2018-19 TOW #27: Bone Health

As we are in the thick of winter and lacking sun, it’s a good time to review optimizing bone health for children. The AAP updated its statement in 2014 with higher RDA levels for vitamin D for children, due in part to no “safe” sun exposure. Nonetheless, outdoor play time is still recommended, and can help with bone health, as Drs. Pooja Tandon and Kyle Yasuda (UW professor emeritus and current AAP president) wrote about recently in the Seattle Times!

Materials for this week:

Take-home points:

  1. What are the optimum levels for intake of calcium and vitamin D? Recommended daily allowances (RDA) for vitamin D for children are 400 IU 0-12 months, 600 IU >1 year. Calcium RDAs also increase with age: 700mg for 1-3 yo, 1000 mg for 4-8 yo, and 1300mg for 9-18.
  2. Why are we concerned about these nutrients? In addition to rickets, low Vit D and calcium intake is linked to increased fractures later in childhood/adolescence (and adulthood). Despite the many studies linking low vit D to a host of other conditions, we do not have reliable evidence that they are in fact causally linked.
  3. Who is at highest risk for low levels? Children at higher risk for low vit D include youth with darker pigmented skin, overweight youth, inadequate dietary intake, living in northern latitudes (>33 degrees -that’s us!), taking certain medications (anticonvulsants, steroids, antiretrovirals). Those at high risk for low bone density include children who do not do bone-density strengthening exercise, particularly children who require wheelchairs.
  4. Who should be screened with blood tests? Testing for Vit D levels is not routinely indicated; AAP recommends only for conditions associated with reduced bone mass (malabsorption syndromes, CP, taking medications that interfere with absorption), or recurrent low-impact fractures. (*note Endocrine society also recommends for children with dark skin or with obesity).
  5. When should we recommend supplements? It’s better to receive Vit D and calcium in dietary sources, but there are few sources of vit D in the diet: mainly fortified milk (and some orange juice and yogurts). Supplements are indicated for breastfed babies (until drinking at least 1L per day of fortified formula/milk), and those with low dietary sources or high risk for low bone density. Among children who do not drink much milk (including one of my own kids), I recommend a multi-vitamin supplement with calcium and vitamin D.

2018-19 TOW #26: Childhood Obesity

As the new year begins, we can harness the season’s focus on wellness to offer families encouragement with healthy behaviors. Obesity prevention and intervention is a topic close to my heart, so I am excited to highlight our great local resources. We have many wonderful obesity research experts in our clinics, including Drs. Lenna Liu, Jay Mendoza, and Pooja Tandon. A big thanks to Dr. Allison LaRoche for her help updating materials for this topic. Feel free to email any of us with questions!

Teaching materials for this week:

Take-home points for this week:

  1. What’s the epidemiology of child obesity?: While some progress is being made, with promising data on declines among preschool youth, overweight/obesity rates remain high at 1 in 3 children with a BMI at or above the 85th percentile. Etiology of obesity is multifactorial including important environmental contributors that are affected by social determinants. As pediatricians, we should acknowledge the equity issues reflected in higher rates of obesity among those with more social disadvantage including low-income families, and Hispanic, African American and American Indian youth.
  2. What focused messages can we share in clinic? Focusing on behaviors/ environments that support healthy weight starts from infancy. Teach the Division of Responsibility for feeding in which “parents provide, and child decides.” The parent is responsible for what, where, and when food is served, and the child is responsible for how much to eat. We can use 5210 goals to help guide healthy weight behaviors: 5 fruits and veggies per day, watch no more than 2 hours of screen time, get 1 hour or more of physical activity, and have 0 sugary drinks. The Let’s Go! 5210 campaign was started by a pediatrician in Maine, and they have some great resources like Phrases that Help and Hinder. Families should choose their own goals through motivational interviewing, which has been shown in randomized trials in pediatrics to work in improving weight trajectories.
  3. How can we address this sensitive topic and avoid weight stigma in our practice? Recognize that obesity is highly stigmatizing and bias for weight is among the strongest biases culturally, even among children. We must be aware of our own biases as we treat patients and adopt inclusive, non-judgmental language, as recommended by Health at Every Size (HAES), which seeks to promote health-affirming behaviors and diversity of size, and to decrease weight stigma and emphasis. It’s helpful to acknowledge there are a lot of things outside the control of families (genes, community environment, etc), while also supporting specific behaviors that make a difference for health.
  4. What are the approaches for overweight and obese? For youth with BMI >85th percentile (overweight), and BMI> 95th percentile (obese), follow weight trajectory and family history to assess risk. Screening labs for metabolic risk factors (lipid panel, liver enzymes and A1c and/or glucose) are recommended starting at age 10 if obese (or overweight+risk factors). To promote healthy behaviors, refer to resources like the YMCA ACT! program – ACT! programs are enrolling this winter for 8-14 year olds around our area. We can also refer to SCH Wellness Clinics for multidisciplinary weight management from age 2 through adolescence. When metabolic problems are identified, see this article on treating comorbidities.
  5. What is the role of physical activity? For children at all weights, regular physical activity reduces the likelihood of comorbidities, even without decreasing BMI. It’s important for us to emphasize helping kids and parents find ways to be active and enjoy movement, no matter their body size.

