11. Endocrinology and Metabolism

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11. Endocrinology and Metabolism


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A Brief Autobiography




Section 1 Basic Science of Clinical Endocrinology

1 Clinical Molecular Endocrinology Laboratory Testing

  Wayne W. Grody

2 Hormone-Resistant States

  Mitchell E. Geffner

3 Genetics of Endocrinology

  Hayk Barseghyan, Rena Ellen Falk, and Eric D. Vilain

4 The Growth Plate

  Francesco De Luca, Ola Nilsson, and Jeffrey Baron


Section 2 Hypothalamic-Pituitary Dysfunction

5 Anterior Pituitary Diseases

  Harold E. Carlson

6 Hypopituitarism after Traumatic Brain Injury

  Norman Lavin

7 Prolactin

  Ignacio Bernabeu and Felipe F. Casanueva

8 Nipple Discharge/Galactorrhea

  Bhavika Kantilal Patel

9 Acromegaly/Gigantism

  Merav Fraenkel and Laurence Katznelson

10 Clinical Disorders of Vasopressin

  Brandon Barthel, Cameron Herr, Sanaa Deshmukh, and James R. Sowers

11 Preoperative, Intraoperative, and Postoperative Management Following Pituitary Surgery

  Andrew R. Conger, Garni Barkhoudarian, and Daniel F. Kelly

12 Growth Hormone in Adults

  Norman Lavin

  1. xip. xii

13 Pituitary Disorders and Tall Stature in Children

  Phillip D. K. Lee

14 Short Stature and Growth Hormone Therapy

  Philippe F. Backeljauw

15 Laron Syndrome

  Zvi Laron

16 Prader–Willi Syndrome

  Mario Carcamo and Norman Lavin

Section 3 Adrenal Disorders

17 The Adrenal Cortex and Mineralocorticoid Hypertension

  Naftali Stern, Etty Osher, and Michael L. Tuck

18 Pheochromocytoma and Paraganglioma

  George T. Georges, Ankur Jindal, L. Romayne Kurukulasuriya, and James R. Sowers

19 Hormonal Hypertension

  Phyllis W. Speiser and YeouChing Hsu

20 Use of Salivary Cortisol Assay to Screen for Cushing Syndrome/Disease

  Swati Ramteke-Jadhav and Nalini S. Shah

21 Adrenal Hormones during Acute and Chronic Illness: Evaluation and Treatment

  Eva Boonen and Greet Van den Berghe

22 Congenital Adrenal Hyperplasia

  Mabel Yau, Ahmed Khattab, Saroj Nimkarn, Karen Lin-Su, and Maria I. New

23 Adrenal Steroid Excess in Childhood

  Kimberly S. Tafuri and Thomas A. Wilson

24 Adrenal Insufficiency in Childhood

  Kimberly S. Tafuri and Thomas A. Wilson


Section 4 Disorders of the Reproductive System

25 Female Reproductive Endocrinology in Adults

  1. Blake Evans, Eric D. Levens, and Alan H. DeCherney

26 Polycystic Ovary Syndrome

  Alice Y. Chang

27 Male Reproductive Disorders in Adults

  Vahid Mahabadi and Ronald S. Swerdloff

28 Disorders of Sexual Development in the Pediatric and Adolescent Male

  Louis C. K. Low, Jennifer K. Yee, and Christina Wang

  1. xiip. xiii

29 Early, Precocious, and Delayed Female Pubertal Development

  Christopher P. Houk and Peter A. Lee

30 Ambiguous Genitalia

  Selma Feldman Witchel and Peter A. Lee

Section 5 Mineral Disorders

31 Disorders of Calciotropic Hormones in Adults

  Sarah Nadeem, Vinita Singh, and Pauline M. Camacho

32 Hypercalcemic Crisis

  Catherine A. Sullivan and Devin Steenkamp

33 Metabolic Bone Disease

  Rod Marianne Arceo-Mendoza, Arshi Basit, and Pauline M. Camacho

34 Parathyroid Hormone-Related Protein

  Farzin M. Takyar and John J. Wysolmerski

35 Common Bone and Mineral Disorders of Childhood

  Michael A. Levine

Section 6 Thyroid Disorders

36 Evaluation of Thyroid Function

  Caroline T. Nguyen and Peter A. Singer

37 Thyroiditis

  Caroline T. Nguyen and Peter A. Singer

