General Topics

Uses and Precautions of Genomic Medicine | Endocrinology

What is genomic medicine?

Genomic medicine is the study of our genes (DNA) and their communication with our health. Genomics investigates how a person’s biological info can be used to improve their clinical care and health outcomes (for example, through real diagnosis and personalized treatment.

While genetics looks at exact genes or groups of ‘letters’ along the DNA chain, genomics refers to the study of a person’s whole genetic makeup. It is about how they tell and react to each other and is associated with conditions that have a wider variety of triggers, such as diabetes, heart disease, cancer, and asthma.

How is genomics used in medicine?

Diagnosis: For example, when the cause of a variety of symptoms cannot be identified by any other means. Prenatal tests are done during pregnancy, either for screening (in case something is wrong with the baby) or when there is already a family history. Helps parents make informed decisions and plans for the future.

When there is a family history of serious genetic disorders, you can tell prospective parents whether they are carriers or not and if they can pass it on to their children. You can also tell someone if you are likely to develop the inherited condition later in life, even if you don’t have any symptoms yet.

To assess risk: A person’s genetic makeup can show their susceptibility to certain diseases, such as heart disease, stroke, and cancer. Maybe they have high cholesterol levels or have vein problems. Possessing this knowledge means that they can achieve risk through medication, medical intervention, or by making positive existence changes.

Advances in genomic medicine

Several notable advances or achievements in genomic medicine are described below. However, further study of these issues beyond that provided in these summaries is warranted.

Precision medicine: The ultimate goal of precision medicine is that instead of a “one size fits all” approach by disease type, medicine will be based on a genetic understanding of the disease. Precision medicine not only involves studying the genome, but it also considers factors such as where a person lives, what they do, and what their family health history is.

The goal is to develop specific prevention or treatment approaches to help specific people stay healthy or get better rather than relying on approaches that are the same for everyone.

Precautions of genomic medicine

There are many aspects of genomic medicine that society must consider. For example, if a genomic medicine causes a disease with no known treatment, does it make sense to test people for that mutation before they develop symptoms? Also, some mutations cause an increased risk of disease, but that increased risk is very small compared to the risks of other factors such as diet and exercise.

Does it make sense to screen people for these kinds of changes when the change may not cause harm? How should this information be used? It is illegal for health insurance companies and employers to use genetic information to limit eligibility, set premiums, or discriminate against people without symptoms.

What is genetic counselling?

There are several types of service providers. In the UK, for example, the National Health Service employs 90 consultant clinical geneticists in 25 centres. They are supported by hundreds of specifically trained staff.5 Referral is usually done through a general practitioner (GP or family doctor) and is available to those concerned about a serious genetic family condition or a family tendency to develop cancer, or for parents of a child with learning disabilities and other developmental problems seeking expert evaluation.

In places where a public service is not available, or for those who choose to seek private healthcare treatment, check that the clinic you are using has the necessary registration (for example in the UK this is through the Care Commission for Quality, also known as CQC6) and the laboratory is also duly accredited.

Whatever the setting, the appointment may take some time and you may need to bring other members of your family with you. Your medical and family history will be mapped and explored, and you will likely have a medical exam as well. Finding out that there may be a life-changing or limiting condition in your future is a serious and, for some, traumatic experience.

Along with counselling, you may be offered tests (including blood tests), with the option to have them done the same day or, if you need time to think about the possible implications, come back at a later date. Results can take weeks or even months to recover (depending on the rarity of the genetic abnormality and how easy it is to find), but the results of prenatal tests will be returned much sooner.

Aftercare depends on the results and the nature of the test. Some people will be referred back to their family doctor along with all the details, or they can continue to receive treatment in a specialized unit. Those without symptoms will receive support and advice on lifestyle changes to minimize their risk, and advice on how to manage their possible condition in the future.

Several private companies offer genetic testing by mail. It involves taking a cheek swab or a blood sample at a local clinic. Then it is sent to the laboratory. The types of things that are tested include genetic risk for diabetes and heart conditions, as well as information about ancestry. Some companies provide more services than others, with counsellors or other healthcare professionals available to help. Convenient (but not necessarily cheap), it should be remembered that this is genetic testing without the usual level of holistic support found in established clinics.

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Overview of Diabetic Microvascular Complications | Endocrinology

Diabetic microvascular complications

Diabetic microvascular disease

The 3 main manifestations of diabetic microvascular disease, retinopathy, nephropathy, and neuropathy are reviewed.

Retinopathy: Diabetic microvascular disease is strongly associated with hyperglycemia. In the range of chronic hyperglycemia commonly seen in practice, there is an 11-fold increase in retinopathy compared to a 2-fold increase in coronary artery disease. Despite the importance of hyperglycemia, some patients may develop early evidence of retinopathy up to 7 years before the development of Frank’s type 2 diabetes mellitus, indicating the contribution of insulin resistance.

In addition to the severity of hyperglycemia and the duration of diabetes mellitus, other factors associated with retinopathy include hypertension, smoking, and dyslipidemia. These and other pathophysiological mechanisms, including insulin resistance and inflammation, contribute to the diabetic microvascular disease process.

The early histopathological sign of retinopathy related to diabetes mellitus is the loss of pericytes. Pericytes surround arterial and capillary endothelial cells and participate in the maintenance of capillary tone, growth, and resistance to damage from oxidative stress. Then the disease is characterized by hardening of the basement membrane, permeability of endothelial cells, and the formation of microaneurysms.

Broadly speaking, there are 2 types of retinopathy, non-proliferative (background), and diffuse. In nonproliferative retinopathy, patients may develop point bleeds, which are small hemorrhages in the middle of the retina surrounded by tight lipid exudates. Retinal edema can also be seen. Proliferative retinopathy is the development of neovascularization in the retina, which is complicated by vitreous hemorrhage. These later changes, without treatment, can lead to vision problems.

According to an analysis of the National Health and Nutrition Survey, the prevalence of retinopathy in the diabetic population is 28.5% and the general risk of vision loss is 4.4%. Male gender, high levels of glycated hemoglobin, long duration of diabetes mellitus, high blood pressure, and insulin use are associated with the development of retinopathy. In a group of 35 studies of people with diabetes from around the world from 1980 to 2008, retinopathy was 35% prevalent in people aged 20 to 79 years, 7% for proliferative retinopathy, and 10% for vision threat.

Rates of retinopathy are higher for patients of African or Caribbean descent compared to Caucasians or South Asians. The presence of the diabetic microvascular disease is also a sign of contagious vascular disease. Diabetic patients with retinopathy have a higher rate of atherosclerosis than diabetic patients without retinopathy.

Diabetic retinopathy is the leading cause of blindness in the United States. It is responsible for 8% of the cases of legal blindness and 12% of the cases of blindness in the United States each year during the last decade of the 20th century. However, newer therapies have improved outcomes with a significantly reduced rate of acute visual impairment. Although the number of patients with diabetes mellitus and diabetic retinopathy has increased from 4 million to మి 5 million in the United States over the past few decades, the number of visually impaired diabetes mellitus patients decreased from 26% in 1997 to ≈19% in 2011, while the general visual disability in the civilian population was 9.3%. It is constant.