2018-19 TOW #16: Precocious Puberty

Time for more talk of puberty – this week we will discuss what happens if there are signs it’s happening too early.

Materials for this week:

Take-home points:

  1. How do we define precocious puberty? Development of pubertal changes occuring 2.5 standard deviations below mean age. Traditionally, that’s been <8 years for girls and <9 years for boys based on data from Europe in the 60’s. More recent cross-sectional data in the US has shown thelarche is occuring up to 2 years earlier in African American girls and 1 year earlier among white girls. However, the timing of menarche has only been about 4 months earlier than in prior studies. There’s less clear evidence of earlier puberty onset for boys. Many endocrinologists still use the <8 year cut-off, but it’s somewhat controversial.
  2. What are factors associated with precocious puberty? These include female sex, family history of early puberty, low birthweight or overweight/obesity in infancy or early childhood, exposure to endocrine disrupting hormones, and international adoption. The link with obesity is especially strong – probably due to effects of multiple hormones including leptin, insulin and estrogen.
  3. What are the types of precocious puberty? Most cases in girls are due to central early activation of the hypothalamic-pituitary axis (also known as gonadotropin dependent or complete precocious puberty). These can be from CNS tumors but are most often idiopathic. Much less common for girls is the peripheral form – sex steroids from ectopic or exogenous sources (also called gonadotropin independent or incomplete precocious puberty). Sources of excess estrogen production include follicular cysts, ovarian tumors and adrenal tumors, severe hypothyroidism. It can also be McCune-Albright syndrome, a rare genetic mutation leading to uncontrolled estrogen that includes café au lait spots, osseous lesions, and multiple endocrinopathies. Boys are more likely to have the peripheral form, especially from congenital adrenal hyperplasia (CAH).
  4. What should evaluation include? Physical exam to assess height, weight, and Sexual Maturation (Tanner) stage, findings of potential endocrinopathy (café au lait spots, acanthosis, signs of hypothyroidism). Females should be examined for estrogenization of the labia and vaginal tissue. A radiographic bone age should be obtained. Consider pelvic ultrasound to view ovaries if peripheral form is suspected. Labs should be obtained in consultation with an endocrinologist and may include early morning plasma estradiol, LH/FSH, and thyroid function. If there is adrenarche, add plasma DHEA, DHEAS, and 17-hydroxyprogesterone. GnRH stimulation test is the gold standard for central precocious puberty. When there is central precocity, especially before age 6, MRI would be used to assess for CNS lesions.
  5. What are adverse outcomes? Biggest are decreased adult height and psychosocial impact such as early sexual activity and drug and alcohol use. When appropriate, we may treat with a GnRH analog like leuprolide to slow central precocious puberty – this is considered generally safe and effective to delay puberty progression and improve adult height.

2018-19 TOW #15: Puberty – Normal and Delayed

It’s time to talk puberty! We will review normal/delayed this week followed by precocious puberty next week. The puberty topic is getting a little more airtime at my house with a 9.5 year old at home. We are gearing up for the highly acclaimed puberty classes, offered through SCH for 10-12 year olds.

Here are the materials for this week:

Normal and delayed puberty take-home points:

