The importance of neoplasms ultimately lies in their effects on patients. Although malignant tumors are of course more threatening than benign tumors, morbidity and mortality may be associated with any tumor, even a benign one. Indeed, both malignant and benign tumors may cause problems because of (1) location and impingement on adjacent structures, (2) functional activity such as hormone synthesis or the development of paraneoplastic syndromes, (3) bleeding and infections when the tumor ulcerates through adjacent surfaces, (4) symptoms that result from rupture or infarction, and (5) cachexia or wasting. The following discussion considers the effects of a tumor on the host, the grading and clinical staging of cancer, and the laboratory diagnosis of neoplasms.
Location is crucial in both benign and malignant tumors. A small (1-cm) pituitary adenoma can compress and destroy the surrounding normal gland, giving rise to hypopituitarism. A 0.5-cm leiomyoma in the wall of the renal artery may encroach on the blood supply, leading to renal ischemia and hypertension. A comparably small carcinoma within the common bile duct may induce fatal biliary tract obstruction.
Signs and symptoms related to hormone production are often seen in patients with benign and malignant neoplasms arising in endocrine glands. Adenomas and carcinomas arising in the beta cells of the pancreatic islets of Langerhans can produce hyperinsulinism, sometimes fatal. Similarly, some adenomas and carcinomas of the adrenal cortex disrupt homeostatic mechanisms by elaborating steroid hormones (e.g., aldosterone, which induces sodium retention, hypertension, and hypokalemia). Such hormonal activity is more likely with a well-differentiated benign tumor than with a corresponding carcinoma.
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A tumor may ulcerate through a surface, with consequent bleeding or secondary infection. Benign or malignant neoplasms that protrude into the gut lumen may become caught in the peristaltic pull of the gut, causing intussusception (Chapter 15) and intestinal obstruction or infarction.
Many cancer patients suffer progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia, and anemia—a condition referred to as cachexia. There is some correlation between the size and extent of spread of the cancer and the severity of the cachexia. However, cachexia is not caused by the nutritional demands of the tumor. Although patients with cancer often are anorexic, current evidence indicates that cachexia results from the action of soluble factors such as cytokines produced by the tumor and the host, rather than reduced food intake. In patients with cancer, calorie expenditure remains high, and basal metabolic rate is increased, despite reduced food intake. This is in contrast with the lower metabolic rate that occurs as an adaptive response in starvation. The basis of these metabolic abnormalities is not fully understood. It is suspected that TNF and other cytokines produced by macrophages in response to tumor cells or by the tumor cells themselves mediate cachexia. TNF suppresses appetite and inhibits the action of lipoprotein lipase, preventing the release of free fatty acids from lipoproteins. There is no satisfactory treatment for cancer cachexia other than removal of the underlying cause, the tumor.
Symptom complexes that occur in patients with cancer and that cannot be readily explained by local or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue of origin of the tumor are referred to as paraneoplastic syndromes. They appear in 10% to 15% of patients with cancer, and their clinical recognition is important for several reasons:
Such syndromes may represent the earliest manifestation of an occult neoplasm.
In affected patients, the pathologic changes may be associated with significant clinical illness and may even be lethal.
The symptom complex may mimic metastatic disease, thereby confounding treatment.