Systemic medical treatment plays an important role in diabetic microvascular disease and will be discussed later. 2 specific eye treatments slow the progression to blindness. Two clinical trials, the Diabetic Retinopathy Early Treatment Study and the Diabetic Retinopathy Study established macular and pan-retinal photocoagulation as the main treatment for these two eye problems. Recently, the use of injected vascular endothelial growth factor antagonists has been shown to improve outcomes in proliferative retinopathy and has become fashionable. The timing, use, and role of this treatment about photocoagulation have not been established and depend on the results of clinical studies.

Nephropathy: The pathophysiology of nephropathy in diabetes mellitus has many similarities to retinopathy, including hardening of the basement membrane and the formation of microaneurysms. Furthermore, glomerular hyperfiltration is associated with the proliferation of the extracellular matrix and the progression of tubular and glomerular sclerosis. These changes can cause albuminuria. Nephropathy is defined as a protein loss> 500 mg/day. Previously, microalbuminuria was defined as a loss of 299 mg / d28.

Neuropathy: The development of diabetic neuropathy is associated with vascular and non-vascular abnormalities. In addition to basement membrane hardening and percussion damage, there is evidence that capillary blood flow to C fibers is reduced, resulting in nerve perfusion and consequent endocrine hypoxia. Neuropathy is characterized by axonal hardening and eventual loss of neurons. Although there are 2 main types, the clinical manifestations of diabetic neuropathy can vary widely.

The most common is length-dependent, symmetric, chronic sensorimotor polyneuropathy, which is associated with the severity and duration of hyperglycemia. The pathophysiology of this subtype is similar to other microvascular manifestations of diabetes mellitus. Polyneuropathies that develop at more unpredictable times during diabetes mellitus are less likely to be symmetrical. Polyneuropathy is often accompanied by pain or spontaneous symptoms and can have a fluctuating course.

Medical therapy and diabetic microvascular disease

Clinical trials have shown that diabetic microvascular disease can be prevented or progressed by aggressive treatment of hyperglycemia and cardiovascular risk factors. Seminal trial Diabetes Control and Complications Trial (DCCT) in glycemic control. In DCCT, 1,441 type 1 diabetic patients, 726 without retinopathy, and 715 with mild retinopathy were randomly assigned to routine or intensive glycemic monitoring and followed for more than 6.5 years.

Median hemoglobin A1c as a result of intensive monitoring was ~ 7%, compared with 9% in the general care group. Intensive treatment is associated with a 76% reduction in the development of retinopathy and a 56% reduction in the need for laser therapy in patients with mild retinopathy at baseline. Similarly, intensive therapy reduced the rate of microalbuminuria by 43% and neuropathy by 69%.

The benefits of lowering glucose in patients with type 2 diabetes mellitus have also been demonstrated in the UK Prospective Diabetes Study (UKPDS). Diabetes and Vascular Disease in More Aggressive Glucose Control Action: Action to Control Cardiovascular Risk in Pretrox and Diamicron Modified Release (Advance) and Diabetes (ACCORD) Controlled Evaluation Trials. In both attempts, the intensive glycohemoglobin target gly6.5% arm was treated, some with modest benefits but not all signs of diabetic microvascular disease, which were not sufficient to change glycemic treatment goals.

Controlling blood pressure also reduces the likelihood of diabetic microvascular disease. A recent meta-analysis examined the effect of blood pressure control on diabetic retinopathy. The improved control of blood pressure resulted in an 18% reduction in the incidence of retinopathy in patients with type 1 diabetes mellitus and a 22% reduction in patients with type 2 diabetes mellitus. In contrast, no one has been identified. benefit in preventing the progression of retinopathy.

For nephropathy, some blood pressure agents are more effective. Angiotensin-converting enzyme (ACE) inhibitors reduce the incidence of nephropathy by 30% as determined by albuminuria42. Although there is no significant difference in blood pressure reduction, ACEIs are superior to calcium channel blockers. In contrast, the data supporting the efficacy of angiotensin receptor blockers are conflicting, with recent data being less positive than the initial studies.

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Overview of Endocrine Neoplasia and Cancer | Endocrinology

What are endocrine neoplasia and cancer?

Endocrine neoplasia refers to growths or tumors that affect the hormone-producing endocrine system. Tumors develop in the adrenal glands, pituitary gland, parathyroid glands, or pancreas and can be cancerous or benign. The Nig Comprehensive Cancer Center‌ Endocrine Neoplasia Program is dedicated to the evaluation and treatment of the structural and hormonal symptoms of these disorders.

Our endocrine neoplasia program is the only one in Connecticut, and our dedicated team of experienced multidisciplinary specialists provides clinical services in the following areas:

  • Thyroid cancer and thyroid nodules
  • Fine injection aspiration biopsy: Thyroid and adrenal
  • Thyroid ultrasound
  • Thyroid carcinoma test: Thyrogen stimulated thyroglobulin and thyroid scan
  • Cancer and benign tumors of the adrenal glands.
  • Invasive radiology including petrous sinus sampling, adrenal vein sampling, and selective infusion of pancreatic calcium
  • Hyperparathyroidism and parathyroid tumors
  • Pituitary adenomas
  • Dynamic endocrine examination
  • Nuclear medicine scan

With specialists in a variety of diagnostic and therapeutic approaches, we work with teams of physicians from other disciplines to treat patients with endocrine neoplasia. Our medical professionals have experience in endocrine surgery, urological surgery, neurosurgery, neuro-ophthalmology, pathology, nuclear medicine, invasive radiology, hypertension, genetics, molecular biology, and endocrinology. They provide state-of-the-art patient care while conducting basic and clinical research to advance treatment options.

Types of endocrine neoplasia and cancer

Tumors can appear in any large endocrine gland, including the thyroid, parathyroid, pituitary, and adrenal glands, and the pancreas. The most common sites are:

  • Thyroid gland: Most endocrine cancers develop in the thyroid gland (a butterfly-shaped organ in the lower neck). Thyroid cancer is more common in women than in men. Statistics show that the annual rate of thyroid cancer is increasing in the United States and around the world. The good news is that most thyroid tumors (called nodules) are not cancerous.
  • Pituitary gland: A pea-sized organ connected to the brain, the pituitary gland produces hormones that affect growth and fertility. Pituitary tumors are almost always benign, but they contain more or less than one or more hormones, which can upset the balance of other glands.
  • Adrenal gland: The two adrenal glands that live above the kidneys produce hormones that regulate metabolism (cortisol), stress response (adrenaline), blood pressure (aldosterone), and certain sexual characteristics (androgens).
  • Pancreas: Although the pancreas plays an active role in the digestive system, it is also a source of important hormones, including insulin. Rare tumors produce too much insulin or other related hormones, which can affect blood sugar levels.

Although some cases are inherited, the cause of most endocrine cancers is generally unclear.

Symptoms of endocrine neoplasia and cancer

Some patients with thyroid tumors notice a lump in the neck. For others, and for other endocrine tumors, the general rules do not apply. Some tumors cause severe hormonal changes or discomfort, while other tumors do not have any symptoms.

So when does a tumor have symptoms? You basically have symptoms if it doesn’t work (makes extra hormones) but is active (doesn’t make them). For example, an adrenal tumor that produces excess testosterone can cause a patient to develop certain male characteristics, such as facial hair. Symptoms also appear as the tumor grows.

A large tumor destroys part of the gland, causing a lack of hormones. It also affects nearby structures. For example, a large pituitary tumor can focus on the nerve that runs between the eyes and the brain, causing vision changes. When endocrine tumors have no symptoms, doctors may randomly notice them and evaluate the patient for another reason.

