Cases reported "Psoriasis"

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1/8. 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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2/8. Acute acral pustulosis.

    We report a patient with a pustular eruption in an acral distribution that developed abruptly 4 days after a streptococcal pharyngitis. The histology showed an intraepidermal vesicle filled with neutrophils with an underlying lymphocytic vasculitis. Direct immunofluorescence demonstrated heavy deposition of C3 within the vessel walls. In addition, circulating immune complexes were found.
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3/8. psoriasis and intraocular inflammation.

    Presented in this series were seven men and three women. Ages when seen, ranged from 32 to 68 years (average 54). psoriasis had begun in childhood in the women and in the late 20's and 30's in the men. Arthritis (ankylosing spondylitis) was present in only one. Their ocular inflammations began from ages 26 to 62 (average 41). The onset of the inflammation was acute iritis in four and in indolent iridocylcitis in six. All but one were bilateral and chronic. The vitreous had heavy debris in nine of the ten patients. The retina was normal in only three. Boggy congestion was present in two with cystoid edema. Patches of edema. fluorescein leaking, depigmentation of both maculae, pars plana exudate, and retinal vessel obliteration to grey-white, shaggy cords was present in at least one of the remaining five patients. Systemic corticosteroid therapy has been used in eight of the ten patients described in this report. Doses no higher than 30 mg of prednisone per day were used to initiate reversal of the inflammatory response. In case 10, knowledge of the sensitivity of the process to steroids led to the successful rapid reversal of a recalcitrant iritis with only 20 mg of prednisone as a first dose and 20 mg per day for less than three weeks. maintenance corticosteroid therapy ranged from 40 mg of prednisone every other day in case 9, prednisone 12.5 mg one day and 5 mg the next in case 8, to 8 mg of Aristocort or methylprednisolone acetate (M-edrol) daily in cases 1 and 2. In summary, these patients are older, have an indolent onset bilateral uveitis with dense vitreous debris, retinal abnormalites, and are extremely sensitive to systemic corticosteroids. Many of these patients had undergone the series of clinical evaluations known as a "uveitis survey." Many different systemic abnormalities were found and merited treatment which rarely made a difference in their ocular disease, though two improved after infected teeth were treated. Assuming that these ocular diseases were related to psoriasis, one can then challenge the value of anything found by a "uveitis survey." The author uses information gained from such studies to insure that the patient is in the best possible heatlh and then makes clinical correlations such as presented in this paper. The rarity of this combination of ocular inflammations in patients with psoriasis makes it risky to propose that this is a significant association. Arguments that this is a disease entity began with the clinical similarities: older age, indolent onset, vitreous and retinal involvement, and the extreme sensitivity to systemic corticosteroids. None of these patients had psoriatic arthritis and only one had ankylosing spondylitis. The best explanation for the fact that this disorder has not been emphasized in the past would be an attitude of ophthalmologists and physicians that the eye and skin disease were coincident.
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4/8. Pigmented villonodular synovitis associated with psoriatic polyarthropathy: and electron microscopic and immunocytochemical study.

    A case of pigmented villonodular synovitis in a patient with psoriatic polyarthropathy was studied by means of light microscopy, electron microscopy and immunocytochemical techniques. The lesion consisted of mononuclear phagocytes with features intermediate between type A and type B cells, two types of multinucleate giant cells, an abnormal vasculature, extravasated fibrin and erythrocytes. An unexpected feature was the presence of a mononuclear cell whose cytoplasm contained intermediate filaments and reacted strongly to antisera to cytokeratins. Such a cell type has not previously been described in this condition and its significance is unclear. The findings support the theory that the pathogenesis of PVNS involves leakage of blood through abnormal vessels resulting in the local accumulation and proliferation of mononuclear phagocytes, connective tissue cells and unidentified cytokeratin positive mononuclear cells. The aetiology of the vascular damage, however, remains unknown.
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5/8. vasculitis as the basis of cutaneous lesions in Reiter's disease.

