No rush to label teens as having PCOS, says expert


Dr Veronique Celine Viardot-Foucault.

Diagnosis of polycystic ovary syndrome (PCOS) is challenging, and there should be no rush to label an adolescent as having the condition before a thorough evaluation of symptoms, according to a leading endocrinologist who was speaking at the RCOG World Congress 2018 in Singapore.

“Common features of PCOS such as hirsutism, acne, and obesity are often present in otherwise ‘normal’ adolescents,” said Dr Veronique Celine Viardot-Foucault from the KK Women’s and Children’s Hospital, Singapore, adding that these features may not necessarily be indicative of PCOS.

Appropriate diagnosis of PCOS in adolescents should involve careful evaluation of symptoms such as menstrual irregularities, hyperandrogenism, and polycystic ovarian morphology, she said. Menstrual irregularities—including secondary amenorrhoea and oligomenorrhoea in girls beyond 2 years after menarche, or primary amenorrhoea in those who have completed puberty—may be indicative of androgen excess. [Horm Res Paediatr 2017;88:371-395]

As symptom such as acne is common in adolescence and usually transient, it may not be indicative of hyperandrogenism, said Viardot-Foucault. Also, isolated cases of acne and/or alopecia should not be considered as diagnostic criteria for PCOS in adolescence, but moderate or severe inflammatory acne that is unresponsive to topical therapy may require investigation of androgen excess. [Horm Res Paediatr 2017;88:371-395]

Another feature commonly seen with PCOS is hirsutism, which can be evaluated using the modified Ferriman–Gallwey (FG) scoring system. “However, the FG scoring system is not applicable to younger, perimenarchal patients [younger than 15 years old],” she advised, pointing out that biochemical evidence of hyperandrogenism is preferred in this group.

As there is no clear cut-off of testosterone levels for adolescents, biochemical hyperandrogenism should be defined based on the methodology used, informed Viardot-Foucault. “Ideally, to establish the existence of androgen excess, assaying for free testosterone levels is the gold standard as it is more sensitive than measuring the total testosterone levels,” she said. “But a downside of this is that it requires equilibrium dialysis techniques which are costly and not widely available.”

However, most commercial laboratories use direct analogue radio-immunoassay, which is notoriously inaccurate for measuring free testosterone, cautioned Viardot-Foucault. “If uncertain regarding the quality of the free testosterone assay, it is preferable to rely on calculated free testosterone, which has a good concordance and correlation with free testosterone levels measured by equilibrium dialysis methods,” she suggested. [J Clin Endocrinol Metab 1999;84:3666-3672]

Also, the value of measuring other androgens besides free testosterone in patients with PCOS is relatively low, although increased levels of dehydroepiandrosterone sulphate (DHEAS) have been observed in 30–35 percent of PCOS patients. [Ann N Y Acad Sci 2006;1092:130-137]

“Transabdominal pelvic ultrasound has a lower diagnostic accuracy,” said Viardot-Foucault. “The presence of polycystic ovarian morphology [on ultrasound] in an adolescent who does not have hyperandrogenism or oligo-anovulation does not indicate a diagnosis of PCOS.”

When menstrual irregularities are concerned, the first-line treatment should be cyclical progestogens when contraception is not required and there are no signs of hyperandrogenism, according to Viardot-Foucault. If there is clinical hyperandrogenism or a need for contraception in those sexually active, third-generation oral contraceptives such as ethinyl estradiol 30 µg can be considered.

“There is room for local treatment of hirsutism such as laser [hair removal, but only for patients beyond] 16 years old and [who are] at least 2 years post-menarche,” she said. “If there are metabolic complications, [patients should be referred] to the endocrinologist.”

Links Between Fatty Liver Disease and Polycystic Ovary Syndrome


The possible link between these two conditions may have a number of implications for the diagnosis and treatment of various diseases among women.

A growing body of research indicates that non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) may be related and, due to shared mechanisms, may increase the risk of type 2 diabetes (T2D) and other cardiometabolic complications. The findings may have a number of implications for the diagnosis and treatment of various diseases.

