Apoptotic cell death in formation of vesicular skin lesions in patients with acquired zinc deficiency

We investigated the role of apoptotic cell death in the production of skin lesions in patients with acquired zinc deficiency. Nuclear condensation of keratinocytes was observed at an early stage of skin lesions in patients with zinc deficiency, especially around vesicular lesions. Nuclei of keratinocytes in perivesicular lesions of the epidermis were positively stained by the nick-end labeling specific for fragmented DNA. Lewis Y antigen was also expressed on perivesicular lesions. On the other hand, there were no such positively stained cells in hyperkeratotic skin lesions of the patients. Therefore, it was suggested that apoptotic cell death might play a role in the formation of vesicular skin lesions in patients with zinc deficiency, but not in the formation of hyperkeratotic skin lesions.     

Skin lesions in acquired zinc deficiency due to parenteral nutrition.

The skin lesions seen in 10 patients who received parenteral nutrition during treatment of chronic enteropathy are described. All of these patients had a lowered serum zinc concentration. The skin lesions were similar to those seen in acrodermatitis enteropathica. After supplementation with zinc sulphate, the skin lesions disappeared completely. A decrease in the serum alkaline phosphatase level can be regarded as a sign of an impending zinc deficiency. Parenteral nutrition formulae should contain a sufficient amount of zinc.     

Dermopathic changes in hypozincemia.

In seven patients with chronic debilitating gastrointestinal disease who were being given total parenteral nutrition using L-amino acids and concentrated dextrose solution, severe hypozincemia (less than 60 micrograms/dL) developed with characteristic skin lesions and alopecia. The lesions were similar to seborrheic dermatitis, and they occurred in areas of high sebaceous gland concentration. Hyperkeratotic lesions were also seen on the extensor surfaces of large joints. The skin lesions and alopecia disappeared when serum zinc values were raised to levels above 60 micrograms/dL, with appropriate zinc sulfate replacement. A hypothesis on the etiology and clinical manifestations is presented.     

Cutaneous manifestations of zinc deficiency in ethylic cirrhosis

Thirty-three patients with alcoholic cirrhosis (AC), selected on widely recognized criteria (16, 57), were investigated prospectively for cutaneous manifestations of zinc deficiency. The patients were divided into 3 groups: group A (n = 12): AC without skin lesions; group B (n = 12): AC with skin lesions responsive to a zinc-free topical treatment or resistant to enteral zinc sulfate intake; group C (n = 9): AC with skin lesions cured by oral zinc replacement therapy alone. The lesions observed in group C were studied microscopically. Data concerning zinc metabolism (Zn concentrations in plasma, red cells, urine and hair; alkaline phosphatase values), biochemical criteria of AC (plasma serum-albumin concentration, IgA/transferrin ratio) and a malabsorption test (xylosemia 120 min after oral absorption of D-xylose 25 g) were compared by the variance analysis method. A control group (D, n = 12) was used as reference. Few cases of cutaneous manifestations of zinc deficiency in AC patients have been published. In more than one half of the 15 or so we found in the literature, an aggravating factor (total parenteral nutrition, digestive tract surgery) had to be taken into account. In this prospective study 9 new cases in which AC was the only cause of zinc deficiency are reported. A clinical picture similar to acrodermatitis enteropathica with peribuccal bullous lesions was observed in only one patient. In all other cases the patients presented with a cracked and reticulated eczema on the extensor aspect of the limbs and (often erosive) in the perianal and genital regions. The eczema was associated with cheilitis, glossitis, stomatitis, alopecia and, seldom, ungual Beau's lines. Disorders of behaviour, diarrhoea and bouts of lever regressing under zinc replacement therapy were frequent. Histology was not very specific, except for the presence of necrotic areas in the stratum germinativum, sometimes associated with small subcorneal pustules containing altered polymorphonuclears. In every case, it was the rapid regression of symptoms under zinc sulfate treatment that confirmed the diagnosis. Plasma zinc concentrations were most significantly decreased in all AC groups as compared to controls (61.2 +/- 19.4 vs 97.8 +/- 10.4 micrograms/100 ml) and also in AC patients with skin manifestations of zinc deficiency as compared to the other AC patients (44.4 +/- 9.2 vs 66.5 +/- 18.8 micrograms/100 ml) table V). Changes in serum-albumin levels and in hepatocellular function were parallel to changes in plasma zinc concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)     