38 Hypothyroidism and Hyperthyroidism

  Jerome M. Hershman

39 Thyroid Tumors in Adults

  Jerome M. Hershman

40 Newborn Thyroid Disorders and Screening

  Stephen A. Huang and Stephen LaFranchi

41 Thyroid Nodules and Thyroid Cancer in Children and Adolescents

  Harvey K. Chiu and Andrew J. Bauer

42 Thyroid Disorders in Children and Adolescents

  Andrew J. Bauer, Kuk-Wha Lee, and Norman Lavin

Section 7 Metabolic Disorders

43 Obesity

  George A. Bray, Richard A. Dickey, and Donna H. Ryan

44 Disorders of Lipid Metabolism

  Stanley H. Hsia

  1. xiiip. xiv

45 Hypoglycemia in Adults

  Mayer B. Davidson

46 Hypoglycemia in Infants and Children

  Molly O. Regelmann, Cem S. Demirci, and Mark A. Sperling

47 Congenital Hyperinsulinism

  Amanda M. Ackermann and Diva D. De Leon

Section 8 Inborn Errors of Metabolism


48 Introduction to Inborn Errors of Metabolism

  Stephen D. Cederbaum and Derek A. Wong

49 Glycogen Storage Diseases

  Joseph I. Wolfsdorf and Paulina Ortiz-Rubio

50 Hypokalemic Paralysis

  Chih-Jen Cheng and Shih-Hua Lin

Section 9 Diabetes Mellitus

51 Etiology, Pathogenesis, and Therapy of Type 1 Diabetes Mellitus

  David A. Baidal and Jay S. Skyler

52 Diagnosis and Management of Type 1 Diabetes Mellitus in Children, Adolescents and Young


  Stuart J. Brink

53 Hypoglycemia-Associated Autonomic Failure (HAAF) in Diabetes Mellitus

  Norman Lavin

54 Diabetic Ketoacidosis

  Benjamin Fass

55 Type 2 Diabetes Mellitus

  Yunying Shi, Stephanie Smooke Praw, and Andrew J. Drexler

56 Glucose Control in Glucocorticoid-Induced Hyperglycemia

  Norman Lavin

57 Bariatric Surgery in Adults with Type 2 Diabetes

  Ali Ardestani, Eric G. Sheu, and Ali Tavakkoli

58 Diabetes Mellitus and the Geriatric Patient

  Alexis M. McKee and John E. Morley

59 Diabetes Mellitus Type 2, Obesity, Dyslipidemia, and the Metabolic Syndrome in Children

  Norman Lavin

60 Type 1.5 Diabetes: Overlay between Type 1 and Type 2 Diabetes

  Roja Fallah and Anna Pawlikowska-Haddal

61 C-Peptide

  Åsa Davis

62 Cystic Fibrosis Related Diabetes

  Katie Larson Ode and Andrew W. Norris

63 Diabetes in Pregnancy

  Samer Hafi, Shreela Mishra, Kate E. Pettit, and Susan E. Kirk

64 Management of Diabetes Mellitus in the Perioperative Period

  Rajesh Garg

65 Diabetes Mellitus: Recent Developments and Clinical Implications

  Roy G. Handelsman and Yehuda Handelsman

66 Artificial Pancreas

  Kathleen H. Ang and Stuart A. Weinzimer

67 Glycated Proteins in the Diagnosis and Management of Type I and Type II Diabetes Mellitus

Norman Lavin

68 Inhaled Insulin

  Maamoun F. Salam and Janet B. McGill

69 The Application of Stem Cells in Diabetes Mellitus

  Arye Lavin

Section 10 Sex Hormone Treatments

70 The Care of Gender-nonconforming and Transgender Youth

  Johanna Olson-Kennedy

71 Hormone Therapy in Transgender Adults

  Steven C. Myers and Joshua D. Safer

72 How to Manage Men with Low Testosterone

  Michael S. Irwig

73 The Use of Hormones in Female Sexual Dysfunction

  Rosemary Basson

74 Menopausal Hormone Therapy

  Khalid Benkhadra and Ekta Kapoor

Section 11 Special Topics in Clinical Endocrinology

75 Endocrine Diseases in Pregnancy

  Martin N. Montoro and Jorge H. Mestman

76 Fetal Endocrinology and Neonatal Emergencies

  Phillip D. K. Lee and C. Joan Richardson

77 Hormones and Aging

  Alexis M. McKee and John E. Morley

78 Neuroendocrine (APUD) Syndromes

  Adrian Langleben

  1. xvp. xvi