Although the etiology of PCOS, one of the most common endocrine disorders in women of reproductive age, is uncertain, obesity and insulin resistance are frequently present in affected individuals, and they play a role in its development. The condition affects 5% to 18% of this population depending on the diagnostic criteria used, and clinical features consist of menstrual dysfunction, infertility, hirsutism, acne, and alopecia.

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Similarly, obesity and insulin resistance appear to contribute to the pathogenesis of NAFLD, which is characterized by increased accumulation of fat in the liver in the absence of significant alcohol consumption. NAFLD includes a range of diseases, from simple steatosis to non-alcoholic steatohepatitis to cirrhosis, and it has an estimated worldwide prevalence of 6.3% to 33.0%; however, if obesity or T2D is involved, the prevalence of NAFLD rises to approximately 75%.

2

A connection, but few reasons as to why

NAFLD and PCOS occur together more frequently than expected, in many cases simply by chance alone. Studies have consistently shown that NAFLD rates are elevated in young women with PCOS, independent of weight and metabolic syndrome features, and limited data suggest that these women have better odds of experiencing more severe forms of NAFLD.

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In one recent study, by Evangeline Vassilatou, MD, PhD, an endocrinologist at the Attikon University General Hospital, in Athens, Greece, NAFLD was detected in 71 of 110 (64.5%) overweight and obese (yet otherwise apparently healthy) premenopausal women, and women with NAFLD were more often diagnosed with PCOS than women without NAFLD (43.7% versus 23.1%, respectively).

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It’s currently unclear how the two conditions may influence each other: Are they a consequence of shared risk factors? Or does one condition contribute to the other independently of these factors? Accumulating evidence indicates that NAFLD may exacerbate insulin resistance and release multiple pro-inflammatory, pro-coagulant, and pro-fibrogenic mediators that could contribute to the pathophysiology of PCOS.

3

On the other hand, insulin resistance and androgen excess are the main characteristics of PCOS that could increase the risk of developing NAFLD.

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To examine the most relevant factors associated with NAFLD in women with PCOS, investigators recently conducted a cross-sectional study including 600 Caucasian women diagnosed with PCOS between May 2008 and May 2013 and 125 women matched for body mass index.

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NAFLD, which was diagnosed by an NAFLD liver fat score, was identified in 50.6% of women with PCOS, compared with 34.0% of controls. Women with PCOS had higher readings for waist circumference, lipid accumulation product (a combination of waist circumference and fasting triglyceride levels), insulin resistance, total cholesterol, and triglycerides than controls. Upon further analysis, insulin resistance and lipid accumulation product were independently associated with NAFLD.

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“This study provided further evidence that PCOS women are more prone to develop NAFLD compared with non-PCOS premenopausal women, and that features of the metabolic dysfunction that characterize PCOS are the main factors implicated in the development of NAFLD in these patients,” says Dr. Vassilatou, who wasn’t involved with the study. “Some research also suggests that androgen excess, which is a key feature of PCOS and is interrelated to insulin resistance, may be an additional contributing factor for the development of NAFLD in PCOS.”

Just scratching the surface

Dr. Vassilatou says that more research is needed to understand the role of androgens, if any, in the pathophysiology of NAFLD in women with PCOS. Also, long-term follow-up studies are necessary to reveal the range of liver-related outcomes in women with PCOS and to determine the natural history of NAFLD in these women—for example, how often it progresses from its early stages to severe liver disease. It will also be important to investigate whether obese patients with PCOS and NAFLD present more frequently with an advanced stage of liver disease, as reported in a few studies.

Although additional studies are needed to clarify the association between PCOS and NAFLD, accumulating data over the past decade indicate that clinicians should at least be aware of this connection. “Thus, these women should be screened for NAFLD, particularly obese patients with features of the metabolic syndrome. Conversely, premenopausal women with NAFLD should be screened for PCOS,” suggests Dr. Vassilatou.

