagonist (1 and 2 mg/kg) did not affect pituitary responses, although the highest dose did cause a significant rise in serum LH. Treatment with a daily dose of 50 ng [d-Ser(But)6]LHRH(1–9)nonapeptide-ethylamide, starting on the day of ovariectomy, markedly attenuated the LH responses to LHRH ex vivo at days 2, 4 and 10 after ovariectomy. In contrast, the analogue treatment did not abolish the rise in LH release but this was proportionately less than in controls.

scholarly journals Frequency of Macroprolactinemia Due to Autoantibodies against Prolactin in Pregnant Women

2001 ◽  
Vol 86 (2) ◽  
pp. 924-929 ◽  
Author(s):  
Dalila Pascoe-Lira ◽  
Genoveva Duran-Reyes ◽  
Iris Contreras-Hernández ◽  
Leticia Manuel-Apolinar ◽  
Francisco Blanco-Favela ◽  
...  
Keyword(s):  
Polyethylene Glycol ◽  
Pregnant Women ◽  
Molecular Mass ◽  
Chromatographic Separation ◽  
Protein A ◽  
Gel Filtration ◽  
Serum Levels ◽  
The Other ◽  
Positive Correlation ◽  
Before And After

The frequency of macroprolactinemia related to the presence of anti-PRL autoantibodies in the serum of 209 healthy women at different stages of pregnancy was studied. Measurements were taken of serum PRL concentrations before and after chromatographic separation (gel filtration and affinity with proteins A and G) and extraction of free PRL with polyethylene glycol (PEG). Sera from 8 of the 209 women (3.8%) were found to have a significantly high proportion of precipitated PRL by PEG (macroprolactinemia); in these patients, gel filtration showed that a substantial amount of big big PRL (molecular mass >100 kDa) was present (19.0–78.2% vs. 3.8–4.9%, P = 0.009 in normal pregnant women with a normal proportion of precipitated PRL by PEG). The presence of macroprolactinemia was attributable to anti-PRL autoantibodies in 5 of the 8 women. Comparison of serum levels of direct and free PRL between women with macroprolactinemia related to anti-PRL autoantibodies and women without macroprolactinemia showed significant differences (direct PRL: 270.2 ± 86.9 vs. 203.4 ± 69.0 μg/L, P = 0.04; and free PRL: 107.0 ± 75.9 vs. 173.3 ± 67.6 μg/L, P = 0.002). On the other hand, there was no difference between women with macroprolactinemia not related to anti-PRL autoantibodies and women with macroprolactinemia caused by anti-PRL autoantibodies, nor was there a difference between women with macroprolactinemia not related to anti-PRL autoantibodies and women without macroprolactinemia. There was a positive correlation between titers of the anti-PRL autoantibody and serum PRL levels (r = 0.82, P = 0.09). The presence of the anti-PRL autoantibody had no relation to the patient’s age, stage of gestation, or number of previous pregnancies. We concluded that the frequency of macroprolactinemia was 3.8% among healthy, pregnant women, which was caused by a anti-PRL autoantibodies in 62.5% of the cases. The autoantibodies were found in the bloodstream, forming a PRL-IgG complex, in accordance with the following observations: 1) immunoreactive PRL on gel filtration was eluted in the fractions corresponding to the molecular mass of IgG (150 kDa); 2) a significantly high proportion of immunoreactive PRL was retained on an affinity gel for IgG (proteins A and G); and 3) a significantly high proportion of serum PRL bound to IgG was precipitated by protein A. There was a positive correlation between titers of anti-PRL autoantibodies and serum PRL levels. Serum levels of total PRL were higher, and serum levels of free PRL were lower, in pregnant women with anti-PRL autoantibodies than in pregnant women without macroprolactinemia.