79 Multiple Endocrine Neoplasia Syndromes

  Vidya Aluri and Joseph S. Dillon

80 Radiology, Nuclear Medicine, and Endocrinology

  Sing-Yung Wu

81 Surgery for Endocrine Disorders

  Jesse D. Pasternak and Orlo H. Clark

82 Surgical Management of Pediatric Endocrine Diseases

  Anna Kundel and Omar Bellorin-Marin

83 Biomarkers Used in the Screening, Diagnosis, Management, and Surveillance of Endocrine


  Colin M. Court and Avital Harari

84 Autoimmune Endocrine Syndromes

  George S. Eisenbarth and Marian Rewers

85 Management of Some Hormone-Dependent Cancers with Analogs of Hypothalamic Hormones

  Norman L. Block, Ferenc G. Rick, and Andrew V. Schally

86 Endocrine-Disrupting Chemicals

  Sheela Sathyanarayana

87 Flushing and Sweating

  Isabel Huguet and Ashley Grossman

88 Intranasal Hormones

  Norman Lavin

89 The Female Athlete

  Stéphane Bermon

 Protocols for Stimulation and Suppression Tests Commonly Used in

Clinical Endocrinology

  Etty Osher and Naftali Stern

Endocrinology and Metabolism

Anabolic androgenic steroids (AASs) are appearance and performance-enhancing drugs (APEDs) used in competitive athletics, in recreational sports, and by body-builders. The global lifetime prevalence of AASs abuse is 6.4% for males and 1.6% for women. Many AASs, often obtained from the internet and dubious sources, have not undergone proper testing and are consumed at extremely high doses and in irrational combinations, also along with other drugs. Controlled clinical trials investigating undesired side effects are lacking because ethical restrictions prevent exposing volunteers to potentially toxic regimens, obscuring a causal relationship between AASs abuse and possible sequelae. Because of the negative feedback in the regulation of the hypothalamic–pituitary–gonadal axis, in men AASs cause reversible suppression of spermatogenesis, testicular atrophy, infertility, and erectile dysfunction (anabolic steroid-induced hypogonadism). Should spermatogenesis not recover after AASs abuse, a pre-existing fertility disorder may have resurfaced. AASs frequently cause gynecomastia and acne. In women, AASs may disrupt ovarian function. Chronic strenuous physical activity leads to menstrual irregularities and, in severe cases, to the female athlete triad (low energy intake, menstrual disorders and low bone mass), making it difficult to disentangle the effects of sports and AASs. Acne, hirsutism and (irreversible) deepening of the voice are further consequences of AASs misuse. There is no evidence that AASs cause breast carcinoma. Detecting AASs misuse through the control network of the World Anti-Doping Agency (WADA) not only aims to guarantee fair conditions for athletes, but also to protect them from medical sequelae of AASs abuse.
Anabolic-androgenic steroids (AAS) are synthetic derivates of testosterone used primarily for hormone replacement in male hypogonadism. However, in many countries, this medication is sold over-the-counter to enhance muscle mass and improve the athletic performance. Physiologically, elevations in testosterone concentrations stimulate protein synthesis resulting in improvements in muscle size, body mass and strength. AAS is by far the most detected doping substance banned by all major sporting bodies. AAS can cause many adverse effects such hepatic failure, endocrine dysfunction, behavioural changes or cardiovascular complications depending on the length and dose-dependent of drug abuse.

