Female Quick Check Basic Panel
The Female Quick Check Basic Panel combines the gonadotrophins FSH and LH with oestradiol, prolactin, TSH, and total testosterone to provide an initial assessment of the hypothalamic-pituitary-ovarian axis and identify common endocrine causes of menstrual disturbance.
6
Biomarkers
Blood (serum)
Sample
2–5 business days
Turnaround
No — fasting is not required, though morning collection is preferred, particularly for prolactin and testosterone which both show diurnal variation
Fasting
What is the Female Quick Check Basic test?
The Female Quick Check Basic Panel provides an initial hormonal assessment in women presenting with menstrual disturbance, suspected hormonal imbalance, subfertility, or symptoms suggesting hyperandrogenism or thyroid dysfunction. It combines the gonadotrophins and oestradiol, which characterise the hypothalamic-pituitary-ovarian axis, with prolactin, TSH, and total testosterone, which identify common endocrine causes of menstrual disturbance that lie outside the ovary itself. Its purpose is to establish where in the axis a problem originates and to identify readily correctable contributors. The single most important determinant of whether this panel can be interpreted is when in the menstrual cycle it is collected. FSH, LH, and oestradiol vary several-fold across the cycle, so a specimen drawn on an unknown cycle day in a menstruating woman produces numbers that cannot be meaningfully interpreted — this is not a refinement but a precondition. For baseline assessment and ovarian reserve, collection on cycle days 2 to 5 is required, counting from the first day of full flow. If the clinical question is whether ovulation has occurred, that requires a mid-luteal progesterone measured approximately seven days before the expected period, which this basic panel does not include. In amenorrhoeic women, pregnancy must be excluded first, after which specimens may be collected at any time since no cycle reference exists. In postmenopausal women, cycle timing is irrelevant and the expected pattern is elevated gonadotrophins with low oestradiol. The panel is designed to sort presentations into recognisable patterns rather than to diagnose a single condition. Raised FSH and LH with low oestradiol indicates primary ovarian insufficiency or menopause. Low or inappropriately normal gonadotrophins with low oestradiol indicates a hypothalamic or pituitary cause, including functional hypothalamic amenorrhoea from low energy availability, excessive exercise, or psychological stress. Raised prolactin points towards hyperprolactinaemia and warrants its own pathway. An abnormal TSH identifies thyroid dysfunction, which is both a common cause of menstrual disturbance and a cause of secondary hyperprolactinaemia — so thyroid status should be established before an isolated raised prolactin is investigated further. Raised testosterone suggests hyperandrogenism, most commonly polycystic ovary syndrome, though marked or rapidly progressive elevation requires exclusion of an androgen-secreting tumour. Two limitations should be understood at the outset. Polycystic ovary syndrome cannot be diagnosed from this panel: the Rotterdam criteria require two of oligo-ovulation, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology on ultrasound, together with exclusion of other causes, so a suggestive result requires ultrasound and clinical correlation. And the analytical performance of immunoassays is poor at the low oestradiol and testosterone concentrations found in women, particularly postmenopausal women, where mass spectrometry is considerably more reliable.
What does the Female Quick Check Basic test measure?
Follicle stimulating hormone is a gonadotrophin secreted by the anterior pituitary under pulsatile gonadotrophin-releasing hormone control, which stimulates ovarian follicular recruitment and granulosa cell oestradiol production. It is regulated by negative feedback from oestradiol and inhibin B, so as the follicular pool declines with age, reduced inhibin B feedback allows FSH to rise. Levels vary markedly across the menstrual cycle, with a follicular baseline, a mid-cycle surge, and a luteal decline.
FSH measured on cycle days 2 to 5 provides a conventional assessment of ovarian reserve, with elevation indicating diminished reserve, and is central to distinguishing primary ovarian insufficiency from hypothalamic or pituitary causes of amenorrhoea. It is interpreted only alongside oestradiol, since a raised oestradiol suppresses FSH and can mask diminished reserve. Anti-Mullerian hormone and antral follicle count are less cycle-dependent and have largely superseded FSH for ovarian reserve assessment in fertility practice.
Luteinising hormone is the second gonadotrophin, secreted in pulses that vary in frequency and amplitude across the cycle. It stimulates ovarian theca cell androgen production and triggers ovulation through a mid-cycle surge, then supports the corpus luteum. Because secretion is pulsatile, a single measurement samples one point in an oscillating signal.
LH is interpreted alongside FSH rather than alone. An elevated LH to FSH ratio has historically been associated with polycystic ovary syndrome, though it is neither sensitive nor specific and is not a diagnostic criterion under the Rotterdam consensus. Both gonadotrophins elevated indicates primary ovarian failure, while both low or inappropriately normal in the presence of low oestradiol indicates a hypothalamic or pituitary cause. Pulsatile secretion limits the interpretive weight of any single value.