    The cutaneous lesions of Reiter's disease (RD) and pustular psoriasis (PP) are said to be histologically similar and often indistinguishable. We encountered three cases of RD in which biopsy specimens of lesions clinically compatible with keratoderma blenorrhagicum showed a pustular psoriasiform tissue reaction in conjunction with a subjacent superficial leukocytoclastic vasculitis (LCV). In an attempt to ascertain if these changes were distinctive and unique to cutaneous RD, the incidence of such changes in lesions of PP was examined using light microscopy and immunohistochemistry. The role of chlamydial infection in the pathogenesis of the observed vascular changes also was explored by assessing for the presence or absence of vascular deposition of chlamydial antigen in cutaneous RD compared with that in a control group that included cases of LCV and PP. In addition to conventional light microscopic analysis, immunoperoxidase studies to identify immunoglobulin deposition were performed on formalin-fixed, paraffin-embedded tissue from two of three patients with RD and on skin biopsy specimens from 11 patients with PP. Direct immunofluorescence (DIF) studies with antibodies to immunoglobulin (Ig)G, IgM, IgA, C3, and chlamydial antigens were performed on frozen tissue from one patient with RD, two patients with PP, three patients with LCV, one patient with nonspecific dermatitis, and one patient with Behcet's disease, who had a high antichlamydia antibody titer. All three specimens of RD showed a pustular psoriasiform diathesis in conjunction with a subjacent superficial LCV that was of maximal intensity in the dermal papillae capillaries. Through an immunoperoxidase technique performed on formalin-fixed tissue, the RD cases for which tissue was available for study demonstrated Ig deposition in injured blood vessels; using the same technique one of 11 PP biopsy specimens showed vascular Ig deposition in concert with LCV. This patient's biopsy was from a lesion of drug-induced LCV. None of the other specimens showed either light microscopic or immunohistochemical evidence of vasculitis. In the one specimen of RD studied by DIF, vascular deposition of IgG, IgM, C3, chlamydia heat shock protein 60 (CHSP60), and chlamydia-specific lipopolysaccharide (LPS) was observed. In the two specimens of PP studied, vascular deposition of C3, fibrin, CHSP 60, and chlamydia-specific LPS was not observed. Two specimens of LCV and the one specimen of dermatitis with concomitant nonspecific vascular injury showed vascular Ig and C3 deposition; in contrast, no vascular deposition of CHSP 60 or chlamydia-specific LPS was observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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6/8. Pustular psoriasis and aseptic purulent arthritis: possible role of leukotrienes B4 and C4 in a flare of synovitis.

    BACKGROUND: Arthritis is a frequent complication of pustular psoriasis. However, the mechanism of onset of this arthritis still remains unclear. OBJECTIVES: The present study was conducted to determine whether leukotriene (LT) B4 or LTC4 is one of the proinflammatory mediators that possibly enhance exacerbation of the arthritis lesions. methods: We investigated the condition of the arthritis and autopsy findings of two cases of generalized pustular psoriasis with the severe complication of aseptic purulent arthritis. We also measured the synovial fluid levels of LTB4 and LTC4 by radioimmunoassay. RESULTS: The collected synovial fluid was purulent, but nonbacterial, and the synovium of the knee joint showed histopathologic evidence of polymorphonuclear leukocyte (PMN) invasion, edema and dilatation of small vessels showing similarity to a histologic reaction in the skin lesions. The immunoreactive (i-) LTB4 and i-LTC4 in the samples significantly exceeded the amount measured in osteoarthritis patients used as the controls. CONCLUSION: Thus, i-LTB4 and i-LTC4 appear to be generated in the arthritis lesions of pustular psoriasis, the former attracting PMNs to the joints and the latter causing exudation of synovial fluid.
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7/8. Pustular vasculitis with clinical feature of pustular psoriasis and sternoclavicular hyperostosis.

    We report the case of a 51-year-old Japanese man with a unique pustulosis. He had multiple erythematous plaques and numerous pinpoint pustules on the trunk and extremities resembling pustular psoriasis. Histologic features revealed a fully developed intraepidermal abscess filled with neutrophils and disrupted epidermal keratinocytes. Mild leukocytosclastic vasculitis was seen in the underlying dermis. A direct immunofluorescence study revealed IgM, Clq, C3 and fibrinogen deposits in the dermal vessels. The patient had also sternoclavicular hyperostosis. We think that this represents a unique type of pustular vasculitis distinct from pustular psoriasis.
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8/8. The clinical and histomorphological features of pityriasis rubra pilaris. A comparative analysis with psoriasis.

    pityriasis rubra pilaris (PRP) is an idiopathic erythematous scaling eruption which can be difficult to distinguish from psoriasis. We explored the clinical features, including background medical illnesses and potential triggers in patients with PRP, and also its histomorphologic spectrum. patients with PRP were selected by natural language search of dermatopathology databases containing 250,000 cases accessioned over a 3-year period. A detailed medical history was obtained on each patient via office chart review and patient interviews. We compared the histologic findings in skin biopsies from patients with PRP to those of biopsies matched for site and age from control patients with psoriasis. Certain aspects of the clinical presentations encountered in the study group patients have not been previously emphasized, including eruptions compatible with a vesiculobullous disorder in 4 patients. Several patients had evidence of underlying iatrogenic or systemic immune dysregulatory states and certain triggers could be isolated such as emotional stress and prior exposure to microbial pathogens. Histomorphologic features predictive of PRP included follicular plugging, an increased granular cell layer, and acantholysis. While seen in a minority of biopsies of PRP, morphologic discriminators supportive of a diagnosis of psoriasis included neutrophils in the parakeratotic scale crust, and dermal papillae capillary ectasia with vessels lying in direct apposition to the epidermis. Other morphologic features were encountered in biopsies of PRP which have received little emphasis in the dermatopathology literature, including epithelial atrophy, significant dermal inflammation, the presence of eosinophils and plasma cells within the inflammatory infiltrates, an abnormal granular cell layer, and epidermolytic hyperkeratosis, albeit none were statistically signficant predictors of PRP over psoriasis. Nevertheless, their identification emphasizes the varied histologic spectrum of PRP. The almost ubiquitous finding of acantholysis and the presence of an abnormal granular cell layer in many biopsies of PRP suggests that abnormal keratins or defects in the retinol signalling pathway may be of pathogenetic importance.
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