Despite the need for greater screening, more work is necessary to identify the most appropriate methods, which could include ultrasound, liver function tests, and algorithms such as the NAFLD liver fat score. Furthermore, because there’s no medical therapy of proven benefit for treating NAFLD, well-designed interventional studies—with lifestyle modifications and/or the use of medical therapy targeting insulin resistance, impaired glucose tolerance, and dyslipidemia—are needed to determine the optimal management of affected patients.

To get a sense of where we are now, diet, weight loss, and exercise are currently the cornerstone of therapy and are often combined with insulin sensitizers, hypolipidemic drugs, and hepatoprotective agents, like antioxidants.

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Published: March 17, 2017

7 Subtle Signs You Could Have PCOS


Experts believe that more than half of women with polycystic ovary syndrome don’t even realize they have it.
PCOS_Feature

If you’ve skipped a period or two (and know you’re not pregnant) and have been breaking out like you’re a teenager again, it’s easy to chalk it all up to stress. But something more serious may be going on, such as polycystic ovary syndrome (PCOS), a stealth health issue caused by a hormonal imbalance and marked by a series of small cysts on the ovaries.

Five to 10 percent of women of childbearing age are affected by the condition, but less than half of women are diagnosed, according to the PCOS Foundation. That means millions of women have PCOS and don’t even know it. To shed some light on this silent disease, here are the most common not-so-obvious signs of the hormonal disorder. If you’re experiencing any of these symptoms, bring them up with your gynecologist or general practitioner and get them evaluated.

1. Your cycle is all over the place.

Unpredictable menstrual cycles or skipping several periods are one of the hallmarks of PCOS. “Our menstrual cycle is like a vital sign,” says Maryam Siddiqui, MD, assistant professor of obstetrics-gynecology at the University of Chicago Medicine. “It tells us if our metabolism is in a good state; if you’re too thin, overweight, or stressed, that can throw your cycles off. Having irregular periods or more likely, skipping multiple periods could be a sign of a hormonal imbalance like PCOS.” Menstrual irregularities like these should raise a red flag and warrant a doctor’s attention.

2. You’re growing hair in unexpected places.

With PCOS, the ovaries produce excessive amounts of a type of hormones called androgens, which stimulate hair growth. We’re not talking about the hairs on your head. “You’ll get hair growth in funny places—around the nipples, on your chest, the inside of your thighs, and your belly,” says Siddiqui. “Places were women don’t typically have a lot of hair growth.”

3. You’re breaking out.

Those same high levels of androgens also trigger acne. The hormones boost sebum production, and the combo of excess oil and old skin tissue plugs pores. To add insult to injury, bacteria that flourish on sebum increase, triggering inflammation.

4. There’s a dark “ring” around your neck.

You might blame it on a cheap necklace leaving a ring of residue on your skin at first, but PCOS can cause a stubborn darkening of the skin around the back of your neck. “It’s a velvety, dark discoloration that doesn’t wash off,” explains Siddiqui. The pigmentation and skin texture changes can also appear under your arms and around the vulva.

5. Your belly is getting bigger and you don’t know why.

Unexplained, persistent weight gain, particularly around the abdomen, is a sign of the hormonal disorder. Although it’s not fully understood why weight gain is a symptom, insulin resistance appears to play a role. “With PCOS, you can have trouble metabolizing blood sugar, known as insulin resistance,” explains Siddiqui. “When you have insulin resistance, your pancreas has to work really hard and make a lot of insulin just to lower your blood sugar. That is linked to weight gain and central obesity.” (Women with PCOS are at higher risk for developing diabetes.)

6. Those annoying skin tags keep popping up.

Although it’s not fully understood why, those flesh-colored nubs of excess skin tend to crop up around the neck area and under the arms of women with PCOS, according to the U.S. Department of Health and Human Services. It’s worth noting, though, that skin tags, which are benign and can be triggered by friction, are also common in people who don’t have PCOS, so don’t automatically freak out if you have them.

7. You’re having trouble getting pregnant.

The hormonal imbalance interferes with the body’s ability to ovulate normally, which is essential for pregnancy to occur. So it’s no surprise that PCOS is one of the most common causes of infertility. In fact, it’s responsible for 70 percent of infertility problems in women who have trouble ovulating, according to the PCOS Foundation.

