Cases reported "Psoriasis"

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1/28. Generalized pustular psoriasis with hypoparathyroidism.

    A 36-year-old Japanese woman with pustular psoriasis associated with hypoparathyroidisum was reported. The patient showed hypocalcemia and was treated with calcium supplements and calcitriol. When the serum calcium level became normal, the pustules disappeared and erythroderma completely resolved. Histopathological features consisted of the formation of intraepidermal pustules including spongiform pustules underneath the stratum corneum, and acantholysis was observed in the epidermis. It was suggested that generalized pustular psoriasis may have been induced by hypocalcemia due to hypoparathyroidism in this case, and that acantholysis may be caused by hypocalcemia, since intercellular junctional components such as cadherins are highly dependent on calcium in the epidermis.
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2/28. Erythema gyratum repens-like psoriasis.

    A 28-year-old man was admitted to our department for investigation in 1992. He presented with a red, scaly, centrifugally spreading eruption, which had appeared in 1990, beginning on the neck and thorax, and later extending to the trunk and limbs. The cutaneous lesions, located mainly on the trunk and proximal upper limbs, were arranged in rings, with a slightly raised prominent scaling edge (Fig. 1a). The characteristic feature was the presence of rings or waves within already existing rings, whereas the central part was flattened, with the texture of normal skin. The concentric figurate lesions resembled a wood grain pattern (Fig. 1b). The clinical picture was strikingly similar to tinea imbricata; there was, however, no itching, and repeated mycologic studies did not disclose trichophyton concentricum. The histology was not characteristic. The epidermis, which was slightly edematous, was covered with a heavy crust. In the dermis, a sparse inflammatory infiltrate, somewhat more pronounced in the subpapillary areas, was composed of lymphocytes with some eosinophils. periodic acid-Schiff (PAS) and other stains for mycotic infection were negative. The general condition was not affected and laboratory studies did not show any abnormalities, except for low serum protein (5.1 g/L) and decreased gamma globulins (10.5%). Cell-mediated immunity was preserved. Immunofluorescence studies (direct and indirect) were negative. In spite of repeatedly negative mycotic examinations and due to the striking similarity to tinea imbricata, we applied various antimycotic therapies (terbinafine, itraconazole), with no effect. The figurate pattern, with normal skin in between, altered from day to day, while new concentric rings appeared within the cleared skin. The migrating rate was about 2-3 cm per 2 weeks. The patient had undergone a thorough search for internal malignancy. During the follow-up period of 1992-98, cutaneous involvement slowly became almost generalized (1996), and the confluent lesions formed large plaques, but still with pronounced concentric rings. Transitional blood eosinophilia (27% in 1993 and 11% in 1996) regressed with no therapy. Since 1995, antibodies to HBs and HBc have been present with no clinical symptoms of liver disease. The blood proteins increased to 7.0 g/L, and gamma globulins to 17.2% (normal). The histology, studied repeatedly, started to display some signs of psoriasis from 1996 and, in 1998, was already consistent with the disease (Fig. 2). RE-PUVA (0.8 mg/kg acitretin and UVA 0.8 J/cm2 ) was applied for 2 weeks before the patient interrupted the therapy. In spite of this, there was further improvement and, in 1999, the patient was almost free of lesions with some abortive rings left. From time to time, single vesicles appeared within the elevated borders of the rings. The histology of such vesicles was consistent with abortive pustular psoriasis (Fig. 3).
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3/28. stevens-johnson syndrome-like exanthema secondary to methotrexate histologically simulating acute graft-versus-host disease.

    A 61 year old male patient suffering from psoriasis vulgaris developed a severe skin reaction with toxic myelosuppression three days after administration of 20 mg methotrexate (MTX) p.o. per week and concomitant 100 mg acetylic salicylic acid (ASA) per day. The skin lesions simulated stevens-johnson syndrome with ulcerations of the oral mucosa and erythema multiforme-like target lesions. The histology of the epidermis resembled an acute graft-versus-host reaction. The increased toxic effect of MTX on keratinocytes in our patient was most likely caused by a lowered plasma binding capacity and reduced renal excretion of MTX due to concomitant administration of ASA. Thus in the treatment of severe forms of psoriasis with MTX, the combined administration of drugs aggravating MTX toxicity, particularly of ASA, should be carefully considered, due to the increased toxicity and risk of severe skin reactions.
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4/28. Oral psoriasis in a patient with hepatitis c virus infection.

    We report a case of 65-year-old patient with psoriasis vulgaris who developed a psoriatic manifestation on his lower lip, along with typical features of psoriasis on his trunk and extremities. Mucous membranes, palate and tongue were not affected. A biopsy specimen from lip showed acanthosis of the epidermis with parakeratosis, and mild cellular infiltrates in the upper dermis. He was also suffering from type C hepatitis, however, he had not been treated with interferons. Oral psoriasis involving the lip is extremely rare.
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5/28. staphylococcal scalded skin syndrome complicating acute generalized pustular psoriasis.