2. Case Report

A 32-year-old patient with episodes of arterial hypertension self-treated with beta blockers, depressive syndrome and frequent consumption, in adolescence and youth, of cocaine, amphetamines and AAS (750 mg of testosterone plus 750 mg nandrolone weekly in alternating cycles of 6 weeks and 3 weeks off from the age of 22) attended to the emergency department due to headache and abdominal pain in association with a hypertensive crisis (220/100 mmHg). The patient had an athletic constitution, with a weight of 109 kg and a body mass index of 33.3 kg/m2, and referred in the last months exercise intolerance attributing his current clinical symptomatology to the intake of undercooked meat (the patient referred to eat 3 kilograms of rice and 2 kilograms of meat, distributed in six meals, every day to gain muscle mass). Three days after requesting voluntary hospital discharge, the patient returned to the emergency department with intense weakness, deep sweating and severe arterial hypotension after beta blocker intake, requiring fluid and catecholamines perfusion for a few hours. Analytically, there was leukocytosis (19.5 10 3/µL) with an impairment of the renal function (creatinine of 1.7 mg/dL), an alteration of the lipid metabolism (total cholesterol of 279 mg/dL, low-density lipoprotein (LDL) of 206 mg/dL, high-density lipoprotein (HDL) of 21 mg/dL and triglyderides of 259 mg/dL) and an elevation of the liver enzymes (glutamic-oxaloacetic transaminase (GOT) of 766 u/L and glutamic-pyruvic transaminase (GPT) of 205 U/L. Basic coagulation study was normal and urine test showed positivity for methamphetamines and barbiturates.

Electrocardiogram was in sinus rhythm and the echocardiogram showed severe left ventricular dysfunction, dilation, hypertrophy and increase in the ventricular mass (an ejection fraction of 20%, a diastolic diameter of 62 mm, an interventricular septum of 17 mm with a posterior wall of 15 mm thickness and a ventricular mass of 553 grams, respectively), mild right ventricular dysfunction (tricuspid annular plane systolic excursion ]TAPSE[ of 15 mm) and no significant valvular regurgitation or ventricular thrombus. Cardiac markers were within normal limits. Abdominal ultrasonography showed increased heterogeneous echogenicity of the liver without associated focal lesions. Metanephrines and catecholamines in urine were checked to rule out pheochromocytoma, as well as thyroid-stimulating hormone (TSH) and antinuclear antibodies, which were all in normal range. Serology for Coxackie B (1-6) and A9 virus, Parvovirus B19 virus, Herpes type 6 virus, Hepatitis B, C and A viruses, human immunodeficiency virus (HIV), Leptospira interrogans, Rickettsia conorii and Coxiella burnetii were negative. The patient was discharged under angiotensin-converting-enzyme inhibitors, beta blockers and anti-aldosterone treatment emphasizing the need for a radical change in the lifestyle, type of physical exercise and eating habits.

Four months after hospital admission, the patient has ceased using anabolic steroids and refers an improvement in his functional class (New York Heart Association functional class II/IV) with weight gain and a decrease in his libido. Echocardiographically, the left ventricular ejection fraction has improved to 40% and the septal thickness has decreased slightly to 15 mm in diameter showing the left ventricular apex a hyperechoic image in relation to a non-mobile thrombus. Meanwhile, analytical data shows normal serum sex-hormone-binding globulin (SHBG) concentrations, normal serum metanephrines and normetanefrines levels and normal catecholamines, metanephrines and normetanefrinas 24-hour urine concentrations.