Polycystic Ovary Syndrome Might Start in the Brain, Not the Ovaries


Finally, some answers.

A new study has found evidence that the common and debilitating reproductive condition, polycystic ovary syndrome, could start in the brain, not the ovaries, as researchers have long assumed.

If verified, the research could change the way we think about the painful and severely misunderstood condition, which affects at least one in 10 women worldwide.

Anyone who has polycystic ovary syndrome (PCOS) – or knows someone with the condition – will be aware of how incredibly frustrating it can be.

Thanks to the variety of symptoms it can cause – from weight gain, large ovarian cysts, difficulty ovulating, acne, facial hair, depression, and agonising and heavy periods – it can take women years to get diagnosed.

Even then, there’s very little in the way of treatment options. Most women are simply told to go on the pill or take other hormonal medications to manage their individual symptoms, but not the underlying cause.

In the long-term, PCOS can lead to metabolic disorders, such as type 2 diabetes, cardiovascular disease, and hormonal dysfunction, including infertility. In fact, PCOS is the cause of more than 75 percent of anovulatory infertility, which is infertility caused by a woman not ovulating.

And yet, despite the severity of the condition, researchers still don’t understand how PCOS arises and how we can treat it.

Now, researchers led by the University of New South Wales in Australia have shown that mice without receptors for androgens – a group of steroid hormones commonly associated with males, such as testosterone – in their brains can’t develop PCOS. But if the androgen receptors in the ovaries are removed, the condition can still arise

 Seeing as mouse and human reproductive systems share many similarities, it’s compelling early evidence that doctors and scientists might have been focussing on the wrong piece of the puzzle all along.

“For the first time we have a new direction of where we should be looking to try and develop treatments that will treat the cause of PCOS, the androgen excess in the ovary but also in the brain,” said lead researcher Kirsty Walters in an emailed press release.

Before this, researchers knew that an increase in androgens, known as hyperandrogenism, was linked to the onset of PCOS. But exactly how and where these androgens act in the body was poorly understood.

“Hyperandrogenism is the most consistent PCOS characteristic; however, it is unclear whether androgen excess, which is treatable, is a cause or a consequence of PCOS,” the researchers write in their paper.

To get a better idea, the researchers took four groups of mice:

  • a control group of normal mice
  • a group of mice genetically engineered to have no androgen receptors (ARs) anywhere in their bodies
  • a group that had been engineered to have no ARs in just their brains
  • a final group that only had ARs missing from their ovaries.

The team then used a high dose of androgen to attempt to trigger PCOS in all four groups of mice.

While the control group developed PCOS as they expected, the mice missing ARs entirely, or just missing them from their brains, didn’t get the condition.

Interestingly, the mice that were only missing ARs from their ovaries still went on to develop PCOS, although at a lower rate than the control group. That means androgens acting on the ovaries can’t be the sole cause of PCOS.

The result suggests two important things: researchers were right about an excess of androgens triggering the condition; and the action of androgens on the brain is important to the development of PCOS.

That means if we can find a way to stop those excess androgens in the brain, it could signal a new way to treat PCOS.

“These data highlight the previously overlooked importance of extraovarian [outside the ovary] neuroendocrine androgen action in the origins of PCOS,” the researchers explain.

To be clear, this study has only looked at mice so far, and the results need to be replicated in humans before we can get an idea of whether the same thing is happening in our own reproductive systems.

But this is a big deal because, until now, the focus when looking for effective treatments and preventions has been on the ovaries – and we haven’t had much luck.

The new study, though it’s still early days, gives researchers a new target to look into, and it could hopefully lead to new, more effective treatments for people with the condition.

Source:http://www.sciencealert.com

Omega-3 fatty acid supplementation does not affect insulin resistance in PCOS


Women with polycystic ovary syndrome likely receive no benefit from daily omega-3 fatty acid supplementation, according to a meta-analysis of three randomized controlled trials.