What are the genes associated with multiple endocrine neoplasias?

Mutations in the MEN1, RET, and CDKN1B genes cause multiple endocrine neoplasms. Mutations in the MEN1 gene cause type 1 multiple endocrine neoplasias. This gene provides instructions for the production of a protein called melanin. Menin acts as a tumor suppressor, which means that it generally prevents cells from growing and dividing too quickly or uncontrollably.

Although the exact function of the meninges is unknown, it is involved in cellular functions such as DNA copying and repair and regulation of the activity of other genes. When mutations inactivate two copies of the MEN1 gene, the meninges are no longer available to control cell growth and division. Loss of functional meninges allows cells to divide more frequently, leading to tumor characterization of multiple endocrine neoplasia type 1. It is not clear why these tumors affect endocrine tissues.

Mutations in the RET gene can cause type 2 multiple endocrine neoplasias. This gene provides instructions for the production of a protein involved in cell signaling. The RET protein stimulates chemical reactions that direct cells to respond to their environment, for example by dividing or maturing. Mutations in the RET gene over-activate the protein’s signaling function, which stimulates cell growth and division in the absence of signals external to the cell. This unproven cell division can lead to the formation of tumors in the endocrine glands and other tissues.

Mutations in the CDKN1B gene cause type 4 multiple endocrine neoplasias. This gene provides instructions for the production of a protein called p27. Like the meaning protein, p27 is a tumor suppressor that helps regulate cell growth and division. Mutations in the CDKN1B gene reduce the number of functional p27 that allows cells to grow and divide without being analyzed. This irregular cell division leads to the development of tumors in the endocrine glands and other tissues.

Diagnosis of endocrine neoplasia and cancer

Doctors can perform several tests to check for a suspected endocrine tumor:

  • A medical history and physical exam to assess for physical or behavioral changes related to hormone function
  • Lab tests to check for abnormal hormone levels in the blood or urine
  • Imaging studies (CT scan, MRI, or ultrasound) to look for evidence of abnormal tissue in the gland
  • A biopsy to obtain a sample of abnormal tissue and analyze it for cancer cells

Treatment for endocrine neoplasia and cancer

For any endocrine tumor, treatment involves surgery to remove it. For people with cancer, another approach that is sometimes used is radiation therapy. Patients sometimes receive hormone therapy to balance the level of hormones in the body. Depending on the type of tumor, your doctor may prescribe other specific rules to meet your individual needs.

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Overview of Female Reproductive Endocrinology | Endocrinology

What is female reproductive endocrinology?

The hormonal interaction between the hypothalamus, the anterior pituitary gland, and the ovaries regulate the female reproductive endocrinology system. The hypothalamus secretes a small peptide, gonadotropin-releasing hormone (GnRH), also recognized as a luteinizing hormone-releasing hormone.

GnRH regulates the release of gonadotropins, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) from specialized (gonadotropic) cells in the anterior pituitary gland (see figure The CNS-hypothalamic-pituitary-gonadal target organ axis). These hormones are released in short bursts (pulses) every 1 to 4 hours. LH and FSH promote ovulation and stimulate the secretion of the sex hormones estradiol (an estrogen) and progesterone from the ovaries.

Estrogen and progesterone circulating in the bloodstream almost completely bound to plasma proteins. Only free estrogen and progesterone appear to be biologically active. They stimulate the target organs of the reproductive system (eg, breasts, uterus, vagina). They are usually inhibitory, but in certain situations (eg, around ovulation), they can stimulate gonadotropin secretion.


Puberty is the order of events in which a child acquires adult physical characteristics and reproductive volume. Circulating levels of LH and FSH are elevated at birth, but drop to low levels within a few months and remain low until puberty. Until puberty, few qualitative variations occur in reproductive target organs.

Age of onset of puberty: The age of onset of puberty and the rate of development through diverse stages are influenced by different factors. Over the past 150 years, the age at which puberty begins has been decreasing, primarily due to better health and nutrition, but this trend has stabilized. Puberty often occurs earlier than average in moderately obese girls and later than average in underweight and malnourished girls.

Such explanations suggest that critical body weight or amount of fat is essential for puberty. Many other factors can influence the onset of puberty and how quickly it progresses. For example, there is some evidence that intrauterine growth restriction, especially when followed by postnatal overfeeding, can contribute to earlier and faster development of puberty.

Puberty occurs earlier in girls whose mothers matured earlier and, for unknown reasons, in girls who live in urban areas or who are blind. The age of onset of puberty also varies between ethnic groups (eg, it tends to be earlier in blacks and Hispanics than in Asian and non-Hispanic whites).

Physical changes of puberty: The physical changes of puberty occur consecutively during adolescence (see figure Puberty, when female sexual characteristics progress). Mammary budding (see figure Schematic representation of Tanner stages I to V of human mammary maturation) and the onset of the growth spurt are generally the first recognized changes.

Subsequently, pubic and axillary hair appear (see figure Schematic representation of Tanner’s stages I to V for pubic hair development in girls), and accelerated growth peaks.

Menarche (the first menstrual period) occurs about 2 to 3 years after the breast buds. Menstrual cycles are typically irregular at menarche and can take up to 5 years to become regular. The growth spurt is limited after menarche. Body habit changes and the pelvis and hips widen. Body fat increases and accumulates on the hips and thighs.

Mechanisms that initiate puberty: The mechanisms that initiate puberty are unclear.

Central influences that regulate GnRH release include neurotransmitters and peptides (eg, gamma-aminobutyric acid [GABA], kisspeptin). These factors can inhibit GnRH release during childhood and then initiate its release to induce puberty in early adolescence. In early puberty, hypothalamic GnRH release becomes less sensitive to inhibition by estrogen and progesterone.

The resulting increase in GnRH release promotes the secretion of LH and FSH, which stimulates the production of sex hormones, primarily estrogen. Estrogen stimulates the development of secondary sexual characteristics.

The growth of pubic and axillary hair can be enthused by the adrenal androgens dehydroepiandrosterone (DHEA) and DHEA sulfate; the manufacture of these androgens increases several years before puberty in a process called adrenarche.

The Hypothalamic Pituitary Gonadal (HPG) Axis of Amphibians

Reproductive endocrinology has been characterized mainly in anurans (frogs, toads) with some corroborative data from urodeles (salamanders, newts). Gymnophionid amphibians (caecilians or apodans) are similar to urodeles, although endocrine details are not well understood.

The hypothalamus controls gonadotropin secretion through the release of GnRH (see Tsai (2011)). Amphibian FSH stimulates spermatogenesis in males, as well as follicle development and estrogen secretion in females.

What regulates the female reproductive endocrinology cycle?

The menstrual cycle is regulated by hormones. Luteinizing hormone and follicle-stimulating hormone, which are bent by the pituitary gland, promote ovulation and kindle the ovaries to produce estrogen and progesterone.

What are the two female reproductive endocrinology cycles?

A fertile woman exhibits two periodic cycles: the ovarian cycle, which occurs in the cortex of the ovary, and the menstrual cycle, which occurs in the endometrium of the uterus. The phases of the menstrual cycle are under the control of the hormones unseen during the different phases of the ovarian cycle.

What are the 2 main female reproductive endocrinology hormones?

The two main feminine sex hormones are estrogen and progesterone. Although testosterone is considered a male hormone, women also produce and need a small amount of it as well.