Oestradiol is the principal circulating oestrogen, produced predominantly by ovarian granulosa cells under FSH stimulation, with smaller contributions from peripheral aromatisation of androgens in adipose tissue. It rises through the follicular phase to a pre-ovulatory peak that triggers the LH surge, falls after ovulation, and rises again in the luteal phase. Most circulating oestradiol is bound to sex hormone binding globulin and albumin.
Oestradiol is essential context for interpreting FSH, since an elevated early-follicular oestradiol suppresses FSH and can conceal diminished ovarian reserve — the two must always be read together. It confirms ovarian activity, assists in distinguishing menopausal status, and is central to the assessment of amenorrhoea. Immunoassay performance is limited at the low concentrations characteristic of postmenopausal women, where mass spectrometry provides better reliability.
Prolactin is secreted by anterior pituitary lactotrophs under predominantly inhibitory dopaminergic control. Pathological elevation suppresses gonadotrophin-releasing hormone and causes secondary hypogonadism, which is the mechanism linking hyperprolactinaemia to menstrual disturbance and infertility. Circulating prolactin includes both biologically active monomeric prolactin and macroprolactin, an immunoreactive but inactive immunoglobulin complex.
Prolactin is included because hyperprolactinaemia is a readily identifiable and treatable cause of oligomenorrhoea, amenorrhoea, galactorrhoea, and infertility. Two analytical pitfalls apply: macroprolactin falsely elevates the measured value in patients without true hyperprolactinaemia and should be excluded by polyethylene glycol precipitation where the result is unexplained, and the high-dose hook effect can produce a falsely low result in the presence of a very large prolactinoma. Venepuncture stress alone raises prolactin, so a mild elevation warrants a rested repeat sample before investigation.
Thyroid stimulating hormone is secreted by anterior pituitary thyrotrophs under negative feedback from circulating thyroid hormones. Because the feedback relationship is log-linear, small changes in free thyroxine produce large amplified changes in TSH, making it the most sensitive first-line indicator of thyroid status in patients with an intact pituitary axis.
TSH is included because thyroid dysfunction is a common and correctable cause of menstrual disturbance, anovulation, and infertility, and because primary hypothyroidism raises prolactin through elevated thyrotrophin-releasing hormone — so an abnormal TSH may explain an abnormal prolactin. It is unreliable in central hypothyroidism, during acute illness, and within six to eight weeks of a thyroid dose change, and pregnancy requires trimester-specific interpretation.
Testosterone in women derives roughly equally from ovarian theca cells and the adrenal cortex, with a further contribution from peripheral conversion of androstenedione and DHEA. Circulating concentrations are approximately one twentieth of male levels, and most is bound to sex hormone binding globulin, leaving a small free fraction that is biologically active.
Total testosterone is measured in the assessment of hirsutism, acne, androgenic alopecia, and suspected polycystic ovary syndrome, and to exclude an androgen-secreting tumour where hyperandrogenism is severe or rapidly progressive. Its principal limitation in women is analytical: female concentrations sit at the lower limit of most immunoassays, where performance is poor, and mass spectrometry is substantially more reliable. Because SHBG is suppressed by insulin resistance, a normal total testosterone can accompany clinically significant free androgen excess, so SHBG or a free androgen index adds interpretive value.
Why is the Female Quick Check Basic test ordered?
- Initial assessment of oligomenorrhoea, amenorrhoea, or irregular cycles, collected on cycle days 2 to 5 where menstruation is occurring and after exclusion of pregnancy
- Baseline hormonal evaluation in subfertility, recognising that confirmation of ovulation requires a mid-luteal progesterone not included in this panel
- Investigation of suspected polycystic ovary syndrome, as a contribution to the Rotterdam assessment alongside ultrasound and clinical evaluation rather than as a standalone diagnostic
- Assessment of hirsutism, acne, or androgenic alopecia, where marked or rapidly progressive hyperandrogenism additionally warrants exclusion of an androgen-secreting tumour
- Evaluation of suspected primary ovarian insufficiency in women under 40 with menstrual disturbance, where raised gonadotrophins with low oestradiol support the diagnosis
- Confirmation of menopausal status where the clinical picture is unclear, particularly in women with a hysterectomy or on hormonal contraception
- Assessment of galactorrhoea or suspected hyperprolactinaemia, alongside thyroid status since primary hypothyroidism raises prolactin
Sample collection and turnaround
Sample type
Blood (serum)
Fasting required
No — fasting is not required, though morning collection is preferred, particularly for prolactin and testosterone which both show diurnal variation
Collection method
Venipuncture at patient service centre
Turnaround
2–5 business days
Collection notes
Collect on cycle days 2 to 5, counting from the first day of full flow, for baseline and ovarian reserve assessment, and record the actual cycle day on the request — results collected on an undocumented cycle day cannot be interpreted. In amenorrhoeic women, exclude pregnancy first, after which collection may occur at any time. Morning collection is preferred, in a calm rested state to avoid stress-related prolactin elevation, and avoid collection immediately after exercise or breast examination. Document hormonal contraception or hormone therapy and any recent cessation, all dopamine antagonist medications, biotin supplementation, pregnancy and lactation status, and thyroid therapy. Where prolactin is unexpectedly raised, request macroprolactin assessment; where hyperandrogenism is suspected, consider adding SHBG.
