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At least 217 records · Page 12Linked to original sources
PubMed1989

Acrodermatitis enteropathica.

Acrodermatitis enteropathica results from a defect in zinc metabolism inherited as an autosomal recessive trait. Zinc is chelated in the gastrointestinal tract by an oligopeptide that is normally destroyed in the bowel. Zinc deficiency results in skin and bowel lesions, as well as alterations in mental status. If the disorder is not treated, death occurs from infection and/or marasmus. Blood zinc levels confirm the diagnosis. Dramatic recovery and normal development occur when dietary zinc is supplemented.

Acrodermatitis↗
PubMed1985

[Papular acrodermatitis of childhood as Gianotti-Crosti syndrome].

A case of a boy with a papular acrodermatitis caused by an Epstein-Barr viral infection is presented. This makes us consider actualized criteria relating to diseases in the Gianotti-Crosti syndrome and its relationship with the presence or absence of Australian antigen.

Acrodermatitis↗
PubMed1985

[The infantile acrodermatitis syndrome and Epstein-Barr virus infection].

Six cases of APVS, associated with Epstein-Barr-Virus-infection are reported, the clinical picture, however, is not diagnosed as it is in acrodermatitis papulosa infantum (API). For this reason, we suggest to look for the signs of a primary viral infection in all cases of acro-localized papulo-vesicular skin manifestations. In contrast of APVS, API is a primary hepatitis B virus infection.

Acrodermatitis↗
PubMed1977

Immune response to hepatitis B virus in children with papular acrodermatitis.

Papular acrodermatitis of childhood (PAC) is characterized by papular eruption of skin, lymphadenopathy, and acute hepatitis B surface antigen (HBsAg)-positive anicteric hepatitis. To study the course of hepatitis B virus infection we followed 16 patients with PAC, 2 to 7 years of age, for periods ranging from 6 to 46 months. All patients tested developed hepatitis B surface antigenemia subtype ay, and produced antibody to hepatitis B core antigen with the highest incidence after 3 to 5 months. Half of the children investigated developed antibody to hepatitis B surface antigen 4 to 18 months (mean, 6.5) after the onset of PAC. At the end of the investigation, 31% of the children were still HBsAg-positive, 50% were antibody to hepatitis B core antigen-positive, and in 43% the activity of serum aminotransferases was abnormal. Liver biopsy repeated in 2 children showed chronic aggressive hepatitis. The pattern of antibody response to hepatitis B virus is similar in both HBsAg-positive hepatitis and PAC. The frequent development of HBSAg carrier state and the high proportion of children with liver abnormalities at the end of the investigation suggest an impaired clearance of hepatitis B virus and a tendency to chronicity.

Acrodermatitis↗
PubMed1986

[Etiology of acrodermatitis chronica atrophicans and erythema chronicum migrans].

In Lyme's disease (LD) as well as in the European form of erythema chronicum migrans (ECM), the etiologic agents are spirochetes. As fas as we know by now, these microbes are closely related but not identical. Consequently, LD and ECM should be regarded as closely related but not as identical diseases. The sera of our 21 patients suffering from acrodermatitis chronica atrophicans (ACA) contained elevated antibody titers directed against the etiological agent found in ECM. These findings strongly suggest that ACA is also induced by spirochetes-possibly by the same microbes found in ECM.

Acrodermatitis↗
PubMed1985

[Acrodermatitis papulosa eruptiva infantum as a prodrome in hepatitis B infection].

We report on a 4-year-old boy suffering from typical infantile papular acrodermatitis with an unusual course. The eruption occurred seven weeks before the signs and symptoms of hepatitis. Only trace concentrations of hepatitis B surface antigen (HBsAg) could be detected after three weeks history of the disease. The lesions which persisted for nine weeks were itching, and there were signs of superinfection. We found only localized lymphadenopathy. The condition developed into a chronic HBsAg carrier state.

Acrodermatitis↗
PubMed1985

[Acrodermatitis chronica atrophicans--a borreliosis!].

Spirochetes were recovered from the skin lesions of two patients with acrodermatitis chronica atrophicans. Both patients assume that they had a tick bite. Sera from both patients showed increased IgG-antibody titers to a Borrelia burgdorferi strain isolated from the skin.

Acrodermatitis↗
PubMed1985

[Pediatric papular acrodermatitis and double primary infection by the hepatitis B virus and the Epstein-Barr virus].

A case of papular infantile acrodermatitis was evaluated in a twenty-two month-old child. Laboratory data showed the presence of a cytolytic hepatitis associated to an increase in circulating monocytes (1.500/mm3) with hyperbasophilic cells. Hepatitis B surface (HBs) antigen was detected in the serum, associated to anti-HBc antibodies of the IgM class, without detectable anti-HBs antibodies. Simultaneously, EBV serologic profiles were consistent with a primary infection. The authors review the clinical presentation of previously described cases according to their suspected cause, and discuss the etiologic role of both EBV and HBV in the hereby reported case.

Acrodermatitis↗
PubMed1977

[Acrodermatitis enteropathica in childhood (author's transl)].