What are the 5 main functions of the endocrine system?

  • Endocrine system function
  • Growth and development
  • sexual function and reproduction
  • heart rate
  • blood pressure
  • sleep and wake cycles
  • body temperature

How does the endocrine system touch the female reproductive endocrinology system?

The endocrine glands release hormones into the bloodstream. This allows hormones to travel to cells in other parts of the body. Endocrine hormones help control mood, growth, and development, the way our organs function, metabolism, and reproduction. The endocrine system regulates the amount of each hormone that is released.

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Control of Obesity and Appetite | Endocrinology

Control of obesity and appetite

Obesity and appetite are one of the main challenges for human health worldwide. However, there are currently no effective pharmacological interventions for obesity. New studies have improved our understanding of energy homeostasis by classifying sophisticated neurohumoral networks that transmit signals between the brain and the gut to control food intake.

The hypothalamus is a key region that has reciprocal connections between higher cortical centers, such as the reward-related limbic pathways, and the brain stem. In addition, the hypothalamus integrates a series of peripheral signals that modulate food intake and energy expenditure. Gut hormones such as peptide YY, pancreatic polypeptide, glucagon-like peptide, oxyntomodulin, and ghrelin, are moderated by acute food ingestion.

In contrast, adiposity signals such as leptin and insulin are involved in energy homeostasis both in the short and long term. In this article, we focus on the role of gut hormones and their related neural networks (the gut-brain axis) in appetite control and their potential as new therapies for obesity.

Regulation of obesity and appetite

The global obesity and appetite epidemic is on the rise, and endocrinologists are at the forefront in diagnosing its underlying causes and prescribing treatment plans. Our latest scientific statements, Obesity Pathogenesis and the Science of Obesity Management provide a comprehensive overview of the state of the science in the field of obesity and identify areas for future research.

Central mechanisms in the regulation of obesity and appetite

In the CNS, the hypothalamus is the key region complicated in the regulation of appetite. It has before been hypothesized that satiety was controlled by the ventromedial hypothalamic nucleus and that eating was controlled by the lateral region. However, this early hypothesis has evolved into a much more complete and complex understanding of the integrated neural network responsible for appetite regulation, involving discrete pathways within specific nuclei of the hypothalamus, and various regulatory modulators.

The regulation of eating, energy intake and expenditure, and Bodyweight is a homeostatic process. General health info is connected predominantly through long-term humoral signals, whereas the initiation and termination of meals are believed to be regulated through short-term signals, such as neural signals from the brain and humoral signals from the brain. intestine.

Intestinal hormones and obesity

The GI tract is the largest endocrine organ in the body and is believed to play an important role in the regulation of appetite as a source of several regulatory peptide hormones. Postprandial satiety is believed to be regulated by a sensory system that communicates between the intestine and the appetite-regulating centers in the brain, the hypothalamus is responsible for the detection of nutrients and energy and the corresponding adjustments in food intake.

In the intestine, there is a set of endocrine cells, which synthesize and release various hormones in response to nutrient and energy intake, and these hormones have been shown to influence appetite in humans and rodents when administered at physiological levels. Distinguishing between genuine satiating effects and reductions in appetite due to nausea or feelings of poor health can potentially confuse experimental results.

Food intake is influenced not only by nutritional status but also by various palatability cues, including taste and smell. Dose administration via oral gavage can be used to mitigate potential taste aversion and/or smell and effectively allow further critical analysis of the results of such studies. Together, unlike leptin and insulin, which have been proposed to signal long-term energy status, gut hormones are believed to play a critical role in the initiation and completion of meals.

Can gut hormones control obesity and appetite?

The current obesity epidemic is driven by the availability of very tasty and high-calorie foods and the low requirement of physical activity in our modern environment. If energy consumption exceeds energy use, the extra calories are stored as body fat. Although the body has mechanisms that work to maintain body weight over time, they mainly defend against starvation and are less robust in preventing the development of obesity.

Information of this homeostatic system that controls body weight has augmented exponentially over the last decade and has revealed new possibilities for the treatment of obesity and its associated comorbidities. A therapeutic target in the development of agents based on gastrointestinal hormones that control appetite.

The serious personal, social, and economic consequences that the continued global increase in the prevalence of obesity heralds are well documented. Currently, licensed non-surgical interventions have limited efficacy. This relative failure of available therapies has prompted work aimed at harnessing the physiological mechanisms of appetite control.

The search for the body’s own satiety signals as therapeutic targets promises effective reductions in body weight with minimal disruption to other systems, avoiding the side effects that occur as an unwanted consequence of therapies targeting ubiquitous receptor and neurotransmitter complexes.

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Causes of Male Reproductive Endocrinology | Endocrinology

What is male reproductive endocrinology?

Male reproductive endocrinology is a sexual development and hormonal function that depends on a complex feedback loop consisting of a hypothalamus-pituitary-testis modulated by the central nervous system. Male sexual dysfunction is second only to hypogonadism, neurovascular disorders, drugs, or other disorders.

Despite the growing interest in men’s health and the growing number of clinics dedicated to male reproductive health, not all providers trust the latest science or use evidence-based methods. We have developed our clinical practice guide on testosterone treatment and other science-based resources to ensure that men with reproductive health problems can receive the best medical diagnosis and care. 

Testosterone and DHT have metabolic and other effects, including

  • Stimulating protein anabolism (increasing muscle mass and bone density)
  • Stimulating renal erythropoietin production (increasing red blood cell mass)
  • Stimulating bone marrow stem cells (modulating the immune system)
  • Causing cutaneous effects (ie, sebum production, hair growth)
  • Causing neural effects (ie, affecting cognition, increasing libido, and possibly aggression)

Testosterone also undergoes conversion to estradiol by the enzyme, aromatase; estradiol mediates most of testosterone’s action on organs such as bones and the brain. Testosterone, DHT, and estradiol provide negative feedback on the hypothalamic-pituitary axis. In males, estradiol is the main inhibitor of LH production, whereas both estradiol and inhibin B, a peptide produced by Sertoli cells of the testes, inhibit the production of FSH.

In the presence of testosterone, FSH stimulates the Sertoli cells and induces spermatogenesis. In spermatogenesis, each germinal cell (spermatogonium), located adjacent to the Sertoli cells, undergoes differentiation into 16 primary spermatocytes, each of which generates 4 spermatids. Each spermatid matures into a spermatozoon. Spermatogenesis takes 72 to 74 days and yields about 100 million new spermatozoa each day.

Upon maturation, spermatozoa are released into the rete testis, where they migrate to the epididymis and eventually to the vas deferens. Migration requires an additional 14 days. During ejaculation, spermatozoa are mixed with secretions from the seminal vesicles, prostate, and bulbourethral glands.

How male reproductive endocrinology is assessed?

If you and your partner are unable to conceive after a year of trying, you should speak with your primary care physician, who can refer you to a fertility specialist. A urologist or reproductive endocrinologist can help diagnose and treat male infertility.

It starts with your doctor’s medical history. Your childhood growth and development, and you may have questions about past infections and surgeries, sexually transmitted diseases, testicular damage, and exposure to harmful chemicals or drugs.

Your doctor will perform a physical exam to check for low testosterone levels or other conditions that affect fertility (such as small or missing testicles). You will have a sperm test (often more than one) to see the size, movement, and shape of the sperm. Blood tests look for a hormone deficiency.

