Search PubMedSearch

PubMed · 96035

Acrodermatitis enteropathica.

Abstract

Acrodermatisis enteropathical has had a remarkable hist orical course beginning only 35 years ago, first passing through a period of empiric management with the 8-hydroxyquinoline drugs and culminating with the discovery of a biochemical effect in zinc absorption. This accomplishment has not only resulted in the cure of a serious and often fatal disease, but has opened the way to an understanding of the vital role played by the trace element zinc in many previously unrecognized areas of human physiology.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K H Neldner, K M Hambidge, P A Walravens. 1978. Acrodermatitis enteropathica.. https://doi.org/10.1111/ijd.1978.17.5.380

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Current aspects of Lyme disease and other Borrelia burgdorferi infections.

Lyme disease, acrodermatitis chronica atrophicans, and borrelial lymphocytoma are caused by species of the spirochete Borrelia burgdorferi. Lyme disease has emerged as the leading vector-borne infectious disease in the United States. This article presents a current review of these entities.

Acrodermatitis

Why is chronic Lyme borreliosis chronic?

Chronic Lyme borreliosis (CLB) can present not only in different organs but also in different patterns. Although many theories exist about the mechanisms leading to CLB, it is known that viable Borrelia burgdorferi can persist for decades and cause late skin manifestations of acrodermatitis chronica atrophicans (ACA). Thus, the immunopathogenetic findings in ACA can serve as a model for studying the chronic course of Lyme borreliosis. Recent findings indicate that the most important cell for antigen presentation, the epidermal Langerhans cell (LC), is invaded by B. burgdorferi in early Lyme borreliosis. Therefore, LCs were stained immunohistochemically with different markers to investigate their functional activity. Numbers of CD1a+ LCs were reduced in erythema migrans but normal or slightly elevated in ACA. In both diseases there was also a marked downregulation of major histocompatibility complex class II molecules on LCs, as measured by staining of human leukocyte antigen DR. This phenomenon might be a mechanism that protects against the presentation of autoantigens and may be the cause of the impaired capacity of LCs to eliminate B. burgdorferi antigens, thus explaining why CLB is chronic.

Acrodermatitis

Pseudo-Kaposi's sarcoma associated with acquired arteriovenous fistula.

Pseudo-Kaposi's sarcoma or acroangiodermatitis usually has underlying conditions of increased venous pressure or circulatory abnormality. We experienced two cases of pseudo-Kaposi's sarcoma in patients with acquired iatrogenic arteriovenous fistula from hemodialysis on their forearms. The patients complained of painful swollen crusted vesicles and purple or erythematous patches or plaques on their hands and fingers. Histologic findings included features of pseudo-Kaposi's sarcoma such as proliferations of small vascular spaces with narrow vascular channels lined by spindle cells, extravasated erythrocytes, and hemosiderin deposits. Percutaneous arteriography performed in Case one excluded the possible coexistence of arteriovenous malformation. In both cases, venous pressure and skin surface temperature were increased around the lesions; these may have played important roles in the development of the lesions. Both cases improved after oral erythromycin treatment, which seemed to be safe and effective for pseudo-Kaposi's sarcoma.

Acrodermatitis