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The marked decrease in estrogen levels in menopausal women can cause bothersome symptoms that affect daily life. More than 75% of women experience menopausal symptoms, which can include vaginal dryness, itching, discharge, dyspareunia, mood changes, hot flushes, and night sweats. Menopausal hormone therapy (MHT) is the most effective treatment for vasomotor symptoms. Benefits include decreased risk of osteoporotic fractures and vaginal atrophy, improved glycemic control, and decreased vasomotor symptoms. However, recent research on risks associated with MHT has shown increased risk of venous thromboembolism and breast cancer. MHT typically is an option for patients younger than 60 years or within 10 years of menopause onset with bothersome vasomotor symptoms. The decision to start MHT should be made on an individual basis after a thorough evaluation and counseling. Oral, intramuscular, transdermal, and intravaginal formulations are available. The goal of therapy is use of the lowest dose for the shortest time that effectively manages symptoms. The patient and physician should regularly assess the risks and benefits associated with MHT and ensure that the benefits of its use continue to outweigh the risks.

Approximately 0.6% of adults (1 to 1.4 million adults) in the United States identify as transgender, and 2% of high school-aged individuals (150,000 to 300,000 individuals). Gender-affirming care for transgender and gender- diverse patients can include support with social transition or physical presentation, legal steps, and medical treatments (eg, hormone therapy) and surgeries. Adolescent and adult patients who request gender-affirming hormone therapy must meet several criteria. One is confirmed persistence of gender dysphoria or gender incongruence. Also, the patient must have reached the age of legal medical consent and be able to consent to therapy. For adolescent patients who are minors, meeting of additional criteria is recommended. In eligible adolescent patients, gender-affirming hormone therapy consists of two phases, pubertal suppression and then feminizing or masculinizing hormone therapy. Before puberty, hormone therapy is not recommended. When puberty begins, patients can receive a gonadotropin-releasing hormone agonist to suppress puberty (ie, puberty blocker). Feminizing or masculinizing hormone therapy, which usually is initiated at age 16 years, consists of estradiol or testosterone, respectively. For adult patients requesting gender-affirming hormone therapy, a thorough evaluation should be performed to assess for contraindications and conditions that may increase therapy-associated risks. Feminizing hormone therapy includes estrogen and an antiandrogen, and masculinizing therapy consists of testosterone. These patients should undergo regular monitoring. Cancer screening is based on risk factors, organ inventory, and screening guidelines.

Testosterone levels decrease as men age. When the testes fail to produce an adequate level of endogenous testosterone, men develop hypogonadism. Although the definition of a low testosterone level varies among guidelines, a serum total testosterone level of less than 300 to 350 ng/dL on two separate morning blood samples is considered a low level. To receive exogenous testosterone replacement therapy (TRT), patients should meet criteria for hypogonadism, which is defined as a low testosterone level and signs or symptoms of hypogonadism. Management discussions should be individualized to address patient needs and goals. Counseling before therapy should include shared decision-making regarding risks, benefits, and expectations. Numerous testosterone formulations are available, ranging from topical gels to intramuscular injections. The choice of formulation depends on factors such as cost and patient preference. Use of TRT is limited by contraindications, adverse effects, and a lack of long-term safety data. Patients receiving this therapy require close monitoring. For patients who wish to avoid use of exogenous hormones, are not candidates for TRT, or are unable to tolerate its adverse effects, several nonhormonal pharmacotherapies are available.

Given their association with aging, growth hormone (GH), dehydroepiandrosterone (DHEA), and melatonin (N-acetyl-5-methoxytryptamine) have been evaluated as potential antiaging treatments. It has been hypothesized that declining endocrine function, specifically the decreases in hormone production and secretion seen with aging, plays a role in development of frailty. This physiologic decrease in hormone levels differs from a pathologic decrease due to a condition or disease. However, the signs and symptoms can be similar. Hormone replacement therapy is a well-established treatment for many conditions, but its role in the healthy aging process remains unclear. Off-label use of these hormones has shown some short-term benefits, such as improved body composition, mood, neurocognition, and sexual function and decreased oxidative stress. However, there are no recommendations for routine measurement of these hormone levels or for hormone replacement therapy because of a lack of high-quality evidence. Long-term studies are needed to evaluate the efficacy and safety of GH, DHEA, and melatonin if they are to be used as antiaging therapies.

