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Zinc deficiency, acrodermatitis enteropathica, optic atrophy, subacute myelo-optic neuropathy, and 5,7-dihalo-8-quinolinols.

Acrodermatitis enteropathica, a heritable disease of zinc deficiency, was formerly amenable to treatment only with dihaloquinolinol drugs. A few cases of optic atrophy were reported in surviving patients and were proposed as examples of ocular drug toxicity, principally because of the association between iodochlorhydroxyquin and subacute myelo-optic neuropathy (SMON) in Japan. An alternate hypothesis is now offered: that the optic atrophy was secondary to the zinc deficiency, which is consistent with diverse evidence cited from the literature. Therefore, it would seem worthwhile to investigate zinc in cases of disk pallor described as idiopathic or drug associated, and to investigate visual function in cases of severe malnourishment.

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Acrodermatitis and acquired zinc deficiency.

A 42-year-old woman had an acquired zinc deficiency. The patient was malnourished, secondary to chronic alcohol (ethanol) abuse and cirrhosis, with associated low serum and urinary levels of zinc. Her acrodermatitis was unresponsive to topically applied triamcinolone acetonide but cleared after oral zinc sulfate therapy.

Acrodermatitis↗

Cystic fibrosis manifesting with acrodermatitis enteropathica-like eruption. Association with essential fatty acid and zinc deficiencies.

A refractory dermatitis resembling acrodermatitis enteropathica was the manifesting sign in a 5-month-old male infant with cystic fibrosis, preceding pulmonary and gastrointestinal tract symptoms by two months. The eruption was clearly nutritionally responsive. Biochemical evidence was shown for deficiencies of zinc, essential fatty acids, and protein. Altered prostaglandin metabolism was also demonstrated.

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[Acrodermatitis induced by zinc deficiency].

A patient with acrodermatitis as a result of zinc deficiency is reported. In spite of the characteristic signs the required substitution of zinc is often delayed, because the entity is confused with other, more common forms of dermatitis.

Acrodermatitis↗

[Zinc-deficiency syndrome with acrodermatitis].

The symptoms of the zinc depletion syndrome are demonstrated in two males and two females. The four patients, 23 to 39 years old, were suffering from ileocolitis Crohn. After three to eight weeks of total parenteral nutrition they showed signs of acrodermatitis. Serum zinc was found considerably below normal levels (0,21--0,68 microgram/ml). After oral nutrition was re-initiated the dermatitis healed within four weeks without zinc oxid or zinc sulphate administration. Serum zinc increased to normal levels.

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Successful treatment of acrodermatitis enteropathica with zinc sulfate.

A case of a 22-month-old child with acrodermatitis enteropathica (AE) is reported. At five months of age, the patient experienced generalized oral and cutaneous candidiasis for which she was treated with nystatin and iodochlorhydroxyquin-hydrocortisone. She then had to be treated for secondary infection of the lesions. After three months, the cycle repeated, and the patient was treated with topical clotrimazole, Mycolog (nystatin, gramicidin, neomycin sulfate, triamcinolone acetonide) and oral nystatin. After a worsening of her condition, she was admitted to a hospital where she was treated initially with procaine penicillin G, then methicillin sodium and gentamicin sulfate. Treatment with zinc sulfate, 50 mg t.i.d., was initiated when laboratory studies showed a serum zinc level of 60 microgram/dl. Skin lesions were 99% resolved and serum zinc increased to 118 microgram/dl after 17 days of zinc sulfate therapy. Previous case reports and studies of the clinical features, treatment and pathogenesis of AE are reviewed.

Acrodermatitis↗

Papular acrodermatitis of childhood and hepatitis B infection.

A case of papular acrodermatitis (PAC) associated with acute anicteric type B hepatitis occurred in a 2-year-old child. Immunocytochemical studies failed to detect the presence of viral antigens in the involved skin lesion. Current knowledge of the hepatitis B viral antigens and of their possible role in PAC is discussed.

Acrodermatitis↗

Acrodermatitis in breast-fed premature infants: evidence for a defect of mammary zinc secretion.

Two 9-week-old, breast-fed premature infants developed acrodermatitis and hypozincemia because of low zinc content in their mothers' breast milk. All symptoms of zinc deficiency disappeared within seven days after the infants were treated orally with zinc and did not recur when zinc was discontinued after 11 months (infant 1) and three weeks (infant 3). After a subsequent term pregnancy, one of the mothers had lower breast milk zinc content (P less than .025) and greater exponential decline (P less than .025) of zinc content through 40 weeks of lactation compared with 34 control subjects. Her second infant (infant 2) had hypozincemia at 7 months of age but did not develop clinical zinc deficiency. When the mothers of the affected infants took oral zinc supplements, there was no increase in their breast milk zinc content. Zinc secretion into breast milk appears to be a controlled process that is independent of maternal zinc intake or serum zinc level. Breast milk may be low in zinc because of defective mammary secretion and this may lead to severe symptomatic zinc deficiency in premature infants.

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[Immunocytoma simulating chronic acrodermatitis atrophicans].

A 76 year old female developed an acrodermatitis-chronica-atrophicans-(ACA)-like lesion on her foot. Histological examination and quantitative determination of immunoglobulins in homogenates from the skin lesion revealed an immunocytoma of the IgM type. Malignant lymphoma originating in ACA lesions or concomitting ACA are well known. The case described here indicates that primary malignant lymphoma of the skin clinically can simulate ACA and creates diagnostic, therapeutic and prognostic problems.