Specimen requirements
Serum volume sufficient for all panel components per Access Medical Laboratories protocol. Separate serum from cells promptly. Specimen stable refrigerated; follow Access Medical Laboratories transport guidelines.
What can affect Female Quick Check Basic results?
FSH, LH, and oestradiol vary several-fold across the cycle, so results collected on an unrecorded cycle day cannot be interpreted. Day 2 to 5 collection is required for baseline and ovarian reserve assessment, and the actual cycle day must be documented on the request.
Combined oral contraceptives suppress gonadotrophins and ovarian oestradiol production and raise sex hormone binding globulin, which lowers free androgen availability. Results obtained on hormonal contraception do not reflect underlying ovarian function, and a washout period is generally required before meaningful assessment.
Pregnancy profoundly alters all components of this panel, raising oestradiol and prolactin markedly and suppressing gonadotrophins, and requires trimester-specific TSH interpretation. Pregnancy must be excluded before interpreting an amenorrhoeic presentation.
Prolactin rises acutely with the stress of venepuncture, with sleep, and with exertion, so a mild elevation frequently resolves on a calm rested repeat sample and should be confirmed before investigation proceeds.
Antipsychotics, metoclopramide, domperidone, some antidepressants, and opioids block dopaminergic inhibition and raise prolactin. Drug-induced hyperprolactinaemia is substantially commoner than prolactinoma and should be excluded by medication review before imaging.
Oestradiol and testosterone concentrations in women, particularly postmenopausal women, fall at the lower limit of immunoassay performance where mass spectrometry is preferred. High-dose biotin additionally interferes with streptavidin-biotin immunoassays and can distort several components of this panel in either direction.
What do Female Quick Check Basic results mean?
Elevated
Raised FSH and LH with low oestradiol indicates primary ovarian insufficiency in women under 40, or physiological menopause in older women, and should be confirmed on a repeat sample. Raised prolactin requires confirmation on a rested sample, then exclusion of pregnancy, medication effect, and hypothyroidism, with macroprolactin assessment where the elevation is unexplained. Raised testosterone suggests hyperandrogenism, most commonly polycystic ovary syndrome, though a markedly raised value or rapidly progressive virilisation requires prompt exclusion of an androgen-secreting ovarian or adrenal tumour. An elevated TSH indicates hypothyroidism and may itself explain both menstrual disturbance and a raised prolactin.
Normal
A normal panel collected on a documented early follicular day makes primary ovarian insufficiency, hyperprolactinaemia, overt thyroid dysfunction, and significant hyperandrogenism less likely, but does not exclude them and does not confirm ovulation. Confirming ovulation requires a mid-luteal progesterone, which this panel does not include. A normal total testosterone does not exclude clinically significant free androgen excess where sex hormone binding globulin is suppressed by insulin resistance, and a normal panel does not exclude polycystic ovary syndrome, which is diagnosed on the Rotterdam criteria including ultrasound.
Reduced
Low oestradiol with low or inappropriately normal gonadotrophins indicates a hypothalamic or pituitary cause rather than ovarian failure, and the commonest explanation is functional hypothalamic amenorrhoea arising from low energy availability, excessive exercise, weight loss, or psychological stress — a diagnosis of exclusion that warrants attention to nutritional and psychological factors. Pituitary causes including hyperprolactinaemia and hypopituitarism should be considered, particularly where other pituitary axes are also affected. A suppressed TSH indicates hyperthyroidism, which is also a recognised cause of menstrual disturbance.
Note: Cycle timing is a precondition for interpretation rather than a refinement: FSH, LH, and oestradiol collected on an unrecorded cycle day cannot be meaningfully assessed. This panel does not confirm ovulation, which requires mid-luteal progesterone, and does not diagnose polycystic ovary syndrome, which requires the Rotterdam criteria including ultrasound and exclusion of other causes. Results obtained on hormonal contraception do not reflect underlying ovarian function. Immunoassay performance is poor at the low oestradiol and testosterone concentrations found in women, where mass spectrometry is preferred, and prolactin carries its own macroprolactin and hook effect pitfalls.
Frequently asked questions
It combines FSH, LH, and oestradiol to characterise the hypothalamic-pituitary-ovarian axis with prolactin, TSH, and total testosterone, which identify common endocrine causes of menstrual disturbance arising outside the ovary.
How to access the Female Quick Check Basic test
The Female Quick Check Basic reference page is free and open to all practitioners. Create a free practitioner account to see pricing, save tests to your list, and generate requisition forms. Verification takes 1–2 business days.
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Published: July 16, 2026
Last reviewed: July 16, 2026
- Teede HJ, et al. Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Hum Reprod. (2018)
- Melmed S, et al. Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. (2011)
- Gordon CM, et al. Functional Hypothalamic Amenorrhea: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. (2017)
- Rosenfield RL, Ehrmann DA. The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited. Endocr Rev. (2016)
This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.
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