A five months old infant is described with acrodermatitis enteropathica. The aetiology, pathogenesis and the clinical course of the disease is reported. It will be discussed the side effects of the oxychinolin therapy, the advantages and benefits of the substitution with zinc.

Acrodermatitis↗
PubMed1978

[Hydroxychinoline- and zinc-treated acrodermatitis enteropathica and electroretinographic findings (author's transl)].

A meanwhile 13 years old boy had to be treated by hydroxychinolines for a severe acrodermatitis enteropathica since his 1st year of life. At the age of 5 years he showed visual deterioration by atrophia optici. Dose reduction and application of different halogen substitutions were tried. Finally, it was daily oral zinc application and continuous control of the serum zinc level which made disappear all cutaneous and mucous symptoms. At an unchanged ophthalmoscopic status, there occurred a slight raise of vision, an enlargement of peripheric campus and a normalization of the electroretinographic potentials.

Acrodermatitis↗
PubMed1984

The spirochetal etiology of acrodermatitis chronica atrophicans Herxheimer.

Spirochetes were recovered from the skin lesion of 1 out of 10 acrodermatitis chronica atrophicans patients (ACA). Spirochetes from this skin isolate and from Ixodes (I.) ricinus and I. dammini spirochetes were used as antigens in indirect immunofluorescence tests. All sera from 17 ACA patients showed high antibody titers to the three antigens. Seven of the 17 sera which had the highest titers had crossreactive antibodies to treponemal antigen detectable in the FTA-ABS test. The results indicate that spirochetes are of importance for ACA and probably the causative agent of this disease. The connection between ACA and tick bites and the relationship to erythema chronicum migrans Afzelius (ECMA) and Lyme disease are discussed. The results are consistent with the hypothesis that ECMA and ACA are different manifestations of the same spirochete, with ACA as a late manifestation.

Acrodermatitis↗
PubMed1983

Bullous acrodermatitis due to zinc deficiency during total parenteral nutrition: an ultrastructural study of the epidermal changes.

A 5 1/2-year-old girl with idiopathic intestinal pseudo-obstruction became severely depleted of zinc during total parenteral nutrition and developed a vesico-bullous rash on face, hands and feet such as is seen in acrodermatitis enteropathica. Light and electron microscopy of a bullous lesion on one foot revealed a pronounced extracellular edema with cyst and cleft formation in the deep part of the epidermis. A few acantholytic cells were seen. In the electron microscope degenerate keratinocytes showed multiple vacuoles in the dark cytoplasm and slender, finger-like protrusions. Desmosomes were few. The basal lamina was well-preserved forming deep invaginations, which may serve to distinguish the condition from other bullous diseases of the skin.

Acrodermatitis↗
PubMed1982

[Clinical aspects, diagnosis and therapy of acrodermatitis enteropathica].

Acrodermatitis enteropathica is a very rare disease, usually occurring during child age, but also in grown-ups. Symptoms are skin lesions localized periorally and acrally, alopecia, diarrhea and psychic alterations. The disease is caused by zinc deficiency due to malabsorption. The diagnosis can be established by decreased plasma levels of zinc; typical changes of the Paneth cells may be demonstrated by electron microscopy. Substitution by supplying zinc will lead to complete clinical healing.

Acrodermatitis↗
PubMed1978

[Acrodermatitis enteropathica. Anatomo-clinical study of 2 familial cases treated with zinc sulfate].

Two familial cases of acrodermatitis enteropathica began at the time of weaning, with characteristic dermatologic lesions and digestive signs, resulting in lack of weight gain: at 13 months of age growth future was evident in the elder child. The anatomic lesions were those of an exophagitis and, in the duodenal mucosa, a dilation of the capillaries of the chorion in the absence of villous atrophy. The ultrastructural study showed inclusions in Paneth's cells, and changes in keratin cells, with intra-cytoplasmic vacuoles and abnormal melanin pigment in the skin. The administration of zinc sulphate induced a rapid recovery of cutaneous lesions and resumption of growth. The interruption of treatment resulted twice in a quite immediate relapse of cutaneous signs in the first patient, which was rapidly reversible with the reintroduction of zinc sulphate.

Acrodermatitis↗
PubMed1984

[Clinical aspects and etiology of acrodermatitis chronica atrophicans].

We followed up nine patients with acrodermatitis chronica atrophicans (ACA) for an average of 2 years (6-44 months). Extradermal symptoms were observed in five patients, three of whom developed systemic signs such as fatigue or general sensitivity to cold; three suffered from cardiac symptoms; and two had joint and/or nervous system involvement. In one patient, erythema migrans and oligoarthralgia preceded the ACA. In most patients, the laboratory tests showed changes often seen in inflammatory diseases; we found an elevation of IgA, IgG and/or IgM in five patients. Using an indirect immunofluorescence test with Ixodes dammini spirochetes as antigen, the patients had more or less elevated IgG antibody titers and insignificant IgM antibody titers; similar results were obtained in some patients when an Ixodes ricinus spirochete isolated in the area of Munich was used as antigen. We believe that ACA is a chronic spirochetosis with manifestations present in the skin, joints, nervous system, and presumably in the heart.

Acrodermatitis↗