“Reducing the levels of serum insulin and increasing insulin sensitivity are considered to be of paramount importance for therapeutic targets in PCOS,”Alirez Sadeghi, of the department of cellular and molecular nutrition at the School of Nutritional Sciences and Dietetics at Tehran University of Medical Sciences, Iran, and colleagues wrote. “Omega-3 fatty acids may lead to insulin sensitivity by producing and secreting anti-inflammatory adipokines, such as adiponectin, and also through reducing inflammation and proinflammatory cytokines. Although it is said that omega-3 fatty acids have positive effects on insulin resistance, various studies have indicated contradictory results.”

Sadeghi and colleagues analyzed data from three studies that measured the association between oral omega-3 supplementation and insulin resistance inwomen with PCOS. Studies were conducted in Australia, Iran and the United States, and included 72 women with PCOS and 73 controls. All studies were double blind and published between 2009 and 2012 with follow-up between 6 and 8 weeks. In all three studies, PCOS groups received 1.2 g to 3.6 g daily omega-3 supplementation containing eicosapentaenoic acid and docosahexaenoic acid (median, 2.7 g); control groups received an oral placebo (olive oil, soybean oil or other placebo). Researchers assessed plasma fatty acid composition in one study; participants maintained their usual diet during intervention in two of the studies; daily energy intake was assessed at baseline and end of intervention in two studies.

In women with PCOS, researchers found that omega-3 fatty acid supplementation did not affect insulin plasma level (mean difference: 6.018; 95% CI, –3.347 to 15.382) or homeostasis model assessment of insulin resistance (HOMA-IR; mean difference: 0.276; 95% CI, –1.428 to 1.981), with high heterogeneity observed for both. The researchers noted that samples sizes in the included studies were low, and further, high-quality randomized controlled trials are needed to validate the findings. – by Regina Schaffer

Metabolic syndrome rate, severity in PCOS reduced following bariatric surgery


Bariatric surgery can improve cardiometabolic health in women with polycystic ovary syndrome and obesity, according to findings of a retrospective cohort study presented here.

McAnto Antony, MBBS, a second-year resident at Medstar Washington Hospital Center in Washington, D.C., and colleagues evaluated data from Medstar facilities on 19 women with PCOS (mean age, 18.4 years; 53% black; 41% white; 6% Asian) who had undergone a bariatric surgical procedure. The most common procedure was gastric sleeve, followed by lap band with fewer Roux-en-Y gastric bypass, according to Antony. Researchers compared BMI, blood pressure, HbA1c, and triglyceride and HDL levels before and at least 6 months after surgery (mean time between surgery and follow-up, 7.9 months).

McAnto Antony

McAnto Antony

Compared with presurgical values, postsurgical reductions were observed in body weight (mean, 271 kg vs. 205.4 kg; P< .0001), BMI (mean, 45.9 kg/m2 vs. 35 kg/m2; P < .0001), systolic BP (mean, 133.4 mm Hg vs. 119.5 mm Hg; P = .0002), diastolic BP (mean, 81.9 mm Hg vs. 73.1 mm Hg; P= .007), triglycerides (mean, 143.2 mg/dL vs. 111.5 mg/dL; P = .04) and HbA1c (mean 6.6% vs. 5.8%; P = .03); mean HDL level increased (44.8 mg/dL vs. 52.5 mg/dL; P = 0.04). Before surgery, participants had a mean 2.7 components of metabolic syndrome on average, which decreased to 1.9 after their procedure (P < .01). Forty-seven percent of participants had at least three of the five components of metabolic syndrome, meeting criteria for the condition, before surgery. Following surgery, prevalence dropped to 21%.

“Bariatric surgery is definitely an option in the obese woman with PCOS to reduce her risk of developing cardiovascular disease in the future,” Antony told Endocrine Today. “ – by Jill Rollet

Fertility in women with PCOS improves with weight loss, exercise


Ovulation in women with polycystic ovary syndrome improves with weight loss and exercise, according to recent study findings published in The Journal of Clinical Endocrinology & Metabolism.