白癜风患者血清及皮肤组织液铜锌含量测定

本文用感应藕合等离子发射光谱仪,测定了27例白癜风患者和36例健康人血清中铜锌两种微量元素的含量,并对其中24例白癜风患者无病变部位和白斑部位的皮肤吸力水疱疱液进行了测定。结果显示白癜风患者血清中铜锌的含量均低于正常对照组,病人白斑部位组织液铜含量明显低于无病变部位,提示白癜风发病与铜锌两种微量元素有关。     

Zinc depletion syndrome with acrodermatitis during longterm intravenous feeding

Two patients suffering from terminal ileitis showed signs of zinc depletion during longterm total intravenous feeding. Initially, the skin lesions resembled seborrhoeic eczema with diffuse loss of hair, scaling in the scalp and erosions around the orifices. Later bullae appeared in the creases of the fingers and around the nails. In both patients serum alkaline phosphatase levels gradually decreased and serum zinc was significantly lowered. A prompt beneficial effect in the patients' general condition and dermatosis was seen following zinc administration, especially intravenously. In one patient, the sites of wound dehiscence and donor skin graft areas healed rapidly after zinc therapy was initiated. It is concluded that the zinc depletion syndrome was primarily caused by lack of zinc in the intravenous feeding. However, latent zinc deficiency due to extensive resections or loss of zinc in the fistular secretion and urine might have enhanced the depletion of zinc still further. Prophylactic zinc should be given to patients who require longterm intravenous feeding.     

Acrodermatitis acidemica secondary to malnutrition in glutaric aciduria type I

We encountered a patient with glutaric aciduria type I (GA-I) associated with skin lesions resembling acrodermatitis enteropathica (AE). This child was being fed with a low-protein diet when the skin disorder developed. A deficiency in plasma levels of essential amino acids, particularly isoleucine, and zinc was confirmed. Supplementation of a high-caloric, protein-rich diet together with zinc, selenium and vitamins led to a prompt improvement of the skin lesions. We assume that in our patient the skin lesions were the result of malnutrition, rather than being primarily associated with the underlying metabolic disease. To our knowledge, no other report is so far available concerning GA-I complicated by skin eruptions.     

Bullous Pemphigoid Induced by Penicillamine in a Patient with Wilson Disease

We report a 47-year-old man with Wilson disease who developed bullous lesions on the trunk and extremities after 20 years of penicillamine treatment. The histologic and immunofluorescence findings were diagnostic of bullous pemphigoid. When penicillamine was replaced by zinc sulfate, the patient’s bullous skin lesions improved rapidly. However, after 2 months of zinc sulfate treatment, the patient’s skin condition remained improved but his neurologic disease became worse and penicillamine was reinstituted. Bullous lesions recurred within 1 week and the diagnosis of penicillamine-induced bullous pemphigoid was confirmed. This is the first report of penicillamine-induced bullous pemphigoid in a patient with Wilson disease.     

A FATAL CASE OF JUNCTIONAL EPIDERMOLYSIS BULLOSA (HERLITZ-PEARSON)

Clinical findings, therapeutic responses and autopsy findings of a case of junctional epidermolysis bullosa were reported. A low serum zinc level was corrected by oral zinc sulphate with little improvement in skin lesions. Early diagnosis and genetle nursing were stressed.     

Zinc deficiency with transitory acrodermatitis enteropathica in a boy of low birth weight

A premature male baby fed on his mother's milk developed zinc deficiency and a skin disorder inseparable from acrodermatitis enteropathica. Following zinc therapy the skin lesions healed. Later the treatment was withheld and no recurrence was seen during 30 months’ observation. The boy's zinc deficiency was thought to be due to a high requirement secondary to rapid growth, to poor zinc supply in food and, possibly, to inefficient zinc absorbtion.     