Also, your doctor may perform a scrotal or transrectal ultrasound. This imaging test looks for varicose veins around the testicles, tumors, or obstruction in the vas deferens. Your partner must have a complete medical history and evaluation at the same time. It gives you a complete picture of your potential as a couple with children.

Causes of male reproductive endocrinology

In about 30 to 40 percent of cases, the problem is in the testicles, the glands that make sperm, and testosterone (the main male sex hormone). Cancer treatments such as damage to the tonsils, infections such as tonsils, radiation or chemotherapy, trauma, or surgery.

Heat affects sperm production. Heat loss occurs when one or both testicles do not descend from the abdomen (where they were before birth) into the scrotum (usually the sac of skin that contains the testicles). Most men dilate the veins around the testicles (called a varicocele), which also raises the temperature in the testicles. If they are very large, a varicocele can lead to less sperm production.

Some inherited (genetic) diseases may or may not cause motility or reduced sperm production. In 10 to 20 percent of cases, the problem is the obstruction in the passage of sperm from the testicles to the penis through tubes called the vas deferens. It can be caused by infection scars, vasectomy (surgery to cut the vas deferens and prevent sperm), or cystic fibrosis (genetic disease). In addition to the penis, the backward movement of sperm into the bladder can also cause infertility.

In rare cases, infertility is caused by a hormonal deficiency. The testes produce luteinizing hormone (LH) and follicle-stimulating hormone (FSH) testosterone and sperm. The pituitary gland in the brain produces these hormones. Any condition that lowers LH and FSH levels, such as a pituitary tumor, can lead to low or low sperm production and low levels of testosterone in the blood.

In 30 to 40 percent of men with infertility, the cause is not found. But, these men usually have abnormal sperm (for example, sperm that are slow-moving, abnormally shaped, or in small numbers). Other problems include reduced sperm production and fertility. These include chronic (chronic) illnesses, total health, late payments, certain prescription drugs, and medications.

Treatment for male reproductive endocrinology treated?

Treatment of male reproductive endocrinology depends on the cause.

Surgery: Obstruction of the sperm transport system can be corrected surgically. Vasectomy can be reversed by surgery in 85% of cases, but most men remain infertile even after the barrier is resolved (other types of barriers are difficult to treat due to past infections). If veins are large and repaired before chronic damage, varicocele repair is likely to restore fertility. Surgery can also repair the varicocele, but it may not restore fertility.

Hormonal therapy: If the cause is due to low testosterone levels, treatment with injections of hormones (LH and FSH) is usually successful. However, hormone therapy can take a year or more to produce enough sperm and regain fertility.

Assisted reproductive technologies: Other options for a couple to achieve pregnancy are assisted reproductive techniques. These treatments involve injecting the collected sperm into the uterus, injecting the sperm with the egg outside the body (in vitro fertilization or IVF), or injecting a sperm into the egg (intracytoplasmic sperm injection or ICSI).

To improve your chances of successful treatment, it is helpful to maintain a healthy lifestyle exercise often, eat a healthy diet, and do not smoke or use recreational drugs. Also, continue treatment for any chronic illness.

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Symptoms of Bone health and Osteoporosis | Endocrinology

What is osteoporosis?

Osteoporosis is a condition that affects the bones. Its name comes from the Latin “porous bones”. The inside of a healthy bone has tiny holes like a honeycomb. Osteoporosis increases the size of these areas, causing loss of strength and bone density. Also, the outside of the bone becomes weak and thin.

Osteoporosis can occur at any age, but it is more common in adults, especially women. More than 53 million people in the United States have or are at risk of developing osteoporosis. People with osteoporosis are at risk for fractures or fractures when they perform normal activities such as standing or walking.  The most commonly affected bones are the ribs, hips, and bones of the wrist and spine.

Bone is biological tissue that is constantly being degraded and replaced. Osteoporosis occurs when the creation of new bone does not sustain the loss of old bone. Osteoporosis affects men and women of all races. But white and Asian women, especially older menopausal women, are at the highest risk. Medications, a healthy diet, and exercise with weights can help prevent bone loss or strengthen already weak bones.

What can I do to keep my bones healthy?

You can take some simple steps to prevent or delay bone loss. For example:

Include a lot of calcium in your diet. For adults ages, 19 to 50 and for men ages, 51 to 70, the recommended daily allowance (RDA) is 1,000 milligrams (mg) of calcium per day. The recommended dose is 1200 mg per day for women over 50 and men over 70.

Good sources of calcium are dairy products, soy products like almonds, broccoli, kale, canned salmon, sardines, and tofu. If you find it difficult to get enough calcium from your diet, ask your doctor about supplements.

Take care of vitamin D Your body needs vitamin D to absorb calcium. For adults ages 19 to 70, the RDA for vitamin D is 600 international units (IU) per day. For adults 71 and older, this recommendation increases to 800 IU per day.

Good sources of vitamin D are fatty fish such as salmon, trout, white fish, and tuna. Also, mushrooms, eggs, and fortified foods such as milk and whole grains are good sources of vitamin D. Sunlight also contributes to the body’s production of vitamin D.

Include physical activity in your daily routine. Weight-bearing exercises, such as walking, jogging, and stair climbing, can help you build strong bones and decrease bone loss.

Stay away from drug abuse. Do not smoke. If you are a woman, have no more than one drink a day. If you are a man, avoid drinking more than two drinks a day.

Importance of bone health

Your bones are constantly changing: new bone is forming and old bone is breaking. As a child, your body makes new bone faster than it breaks down old bone and increases your bone mass. Most people reach bone mass in their 30s. After that, the bone reconstruction will continue, but you will lose a little more bone mass than you gained.

A condition that causes bones to become weak and brittle (how likely you are to develop osteoporosis) depends on how much bone mass you gain when you reach your 30s and how quickly you lose it after that. At your peak bone mass, you have more bone on the “bank” and are less likely to develop osteoporosis as you age.

Does it affect bone health?

Bone health is affected by many factors. For example:

The amount of calcium in your diet. A diet low in calcium contributes to a decrease in bone density, a risk of early bone loss and fractures.

Physical activity: Those who are physically inactive are at a higher risk of developing osteoporosis than their active counterparts.

Tobacco and alcohol: Research suggests that tobacco use contributes to weak bones. Similarly, more than one alcoholic drink a day for women on a regular basis or two alcoholic drinks a day for men increases the risk of osteoporosis.

Gender: If you are a woman, you are at risk of developing osteoporosis because women have less bone tissue than men.

Size: If you are very thin (with a body mass index of 19 or less) or have a small body frame, you are at risk because your bone mass is lower than your age.

Years: As you get older, your bones become thinner and weaker.

Ethnic and family history: If you are white or of Asian descent, you are at risk of developing osteoporosis. Also, having parents or siblings with osteoporosis puts you at higher risk, especially if you also have a family history of fractures.

Hormone levels: Too much thyroid hormone can cause bone loss. In women, decreasing estrogen levels can significantly increase bone loss at menopause. The absence of premenopausal amenorrhea also increases the risk of osteoporosis. In men, low testosterone levels lead to loss of bone mass.

Eating disorders and other conditions: People with anorexia or bulimia are at risk for bone loss. Also, conditions such as stomach surgery (gastrectomy), weight loss surgery, and Crohn’s disease, celiac disease, and Cushing’s disease can affect the body’s ability to absorb calcium.