  1. What is puberty and what triggers it? Puberty is the process of normal sexual maturation culminating in full reproductive capability. Pubertal changes are due to increased secretion of sex steroids (gonadarche) triggered by the release GnRH from the hypothalamus and release of LH and FSH from the anterior pituitary. The genetic trigger for puberty is still not well understood. NOTE – Terminology is changing now: what used to be “Tanner Staging” is now more often being referred to in the literature as “Sexual Maturation Rating (SMR)” – see article for updates.
  2. When does puberty start for girls and what is the sequence? For females, average puberty onset is 11 years, but normal range is considered from 8-14 years. The average duration of pubertal development is 3 years (range of 2-6 years). Thelarche, the onset of breast development, is usually the first visible evidence of puberty in girls. The growth of pubic hair usually follows within the next 6 months, along with a growth spurt. Menarche usually occurs 2 years after the onset of pubertal breast growth and coincides with SMR (aka Tanner) Stage IV. After menarche, girls grow 4-6 cm on average (varies a lot), and finish growing within two years. Generally, early menarche is correlated with shorter adult height.
  3. When does puberty start for males and what is the sequence? For males, average puberty onset is 12 years (normal range 8-14). Increased LH, FSH, and testosterone cause testicular maturation and enlargement. Increased testicle size is the first visible evidence of gonadarche, though often not recognized until the growth of penile length and pubic hair, typically within 6 months. As the testicles mature, other physical features virilize including increased muscle mass and voice deepening. Facial hair growth usually happens 3 years after pubic hair onset. Pubertal growth spurt is later in males, and puberty lasts longer (typically 5 years).
  4. How do we identify delayed puberty? Delayed puberty is more common in boys than girls. Delay is considered as no pubertal changes by 13 in girls and 14 in boys. Work-up for both sexes includes reviewing weight gain and linear growth, obtaining a bone age, and looking for other evidence of endocrinopathy such as panhypopituitarism or hypothyroidism. Laboratory studies include serum LH and FSH levels, growth hormone secretion, thyroid function and, in males, a morning testosterone level. Typically, these patients should be referred to endocrinology.
  5. What are the causes of delayed puberty? Delayed puberty is divided into causes based on serum LH/FSH levels: 1) normal/low (constitutional delay and hypogonadotropic hypogonadism (e.g., CNS tumors, endocrinopathies) and 2) elevated (hypergonadotropic hypogonadism or gonadal failure)-most common cause among these is Klinefelter Syndrome in boys and Turner Syndrome in girls.

TOW #39: Adolescent sexuality

One of the joys of general pediatrics is the opportunity to see children across the lifespan. After some recent infant-focused TOW’s, it’s time to shift gears to adolescents and review an important topic to them: sexuality! We have the privilege to help teens and their parents navigate through an incredibly important (albeit challenging) phase in life. So, here are some materials to get us comfortable with the sex talks.

Materials for this week:

Key take-away points on adolescent sexuality:

  1. Importance of discussing conditional confidentiality: When meeting with adolescents, we need to review why we are having these conversations and that our discussions are confidential except for situations of abuse or self-harm (when we are mandated reporters). Some helpful wording: “I need to ask you some personal questions that I ask all of my patients so that I can the best take care of your health. When we talk our conversation is confidential. This means that what we talk about is between you and me, and I won’t tell other people, such as your parents, unless you want them to know. One exception to this is if I am concerned someone has abused or hurt you. Another exception is if I am concerned you are at risk of hurting yourself or someone else.” It’s also good to specify that patients do not have to answer any question that they don’t want to answer.
  2. How to broach the subject of sexuality/sexual orientation: we want to normalize the conversation as much as possible and put our patients at ease. “Many teens your age have romantic interests and develop attraction to other people. Have you been attracted to anyone? Do you find yourself attracted to guys, girls, both?” This can be followed by more specific questions about sexual activity. Remember, sexual attractions can be evolving throughout adolescence so you should continue to ask as this may not be a fixed preference.
  3. Asking about sexuality activity: Some prefer to start by asking what questions the teen may have: “What questions do you have about sex that you’ve never really had the chance to ask?” Others prefer to start by asking directly about types of sexual activity. Dr. Shafii reminds us we will not find out unless we ask, and we have to ask direct questions to find out about different behaviors and STI risks. “There are different ways people have sex like oral, vaginal, and anal sex. Have you ever had any of these types of sex?” and “Now or in the past have you had sex with males, females, or both?”
  4. Screen for unwanted sexual activity: As mandated reporters, we need to ask about a history of sexual abuse with a question like: “Has anyone touched you in a way you didn’t want to be touched?” “Have you ever felt forced or pressured into having sex with anyone?”
  5. Counsel on contraception: Discussing contraception and pregnancy prevention is so important for us to do: in one US study, 46% of males and 33% of females did not receive formal education about contraception before their sexual debuts. Contraception should be discussed with both males and females regardless of whether they have started having sex. Helpful wording includes “What are you doing to protect yourself from pregnancy?” or “What are you doing to protect yourself from sexually transmitted infections?”