Necrolytic acral erythema: a variant of necrolytic migratory erythema or a distinct entity?

BACKGROUND: Hepatitis C is a major health problem in Egypt. Necrolytic acral erythema (NAE) is a recently described necrolytic erythema that has a distinctive acral distribution and a uniform association with hepatitis C. Some authors believe that NAE is a distinct entity and others consider it as a variant of necrolytic migratory erythema (NME). METHODS: Five patients with clinical features consistent with NAE were included in this study. The patients were subjected to skin biopsy examination, CT scan of the pancreas and a liver biopsy. Liver function tests, serum glucagon, glucose, amino acids and zinc were measured. All patients were tested for hepatitis C by enzyme-linked immunosorbent assay (ELISA) and by polymerase chain reaction (PCR). RESULTS: Three patients presented with early (acute) lesions and two patients with chronic lesions. The distribution of the lesions was almost exclusively on the dorsae of the feet. Histopathological findings were similar to those of other necrolytic erythemas. Hepatitis C virus was uniformly detected in all patients. Serum glucagon was high in two patients, serum glucose was high in four patients, serum amino acids were low in three cases and serum zinc and albumin were low in two cases. Little or no improvement was reported after oral amino acid supplementation, while the response to oral zinc sulfate was moderate to good. CONCLUSION: Necrolytic acral erythema is closely associated with hepatitis C infection. Many findings indicate that NAE seems to be a variant of NME rather than a distinct entity. Hence, an alternative proposed term could be acral NME.     

Venous leg ulceration: skin and serum zinc concentrations.

Zinc was measured in serum and in thigh skin in patients with venous leg ulceration and also in controls. Skin zinc concentrations were expressed in terms of area and dry weight. The mean serum zinc concentration was significantly lowered in the ulcer group. The thigh skin zinc concentration was elevated in patients with chronic venous leg ulceration. The difference was more marked if the zinc concentration was calculated per surface area of skin, but did not reach statistical significance.     

Diagnosis and therapy of the zinc deficiency syndrome during total parenteral feeding. Review with report of a case]

A 47-year-old man with ulcerative colitis developed severe zinc deficiency during longterm intravenous feeding. Early symptoms included seborrhoeic lesions in the face and scalp. Later on his general condition deteriorated, and erythema and bullae erupted in the fingers, together with an erosive area with a marked border in the perianeal and scrotal regions. The symptomatology was suggestive of zinc depletion syndrome, a recently recognised acrodermatitis-enteropathica-like disorder in patients receiving longterm total intravenous feeding. A significantly lowered serum zinc level and a prompt beneficial response to intravenous zinc therapy (20 mg Zn2+ daily for one week) substantiate the provisional clinical diagnosis. As zinc depletion is caused by a zinc free parenteral alimentation this serious complication should be avoided by adding zinc to the infusions. Serum zinc determinations should be carried out as a control of the prophylactic zinc supply. Possibly, zinc plays a role in the symptomatology of various disorders with skin and bowel symptoms.     

Acquired zinc deficiency mimicking glucagonoma dermatitis. Histology and electron microscopy

A 47-year-old man suffering from colitis ulcerosa developed serious anaemia, oedema, stomatitis with burning tongue, dry skin and erosive lesions with peripheral spreading on the ankles. Histology and electron microscopy showed characteristic signs for necrolytic migratory erythema, zinc deficiency acrodermatitis, or pellagra. Decreased serum zinc level and response to oral zinc substitution finally proved the diagnosis of acquired zinc deficiency.     