    A 60-year-old woman with psoriasis vulgaris treated with oral cyclosporin and acitretin developed an acute generalized pustular eruption with erythema and associated fever consistent with acute generalized pustular psoriasis. She was admitted to hospital and, despite intravenous fluid replacement, developed acute renal failure. In addition, she developed staphylococcal septicaemia. After transfer to the intensive care unit because of deteriorating renal function, a sudden onset of widespread flaccid blistering (Nikolsky sign positive) and superficial erosions was noted. histology of a biopsied blister revealed subcorneal splitting of the epidermis consistent with staphylococcal scalded skin syndrome. The patient was treated with intravenous dicloxacillin and the blistering gradually improved over 10 days.
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6/28. The pustule in palmoplantar psoriasis: transformed vesicle or mature microabscess? A three-dimensional study.

    psoriasis on the palms and soles is characterized by pustules, vesicles and hyperkeratotic plaques. Several studies have postulated that the pustules and vesicles are round or egg-shaped. This three-dimensional study reveals that neither pustules nor vesicles have a regular spherical morphology. The vesicles are located in the upper and middle layers of the epidermis and may exhibit dumb-bell- or banana-shaped lumina. The pustules consist of different compartments combining characteristics of a dyshidrotic vesicle with those of a microabscess of Munro.
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7/28. Annular psoriasiform eruption with lymphocytic infiltration of the epidermis: a variant of acute psoriasis?

    Disseminated annular psoriasiform lesions developed over a period of 2 months in a 48-year-old man with no preceding psoriatic history of drug intake, being accompanied by general dullness and arthralgia. etretinate was effective for both skin eruption and arthralgia; only the latter recurred on its cessation 5 months later. However, histologic features examined by serial sections totally lacked those of pustular psoriasis; there were no neutrophils in the epidermis where massive T lymphocyte infiltration existed instead, in a fashion similar to that of early psoriatic lesions. We differentiated this peculiar annular psoriasiform eruption from the annular erythematous lesions noted in pityriasis rosea, erythema annulare centrifugum, subacute cutaneous lupus erythematosus, annular erythema associated with sjogren's syndrome and erythema chronicum migrans. It is our speculation that this dermatosis represents a variant of acute psoriasis, rather than annular pustular psoriasis. The histopathologic and immunohistologic findings suggest ongoing cellular immune responses in these lesions where some unknown inhibitory mechanisms might be operative against further production of neutrophil chemotactic factors that usually takes place in psoriatic lesions.
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8/28. Eosinophilic pustular folliculitis starting initially only with palmoplantar pustular lesions. Report of a case and review of the literature.

    We report a 23-year-old Japanese male with eosinophilic pustular folliculitis (EPF) that had started with palmoplantar rash. Only when follicular pustules appeared on the bilateral cheek 31 months later, we revised our initial diagnosis of pustulosis palmaris et plantaris (PPP) to EPF, and all the skin eruptions cleared mostly with indomethacin. A review of the Japanese literature for the past 20 years disclosed that in 207 cases of EPF so far reported, palmoplantar pustular lesion was noted in 38 (18%). Among them, in 16 cases (8%) the skin lesions started first from the palmoplantar region with the average period of 26 months until the appearance of other eruptions of EPF. None of them was diagnosed as EPF when skin lesions were localized only to the palmoplantar region. When we find pustules on the palmoplantar region, we should suspect the possibility of early lesions of EPF as well as PPP. Histopathologic demonstration of multilocular pustules located in the upper epidermis containing numerous eosinophils in the palmoplantar pustular lesions, together with the dramatic therapeutic response to indomethacin greatly favor the diagnosis of EPF.
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9/28. Granulocyte colony-stimulating-factor-induced psoriasiform dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation.

    psoriasis is a chronic inflammatory skin disorder characterized by accumulation of Th1-type T cells and neutrophils, regenerative keratinocyte proliferation and differentiation, and enhanced epidermal production of antimicrobial peptides. The underlying cause is unknown, but there are some similarities with the immunologic defense program against bacteria. Development of psoriasiform skin lesions has been reported after administration of granulocyte colony-stimulating factor (G-CSF), a cytokine induced in monocytes by bacterial antigens. To further investigate the relation between this type of cytokine-induced dermatitis and psoriasis, we analyzed the cutaneous cytokine profile [tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), IL-12p35 and p40, and IL-8] and expression of markers of epidermal activation [Ki-67, cytokeratin-16, major histocompatibility complex (MHC) class II, intercellular adhesion molecule-1 (ICAM-1)] in a patient who developed G-CSF-induced psoriasiform dermatitis by using quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistology. The histologic picture resembled psoriasis with regard to epidermal hyperparakeratosis and the accumulation of lymphocytes in the upper corium. CD8( ) T cells were found to infiltrate the epidermis which was associated with an aberrant expression of Ki-67, cytokeratin-16, MHC class II, and ICAM-1 on adjacent keratinocytes. As compared to normal skin (n = 7), there was an increased expression of TNF-alpha, IL-12p40, and IL-8, a decreased expression of TGF-beta1, and a lack of IL-10, similar to the findings in active psoriasis (n = 8). Therefore, G-CSF may cause a lymphocytic dermatitis that, similar to psoriasis, is characterized by a pro-inflammatory Th1-type cytokine milieu and an epidermal phenotype indicative of aberrant maturation and acquisition of non-professional immune functions.
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10/28. Psoriasiform eruption induced by propranolol.

    The appearance of a psoriasiform eruption in a seventy-eight year old patient after one year of treatment with propranolol is presented herein. The histologic picture was not compatible with psoriasis vulgaris, although it contained some of the same features. Immunologic investigation revealed immune deposits at the junction of the dermis and epidermis and in blood vessel walls as well as monoclonal gammopathy. The rash, which was followed by a reduction in tear secretion, is suggested to have been a drug reaction associated with propranolol. This is supported by the positive results of a migration inhibiting factor test towards propranolol, the clearing of the eruption which took place three weeks after withdrawal of the drug, and the negative result of the same test obtained soon afterwards.
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