TOW#36: Short stature

This week we review another very relevant growth topic, short stature, that may cause disproportionate parental concern. Let’s review definitions and most common causes/ concerning findings related to evaluation of short stature.

Materials for this week:

Take-home points for short stature in childhood:

  1. Epidemiology: Most short stature represents familial short stature or constitutional growth delay. Incidence of growth hormone deficiency is pretty rare at 1 in 4,000 to 10,000 short children.
  2. What’s the clinical definition of short stature?: Short stature refers to a child who is 2 standard deviations below the mean height for age and sex (<3rd percentile).
  3. What are patterns of growth with familial short stature and constitutional growth delay? Familial short stature typically follows a pattern of proportional wt/ht growth along a curve below normal that starts before age 3, but with a normal bone age and, ultimately, shorter adult height. Children with constitutional growth delay (“late bloomers”) also slow down before age 3, but follow a normal rate of growth around 5th percentile and catch up later. They often have delayed puberty and below-normal bone age, but ultimately adult height in the normal range. Use mid-parental height to determine what is expected height growth (most children are within 10cm of mid-parental height).
  4. When to do a work-up? Work-up is recommended when the child’s height deficit is severe (<1st percentile for age), the child falls off the curve, especially after age 3 (more concerning for acquired growth hormone deficiency), the growth rate is abnormally slow (<10th percentile for bone age), predicted height differs substantially from mid-parental height, or body proportions are abnormal. Work-up includes bone age x-rays, may include labs (if suspicious for another diagnosis: CBC, ESR, renal function, calcium, phosphorus, TFTs, TTG antibody, sweat test, karyotype, IGF-1, IGFBP-3), referral to endocrinologist.
  5. How do we treat? Most children with short stature can be observed and offered reassurance. Evidence is lacking that short stature causes psychological harm or that there is a long-term psychosocial benefit with growth-enhancing therapy. In a few children who are very short, hormone treatment may be helpful. Human growth hormone treatment increases the growth rate, modestly increases adult height, and is mostly considered safe, but it is expensive (~$50K per inch of height!) and the long-term risk:benefit ratio for essentially healthy children remains unclear. Low-dose oral oxandrolone is a relatively inexpensive option to accelerate growth, but has not been shown to increase adult height. It’s important to support children who may be smaller than classmates; some may need extra help coping with differences based on size.

TOW #48: Menstrual disorders

As we help with the process of puberty, addressing the challenges that arise with menarche and menstrual disorders in adolescents is a common issue we see in primary care. For those of you who have had your adolescent rotation, this is a great topic for you to facilitate.

Materials for this week:

Take-home points for this week:

  1. How is the menstrual cycle different for adolescents than fully mature females? In adolescents the hypothalamic-pituitary-ovarian (HPO) axis feedback loops are not yet mature. For the first 1-2 years after menarche, steroid hormones do not yet regularly have coordinated negative and positive feedback loops to cause ovulation, so menstrual cycles may be anovulatory or infrequent /irregular (oligoovulation). In the first year after menstruation, ~50% of cycles are anovulatory. One of the most difficult aspects of these cycles for teens is that they can cause prolonged and/or unpredictable bleeding.
  2. What's considered a "normal" cycle for a teen? AAP and ACOG define normal menstrual cycles for adolescents as having an interval of 21–45 days with the duration of flow lasting <=7 days, and average product use of 3-6 pads/tampons per day. We should be concerned when there's heavier bleeding (soaking through products after 1-2 hours), cycles >90 days apart for even one cycle, or a change from regular to very irregular.
  3. What defines "abnormal uterine bleeding (AUB)"? Bleeding that's heavy or prolonged or occurs outside normal menstrual cycles. Ovulatory AUB, or heavy menstrual bleeding, occuring as part of the usual cycle, is most commonly caused by uterine problems (i.e., endometrial polyps, leiomyomas, malignancy) or bleeding disorders. Ovulatory dysfunction is AUB that presents as irregular, heavy, or frequent episodes of bleeding without a clear pattern. While this is usually from anovulatory cycles, it's considered a diagnosis of exclusion; other causes to consider would be endocrine disorders, pregnancy and infection.
  4. When working up AUB, what are key parts of the history and physical? In addition to regular elements of H&P, we should obtain 1) Menstrual history: timing of menarche, usual frequency, duration, and volume of bleeding, presence of menstrual cramps, when/how did menstrual bleeding change, and any medical problems or lifestyle changes or other events that coincided with the change; 2) confidential HEADSSS review of substance use, sexuality, sexual activity, exposure to STIs, contraception, and any history of sexual abuse; 3) related ROS including symptoms of PCOS, thyroid disease, bleeding disorders, pelvic infection, anemia, psychosocial dz like eating disorders/female athlete triad; and 4) physical exam including external genitalia; consider a full pelvic exam in sexually active females.
  5. What tests would you obtain? Depending on the presentation, appropriate lab testing could include a urine pregnancy test or quantitative hCG level, CBC, TSH, and iron studies. If there's heavy bleeding, check coagulation studies including von Willebrand panel and possibly platelet function. An androgen panel would be useful if a patient is hirsute or has significant acne. An ultrasound would be done to help evaluate pelvic anatomy, uterine abnormalities and endometrial thickness – usually it could be done transabdominally, but transvaginal can provide better anatomy if patient is sexually active and more detail is needed.