Some drugs: Long-term use of corticosteroid medications such as prednisone, cortisone, prednisolone, and dexamethasone can cause bone damage. Other medications that increase the risk of osteoporosis include aromatase inhibitors, selective serotonin reuptake inhibitors, methotrexate, phenytoin (Dilantin), and some anti-seizure medications such as phenobarbital and proton pump inhibitors to treat breast cancer.

Symptoms of osteoporosis

In general, there are no symptoms of osteoporosis. This is why it is sometimes called a silent disease. However, you should look for the following:

  • Loss of height (decrease of an inch or more)
  • Change of posture (stooping or leaning forward)
  • Piri of respiration (capacity of the small lungs due to compressed discs)
  • Bone fractures
  • Pain in the lower back

Causes of osteoporosis

Your bones are in a constant state of restoration: new bone is formed and old bone is broken. When you are a child, your body makes your bone faster than it breaks an old bone, and your bone mass increases. This process slows down in their early 20s, and most people reach their peak bone mass in their 30s. As people age, bone mass is lost faster than it was created.

How likely you are to develop osteoporosis depends on the amount of bone mass you have achieved as a youth. Peak bone mass is inherited in some way and the species group also varies. At your peak bone mass, you have more bone on the “bank” and are less likely to develop osteoporosis as you age.

Risk factors of osteoporosis

There are many risk factors that increase your chances of developing osteoporosis, two of which are sex and age.

Osteoporosis is a disorder that affects more and more people. However, women over the age of 50 or postmenopausal women are at higher risk of osteoporosis. During the first 10 years after menopause, women experience a rapid loss of bone mass because menopause reduces the production of a hormone called estrogen, which protects against excessive loss of bone mass.

Age and osteoporosis affect men too. You might be surprised that men over the age of 50 are more likely to develop osteoporosis-induced fractures than those with prostate cancer. An estimated 80,000 men a year break their hips and women are more likely to die in the year following a hip fracture.

The risk of developing osteoporosis is also related to race. Caucasian and Asian women are more likely to develop osteoporosis. However, African American and Hispanic women are still at risk. In fact, African American women are more likely than white women to die after a hip fracture.

Another factor is bone structure and body weight. Small and thin people are at higher risk of developing osteoporosis because they lose less bone than people with higher body weight and larger frames. Family history also influences the risk of osteoporosis. If your parents or grandparents have signs of osteoporosis, such as a broken hip after a minor fall, you are at risk for the disease.

Finally, certain medical conditions and medications can increase your risk. If you have any of the following conditions, some of which are related to irregular hormone levels, you and your healthcare provider may want to consider screening for osteoporosis.

  • An overactive thyroid, parathyroid, or adrenal glands.
  • History of bariatric surgery (weight loss) or organ transplantation.
  • History of hormone therapy or missed periods due to breast or prostate cancer.
  • Celiac disease or inflammatory bowel disease.
  • Blood diseases such as multiple myeloma.

Some medications can cause side effects that can damage bones and lead to osteoporosis. These include steroids, breast cancer treatments, and medications to treat seizures. You should talk to your healthcare provider or pharmacist about the bone effect of your medication.

Each risk factor may seem related to something beyond your control, but it is not. You have control over some of the risk factors for osteoporosis. You can discuss drug-related problems with your healthcare provider. And you are responsible for:

Eating habits: If your body does not have enough calcium and vitamin D, you are more likely to develop osteoporosis. Although eating disorders such as bulimia or anorexia are risk factors, they can be treated.

Lifestyle: People who lead a sedentary (inactive) lifestyle are at risk of developing osteoporosis.

Tobacco use: Smoking increases the risk of cracking.

Alcohol consumption: having two drinks (or more) a day increases the risk of osteoporosis. 

Treatment for osteoporosis

If your test reveals that you have osteoporosis, your doctor will work with you to create a treatment plan. Your doctor can also prescribe medications and lifestyle changes. These lifestyle changes can increase your intake of calcium and vitamin D, as well as get adequate exercise.

There is no cure for osteoporosis, but proper treatment can help protect and strengthen your bones. These treatments can help slow bone breakdown in your body, and some treatments can increase the growth of new bone.

Medications for osteoporosis: The most common medicine used to treat osteoporosis is called bisphosphonates. Bisphosphonates are used to prevent bone loss. They can be taken orally or by injection. Among them are:

  • Alendronate (Fosamax)
  • Ibandronate (Boniva)
  • Rhysdronate (octonel)
  • Zoledronic acid (regeneration)
  • Other medications can be used to prevent bone loss or to stimulate bone growth. Among them are:
  • Testosterone
  • In men, testosterone treatment can help increase bone density.

Hormonal therapy: For women, the estrogen used during and after menopause can help reduce bone density. Unfortunately, estrogen therapy also increases the risk of blood clots, heart disease, and some types of cancer.

  • Raloxifene (Evista)
  • Although there is still a risk of blood clots, these drugs have been found to provide the benefits of estrogen without much risk.
  • Denosumab (Prolia)
  • This injection is given by injection and is more promising than bisphosphonates in reducing bone loss.
  • Teriparatide (Forteo)
  • This medicine is also given by injection and stimulates bone growth.
  • Calcitonin Salmon (Fortical and Miocalcin)
  • This medicine is taken as a nasal spray and reduces bone resorption. Talk to your doctor about the risk of cancer with this drug.
  • Romosozumab (evidence)

The drug was approved by the FDA in April 2019 to treat women experiencing menopause and at risk of fractures.

12 medications are given under the skin in two injections (in one session) once a month for 12 months or less. It has a “black box” warning because it increases the risk of heart attack or stroke, so it is not recommended for people with a history.

Natural remedies for osteoporosis: Since osteoporosis medications can cause side effects, you can try other treatments instead of medications. Many supplements such as red clover, soy, and black cohosh can be used to help promote bone health.

However, before using these supplements, be sure to speak with your doctor or pharmacist. This is for two main reasons. There are very few studies to support the use of these substances in the treatment of osteoporosis. As a result, we have no evidence that they work.

These medications can cause side effects in addition to interacting with the medications you are taking. You need to make sure you know what side effects are occurring and if you are taking medications that can interact with the supplement.

All of them report good results with natural treatments.

Exercises for osteoporosis: What you can do to help keep your bones healthy is not the right thing to do. Exercise is very important, especially exercises with weights.

Weight-bearing exercises involve placing your feet or hands on the floor or another surface. Examples:

  • Climbing stairs
  • Leg presses
  • Squats
  • Lizards
  • Resistance bands
  • Dumbbells
  • Heavy-duty exercise machines

These exercises help because they make your muscles push and pull on your bones. This action tells your body to form new bone tissue, which makes your bones stronger.

This isn’t your only benefit from exercise, however. In addition to its many positive effects on weight and heart health, exercise can also improve your balance and coordination, which can help you avoid falls.

Prevention of osteoporosis

Your bones need good nutrition and regular exercise to stay healthy throughout your life.

Protein: Protein is one of the building blocks of bones. However, there is conflicting evidence on the effect of protein intake on bone density. Most people eat a lot of protein in their diet, but some don’t. Vegetarians and vegans can deliberately get enough protein in their diet if they want adequate sources such as soy, nuts, legumes, seeds for vegetarians and vegans, and dairy and eggs for vegetarians.