However, testosterone levels were low (0.82 ng/mL having the external genitalia with a normal appearance.
However 2 weeks later the patient was readmitted to the hospital due to critical ischemia of the lower limbs. Systemic heparinization associated with intravenous prostaglandin was started, presenting the patient an improvement of his symptoms with recovery of the mobility and the sensitivity. Control echocardiography showed severe global left ventricular dysfunction with a pedunculated mobile thrombus adhered to the ventricular septum. Arteriography of the lower limbs showed right popliteal artery and left superficial femoral artery occlusion with a poor collateral circulation. Given the improvement and little chance of surgical treatment due to the severe distal obliterations, conservative treatment and outpatient control was decided under oral anticoagulation treatment.

Anabolic steroids have become a popular drug among athletes and are known to have a multitude of pathological effects when administered in suprapharmacological doses. Serious adverse effects include hepatic and endocrine dysfunction, behavioral changes and cardiovascular complications such as arterial hypertension, especially in those with pre-existing hypertension, myocardial infarction, myocardial hypertrophy with diastolic dysfunction, congestive heart failure, ventricular arrhythmias, sudden death, arterial and ventricular thrombosis, stroke and dyslipidemia. In fact, changes in the concentration of blood lipoproteins, particularly an increase in LDL and a reduction in HDL cholesterol, can lead to early atherosclerosis. However, and because of their youth, myocardial infarction in AAS consumers usually occur due to endothelial dysfunction, vasospasms or hypercoagulability.

Meanwhile, left ventricular hypertrophy (LVH) differential diagnosis may be considered in arterial hypertension, hypertrophic cardiomyopathy, accumulation myocardial diseases, non-compact myocardium, valvular and combined cardiac pathology, compensatory LVH in athletes and the consumption of anabolic steroids. In this context, Nieminen et al. reported four patients with large doses of anabolic steroids abuse and myocardial hypertrophy, of which two patients had symptoms and signs of heart failure, and one of these two had a massive thrombosis in both the right and the left ventricles. However, after cessation of the use of anabolic steroids left ventricular and wall thickness reduced quickly and left ventricular ejection fraction increased. Endomyocardial biopsy revealed increased fibrosis in the myocardium in two of the three cases. On the contrary, Urhausen et al. found, several years after discontinuation of anabolic steroid abuse, that strength athletes still showed a slight concentric LVH in comparison with anabolic androgenic steroids-free strength athletes. Similarly, D’Andrea et al. in a study to investigate left ventricular dysfunction, after chronic misuse of AAS in athletes, showed that power athletes had a subclinical impairment of both systolic and diastolic myocardial functions, being the dysfunction associated with mean dosage and duration of AAS use. In fact, anabolic steroids consumers administer them in alternating cycles, and at doses much higher than usual, to maximize end-organ effects, to prevent gradual loss of benefits with chronic usage and to avoid detection on drug testing. In this context, the pituitary–testicular axis frequently becomes suppressed resulting in testicular atrophy, azoospermia, gynecomastia, hot flushes and fluid retention.

Also, unfavorable cardiovascular events have been linked to both cocaine and anabolic-androgenic steroid abuse in healthy, physically active individuals. Cocaine can cause myocardial infarction in the context of coronary arteries spasms, enhanced myocardial oxygen demand and a procoagulant effect. Meanwhile, global ventricular dysfunction has been related to the cardiotoxic effects of the catecholamines on the heart. Similarly, the main cardiovascular manifestations of methamphetamine abuse encompass tachycardia, atrioventricular arrhythmias, myocardial ischemia and hypertension.

It is also important to draw attention to the fact that drug abuse addictions and psychiatric disorders often occur at the same time having certain mental conditions such as depression, bipolar disorders, psychosis, aggression and violence, mania, suicide and symptoms of dependence and withdrawal on discontinuation associated with AAS consumption.

Because the over-the-counter availability and unrestrained self-medication with products containing AAS create a heightened potential for serious side effects, we should be aware of those bodybuilder patients, especially if they have a psychiatric disorder background with the consumption of other types of drugs.



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