Fecal impaction is a common disorder with variable presentation and many potential complications. Its pathophysiology is complex, and the treatment is often difficult and frustrating. Preventive measures are likely to be cost effective in populations at high risk, such as institutionalized or debilitated elderly people, mentally ill patients, those with chronic renal failure or cancer, and those who are neurologically impaired.

Within the last decade, Lyme borreliosis has emerged as a complex new infection whose distribution is worldwide. The disorder is caused by a recently recognized spirochete, B. burgdorferi, transmitted by ticks of the I. ricinus complex. Certain species of mice are critical in the life cycle of the spirochete, and deer appear to be crucial to the tick. Although the disorder's basic outlines are similar everywhere, there are regional variations in the causative spirochete, animal hosts, and clinical manifestations of the illness. In the United States, Lyme disease commonly begins in summer with a characteristic skin lesion, erythema migrans, accompanied by flu-like or meningitis-like symptoms. Weeks or months later, the patients may have neurologic or cardiac abnormalities, migratory musculoskeletal pain, or arthritis, and more than a year after onset, some patients have chronic joint, skin, or neurologic abnormalities. After the first several weeks of infection, almost all patients have a positive antibody response to the spirochete, and serologic determinations are currently the most practical laboratory aid in diagnosis. Treatment with appropriate antibiotics is usually curative, but longer courses of therapy are often needed later in the illness, and some patients may not respond.

Islet-amyloid deposits, which are a common feature of Type II diabetes mellitus, are derived from the polymerization of a putative hormone identified as IAPP. IAPP is synthesized by normal islet beta cells and probably is cosecreted with insulin. Although the physiologic function of IAPP and its role in the pathogenesis of Type II diabetes mellitus are just beginning to be unraveled, IAPP may play an important part in the development of this most common form of diabetes mellitus by opposing the action of insulin in peripheral tissues. The polymerization of IAPP to form extracellular islet-amyloid deposits may further contribute to the development of Type II diabetes mellitus by destroying islet cells and by disrupting the passage of glucose and hormones to and from them. Substantial evidence indicates that the propensity of IAPP to polymerize and form extracellular amyloid deposits in only certain species (e.g., humans, cats, and raccoons) is directly associated with an intrinsically amyloidogenic part of the molecule--i.e., positions 20 through 29 of IAPP. The inherent amyloidogenicity of IAPP in these species may be further facilitated by increased beta-cell production of IAPP, leading to a high local concentration that predisposes to polymerization. The latter possibility is supported by studies demonstrating that IAPP production by islet beta cells is increased in normoglycemic cats with impaired glucose tolerance. Although increased production of IAPP may initially cause insulin resistance, prolonged overproduction of IAPP may ultimately impair insulin secretion by leading to the progressive deposition of insoluble islet amyloid, a finding apparent in most subjects with overt diabetes. If, as these studies suggest, increased IAPP production is linked to the development of Type II diabetes mellitus, further studies must address the genetic and nongenetic factors that influence this important biologic change in humans and some animal species.

Lipoprotein lipase is an important regulator of lipid and lipoprotein metabolism. It also contributes to the lipid and energy metabolism of different tissues in varying ways. Although the synthesis, manner of secretion, and mechanism of endothelial binding of lipoprotein lipase appear similar in all tissues, the factors that control gene expression and posttranslational events related to processing vary from tissue to tissue. The actual molecular events that determine this tissue specificity are not yet understood. In the future, however, it may be possible to stimulate or inhibit the activity of lipoprotein lipase in specific tissues and to alter metabolic processes so as to improve the quality and length of life in patients with metabolic diseases such as hypertriglyceridemia, HDL2 deficiency, and obesity.