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Biomedical subjects

A N Crowson

Publications and source records attributed to A N Crowson.

52 records · Page 3Linked to original sources
PubMed1996

The use of antibody to C5b-9 in the subclassification of lupus erythematosus.

Fifty-five patients with biopsy-proven cutaneous lupus erythematosus (LE) were identified in whom a prospective and retrospective review of the clinical and laboratory data allowed subclassification into systemic (SLE), subacute (SCLE), or discoid (DLE) variants. In addition to conventional direct immunofluorescence, an indirect immunofluorescent technique, using a monoclonal antibody, was employed to assess deposition of the membranolytic attack complex (C5b-9) in skin lesions. Deposition of C5b-9 within the epidermis correlated with a diagnosis of SCLE with or without antibodies to Ro and was seen in SLE patients with antibodies to extractable nuclear antigens Ro, La, Sm, and RNP, and in DLE patients with positive antinuclear antibodies and/or extracutaneous manifestations. In the SLE group, vascular C5b-9 deposition was present in six patients. Of these, four had circulating lupus anticoagulant, one had lymphocytic vasculitis, and two had antibodies to Ro. In two patients with SLE there was keratinocyte decoration for immunoglobulin G but not for C5b-9, in the absence of seropositivity for antibodies to Ro, La, Sm, and ribonucleoprotein (RNP). The immunohistological examination of skin lesions using a monoclonal antibody to C5b-9 is a valuable adjunct in the subclassification of LE. The presence of C5b-9 within skin lesions of patiens with LE implies a pathogenic role for complement-mediated pore formation.

Biomarkers↗
PubMed1995

Antidepressant therapy. A possible cause of atypical cutaneous lymphoid hyperplasia.

BACKGROUND: Cutaneous pseudolymphomas were encountered in eight patients who were receiving the antidepressant (AD) medications fluoxetine hydrochloride and amitriptyline hydrochloride, which promote tumor growth and suppress certain lymphoid functions by inhibiting the binding of endogenous histamine to an intracellular histamine receptor designated HIC. OBSERVATIONS: Lesions appeared in all patients following the start of AD therapy and resolved or improved in all seven who discontinued AD therapy. Skin lesions were solitary in three patients and multiple in five. Four patients were being treated with other drugs that altered lymphocyte function, and three had underlying systemic diseases that were associated with immune dysregulation. There were four histological patterns: mycosis fungoides-like, lymphocytoma cutis, lymphomatoid vascular reaction, and follicular mucinosis. Common to the first group were histological features of delayed-type hypersensitivity reactions that enabled distinction from mycosis fungoides. More problematic was the distinction of lymphocytoma cutis lesions from low-grade lymphocytic neoplasms. The lymphocytoma cutis lesions were rich in B cells; the other cases were dominated by T lymphocytes. CONCLUSIONS: Cutaneous pseudolymphomas are associated with AD therapy, possibly reflecting perturbation of lymphoid function. Concomitant therapy with agents that have additive or synergistic immunomodulatory effects or an immune-dysregulating systemic disease may increase a patient's susceptibility to developing atypical cutaneous lymphoid hyperplasia while the patient is receiving AD therapy.

Adult↗
PubMed1995

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 Behçet'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)

Adult↗
PubMed1995

Drugs with antihistaminic properties as a cause of atypical cutaneous lymphoid hyperplasia.

BACKGROUND: Although an association between antihistaminic drugs and atypical cutaneous lymphoid infiltrates has not been reported previously, in vitro evidence suggests that these agents perturb certain lymphoid functions through binding to histamine receptors, including a novel growth-promoting intracellular histamine receptor, designated HIC. OBJECTIVE: We studied the clinical findings and histopathologic findings in 14 patients taking antihistaminic drugs in whom atypical cutaneous lymphoid infiltrates developed. METHODS: We retrospectively reviewed the clinical and histologic features of these patients' skin lesions. RESULTS: The clinical presentations included solitary or multiple nodules and plaques, and multiple papules. In some patients a temporal association between drug therapy and clinical course was observed, as the lesions improved or resolved after a decrease or discontinuation of the drug. Eleven patients were taking two or more medications that in vitro are associated with alterations in lymphocyte function, including agents without antihistaminic properties. A diagnosis of pseudolymphoma seemed clinically apposite in seven of the 14 patients on the basis of either resolution of the eruption or presentation of a solitary nodule that did not recur after excision. Histologic analysis showed four distinct morphologies: mycosis fungoides-like, nodular dermal infiltrates consistent with either lymphocytoma cutis or lymphoma cutis, lymphomatoid vascular reaction, and follicular mucinosis. Common to cases showing the first pattern were histologic features suggesting a delayed-type hypersensitivity reaction, thus enabling their distinction from mycosis fungoides. The infiltrates were predominantly of T-cell phenotype. CONCLUSION: Antihistamines are associated with atypical lymphoid hyperplasia in some patients. The antihistaminic drug may not be the provocative agent per se; rather, a drug-induced immunodysregulatory state may render an abnormal immune response to some other exogenous antigen. Multidrug therapy with these and other agents known to exert immunomodulatory effects may increase susceptibility to the development of atypical lymphoid hyperplasia and malignant lymphoma.