“The findings confirm what we have long suspected — that exercise and a healthy diet can improve fertility in women who have PCOS,” Richard S. Legro, MD, vice chair of research and professor of obstetrics and gynecology and public health sciences at Penn State College of Medicine, said in a press release. “Making preconception lifestyle changes is beneficial, either alone or in combination with other pretreatment options.”

Richard Legro

Richard S. Legro

Legro and colleagues evaluated 149 women aged 18 to 40 years with overweight or obesity and infertility due to PCOS to determine the efficacy of preconception intervention on reproductive and metabolic abnormalities. Main outcome measures were weight, ovulation and live birth.

During the preconception intervention, women were randomly assigned to 16 weeks of one of the three following treatments: continuous oral contraceptive pills (pills; n = 49); lifestyle modification consisting of caloric restriction with meal replacements, weight-loss medication and increased physical activity to promote a 7% weight loss (lifestyle; n = 50); or combined treatment with both oral contraceptive pills and lifestyle modification (combined; n = 50).

Participants underwent standardized ovulation induction with clomiphene citrate, as well as timed intercourse for four cycles after the intervention, and pregnancies were followed at trimester visits until delivery.

Compared with the pill group, the lifestyle and combined groups achieved weight loss (P < .0001) and a decrease in waist circumference (P = .03) after intervention.

Compared with baseline, there was a significant increase in metabolic syndrome within the pill group (OR = 2.47; 95% CI, 1.42-4.27); no changes were found with the lifestyle or combined groups.

The combined group achieved ovulation more commonly than the pill group (P < .05). The rate of live births nearly reached statistical significance after combining the lifestyle and combined groups compared with the pill group (P = .05). Among patients who ovulated, fecundity was higher among the lifestyle group compared with the pill group (P = .04).

“The research indicates preconception weight loss and exercise improve women’s reproductive and metabolic health,” Legro said. “In contrast, using oral contraceptives alone may worsen the metabolic profile without improving ovulation. Lifestyle change is an important part of any fertility treatment approach for women with PCOS who are overweight or obese.” – by Amber Cox

CVD risk higher for women aged at least 30 years with PCOS


Among women with polycystic ovary syndrome, those aged 30 years or older are potentially at higher risk for developing early atherosclerosis, based on elevated lipid levels, lipid ratios and hypertension rates, compared with younger women with or without polycystic ovary syndrome, according to research in the International Journal of Endocrinology.

Subclinical cardiovascular disease was more prevalent in women aged at least 30 years with PCOS regardless of BMI, according to researchers.

“If we consider that women with PCOS are exposed to risk factors for CVD early in life, the diagnosis of subclinical atherosclerosis in this population would be of importance,” the researchers wrote.

Djuro Macut, MD, of the University of Belgrade, Serbia, and colleagues compared data from 100 women with PCOS (26.32 ± 5.26 years; BMI, 24.98 ± 6.38 kg/m²) with 50 healthy women (27.96 ± 5.6 years; BMI, 24.66 ± 6.74 kg/m²). Baseline blood samples collected after 12 hours of fasting during the follicular phase of the menstrual cycle, or randomly in the case of amenorrhea, were analyzed for levels of total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, apolipoprotein A, ApoB, glucose, insulin, total testosterone, sex hormone-binding globulin, androstenedione and dehydroepiandrosterone sulfate.

Patients aged at least 30 years with PCOS (n = 24) had higher BMI (P < .001) waist-to-hip ratio (P = .008), systolic blood pressure (P < .001), diastolic BP (P < .001), all lipids and their ratios, and ApoB (P = .014) than younger women with PCOS (n = 76), according to researchers. After adjustment for BMI, significant differences remained for systolic BP (P = .003), diastolic BP (P = .003), triglycerides (P = .05), insulin (P = .028) and free androgen index (P = .043).

In the older subgroups, women with PCOS had a significantly higher prevalence of hypertension than women without PCOS (n = 18; 61% vs. 17%, P = .003).