Older people can eat less protein for a number of reasons. If you think you are not getting enough protein, ask your doctor if supplementation is an option.

Bodyweight: Being underweight increases your risk of bone loss and fractures. Being overweight now increases your risk of arm and wrist fractures. Therefore, maintaining appropriate body weight is good for your bones, as well as your overall health.

Calcium: Women between the ages of 18 and 50 need 1,000 milligrams of calcium per day. This daily increase to 1,200 milligrams when women turn 50 and men turn 70.

  • Good sources of calcium
  • Low-fat dairy products
  • Dark green leafy vegetables
  • Canned salmon or sardines with bones
  • Soy products like tofu
  • Calcium-fortified whole grains and orange juice

If you find it difficult to get enough calcium from your diet, consider taking calcium supplements. However, too much calcium is associated with kidney stones. Although it is not yet clear, some experts suggest that calcium may increase the risk of heart disease, especially in supplements.

The Department of Health and Medicine of the National Academy of Sciences, Engineering, and Medicine (formerly Institute of Medicine) recommends that total calcium intake, including supplements and diet, should not exceed 2,000 milligrams per day for those over 50 years.

Vitamin D: Vitamin D improves your body’s ability to absorb calcium and improves bone health in other ways. People can get some of their vitamin D from sunlight, but it is not a good source if you live in high latitude, are at home, or use sunscreen regularly, or avoid the sun due to the risk of skin cancer.

To get enough vitamin D to maintain bone health, it is recommended that adults ages 51 to 70 take 600 international units (IU) and 800 IU after age 70 through diet or supplements. Those who have no other sources of vitamin D and especially those with limited sunlight need supplementation. Most multivitamin products contain 600 to 800 IU of vitamin D. Up to 4,000 IU of vitamin D per day is safe for most people.

Exercise: Exercise can help you build strong bones and slow them down. Exercise can benefit your bones when you start out, but there are many benefits to you if you start exercising regularly as a child and continue to exercise throughout your life.

Combine strength training exercises with weight lifting and balance exercises. Strength training can help strengthen the muscles and bones in your arms and upper spine. Weight-bearing exercises (walking, jogging, running, stair climbing, rope skiing, skiing, and impact sports) primarily affect the legs, hips, and backbones.

Balance exercises like tai chi reduce the risk of falls, especially as you age. Swimming, cycling, and exercising on machines like ellipticals provide good cardiovascular exercise, but they do not improve bone health.


Overview of Endocrinologist | Endocrinology

What is an endocrinologist?

An endocrinologist is a doctor who specializes in the glands and the hormones they produce. They deal with metabolism or all the biochemical processes that make up your body, including how your body converts food into energy and how it grows.

It is related to the expansion, growth, and differentiation of developmental events and metabolism, growth and development, tissue function, sleep, digestion, respiration, excretion, mood, stress, breastfeeding, mental or behavioral movement, and reproduction. Activities. And hormone-induced sensory perception. Specialties in Behavioral Endocrinology and Comparative Endocrinology.

The endocrine system contains many glands in different parts of the body that secrete hormones directly into the bloodstream rather than the vascular system. Therefore, endocrine glands are considered ductless glands. Hormones have many different functions and modes of action; A hormone has many effects on different target organs and, conversely, the target organ is affected by more than one hormone.

Endocrinology is the study of medicine for the endocrine system, a system that regulates hormones. Endocrinologists are specially trained doctors who diagnose glandular diseases. Because these doctors specialize in these conditions, it can be complex and invasive.

The endocrinologist is your best advocate when it comes to hard-to-detect symptoms and hormonal problems.

Most patients begin their journey to the endocrinologist with a visit to their GP. This doctor will run a series of tests to find out what potential problems the patient is facing. If a problem with hormones is suspected, the primary care physician will provide a referral. The goal of the endocrinologist is to restore hormonal balance in the body.

What do endocrinologists do?

They cover a large amount of ground, diagnosing and treating conditions that affect you:

  • Diabetes mellitus type 1 and type 2
  • Thyroid disorders
  • Hypothyroidism
  • Hyperthyroidism
  • Goiter

Other diseases that an endocrinologist treats include:

  • Polycystic ovarian disease (PCOD)
  • Addison’s disease (deficiency of hormones of adrenal glands)
  • Cushing’s syndrome (excessive production of the hormone cortisol which leads to weight gain and puffy face)
  • Gigantism (a child whose bones and body parts grow abnormally fast)
  • Dwarfism (abnormally short stature)
  • Infertility
  • Certain cancers of the endocrine glands


The treatments used in endocrinology are as far-reaching as the diseases involved. Most disorders can be treated with hormone replacement therapies (HRT) that use oral or injected medications to overcome diagnostic deficiencies. In all of them:

  • Glucocorticoid tablets can replace hormones in people with dysfunctional adrenal or pituitary glands.
  • Growth hormone therapy with injections of growth hormone (GH) is sometimes used to treat growth disorders in children and GH disorders in adults.
  • Hormonal contraceptives can be used to treat PMS, PCOs, and endometriosis or to prevent postmenopausal osteoporosis.
  • Insulin and other diabetes medications can help normalize blood sugar in people with diabetes.
  • Testosterone replacement with injections, patches, tablets, and gels can be used in men or women with low levels of testosterone (hypogonadism).
  • Thyroid replacement medications, including syntroid (levothyroxine) and cytomegalovirus (leothyronine), can be used to restore thyroid function in people with hypothyroidism.

When to see an endocrinologist for diabetes

Your GP can treat diabetes, but when you are referred to an endocrinologist:

  • You are new to diabetes and need to learn how to control it
  • They do not have a lot of experience in treating diabetes
  • You take too many injections or use an insulin pump
  • Your diabetes has become more difficult to control or your treatment is not working
  • You have diabetes problems

You can always ask to see an endocrinologist, even if your doctor did not prescribe it for you at first. When you see one, you should also visit your primary care doctor. They work together.

What do endocrinologists do?

Endocrinologists are trained to diagnose and treat hormonal imbalances and problems by helping to revive the traditional balance of hormones within the body. Common diseases and disorders of the system treated by endocrinologists DM and thyroid disorders


Overview of Pediatric Endocrinologist | Endocrinology

What is a pediatric endocrinologist?

A pediatric endocrinologist looks after patients from infancy to late adolescence and early adulthood supported the age range of the patients they treat.

The most common disease within the specialty is type 1 diabetes, which usually represents a minimum of 50% of general clinical practice. The latter is the commonest complication of growth disorders, especially somatotropin treatment. Pediatric endocrinologists are often the first care physicians involved in the care of infants and youngsters with intersex defects.

This specialty deals with hypoglycemia in childhood and other sorts of hyperglycemia, variants of adolescence, also as other adrenal, thyroid, and pituitary problems. Many pediatric endocrinologists have an interest and expertise in internal disorders of bone metabolism, lipid metabolism, gynecology, or adolescent metabolism.

Pediatric endocrinology training includes a 3-year fellowship upon completion of a 3-year pediatric residency. The fellowship and specialty strongly research and academic-oriented, but less so now than in previous decades.

When it is performed?