Inhibition of luteinizing hormone, follicle-stimulating hormone and sex-steroid levels in men and women with a potent antagonist analog of luteinizing hormone-releasing hormone, Cetrorelix (SB-75)

1994 ◽  
Vol 131 (3) ◽  
pp. 286-292 ◽  
Author(s):  
David Gonzalez-Barcena ◽  
Manuel Vadillo Buenfil ◽  
Emilo Garcia Procel ◽  
Laura Guerra-Arguero ◽  
Imelda Cardenas Cornejo ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Free Testosterone ◽  
Serum Levels ◽  
Routes Of Administration ◽  
Serum Lh ◽  
The Mean ◽  
Potent Antagonist ◽  
Normal Men ◽  
Stimulating Hormone

Gonzalez-Barcena D, Vadillo Buenfil M, Garcia Procel E, Guerra-Arguero L, Cardenas Cornejo I, Comaru-Schally AM, Schally AV. Inhibition of luteinizing hormone, follicle-stimulating hormone and sex-steroid levels in men and women with a potent antagonist analog of LH-RH, Cetrorelix (SB-75). Eur J Endocrinol 1994;131:286–92. ISSN 0804–4643 Cetrorelix (SB-75; [Ac-d-Nal(2)1, d-Phe(4Cl)2, d-Pal(3)3, d-Cit6, d-Ala10] luteinizing hormone-releasing hormone (LHRH)) is a new highly potent antagonist analog of LHRH containing the d-ureidoalkyl amino acid d-citrulline at position 6 and is free of allergenic effects. This study shows the inhibition of LH and follicle-stimulating hormone (FSH) release in normal men, postmenopausal women and patients with gonadal dysgenesis, using different doses and im, sc and iv routes of administration of SB-75. The mean serum levels of LH and FSH in normal men who received one single dose of 300 μg of SB-75 sc started to decline rapidly 1 h after its administration; the LH suppression was sustained for 14 h and that of FSH up to 24 h or longer as the samples were obtained only up to this time. The nadir for LH was reached at 14 h and that for FSH at 24 h or later after administration of the antagonist (p < 0.05). Serum levels of total and free testosterone decreased after the first hour and this inhibition was maintained for up to 14 h. The nadir for total testosterone was at 6 h and that for free testosterone was at 8 h (p < 0.001), corresponding to 56% and 60% of inhibition, respectively. In postmenopausal women, inhibition of the elevated basal serum LH and FSH levels occurred after a single injection of the antagonist analog SB-75 in doses of 75, 150, 300, 600 and 1200 μg using im, sc and iv routes of administration. The mean resting levels of serum LH and FSH showed a significant decrease for all doses and routes of administration of SB-75 (p < 0.01). Maximal inhibition was observed 6–12 h after administration. After administration of 300 μg of SB-75 sc every 12 h for 3 days, serum LH and FSH continued to be secreted but a marked decrease in the basal levels of both gonadotropins was observed. A fall in LH and FSH also was produced in patients with gonadal dysgenesis who were given 300 μg of SB-75. The nadir of serum LH was 61 ± 9.6% for the iv route and 58.5 ± 7.5% for the sc route (p < 0.01); for serum FSH it was 51 ± 7.5% and 48.5 ± 7.5% (p < 0.01), respectively, of the baseline levels. These results show that the antagonistic analog SB-75 is devoid of allergenic effects, extremely active in small doses and can be administered safely to humans. The development of sustained delivery systems for SB-75 should facilitate the clinical use of this powerful LHRH antagonist. David Gonzalez-Barcena, Hospital de Especialidades Centro Medico La Raza, Seris Y Zaachila, Col. La Raza, Mexico D.F.

ABSENCE OF INHIBITION BY HYPERPROLACTINAEMIA ON OVARIAN RESPONSE TO EXOGENOUS GONADOTROPHIN

1978 ◽  
Vol 89 (1) ◽  
pp. 142-148 ◽  
Author(s):  
Toshihiro Aono ◽  
Motoi Yasuda ◽  
Takenori Shioji ◽  
Kunio Kondo ◽  
Keiichi Kurachi
Keyword(s):  
Menstrual Cycle ◽  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Ovarian Response ◽  
Serum Levels ◽  
Control Group ◽  
Serum Lh ◽  
Human Menopausal Gonadotrophin ◽  
Injection Control ◽  
The Mean

