Can diagnostic imaging help improve elder abuse detection?

Elder abuse is an underdetected, under-reported issue with severe consequences. Its detection presents unique challenges based on characteristics of this vulnerable population, including cognitive impairment, age-related deconditioning, and an increased number of co-morbidities, all of which predispose to increase vulnerability to injury. While radiologists play a critical role in detection of child abuse, this role is currently not paralleled in detection of elder abuse. We conducted a thorough review of the literature using MEDLINE to describe the current knowledge on injury patterns and injury findings seen in elder abuse, as well as barriers to and recommendations for an increased role of diagnostic imaging in elder abuse detection. Barriers limiting the role of radiologists include lack of training and paucity of rigorous systematic research delineating distinctive imaging findings for physical elder abuse. We outline the current ways in which imaging can help raise clinical suspicion for elder abuse, including inconsistencies between purported mechanism of injury and imaging findings, injury location, multiple injuries at differing stages of healing, and particular patterns of injury likely to be intentionally inflicted. We additionally outline the mechanism by which medical education and clinical workflow may be modified to increase the role for imaging and radiologist participation in detecting abuse in older adult patients, and identify potential future directions for further systematic research.

Acne vulgaris: therapy directed at pathophysiologic defects.

An effective therapeutic regimen for the treatment of acne vulgaris is presented. The emphasis is based upon correcting a defect in keratinization of the sebaceous follicles with a combination of vitamins A and E. This prevents the formation of milia and comedones, thus depriving the Propionibacterium acnes of a culture medium. Vitamin E also prevents irritating lipid peroxidation of sebum, damaged by bacterial growth, which may be responsible for the inflammatory aspects of acne. No antibiotics were employed in the series of 98 consecutive cases examined herein.

Facial dermatitis following friction treatment of acne.

A case report is presented herein of a twenty year old woman in whom an acute dermatitis of the face developed, which may have been caused by the use of a skin machine, possibly in combination with the use of a topical medication.

Synergism of vitamins A and E with dermatologic applications.

A synergism between vitamins A and E has been demonstrated by a number of investigators, notably Stanley R. Ames, who showed that in rats on a vitamin E deficient diet, the serum vitamin A level remained low, no matter how much vitamin A was given by mouth, or even by injection, but that adding vitamin E to the diet restored the vitamin A serum level to normal. We have utilized these observations with a high degree of success where vitamin A alone had failed to control three dermatologic conditions involving a defect in keratinization, namely, keratosis follicularis (Darier's disease), pityriasis rubra pilaris, and acne vulgaris. It is possible that a number of additional dermatoses characterized by dyskeratosis or hyperkeratosis might also be benefited by this combination.

Lupus erythematosus and vitamin E: an effective and nontoxic therapy.

Despite conflicting opinions, our personal experience and a number of reviewed clinical reports indicate that vitamin E, properly administered in adequate doses, is a safe and effective treatment for chronic discoid lupus erythematosus, and may be of value in treating other types of the disease. A possible mechanism leading to the development of autoimmune diseases, including lupus erythematosus, is discussed, together with a rational approach aimed at the cellular level, rather than at attacking the body's immune defenses, which could lead to increased susceptibility to malignant and infectious diseases.

Porphyria cutanea tarda: response to vitamin E. A review and two case reports.

Porphyria cutanea tarda is a disease characterized by a triad of cutaneous manifestations: "fragile" skin, usually involving the dorsal aspects of the hands, forearms, legs, or feet; mild hyperpigmentation; and hypertrichosis, especially of the face. The condition is due to a metabolic defect of liver function involving heme synthesis, resulting in the formation of abnormal amounts of uroporphyrin, and sometimes, coproporphyrin or both, which can be measured quantitatively in the urine. Present methods of treatment, including repeated phlebotomy, alkalinization, or chloroquine leave much to be desired. Based on recent experimental and clinical reports and on our personal experience with two patients, we suggest a more logical therapeutic approach in the form of large doses of vitamin E, which apparently corrects the metabolic defect causing the disease.

Is vitamin E involved in the autoimmune mechanism?

Autoimmune diseases are characterized by an alteration of the body's defense mechanism, designed for protection against infections and toxic injuries, which for unknown reasons attacks and destroys normal tissue. Some evidence strongly suggests that such diseases are the result of hydrolytic enzymes that escape from lysosomes whose membranes have been damaged by lipid peroxidation or other causes and that combine with and denature normal tissue proteins--in effect converting them into foreign proteins--to which the body then reacts by producing antibodies. During the past ten years, in a private dermatologic practice, we have conducted clinical investigations on the possible therapeutic value of vitamin E in the management of a number of disabling skin diseases of unknown etiology as well as several muscular disorders. Among the diseases that were successfully controlled were a number in the autoimmune category, including scleroderma, discoid lupus erythematosus, porphyria cutanea tarda, several types of vasculitis, and polymyositis. Since vitamin E is a physiologic stabilizer of cellular and lysosomal membranes, and since some autoimmune diseases respond to vitamin E, we suggest that a relative deficiency of vitamin E damages lysosomal membranes, thus initiating the autoimmune process.

Polymyositis: response to vitamin E.

A 70-year-old woman with polymyositis was treated with three different immunosuppressive drugs. Her condition deteriorated over a three-month period until she became totally helpness. She then made a dramatic improvement when large doses of vitamin E (d, alpha-tocopheryl acetate) were administered. Current knowledge regarding the nature of polymyositis and the rationale for using vitamin E to treat it are discussed.