Consider getting care from a pediatric endocrinologist in the following situations:

  • Your child has an endocrine disorder but is now having trouble controlling
  • Your child has more than one endocrine problem or complex or complicated endocrine disorders
  • Your child has recently been diagnosed with the endocrine disease and needs expert treatment recommendations
  • Your child needs an expert diagnosis for the new endocrine disorder symptoms

Procedure for a pediatric endocrinology

Pediatric endocrinologists prescribe or perform various procedures and treatments to control endocrine and hormonal conditions in children and adolescents. However, a pediatric endocrinologist is not a surgeon. If your child needs surgery, your doctor may refer you to a general surgeon or specialist surgeon, depending on your child’s condition. For example, a neurosurgeon specializes in performing surgery on the pituitary gland at the base of your brain. General procedures and treatments:

  • Ese counseling including behavior changes for overweight and obese patients
  • A diet that includes bariatric medicine treatments and nutritional education
  • An exercise that includes weight training and cardiovascular conditioning

Drugs including hormone therapy, hormone replacement therapy, hormone blockers, physiological antagonists (anti-hormone drugs), vitamins, diabetes medications, insulin injections, insulin pumps, and cancer chemotherapy.

Radiation including radioactive isotopes, radiation therapy such as radiation therapy, and gamma knife surgery.

Recommendations and indications for surgery, including partial or complete removal of the endocrine gland, weight loss surgery (bariatric), and surgery to remove cancer and non-cancerous tumors.


Children aren’t the sole little adults. As growing individuals, they need special needs associated with growth and development. Also, their psychological needs are different from the requirements of adults.

The pediatric endocrinologist will look after your baby in an environment suitable for youngsters and adolescents. Support staff, nurses, psychologists, pediatric diabetes educators, and nutritionists serve the requirements of youngsters and adolescents.

Pediatric endocrinologists must work with medical care pediatricians to supply a coordinated and comprehensive look after children with special needs. Pediatric endocrinologists have extensive training and knowledge in handling children and treating children with endocrine disorders and hormonal problems. If your pediatrician recommends seeing your child’s pediatric endocrinologist, you’ll make certain your child will get the simplest car possible.


Overview of Positron Emission Tomography (PET Scan) | Endocrinology

What is positron emission tomography (PET Scan)?

A positron emission tomography (PET scan) scan is an imaging test that helps reveal how your tissues and organs are working. The PET scan uses a radioactive drug (tracer) to show this activity. This scan can sometimes find disease before it shows up on other imaging tests.

The tracer can be injected, swallowed, or inhaled depending on the organ or tissue being studied. The marker accumulates in areas of your body that have high levels of chemical activity, often corresponding to diseased areas. On a pet scan, these areas appear as bright spots.

A positron emission tomography scan can be used to reveal or diagnose a number of conditions, including many cancers, heart disease, and brain disorders. PET images are often combined with CT or MRI scans to create unique views.

Why is it done?

A positron emission tomography scan is an effective way to check chemical reactions in parts of your body. It can help diagnose a wide variety of conditions, including many cancers, heart disease, and brain disorders. Images from a PET scan may provide different information than other types of scans, such as computed tomography (CT) or magnetic resonance imaging (MRI).

Positron emission tomography (PET) or computed tomography (PET) scan allows your doctor to better diagnose the disease and evaluate your condition.

Cancer: Cancer cells appear as bright spots on positron emission scans because they have a higher metabolic rate than normal cells. Positron emission tomography scans can help:

  • Detecting cancer
  • Reveal if your cancer has spread
  • Check if cancer treatment is working
  • Detect cancer recurrence

Positron emission scans need to be understood carefully because non-cancerous conditions are like cancer and some cancers do not show up on positron emission scans. Positron emission tomography scans show several types of solid tumors, including:

  • Cervical
  • Colorectal
  • Esophagus
  • Head and neck
  • Lung
  • Lymphoma
  • Melanoma
  • Pancreatic
  • Prostate
  • Thyroid
  • Heart disease

PET scans reveal areas of reduced blood flow to the heart. This information can help you and your doctor, for example, if you may benefit from a procedure to open a blocked coronary artery (angioplasty) or coronary artery bypass surgery.

Uses of PET scan

  • Diagnose cancer
  • Determine if cancer has spread throughout the body
  • Evaluate the effectiveness of the treatment
  • Find out if cancer has come back after treatment
  • Assess the prognosis
  • Assess the metabolism and viability of tissues
  • To determine the effects of myocardial infarction in areas of the heart
  • Identify areas of the heart muscle that may benefit from angioplasty or coronary artery bypass surgery (including myocardial perfusion scan)
  • Evaluate brain abnormalities such as tumors, memory impairment, seizures, and other central nervous system disorders
  • Map the normal functioning of the human heart and brain

The procedure of PET scan

Nuclear medicine imaging is performed on patients and hospitalized patients.

  • You lie on the exam table. If needed, a nurse or technician can insert an intravenous (IV) catheter into your arm or arm.
  • Positron emission tomography scans only use radiotracer injections.
  • Radioradiotherapy usually takes 30 to 60 minutes to travel through the body and is absorbed by the area examined. You are asked to rest quietly and not move or speak.
  • You may be asked to drink some contraindications that are localized to the intestines and will help the radiologist who will describe the test.

You will be transferred to a PET / CT scanner to begin imaging. It should still be there during the imaging. A CT scan is done first, followed by a PET scan. Sometimes a second CT scan followed by a PET scan with IV contrast. For more information on how a CT scan is done, see CT Scan. The CT scan takes less than two minutes. The pet scan takes 20-30 minutes. The total scan time is usually 30 minutes.

Depending on the area being tested, additional tests with other tracers or medications may be used. This can extend the processing time to three hours. For example, if you are being tested for heart disease, you may have a positron emission tomography before and after exercise or before and after receiving IV medications, which can increase blood flow to the heart.

When the test is complete, the technician may ask you to wait until the images are verified if more images are needed. Sometimes more images are obtained to clarify or better visualize certain areas or structures. The need for more images does not mean that there was a problem with the test or that something unusual was found. This should not worry you.

If you insert an intravenous (IV) line for the procedure, it will be removed if you don’t schedule another procedure that requires an IV on the same day.

During and after the PET scan

With the exception of intravenous injections, most nuclear medicine procedures are painless. They are rarely associated with significant discomfort or side effects. When the radiotracer is given intravenously, you feel a slight sting when a needle is inserted into the vein for the IV.

You may feel a cold sensation when moving your hand up when injecting the radiotracer. In general, there are no other side effects. Positron emission tomography scans only use radiotracer injections. With some procedures, a catheter can be inserted into the bladder. This can cause temporary discomfort.

It is important to stay calm during the test. Nuclear imaging is also painless. However, staying stable or in a certain position while taking pictures can cause discomfort. If you are afraid of confined spaces, you may feel anxious during the test. If your doctor doesn’t tell you, you can resume your normal activities after the test. The technician, nurse, or doctor will give you the specific instructions you need before you leave.

A small amount of radiotracer in your body loses its radioactivity over time through the natural process of radioactive decay. During the first hours or days after the test, it can pass out of your body through urine or stool. Drink lots of water to help flush radioactive material from your body.

Results of PET scan

Pictures from a positron emission tomography scan display bright spots where the radioactive tracer collected. These spots reveal higher levels of chemical activity and details about how your tissues and organs are functioning. A doctor specially trained to interpret scan images (radiologist) will report the findings to your doctor.

The radiologist may also compare your positron emission tomography images with images from other tests you’ve undergone recently, such as computerized tomography (CT) or magnetic resonance imaging (MRI). Or the pictures may be combined to provide more detail about your condition.