Adult↗
PubMed1995

A case of necrotizing fasciitis due to Streptococcus pneumoniae.

We report a patient suffering from necrotizing fasciitis. The principal pathogen was Streptococcus pneumoniae. As far as we are aware, this is the first reported case of necrotizing fasciitis (NF) attributable to this organism. We discuss the pathogenesis of NF, and review the literature relating to this disorder.

Adult↗
PubMed1994

Esophageal perforation in recessive dystrophic epidermolysis bullosa.

Recessive dystrophic epidermolysis bullosa is an inherited mechanobullous disease characterized by skin blistering and esophageal bullae. In response to minor trauma, a split in the dermis or esophageal subepithelium occurs. Esophageal perforation is a rare complication. Because the esophagus is diseased in these patients, we believe that esophagectomy rather than repair is the treatment of choice for esophageal perforations. We report a patient for whom early primary repair failed and esophagectomy was required.

Adult↗
PubMed1994

Woringer-Kolopp disease. A lymphomatoid hypersensitivity reaction.

We report two cases of unilesional pagetoid reticulosis (Woringer-Kolopp disease). Histopathological, immunohistological, ultrastructural, and genotypic studies showed both lesions to be lymphomatoid hypersensitivity reactions, as characterized by polyclonal proliferations of T-lymphocytes; CD8+ T cytotoxic-suppressor (Tc/s) lymphocytes were predominant in one case, whereas CD4+ T helper (Th) lymphocytes were predominant in the other. The nosology of Woringer-Kolopp disease is discussed.

Adult↗
PubMed1994

Eosinophilic pustular follicular reaction: a paradigm of immune dysregulation.

BACKGROUND: We encountered 10 patients whose biopsies showed an eosinophilic pustular follicular reaction, a histomorphology alleged to be pathognomonic of eosinophilic folliculitis (EF). Only seven of these patients fell within the clinical spectrum of EF. Seven patients had conditions associated with immune dysfunction, including three patients with an atopic history. Potential antigenic stimuli could be elicited in six cases. METHODS: Formalin-fixed biopsy specimens from all 10 patients were available for examination. Hematoxylin and eosin-, alcian blue-periodic acid-Schiff (PAS)- and PAS-diastase-stained sections cut from paraffin-embedded tissue were examined by light microscopy. Immunoperoxidase preparations with antibody to IgE were performed on paraffin sections and the number of IgE-decorated cells quantitated in each case. Four patients also had biopsy material submitted in Michel's medium, on which direct immunofluorescent studies were conducted. RESULTS: IgE-coated mononuclear cells were present in patients whose lesions would logically be expected to derive from dominant type I hypersensitivity mechanisms and absent or minimal in biopsies from those patients in whom the pathogenetic basis of lesions derived principally from cell-mediated immunity. CONCLUSIONS: The eosinophilic pustular follicular reaction, while characteristic of EF, is not exclusive to that entity. It represents an expression of an excessive immediate or delayed-type hypersensitivity reaction to various auto-, epicutaneous, or ingested stimuli. A background of immune dysregulation may be contributory.

Adolescent↗
PubMed1994

An Id reaction to Mycobacterium leprae: first documented case.

We present a case of generalized sarcoidal dermatitis in a patient with tuberculoid leprosy. After careful consideration of the reactional states in leprosy and recognizing that id reactions occur in other mycobacterial infections, we concluded that the patient's eruption was likely an id reaction to his Mycobacterium leprae infection. It was most reminiscent of the tuberculids: lichenoid tuberculid and lichen scrofulosorum. However, its histomorphologic appearance was distinctive, showing elongated granulomata along with foci of incipient perineural granuloma formation, similar to the histomorphologic appearance of tuberculoid leprosy. A pathogenetic mechanism for this unique eruption is reviewed briefly.

Aged↗