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Biomedical subjects

C M Magro

Publications and source records attributed to C M Magro.

At least 55 records · Page 3Linked to original sources
PubMed1996

Differential expression of the bcl-2 oncogene in human basal cell carcinoma.

The bcl-2 protein increases cell longevity and reduces apoptosis. Expression of the bcl-2 oncogene is reported in certain low grade neoplasms including basal cell carcinomas (BCCs). The authors postulated that the indolent variants of BCC, namely, the superficial and circumscribed subtypes, might exhibit greater bcl-2 expression than their aggressive counterparts, and used a monoclonal antibody to identify its protein product in formalin-fixed tissue from 30 BCCs. Expression of bcl-2, observed in 28 to 30 BCCs, was greatest in indolent-growth BCCs and weakest in the aggressive-growth variants (P = .005). Variable bcl-2 expression is seen in BCC and may be integral to both its pathogenesis and its biological behavior.

Antibodies, Monoclonal↗
PubMed1996

The role of microvascular injury in the pathogenesis of cutaneous lesions of dermatomyositis.

Although microvascular injury has been postulated as the pathogenetic basis of skeletal muscle injury in dermatomyositis (DM), its role in the genesis of the skin lesions, which are said to be difficult to distinguish light microscopically from systemic lupus erythematosus (SLE) and subacute lupus erythematosus (SCLE), has not been analyzed. The authors' intention was to assess the role of microvascular injury in the pathogenesis of skin lesions in DM, SLE, and SCLE. Light microscopic features of biopsies of lesional skin from 20 patients with myopathic DM and 11 with amyopathic DM were compared to eight lesional skin biopsies from eight patients with SLE and 12 lesional skin biopsies from 12 patients with SCLE. Vascular density was compared in the three groups using an immunohistochemical preparation with an antibody to factor VIII. In 12 biopsies from the DM group, and in 19 of 20 lupus erythematosus (LE) specimens, frozen tissue was available. An indirect immunofluorescence methodology was used to detect C5b-9 deposition, and direct immunofluorescence studies for other immunoreactants were performed in standard fashion. Compared with LE, lesions of DM showed a greater degree of endothelial injury, vascular ectasia, and vascular fibrin deposition; there were no differences between myopathic versus amyopathic DM. C5b-9 deposition in vessels was significantly greater in DM than in LE. The superficial vascular plexus density was reduced in lesions of DM versus LE control groups with the greatest reduction observed in myopathic DM. Epithelial injury and mucin was greatest in myopathic DM. Microvascular injury is the apparent pathophysiological basis of skin lesions in DM. Careful attention to microvascular pathology enables distinction of DM from SLE and SCLE. Indirect immunofluorescence testing using a monoclonal antibody to C5b-9 is a valuable tool to distinguish DM from LE in biopsies of lesional skin.

Adult↗
PubMed1996

Granuloma annulare and necrobiosis lipoidica tissue reactions as a manifestation of systemic disease.

Granuloma annulare (GA) and necrobiosis lipoidica (NL) are generally considered to be idiopathic cutaneous palisading granulomatous dermatitides. There are sporadic reports of such lesions occurring in patients with coexistent systemic diseases other than diabetes mellitus. Having encountered 49 patients whose skin biopsies showed GA or NL lesions in the setting of extracutaneous disease, the authors set out to assess their clinical and histopathological findings to determine if any parameters were predictive of underlying systemic disease. Fifty-two skin biopsies from 49 patients having either GA or NL in whom there was a clinical history of an associated systemic disease were analyzed by light microscopy. The main systemic disease associations were rheumatologic, endocrine, hematologic, infectious, and inflammatory bowel diseases, ANCA positive vasculitic syndromes, and sarcoidosis. The clinical and histomorphological features were compared with those of a control group of patients whose skin biopsies showed GA or NL and in whom there was no history of extracutaneous disease. For the systemic disease group, patients were selected either retrospectively or prospectively from 160,000 cases accessioned in a 24-month period in the dermatopathology databases of Pathology Services, Inc (Cambridge, MA) and Central Medical Laboratories (Winnipeg, Canada). All systemic disease cases from the former service were analyzed blindly by the second author and from the latter service were analyzed blindly by the first author. Patients in the control group were obtained retrospectively from the Pathology Services Inc. database by the authors. The location of the lesions was atypical in 30 of 34 biopsies from systemic disease patients with a GA tissue reaction versus 10 of 22 biopsies of GA in the control group (P = .001). Six of 18 biopsies from patients with NL tissue reactions in the systemic disease group showed an atypical location, versus only 1 of 9 biopsies of NL from the control group (P = .19). The clinical diagnostic considerations were much broader in the systemic disease group versus the control group and included vasculitis, panniculitis, and connective tissue diseases including morphea in the former. In 22 of 34 GA biopsies and 16 of 18 NL biopsies from the systemic disease group, an active vasculopathy of leukocytoclastic, granulomatous, or thrombogenic subtypes was demonstrable. None of the GA or NL biopsies from the control group showed a similar active vasculopathy. An active vasculopathy was predictive of systemic disease in patients having either a GA-like or an NL-like tissue reaction (P < .001). Fifteen of 34 GA and 7 of 18 NL biopsies in the systemic diseases group showed extravascular neutrophilia in contrast to 3 of 22 GA (P = .02) biopsies and 2 of 9 NL (P = .33) biopsies in the control group. The finding of an active vasculopathy in a skin biopsy specimen showing a GA- or NL-like tissue reaction, particularly in the setting of an atypical clinical presentation both with respect to the location and appearance of lesions, should prompt consideration of an underlying systemic disease, as should extravascular neutrophilia in a skin biopsy showing a GA-like tissue reaction.

