Calcium is an essential element for normal physiologic function. Normal serum calcium is maintained within a close range of 8.4 to 10.4 mg/dL, and acute or severe changes can result in serious cardiac, musculoskeletal, and neurologic consequences. Normal calcium levels are maintained by interactions of parathyroid hormone and vitamin D. Parathyroid hormone regulates calcium levels via bone resorption, renal calcium reabsorption, and enhanced calcium absorption in the small intestine. Causes of hypocalcemia include hypoparathyroidism (often postsurgical), severe chronic kidney disease, and vitamin D deficiency. Laboratory testing for serum parathyroid hormone, kidney function, vitamin D metabolites, and serum phosphorus can help differentiate among causes. Acutely symptomatic patients require inpatient treatment with intravenous calcium gluconate, cardiac monitoring, and correction of hypomagnesemia. Hypercalcemia is most often due to primary hyperparathyroidism or malignancy. In the evaluation, hypercalcemia should first be confirmed by measurement of ionized calcium or repeat measurement of total serum calcium and correction for albumin. Obtaining a serum parathyroid hormone level is the next step. Asymptomatic, chronic mild hypercalcemia is often caused by primary hyperparathyroidism, which can be observed or treated surgically. Patients with severe hypercalcemia may have profound dehydration and require inpatient treatment with intravenous fluids, bisphosphonates, and calcitonin.
Prostate cancer is the second most common cancer in US men. Guidelines for screening vary, underscoring the need to engage patients in shared decision-making and counsel them about potential benefits and harms. When screening is undertaken, it is based on the prostate-specific antigen test, with digital rectal examination used selectively as an adjunct. Men with an abnormal prostate-specific antigen level should have a repeat test within a few months, before proceeding to biomarker testing, referral to urology, biopsy, and potentially imaging. Patients with newly diagnosed prostate cancer should be risk-stratified using clinical tumor (T) stage as determined by digital rectal examination, International Society of Urological Pathology grade group (Gleason score), prostate-specific antigen level, and tumor volume on biopsy. Treatment options vary by risk. Active surveillance is recommended for patients with low-risk disease, typically those with grade group 1/Gleason score of 6 (3 + 3). For patients with favorable intermediate-risk prostate cancer, treatment options are active surveillance, radiation therapy, or radical prostatectomy. For patients with unfavorable intermediate- or high-risk prostate cancer and estimated life expectancy greater than 10 years, options are radical prostatectomy or radiation therapy plus androgen deprivation therapy. For patients with prostate-specific antigen levels greater than 40 ng/dL, a Gleason score of 9 or higher, or locally advanced prostate cancer, treatment with radiation therapy and androgen deprivation therapy can additionally include concurrent abiraterone plus prednisone for 2 years. Focal ablation is also an option for some patients. Prognosis varies by disease features; men with low-risk prostate cancer are much more likely to die from other causes, whereas those with distant metastases have a 5-year relative survival rate of 38.3%.
Chronic prostatitis/chronic pelvic pain syndrome is a common male genitourinary condition comprising urinary, musculoskeletal, gastrointestinal, and/or psychological concerns with pain as a prominent feature. It is a diagnosis of exclusion. Physicians should use validated patient questionnaires to inventory presenting symptoms and symptom evolution over time. Questionnaires, such as the National Institutes of Health Chronic Prostatitis Symptom Index, can be particularly helpful in monitoring treatment effect on symptoms. Standardized classification systems can prove useful in choosing therapeutic modalities. Treatment should be individualized for each patient and multimodal; it should focus on symptomatic improvement, with a 25% or 6-point reduction in the National Institutes of Health Chronic Prostatitis Symptom Index score being defined as success. Chronic prostatitis/chronic pelvic pain syndrome is a chronic pain condition. Although pharmacologic and nonpharmacologic treatment modalities have variable proven benefit, few are supported by robust evidence. Chronic prostatitis/chronic pelvic pain syndrome does not predispose men to prostate cancer, but it may be associated with male infertility. Physicians should also be alert for its mental health effects on men.
Lower urinary tract symptoms that significantly impair quality of life in men may result from benign prostatic hyperplasia, overactive bladder, or a combination of both conditions. The diagnosis of benign prostatic hyperplasia, a voiding dysfunction due to outlet obstruction, can be made with a thorough history and physical examination. A validated questionnaire should be used to make an accurate initial diagnosis and to monitor treatment effect over time. Selective alpha-1 blockers are an appropriate first-line drug choice for most patients; however, 5-alpha reductase inhibitors and phosphodiesterase type 5 inhibitors may also be used, alone or in combination with each other, depending on symptom severity and if alternative treatment options are needed. If medical therapy is ineffective, surgical and interventional procedures aimed at opening the prostatic urethra are available to ameliorate symptoms. Overactive bladder manifests with urinary urgency, frequency, and nocturia with or without incontinence. The diagnosis of this storage dysfunction due to detrusor overactivity can be made with a thorough history, physical examination, urinalysis, and assessment of the residual volume of urine in the bladder after voiding. First-line treatment for overactive bladder includes beta-3 agonists as well as pelvic floor physical therapy and behavioral interventions. If left untreated, benign prostatic hyperplasia and overactive bladder can result in significant social isolation and relationship strain.
Although metabolic, viral, and drug- and alcohol-related etiologies are a familiar part of the evaluation of elevated liver enzymes, less common causes include autoimmune hepatitis, Wilson disease, and hereditary hemochromatosis. Each has a progressive course to end-organ damage underscoring the importance of early recognition, as effective therapies are available. Autoimmune hepatitis is an immune-mediated liver disease, with a female predominance and autoantibodies present in about 80% of cases. It can progress rapidly without treatment. Liver biopsy featuring lymphoplasmacytic hepatitis is needed for diagnosis and to determine the intensity of immunosuppression. Wilson disease is caused by biallelic variants in the ATP7B gene resulting in copper accumulation in the liver, brain, kidneys, and corneas. Diagnosis relies on clinical findings, laboratory data, and genetic testing results. Lifelong chelation therapy is required. Hereditary hemochromatosis is characterized by iron overload, usually due to a common variant in the HFE gene with variable disease penetrance; it is prevalent in people of Northern European ancestry. Untreated hemochromatosis leads to cirrhosis and hepatocellular carcinoma. Early diagnosis and initiation of phlebotomy can result in normal life expectancy. To facilitate early diagnosis, genetic testing of first-degree relatives is recommended for those with Wilson disease or hemochromatosis.