Evaluation of zinc level in skin of patients with necrolytic acral erythema

Summary Background Necrolytic acral erythema (NAE) is considered a cutaneous sign of hepatitis C virus infection. Its exact pathogenesis is still not fully understood, with some reports about decreased serum zinc levels but none about its level in the skin. Objectives To assess skin (lesional and perilesional) and serum zinc levels in patients with NAE and compare them with levels in control subjects. Methods Fifteen patients with NAE and 10 healthy controls were included in this study. Assessment of zinc level, in serum by graphite furnace atomic absorption spectrophotometry and in lesional and perilesional skin biopsies by flame atomic absorption spectrometry, was done in all subjects. Re‐evaluation of serum and lesional skin zinc level was done after oral zinc treatment. Results Mean ± SD zinc levels were significantly lower in patients (serum 0·44 ± 0·13 mg L^?1; lesional skin 42·6 ± 18·9 mg L^?1; perilesional skin 32·5 ± 17·2 mg L^?1) than controls (serum 1·17 ± 0·29 mg L^?1; skin 100·1 ± 2·77 mg L^?1), with a positive correlation between lesional and perilesional skin zinc (r = 0·91, P < 0·01). Oral zinc supplementation significantly increased serum and skin zinc levels (by 159% and 4%, respectively; P < 0·05). Conclusions NAE is associated with decreased serum and skin zinc levels. Oral zinc supplementation corrects decreased levels of plasma and skin zinc much earlier than the desired clinical benefits appear.     

Acrodermatitis-enteropathica-ähnliche Hautveränderungen bei Morbus-Crohn-bedingtem Zinkmangel

We report a case of acrodermatitis enteropathica-like skin eruptions presenting with alopecia, perlèche, glossitis, and genital erosions as well as multifocal eczematoid, psoriasiform, and bullous skin lesions due to zinc deficiency in Crohn's disease.     

Erosive pustulosis of the scalp: 3 cases

BACKGROUND: Erosive pustulosis of the scalp is a rare entity of unknown etiology mainly affecting elderly people. It is often triggered by local trauma and features chronic pustules of the scalp evolving toward scarring alopecia. Its treatment is not yet codified. OBSERVATIONS: Two patients (66 and 87 years old) presented with crusted and erosive pustules of the scalp following surgical removal of actinic keratosis and total skin graft. In a third patient, similar lesions appeared after hair grafting. Clinical features were consistent with the clinical pattern of erosive pustulosis of the scalp. In all three patients, oral zinc gluconate in combination with topical steroids associated resulted in significant improvement. CONCLUSION: An association of topical steroids and oral zinc gluconate might be an interesting therapeutic option in this chronic, often disabling affection.     

Acrodermatitis enteropathica-like eruptions in a child with Hartnup disease

Acrodermatitis enteropathica-like eruptions, not related to zinc deficiency, have been rarely reported in some metabolic disorders. Reported patients usually had low levels of essential amino acids, particularly isoleucine. Here we report a girl who first presented with an acrodermatitis enteropathica-like eruption and eventually had the diagnosis of Hartnup disease with a normal isoleucine level. We discuss the probable cause of her skin lesions and the differential diagnosis with pellagra.     

Zinkverteilungsstörung bei psoriasis

Zusammenfassung An 64 Psoriatiker fand sich eine statistisch signifikante Erhöhung des Zinkspiegels im Plasma und eine ebenfalls statistisch signifikante Minderung des Zinkgehalts in den Bluterythrocyten, verglichen mit 54 gesunden Personen. Die erhobenen Befunde zeigten keine Relation zur Ausdehnung der Hautkrankheit. Die Verteilungsstörung dieses Spurenelements bei Psoriasis könnte auf eine Störung des Histidin-Stoffwechsels oder auf Veränderungen der Erythrocytenmembran beruhen.

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Zinc distribution disorder in psoriasis

Summary In 64 patients with psoriasis and in 54 persons without any skin disease the amount of zinc was estimated in plasma and in the erythrocytes using atomic absorption spectrophotometry. The findings showed an elevated plasma level and a lower zinc content of blood erythrocytes in psoriasis. Both values were statistically significant. No relation was found between these changes and the percentage skin surface covered by psoriatic lesions. The disturbed distribution of zinc in psoriasis may be due to disturbances of histidine metabolism or to changes of the permeability of the cell membranes associated with this skin disease.

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Herrn Prof. Dr. J. Capetanakis, Direktor der Universitäts-Hautklinik Athen, zum Geburtstag gewidmet