“A more proper assessment of the clinical phenotypes and use of specific metabolic indicators could be a valuable tool for the evaluation of [CV] potential and outcomes in future randomized studies on women with PCOS,” the researchers wrote. – by Regina Schaffer

High testosterone, dihydrotestosterone linked to adverse metabolic phenotype in patients with PCOS


Patients with polycystic ovary syndrome who have a high testosterone to dihydrotestosterone ratio appear to be more likely to have an adverse metabolic phenotype, according to recent findings.

In the study, researchers evaluated 275 premenopausal women aged 16 to 48 years with PCOS and 35 BMI-matched, premenopausal, health women aged 21 to 50 years as controls. The researchers recorded anthropometric data for all participants, including height, weight, waist circumference and hip circumference.

Researchers recorded systolic and diastolic blood pressure measurements and calculated BMI. Fasting blood samples were taken to evaluate basal hormone serum levels. Additionally, an oral glucose tolerance test was performed, and blood samples were collected at 30, 60 and 120 minutes to determine glucose and insulin concentrations.

A routine method for liquid chromatography/mass spectrometry was used to determine total testosterone (T), total dihydrotestosterone (DHT), androstenedione and dehydroepiandrosterone (DHEA).

The researchers found that patients with PCOS had significantly higher levels of total T (P<.001), free testosterone (P<.001) and free DHT (P<.001) vs. healthy controls. Additionally, patients with PCOS had a significantly higher total T/DHT ratio (P<.001). No difference was found between PCOS and control participants in terms of total DHT levels (P=.072).

An analysis of just patients with PCOS revealed a significantly higher total T/DHT ratio in patients with obesity (P<.001) as well as those with metabolic syndrome (P<.001), impaired glucose tolerance (P<.001) or insulin resistance (P<.001).

The researchers also found significant association between total T/DHT ratio and various adverse anthropometric, hormonal, lipid and liver measures, and measures of glucose tolerance.

“This correlation was only found in PCOS patients, suggesting the [total] T/DHT ratio is a new biomarker for an adverse metabolic phenotype in PCOS patients,” the researchers wrote. “Nevertheless, future studies and larger trials are needed for the evaluation of results.”

High testosterone, dihydrotestosterone linked to adverse metabolic phenotype in patients with PCOS


Patients with polycystic ovary syndrome who have a high testosterone to dihydrotestosterone ratio appear to be more likely to have an adverse metabolic phenotype, according to recent findings.

In the study, researchers evaluated 275 premenopausal women aged 16 to 48 years with PCOS and 35 BMI-matched, premenopausal, health women aged 21 to 50 years as controls. The researchers recorded anthropometric data for all participants, including height, weight, waist circumference and hip circumference.

Researchers recorded systolic and diastolic blood pressure measurements and calculated BMI. Fasting blood samples were taken to evaluate basal hormone serum levels. Additionally, an oral glucose tolerance test was performed, and blood samples were collected at 30, 60 and 120 minutes to determine glucose and insulin concentrations.

A routine method for liquid chromatography/mass spectrometry was used to determine total testosterone (T), total dihydrotestosterone (DHT), androstenedione and dehydroepiandrosterone (DHEA).

The researchers found that patients with PCOS had significantly higher levels of total T (P<.001), free testosterone (P<.001) and free DHT (P<.001) vs. healthy controls. Additionally, patients with PCOS had a significantly higher total T/DHT ratio (P<.001). No difference was found between PCOS and control participants in terms of total DHT levels (P=.072).

An analysis of just patients with PCOS revealed a significantly higher total T/DHT ratio in patients with obesity (P<.001) as well as those with metabolic syndrome (P<.001), impaired glucose tolerance (P<.001) or insulin resistance (P<.001).

The researchers also found significant association between total T/DHT ratio and various adverse anthropometric, hormonal, lipid and liver measures, and measures of glucose tolerance.

“This correlation was only found in PCOS patients, suggesting the [total] T/DHT ratio is a new biomarker for an adverse metabolic phenotype in PCOS patients,” the researchers wrote. “Nevertheless, future studies and larger trials are needed for the evaluation of results.”

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