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Hereditary acrodermatitis enteropathica in an adult.

The condition of a 33-year-old woman who had a history of blisters following trauma on the hands, knees, and feet since 1 year of age previously had been diagnosed as epidermolysis bullosa. She also had psoriasiform plaques, a pustular crusted periorificial eruption, paronychia, alopecia, and photophobia. She had had minimal history of diarrhea. A markedly decreased serum zinc level was found, and treatment with zinc sulfate was instituted, resulting in clearing of all clinical manifestations. Since patients with hereditary acrodermatitis enteropathica may have minimal or no diarrhea and the correct diagnosis may be long delayed, the condition should not be considered strictly a disease of children.

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[Enteropathic acrodermatitis treated with zinc sulfate].

A six month old baby with acrodermatitis enteropathica was treated successfully up to the age of 2 1/2 years with oral zinc sulphate, 100 mg daily. No complications were seen but there were two relapses. The first was at the age of 15 months when the dose of zinc sulphate was reduced to 50 mg daily and the second at 20 months when the zinc was stopped by mistake.

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Gluconate zinc in acrodermatitis enteropathica.

Two children with characteristic findings of acrodermatitis enteropathica were found to have low serum zinc levels prior to therapy. Treatment with zinc gluconate in low dosages resulted in an increase in serum zinc levels and clinical improvement. All family members studied had low serum zinc levels. In addition, we noted a change of hair color to red and excessive drooling just prior to exacerbations in these two patients. The hair color returned to normal with remission.

Acrodermatitis↗

Clinical, biochemical and histochemical studies on infants with Acrodermatitis enteropathica chronica.

7 infants diseased with Acrodermatitis enteropathica and 10 normal controls were included in this study. The values of anthranilic acid glucuronide, 6- aminohippuric, anthranilic acid, N-acetyl Kneurine, Kneurine and 30 H Kneurenine, were estimated in mg/24 hours urine, both basal and after tryptophane load. In addition, histopathological and histochemical studies for lactase, succinic dehydrogenase, alkaline phosphatase, acid phosphatase, and alpha-non-specific esterases activities were done for the intestinal mucosal biopsies. All the previous investigations were then repeated after two months treatment with 500 mg/day diiodohydroxyquinoline. The tryptophan metabolites were significantly low in the diseased infants, both basal and after tryptophan load. Moreover, the intestinal enzymes activities were altered. After 2 months treatment with diiodohydroxyquinoline the diseased infants became clinically improved, tryphtophan metabolites became normal, but the activities of the intestinal enzymes were not altered. The biochemical and histochemical findings were discussed, giving the possibility of competitive inhibition of the diiodohydroxyquinolines and the by-product 8 OH Quinololic acid resulting in more degradation of Kneurine and 3 OH Kneurenine to nicotinamide adenine dinucleotide.

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[Acrodermatitis enteropathic treated with zinc sulfate. Report of a case].

A case is reported of a girl with acrodermatitis enteropathica who was treated succesfully with zinc sulfate at 75 mg/day PO. A remarkable increase in weight was evident through the course of 12 months of treatment, reaching the percentile 50 by the age of 3 years; however the height remained close to percentile 3. Possibly, the zinc deficiency is secondary to a selective defect in the metal absorption. Treatment with zinc sulfate in these patients substitutes with greate advantages the use of diiodohydroxyquin. Possibly, zinc supplements must be given for a life time to these patients.

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Zinc correction of defective chemotaxis in acrodermatitis enteropathica.

Three patients with acrodermatitis enteropathica (AE), a disorder of zinc metabolism, demonstrated a zinc-responsive defect in chemotaxis of neutrophils and monocytes. Monocyte chemotaxis was depressed during a controlled period of zinc deficiency and increased to normal values after administration of oral zinc sulfate supplements that was sufficient to restore normal plasma zinc levels. In the only patient in whom neutrophils were also studied, a similar defect in chemotaxis of neutrophils was corrected by administration of zinc sulfate supplements. Preincubation of defective cells in vitro with zinc sulfate increased chemotaxis in an almost linear dose-response relationship. These findings suggest an important role for zinc in neutrophil and monocyte chemotaxis and demonstrate a correctable immune defect in AE.

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Acrodermatitis continua of Hallopeau in a patient with myelodysplastic syndrome.

Acrodermatitis continua of Hallopeau (ACH) is a rare manifestation of pustular psoriasis which may considerably disable affected patients. In this case report we confirm the efficacy of acitretin in the treatment of ACH and, in addition, describe the course of the myelodysplastic syndrome (MDS) from which the patient was suffering. During acitretin treatment, there was a transformation into acute myeloid leukaemia. We discuss the effect of retinoids on the bone marrow of normal subjects, patients with MDS, and patients with acute myeloid leukaemia. Our experience in the present case, and the information from the available literature, lead us to advise against the use of the aromatic retinoids, acitretin and etretinate, in patients with MDS. If such treatment is indicated, intensive haematological supervision is mandatory.

Acitretin↗

Successful treatment for acrodermatitis continua of Hallopeau using topical calcipotriol.

We report a 71-year-old woman who had severe inflammatory acrodermatitis continua of Hallopeau. The administration of local remedies, soft X-rays and a number of systemic treatments resulted only in transient and incomplete resolution of the lesions. The pustules, increased skin fragility, tender oedema and erythema were successfully controlled by the local administration of calcipotriol.

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