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[Infantile papular acrodermatitis. Acrodermatitis papulosa and the infantile papulovesicular acrolocalized syndrome].

Papular acrodermatitis of childhood is an infectious disease characterized by a non-relapsing, non-itching, monomorphic erythemato-papular dermatitis limited to the face and limbs. It is always associated with anacute hepatitis, with hepatitis B antigen in the serum and with a reactive reticulohistiocytic lymphadenitis. In childhood other types of papular or papulovesicular acro-located eruptions, itching or non-itching, associated with reactive lymphadenitis, are observed, in the course of known diseases and with unknown cause. These acro-located cutaneous eruptions of unknown origin, which show varying features, should be classified as "papulovesicular acrolocated syndrome" until their ethiopathogenesis is known.

Acrodermatitis

[Acrodermatitis enteropathica--zinc as a life-saving drug].

Formerly acrodermatitis enteropathica was treated with oxiquinoline without full control of the disease and with the danger of blindness. Moynahan has introduced zinc into the treatment with excellent results, based on the finding that acrodermatitis enteropathica is a zinc-deficiency disorder. Other authors and own observations have confirmed the findings of Moynahan. There are clinical, genetical, immunological and therapeutical parallels between the acrodermatitis enteropathica of man and the so-called hereditary parakeratosis of calves which also is a hereditary disturbance of zinc metabolism. The treatment of acrodermatitis enteropathica with zinc is furthermore a great success in the prevention of blindness, as zinc is not dangerous to the retina and the optic nerve.

Acrodermatitis

[Acrodermatitis enteropathica--a disturbance of zinc metabolism with zinc malabsorption (author's transl)].

The intestinal resorption of zinc using 65ZnCl2 was estimated in 3 patients with acrodermatitis enteropathica, 2 healthy controls, and 3 heterozygotes. After oral application of 65Zn the whole body activity was measured by a whole body counter for 34 days. The 65Zn resorption of the patients amounted to 16, 42 and 30% of the applied dose, whereas the resorption values of the heterozygotes and the controls were in the range of 58 and 77%. The elimination of 65Zn from the body amounted to about 0.7% of the applied dose with no difference between controls and patients with acrodermatitis enteropathica. Before therapy the serum-zinc levels of patients were markedly decreased. After oral application of high doses of zinc aspartate (2 times 400 mg/day) all clinical symptoms disappeared within a week. The results point at a causal connection between zinc and the pathogenesis of acrodermatitis enteropathica. Ultrastructural alterations of the Paneth cells of the intestines are also shown in this disease [12] as have also been seen in Paneth cells of zinc deficient rats [Beitr. Path. 145, 336 (1972)].

Acrodermatitis

[Zinc treatment of acrodermatitis enteropathica (author's transl)].

Treatment of acrodermatitis enteropathica with zinc sulfate, first described by Moynahan and Barnes in 1973, has been widely accepted. We have treated a case of acrodermatitis enteropathica successfully with this drug. The 14-year old boy had to discontinue clioquinol because of a partial opticus atrophy. The skin lesions deteriorated acutely. Following zinc sulfate treatment the lesions rapidly disappeared and the general health of the patient greatly improved. Small doses of zinc sulfate are sufficient for maintenance therapy. The pathogenesis of acrodermatitis enteropathica is reviewed and the modes of action of zinc therapy are considered.

Acrodermatitis

Acrodermatitis enteropathico. Abnormalities of fat metabolism and integumental ultrastructures in infants.

Acrodermatitis enteropathica is a rare disease of childhood, characterized by periorificial and perioral dermatitis, acrodermatitis, diarrhea, and alopecia. Two patients were successfully treated with diiodohydroxyquin (Diodoquin). Lipid concentrations disclosed abnormal distribution of fats that resembled those of less mature infants fed diets low in linoleic acid even though the patients were actually on diets with high linoleic acid levels. Fatty acid distribution showed increased levels of linoleic acid that correlated with clinical improvement in the patient who was more ill. Skin fatty acids showed decreased levels of linoleic acid. Electron micrographs and histochemical staining disclosed increased lipids droplets in epidermal cells. Linoleic acid and zinc may have a role in the origin of the disease, and measurement of both skin and serum linoleic acid is suggested in the evaluation of its progress.

Acrodermatitis

Acrodermatitis enteropathica. Corneal involvement with histochemical and electron micrographic studies.

A case of acrodermatitis enteropathica occurred with corneal changes consisting of linear subepithelial corneal opacities. From the results of histochemical and electronmicrographic studies on a biopsy specimen of the corneal lesion, no definite conclusion may be drawn as to whether the corneal changes are a manifestation of acrodermatitis enterophathica or a result of iodochlorhydroxyquin therapy.

Acrodermatitis

Oral treatment of acrodermatitis enteropathica with zinc sulfate.

In a 7-year-old boy with acrodermatitis enteropathica, oral administration of zinc sulfate brought about complete relief of symptoms and signs, with clearing of the skin lesions, arrest of diarrhea, and growth of new hair. Considering the dramatic results obtained, we believe that oral treatment with zinc sulfate is an innocuous, inexpensive, and very effective medication for acrodermatitis enteropathica, which can replace the previously used and toxic diiodohydroxyquin-like drugs.