TOW #27: Childhood obesity

In this time of new year's resolutions, we can harness the focus on wellness to offer encouragement for families facing challenges with weight. Obesity prevention and intervention is a topic close to my heart, so I am excited to highlight the great local resources we have including the ACT! program, in partnership with the YMCA, and the Child Wellness and Adolescent Wellness Clinics at SCH. We have many wonderful local obesity research experts in our clinics, including Drs. Lenna Liu, Jay Mendoza, and Pooja Tandon. A big thanks to Dr. Allison LaRoche for her help updating materials for this topic. Feel free to email any of us with questions.

Teaching materials for this week:

Take-home points for this week:

  1. What's the epidemiology of child obesity?: Childhood obesity is recognized as one of the most important issues of our time. While some progress is being made, with promising data on declines among preschool youth, we still have a long way to go with overweight/obesity rates persistently high at 1 in 3 children, and even higher among some demographic groups. Etiology of obesity is multifactorial, with higher rates among low-income families, and certain racial-ethnic groups including Hispanic, African American and American Indian youth. Prevention is much easier than weight loss, so focusing on behaviors/ environments that support healthy weight starts from infancy.
  2. What focused messages can we share in clinic? Learn the Division of Responsibility for feeding ("parents provide, child decides" – parent is responsible for what, where, when food is served and child is responsible for how much to eat). Use 5210 goals to help guide healthy weight behaviors among our children: 5 fruits and veggies per day, watch no more than 2 hours of screen time, get 1 hour or more of physical activity, and have 0 sugary drinks. The 5210 Let's Go! campaign was started by a pediatrician in Maine and was adopted to help families learn healthier habits. It can be helpful to let families choose their goals through motivational interviewing, which has been shown to work in decreasing weight in an RCT in pediatric practices.
  3. How can we address this sensitive topic and avoid weight stigma in our practice? Recognize that obesity is highly stigmatizing-bias for weight is among the strongest biases culturally, even among children. We must be aware of our own biases as we treat patients. We want to use sensitive language to be supportive of families and keep them engaged: discuss “healthier weight/ unhealthy weight” and specific behaviors rather than a focus on being overweight/obese. It's helpful to acknowledge there are a lot of things outside the control of families (genes, community environment, etc), AND there are behaviors families can adopt that make a difference for health. 
  4. What are the approaches for overweight and obese? For youth with BMI >85th percentile (overweight), follow weight trajectory and family history to assess risk. Screening labs (lipids, liver enzymes and A1c and/or glucose) are recommended to assess metabolic complications among overweight children with higher risk. Refer to resources like the YMCA ACT! program – ACT! programs are enrolling this winter for 8-14 year olds around our area. For youth with BMI> 95th percentile (obese), do screening labs starting at age 10 (or earlier if BMI>99th percentile), offer the ACT! program, as well as early referral to SCH Wellness Clinics for multidisciplinary weight management from age 2 through adolescence. When metabolic problems are identified, see the above article on management of comorbidities.
  5. What is the role of physical activity? For children at all weights, regular physical activity reduces the likelihood of comorbidities, even without necessarily decreasing BMI. It's important for us to emphasize helping kids and parents find ways to be active and fit, no matter what their body size.

TOW #20: Precocious puberty

It's time for more talk of puberty – this week we will discuss what happens if there are signs it's happening too early.