Macrocytic anemia is divided into megaloblastic and nonmegaloblastic causes, with the former being more common. Megaloblastic anemia results from impaired DNA synthesis, leading to release of megaloblasts, which are large nucleated red blood cell precursors with chromatin that is not condensed. Vitamin B12 deficiency is the most common cause for megaloblastic anemia, although folate deficiency also can contribute. Nonmegaloblastic anemia entails normal DNA synthesis and typically is caused by chronic liver dysfunction, hypothyroidism, alcohol use disorder, or myelodysplastic disorders. Macrocytosis also can result from release of reticulocytes in the normal physiologic response to acute anemia. Management of macrocytic anemia is specific to the etiology identified through testing and patient evaluation.

Microcytic anemia is defined as anemia with a mean corpuscular volume (MCV) of less than 80 mcm3 in adults. Age-specific parameters should be used for patients younger than 17 years. The cause of microcytic anemia includes acquired and congenital causes, which should be considered separately according to the age of the patient, risk factors, and coexisting signs and symptoms. The most common cause of microcytic anemia is iron deficiency anemia; it can be managed with oral or intravenous iron, depending on the severity and comorbid conditions of the affected individual. Pregnant patients and patients with heart failure with iron deficiency anemia require special considerations to prevent significant morbidity and mortality. The wide spectrum of thalassemia blood disorders should be considered in patients with a particularly low MCV in the absence of systemic iron deficiency. Iron chelation may be required for some of these patients. Sickle cell anemia and sideroblastic anemia are important inherited causes of microcytic (as well as normocytic) anemia. Promising treatments are being developed for patients with transfusion-dependent thalassemia and sickle cell anemia.

Anemia is a common condition encountered in inpatient and outpatient primary care settings. When anemia is detected, it is essential to investigate the cause to provide appropriate treatment. Patients may present with symptomatic anemia (eg, fatigue, weakness, shortness of breath), or anemia may be an incidental finding on laboratory evaluation. Initial evaluation consists of a thorough history and physical examination and a complete blood cell count (CBC). Careful examination of the CBC and the mean corpuscular volume provides important clues to the classification and cause of anemia. Supplemental tests may include a peripheral blood smear; reticulocyte count; iron panel (ie, ferritin and iron levels, total iron-binding capacity, transferrin saturation); and levels of vitamin B12, folate, lactate dehydrogenase, haptoglobin, and bilirubin.

Normocytic anemia is anemia with a mean corpuscular volume of 80 to100 mcm3. Its causes include anemia of inflammation, hemolytic anemia, anemia of chronic kidney disease, acute blood loss anemia, and aplastic anemia. In most cases, correction of the anemia should focus on managing the underlying condition. Red blood cell transfusions should be limited to patients with severe symptomatic anemia. Hemolytic anemia can be diagnosed based on signs and symptoms of hemolysis, such as jaundice, hepatosplenomegaly, unconjugated hyperbilirubinemia, increased reticulocyte count, and decreased haptoglobin levels. Use of erythropoiesis-stimulating agents in patients with anemia due to chronic kidney disease should be individualized, but these agents should not be initiated in asymptomatic patients until the hemoglobin level is less than 10 g/dL. Cessation of bleeding is the focus of acute blood loss anemia, and management of the initial hypovolemia typically should be with crystalloid fluids. A mass transfusion protocol should be initiated if the blood loss is severe and ongoing with hemodynamic instability. Aplastic anemia management focuses on improving blood cell counts and limiting transfusions.