Acrodermatitis

Zinc therapy of depressed cellular immunity in acrodermatitis enteropathica. Its correction.

A child with hypogammaglobulinemia and intractable diarrhea underwent parenteral alimentation for five months. A clinical syndrome of acrodermatitis enteropathica subsequently developed associated with a depression in thymus-dependent lymphocyte (T cell) numbers, abnormal T-cell mitogen-induced blast transformation, and anergy to skin test antigens. Plasma zinc levels were found to be abnormally low. Zinc therapy resulted in dramatic resolution of the clinical manifestations of acrodermatitis enteropathica. Cell-mediated immune function was also restored to normal, suggesting an important role for zinc and possibly other trace metals in cellular immune responses.

Acrodermatitis

Zinc therapy of acrodermatitis enteropathica.

The therapeutic effect of orally administered zinc was evaluated in an adult woman with acrodermatitis enteropathica. When she was off therapy and in clinical relapse the plasma zinc concentration (10 mug per 100 ml), serum alkaline phosphatase (3 1U per liter) and urine zinc excretion rate (39 mug per 24 hours) were extremely low. Di-iodohydroxyquin therapy was accompanied by a modest increase in plasma zinc concentrations. Oral zinc sulfate (220 mg three times a day or 50 mg twice a day) resulted in rapid and complete clinical remission, and in a return of plasma zinc, serum alkaline phosphatase and urinary zinc excretion to normal. These data are compatible with a severe zinc deficiency state and indicate that the inherited defect in this disease is either in or closely related to zinc metabolism. The beneficial effects of zinc therapy in this patient provide further confirmation of the efficacy of oral zinc in the treatment of acrodermatitis enteropathica.

Acrodermatitis

Hypertension in a patient with acrodermatitis enteropathica.

One patient with acrodermatitis enteropathica complicated by hypertension is presented. The pathogenesis of the markedly elevated blood pressure is unknown. The acrodermatitis healed completely on zinc therapy and parallel to this improvement the hypertension could easily be controlled with a gradually decreased antihypertensive drug dosage.

Acrodermatitis

Peripheral neuropathy in acrodermatitis chronica atrophicans (Herxheimer).

Acrodermatitis chronica atrophicans is a dermatological condition that takes a chronically progressive course and finally leads to a widespread atrophy of the skin. Involvement of the peripheral nervous system is frequently observed, predominantly a sensory polyneuropathy. General reactions, the effect of penicillin treatment, the histological findings, and reports concerning a communicable agent transmittable from human to human as well in tissue cultures point to an infectious disease. Acrodermatitis chronica atrophicans follows a peculiar geographical distribution forming clusters of high prevalence in certain regions. Transmission by ticks is suggested.

Acrodermatitis

Acrodermatitis enteropathica-like eruption association with parenteral nutrition.

This is a case report of a patient with acrodermatitis enteropathica-like eruption that occurred during parenteral nutrition. The skin lesions were similar to those of acrodermatitis enteropathica, but there were no other major symptoms such as diarrhea and alopecia. It was noticed that the lack of linoleic acid in the diet might be the cause of lesions.

Acrodermatitis

[Zinc therapy in acrodermatitis enteropathica].

Report of two patients with acrodermatitis enteropathica, one of them 20 years old and with very severe symptoms of the disease. Oral therapy with zinc resulted in complete cure within two months. The theory about chelating of dietary zinc in patients with acrodermatitis enteropathica is discussed.

Acrodermatitis

Hereditary zinc deficiency (Adema disease) in cattle, an animal parallel to acrodermatitis enteropathica.

Adema disease and acrodermatitis enteropathica, two parallel syndromes in calves of Friesian descent and in man, are described. Both are congenital zinc deficiency disorders with a lethal course if left untreated. Complete recovery follows oral zinc therapy. Symptoms and findings are set out in Table I. Diseased calves may serve as animal models for further studies on acrodermatitis enteropathica and the biological role of zinc.

Acrodermatitis

[Acrodermatitis enteropathica; zinc sulfate therapy].

We present the case of two siblings with acrodermatitis enteropathica. Zinc levels were low. Oral administration of 100 mg of zinc sulfate allowed total regression of all signs. When zinc therapy was interrupted, the manifestations reappeared and disappeared again when treatment was resumed. A defect of genetic origin in digestive zinc absorption is suggested. Mohnahan's advocated zinc treatment of acrodermatitis enteropathica in 1973; it is a non-toxic treatment, which is always active and be considered as a diagnostic test.

Acrodermatitis

Treatment of acrodermatitis enteropathica with zinc sulfate.

Control of a case of acrodermatitis enteropathica was achieved initially after three months of treatment with diiodohydroxyquin (Diodoquin). Reexacerbation of acrodermatitis enteropathica was noted two months after diiodohydroxyquin was discontinued. Treatment with zinc sulfate was substituted and resulted in dramatic and complete resolution of disease within 48 hours.

Acrodermatitis