American family physician最新文献

Iron deficiency anemia is common worldwide. In adult patients without inflammation, a ferritin level of less than 45 ng/mL or ferritin level of 46 to 99 ng/mL plus a transferrin saturation of less than 20% is diagnostic of iron deficiency. In patients with inflammation, a ferritin level of less than 100 ng/mL is diagnostic. Risk factors for iron deficiency anemia include low socioeconomic status, female sex, age younger than 5 years, and chronic inflammation. Underlying causes should be investigated. Recurrent blood loss is responsible for 94% of cases. In younger patients with a plausible cause of iron deficiency anemia (eg, heavy menstrual bleeding), a reasonable approach is to treat the bleeding and provide iron supplementation. In men and postmenopausal women, bidirectional endoscopy should be performed. Noninvasive testing for Helicobacter pylori infection and celiac disease is recommended because both are common causes of iron deficiency anemia. Oral iron replacement is the first-line treatment for most patients. However, intravenous iron is recommended in patients with heart failure to increase exercise capacity. Every-other-day dosing of oral iron improves absorption. Approximately 50% of patients have decreased adherence due to adverse effects. Patients taking oral iron therapy should be evaluated for response in 2 to 4 weeks. Patients who cannot tolerate oral iron or do not have adequate response should receive intravenous iron. Hypersensitivity to newer formulations of intravenous iron is rare (less than 1%).

Clinicians often need to differentiate between benign, self-limited variations of pubertal development and more serious underlying causes. Precocious puberty should be considered when thelarche occurs in female patients before 8 years of age or when testicular enlargement occurs in male patients before 9 years of age. Delayed puberty should be considered in female patients who lack breast development by 13 years of age or do not experience menarche by age 15 and in male patients who lack testicular growth by age 14. Assessment should focus on clinical and family history, growth, and pubertal examination to rule out benign pubertal variations. Further laboratory and radiographic workup may include early morning testing of luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone (thyrotropin), total testosterone (in male patients), and estradiol (in female patients), as well as left-hand bone age radiography. Neuroimaging with contrast-enhanced magnetic resonance imaging of the brain should be obtained in all patients with central precocious puberty who have neurologic signs or symptoms; are female and younger than 6 years; or are male and younger than 9 years. Specialist evaluation by pediatric endocrinology is often indicated when examination results are not consistent with a benign variation of puberty.

To care for patients at the end of life, family physicians should be able to evaluate the causes of symptoms, differentiate between distressing symptoms and common end-of-life changes, and balance treatment effectiveness with potential adverse effects, while ensuring alignment with the patient's values and wishes. For severe pain and dyspnea, opioids are the mainstay of treatment. Palliation of pain with adjuvant medications and nonpharmacologic measures may delay or decrease the need for opioids. Nausea can be treated by reducing exacerbating factors and choosing agents that target the specific receptor site affected. Constipation should be prevented or treated quickly with osmotic and stimulant laxatives. Severe opioid-induced constipation may require enemas, prokinetics, or mu-opioid antagonists. Anorexia is extremely common at the end of life and may not warrant specific treatment in the absence of distress. Appetite stimulants can be considered after dysphagia, dyspepsia, nausea, and constipation are addressed. Early recognition of delirium, reduction of offending medications, and frequent reorientation may reduce the need for psychotropic medications. Mood disturbances should be distinguished from grief and cognitive loss, and treatment should consider prognosis and time to benefit.

Acute low back pain falls into two causal categories: specific and nonspecific. Specific causes can be intrinsic to the spine, from systemic disease, or referred pain from other organs. However, acute low back pain typically is nonspecific. Aside from recent trauma, most patients with acute low back pain do not require imaging unless history reveals red flag findings. Those with red flag findings require immediate evaluation and treatment, including imaging and specialty referral or consultation. For patients with nonspecific low back pain, first-line treatment involves maintaining activity, use of heat therapy, and other nonpharmacologic treatments (eg, dry needling, transcutaneous electrical nerve stimulation, acupuncture). Pharmacotherapy options include nonsteroidal anti-inflammatory drugs, trigger point injections, and possibly systemic corticosteroids for radicular low back pain. Drugs that should not routinely be used include benzodiazepines, gabapentin, pregabalin, opioids, and acetaminophen. Physicians should address comorbid conditions that increase the risk of acute low back pain becoming chronic. Patients with pain persisting beyond 8 weeks despite appropriate therapy should be considered for imaging and laboratory evaluation to identify specific causes.