Materials for this week:

Take-home points:

  1. How do we define precocious puberty? Development of pubertal changes occuring 2.5 standard deviations below mean age. Traditionally, that's been <8 years for girls and <9 years for boys based on data from Europe in the 60's. More recent cross-sectional data in the US has shown thelarche is occuring up to 2 years earlier in African American girls and 1 year earlier among whites. However, the timing of menarche has only been about 4 months earlier than in prior studies. There's less clear evidence of earlier puberty onset for boys. Many endocrinologists still use the <8 year cut-off, but it's somewhat controversial.
  2. What are factors associated with precocious puberty? These include female sex, family history of early puberty, low birthweight or overweight/obesity in infancy or early childhood, exposure to endocrine disrupting hormones, and international adoption. The link with obesity is especially strong – probably due to effects of multiple hormones including leptin, insulin and estrogen. 
  3. What are the types of precocious puberty? Most cases in girls are due to central early activation of the hypothalamic-pituitary axis (also known as gonadotropin dependent or complete precocious puberty). These can be from CNS tumors but are most often idiopathic. Much less common for girls is the peripheral form – sex steroids from ectopic or exogenous sources (also called gonadotropin independent or incomplete precocious puberty). Sources of excess estrogen production include follicular cysts, ovarian tumors and adrenal tumors, severe hypothyroidism, and rarely McCune-Albright syndrome (a genetic mutation leading to uncontrolled estrogen and includes café au lait spots, osseous lesions, and multiple endocrinopathies). Boys are more likely to have the peripheral form, especially from congenital adrenal hyperplasia.
  4. What should evaluation include? Physical exam to assess height, weight, and Tanner stage, findings of potential endocrinopathy (café au lait spots, acanthosis, signs of hypothyroidism). Females should be examined for estrogenization of the labia and vaginal tissue. A radiographic bone age should be obtained. Consider pelvic ultrasound to view ovaries if peripheral form is suspected. Labs should be obtained in consultation with an endocrinologist and may include early morning plasma estradiol, LH/FSH, and thyroid function. If there is adrenarche, add plasma DHEA, DHEAS, and 17-hydroxyprogesterone. GnRH stimulation test is the gold standard for central precocious puberty. When there is central precocity, especially before age 6, MRI would be used to assess for CNS lesions.
  5. What are adverse outcomes? Biggest are decreased adult height and psychosocial impact such as early sexual activity and drug and alcohol use. When appropriate, we may treat with a GnRH analog like leuprolide to slow central precocious puberty – this is considered generally safe and effective to delay puberty progression and improve adult height. 

TOW #18: Delayed puberty

Ah, the fun topic of puberty – always a good one to review in general pediatrics!

Here are the materials for this week:

Normal and delayed puberty take-home points:

  1. What is puberty and what triggers it? Puberty is the process of normal sexual maturation culminating in full reproductive capability. Pubertal changes are due to increased secretion of sex steroids (gonadarche). The genetic trigger for puberty is still not well understood.
  2. When does puberty start for girls? For females, average puberty onset is 11 years, but normal range is considered from 8-14 years. The average duration of pubertal development is 3 years (range of 2-6 years). Thelarche, the onset of breast development, is usually the first visible evidence of puberty in girls. The growth of pubic hair usually follows within the next 6 months, along with a growth spurt. Menarche usually occurs 2 years after the onset of pubertal breast growth and coincides with Tanner Stage IV. After menarche, girls grow 4-6 cm on average (varies a lot), and finish growing within two years. Generally, early menarche is correlated with shorter adult height.
  3. When does it start for males? For males, average puberty onset is 12 years (normal range 8-14). Increased LH, FSH, and testosterone cause testicular maturation as well as virilization of physical features including increased muscle mass and voice deepening. Increased testicle size is the first visible evidence of gonadarche, though often not recognized until the growth of pubic hair, typically within 6 months. Facial hair growth usually happens 3 years after pubic hair onset. Pubertal growth spurt is later in males, and puberty lasts longer (typically 5 years).
  4. How do we identify delayed puberty? Delayed puberty is more common in boys than girls. Delay is considered no pubertal changes by 13 in girls and 14 in boys-these patients should be referred to endocrinology. Work-up for both sexes includes reviewing weight gain and linear growth, obtaining a bone age, and looking for other evidence of endocrinopathy such as panhypopituitarism or hypothyroidism. Laboratory studies include serum LH and FSH levels, growth hormone secretion, thyroid function and, in males, a morning testosterone level.
  5. What are the causes of delayed puberty? Delayed puberty is divided into causes based on serum LH/FSH levels: 1) normal/low (constitutional delay and hypogonadotropic hypogonadism (e.g., CNS tumors, endocrinopathies) and 2) elevated (hypergonadotropic hypogonadism or gonadal failure)-most common cause is Klinefelter Syndrome in boys and Turner Syndrome in girls.