Adult↗
PubMed1996

A morphological study of penile chancroid lesions in human immunodeficiency virus (HIV)-positive and -negative African men with a hypothesis concerning the role of chancroid in HIV transmission.

Chancroid, the most common cause of genital ulceration in Africa, is known to be associated epidemiologically with heterosexual transmission of human immunodeficiency virus (HIV). The pathophysiological mechanisms by which chancroid might facilitate the spread of HIV are obscure. To investigate the role of chancroid in HIV transmission, the authors studied the histological features of biopsies from 11 men with penile chancroid lesions including five who were serologically positive for HIV. The histomorphologic and immunophenotypic nature of the inflammatory infiltrates suggests that there is a significant role for cell-mediated immunity in the host response to Hemophilus ducreyi infection. This response may be critical to the role of chancroid in HIV transmission.

Black or African American↗
PubMed1996

Drug-induced immune dysregulation as a cause of atypical cutaneous lymphoid infiltrates: a hypothesis.

The authors encountered 22 patients in whom a skin biopsy showed atypical lymphoid hyperplasia and in whom a subsequent drug history showed indigestion of one or more agents before lesional onset. In 13 patients, the biopsy had been performed to rule out a diagnosis of malignant lymphoma, whereas the other nine the clinical impression was that of a drug eruption. Among the more frequently prescribed agents were calcium-channel blockers, angiotensin-converting enzyme (ACE) inhibitors, antidepressants, antihistamines, beta-blockers, benzodiazepines and lipid-lowering agents, all of which are either known to perturb lymphocyte function or have been implicated as a cause of pseudolymphomata. Twelve of the patients were on two or more of these drugs. The effect of drug modulation on the clinical course was assessed. The clinical presentations were as one or more erythematous plaques or multiple infiltrative papules, or as solitary nodules. The patient had been on one or more of the aforementioned drugs from 2 weeks to 5 years before developing the lesions. Resolution of the eruptions occurred in 17 patients within 1 to 32 weeks (mean, 7 weeks) of discontinuing the medication. Five additional patients had complete excision of solitary lesions without recurrence. A history of atopy, autoimmune disease, or previous carcinoma was elicited in five patients. All biopsy specimens showed atypical lymphoid infiltrates, which assumed one or more of the following patterns: mycosis fungoides (MF)-like, a lymphomatoid vascular reaction, lymphocytoma cutis and follicular mucinosis. Based on the histopathology of the biopsied lesions and the clinical course being one of lesional resolution after cessation of drug therapy or excision of a solitary lesion without subsequent recurrence, a diagnosis of drug-associated lymphomatoid hypersensitivity was established in all specimens. A diagnosis of drug-associated pseudolymphoma should be excluded before a diagnosis of cutaneous lymphoma is rendered, and should be considered if the patient is on a drug known to alter lymphocyte function, particularly in the setting of systemic immune dysregulation or multidrug therapy where agent may act synergistically or cumulatively to alter lymphoid function. The authors postulate that the drug may promote an aberrant immune response to an antigen that may be the drug itself or some other stimulus. A skin biopsy may be particularly helpful, as the lesions of drug-associated pseudolymphoma have a morphology distinctive from malignant lymphoma.

Adult↗
PubMed1996

Basal cell carcinoma arising in association with desmoplastic trichilemmoma.

We encountered three cases of basal cell carcinoma (BCC) and one case of an atypical basaloid proliferation best classified as a BCC arising in association with desmoplastic trichilemmomata. Desmoplastic trichilemmoma is a benign tumoral lesion with a pseudomalignant appearance that combines histomorphological features of an infiltrating neoplasm with those of a benign trichilemmoma.

Adolescent↗
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

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

Comparison of magnetic resonance imaging and endoscopy in distinguishing the type and severity of inflammatory bowel disease.

Twenty consecutive patients with first-time presentation of suspected inflammatory bowel disease underwent both endoscopy with biopsy and magnetic resonance imaging (MRI) within a 3-day period; the relative abilities of endoscopy and MRI to distinguish ulcerative colitis (UC) from Crohn's disease (CD) and to determine the severity of the disease process were compared. In 18 of 20 patients, a diagnosis of UC or CD could be made on histological specimens. MRI correctly diagnosed 17 of these 18 patients using T1-weighted fat-suppressed spin echo and gadolinium enhancement. Endoscopy correctly diagnosed 15 patients. Overall, MRI was not significantly better (p > 0.05) than endoscopy in distinguishing UC from CD. MRI correctly graded the severity of inflammatory changes in 13 of 20 patients, and endoscopy did so in 11 of 20. MRI and endoscopy findings were within one grade of histology findings in seven patients each. No significant difference (p > 0.05) was found between MRI and endoscopy in the ability to estimate the severity of the disease (as determined from biopsies). Bowel wall thickness measured on MR images demonstrated good correlation with percentage of contrast enhancement: r = 0.61; p = 0.003. In sum, magnetic resonance imaging was shown to be comparable with endoscopy in differentiating UC from CD and in gauging the severity of disease. Transmural assessment, sagittal imaging, and the lack of invasiveness were attractive features of MRI.

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↗