ABSTRACT In order to assess the effect of hyperprolactinaemia on the ovarian response to exogenous gonadotrophin, serum oestrogen levels were determined in 6 normal females. Two hundred and twenty-five IU of human menopausal gonadotrophin (hMG) was im injected daily for 3 days from the 4th day of the menstrual cycle, and the serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and oestradiol-17β were determined by radioimmunoassay daily for 7 days starting from the first day of injection (control cycle). After 2 months the same schedule was applied to the previous 6 subjects and in addition sulpiride 100 mg bid was given orally during the course of the study (sulpiride cycle). There was a significant increase in serum FSH and a decline in serum LH during hMG treatment in both groups. The mean (± se) serum levels of PRL in the sulpiride group increased gradually from 24.5 ± 3.8 ng/ml (1st day) to 56.2 ± 3.4 ng/ml (7th day). All these levels were significantly higher than those of the control group. The mean (± se) serum oestradiol increments by hMG stimulation in control and sulpiride groups showed a peak on the 5th day with respective levels of 757.2 ± 202.3 and 845.3 ± 263.3 pg/ml. No significant differences in the mean oestradiol increment were found between the two groups on any day. These results indicate that acute hyperprolactinaemia does not appear to induce ovarian refractoriness to exogenous gonadotrophin in normal cyclic women.

Revisiting the serum level of anti-Müllerian hormone in patients with functional hypothalamic anovulation

2021 ◽  
Author(s):  
Sarah Makolle ◽  
Sophie Catteau-Jonard ◽  
Geoffroy Robin ◽  
Didier Dewailly
Keyword(s):  
Polycystic Ovary ◽  
Serum Levels ◽  
Total Testosterone ◽  
Strong Positive Correlation ◽  
Polycystic Ovaries ◽  
Positive Correlation ◽  
Serum Lh ◽  
Significant Difference ◽  
Registration Number ◽  
Competing Interest

Abstract STUDY QUESTION Are serum levels of anti-Müllerian hormone (AMH) normal in patients with functional hypothalamic anovulation (FHA)? SUMMARY ANSWER Our study confirms that in the general FHA population, serum AMH levels are not decreased, but if patients with polycystic ovarian morphology (PCOM) are excluded, levels become significantly lower, as in other situations of gonadotropic insufficiency. WHAT IS KNOWN ALREADY In most situations of low LH (physiological, pharmacological or pathological), serum AMH levels are low. However, paradoxically, many publications have reported normal or even increased serum AMH levels in FHA patients. STUDY DESIGN, SIZE, DURATION Retrospective observational study conducted in an academic centre. The data concerning the study population was collected between 2006 and 2015 from a database including clinical, biological and ultrasound information. PARTICIPANTS/MATERIALS, SETTING, METHODS A total of 45 FHA patients were compared to 37 controls matched based on age and body mass index (BMI). Serum LH, FSH, androstenedione, total testosterone, prolactin and AMH levels were measured by immunoassay. We defined PCOM with strict criteria: a follicle number per ovary (FNPO) ≥ 12 or ≥ 19 per ovary, depending on the date on which the assessment was carried out and the ultrasound device. An AMH level ≥ 35 pmol/l could be a substitute for an excess FNPO. Controls meeting these criteria were not included in this study. MAIN RESULTS AND THE ROLE OF CHANCE There was no significant difference in the ranges of AMH levels between FHA and controls. Using strict criteria to define PCOM status, 46.7% of FHA patients had PCOM. After excluding these patients, the levels of AMH were significantly lower (P &lt; 0.002) in FHA patients compared to controls. Within the FHA group, patients with PCOM had significantly higher ranks of AMH levels and BMI than those without PCOM. However, within the PCOM+ subgroup, the ranks of LH, FSH and A levels were still lower than in controls (P  &lt; 0.0001, &lt;0.002 and &lt;0.05, respectively). The positive correlation between AMH and LH was significant in the controls but not in the FHA group. However, in the FHA PCOM+, there was a strong positive correlation between BMI and LH. LIMITATIONS, REASONS FOR CAUTION This is a retrospective study; our controls did not represent the general population as they were recruited in an ART centre; we used a modified classification for PCOM using follicle count and/or AMH level with in-house thresholds to define the follicle excess; the AMH assay used is no longer commercially available. WIDER IMPLICATIONS OF THE FINDINGS Besides biasing the results of AMH assay in FHA patients, the presence of PCOM in FHA patients despite low gonadotropin and androgen levels raises the issue of epigenetically acquired amplification of androgen and/or FSH sensitivity within granulosa cells from polycystic ovaries. In terms of clinical practice, it seems important not to diagnose a low ovarian reserve in FHA patients too quickly on the basis of a decreased AMH level alone. On the contrary, a high AMH level in the context of a menstrual disorder and PCOM should not lead to a misdiagnosis of polycystic ovary syndrome (PCOS) if the basal LH is low. STUDY FUNDING/COMPETING INTEREST(S) None TRIAL REGISTRATION NUMBER N/A

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