Parvovirus B19 and systemic sclerosis.
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DNA, Viral↗
Biomedical subjects
C M Magro
Publications and source records attributed to C M Magro.
Plasma cell mucositis of the distal airways.
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Bronchitis↗
Tick mouth parts occlusive vasculopathy: a localized cryoglobulinemic vasculitic response.
BACKGROUND: The histologic hallmark of most arthropod bite reactions is a deep, wedge-shaped perivascular and interstitial infiltrate comprising lymphocytes, neutrophils, and eosinophils. METHODS: We present a case series of six patients in whom tick bite reactions, when examined microscopically, were found to mimic mixed cryoglobulinemic vasculitis. RESULTS: Though different in histology, clinically these lesions were indistinguishable from typical tick bite reactions. CONCLUSION: As five of our six biopsy specimens were found to still harbor retained tick parts, it is possible that the actual retention of tick parts was involved in evoking this localized cryoprecipitate reaction.
Adult↗
The spectrum of cutaneous lesions in rheumatoid arthritis: a clinical and pathological study of 43 patients.
INTRODUCTION: Rheumatoid arthritis (RA) is an idiopathic arthropathy syndrome that has a propensity to affect the small joints of the hands and feet with extra-articular manifestations comprising skin lesions, neuropathy, pericarditis, pleuritis, interstitial pulmonary fibrosis and a systemic polyarteritis nodosa (PAN)-like vasculitic syndrome. The most widely recognized skin lesion is the rheumatoid nodule. Other skin manifestations are poorly defined. MATERIALS AND METHODS: Using a natural language search of the authors' outpatient dermatopathology databases, skin biopsies from 43 patients with RA were selected for retrospective analysis in an attempt to define the dermatopathological spectrum of RA and its clinical correlates. RESULTS: The biopsies were categorized by the dominant histologic pattern, recognizing that in most cases there were additional minor reaction patterns. Palisading and/or diffuse interstitial granulomatous inflammation was the dominant pattern seen in 21 patients; the lesions included nodules, plaques and papules with a predilection to involve skin over joints. Besides interstitial histiocytic infiltrates and variable collagen necrobiosis, these cases also showed interstitial neutrophilia, vasculitis and pauci-inflammatory vascular thrombosis. The dominant morphology in 11 other patients was vasculopathic in nature: pauci-inflammatory vascular thrombosis, glomeruloid neovascularization, a neutrophilic vasculitis of pustular, folliculocentric, leukocytoclastic or benign cutaneous PAN types, granulomatous vasculitis, and lymphocytic vasculitis and finally occlusive intravascular histiocytic foci for which the designation of "RA-associated intravascular histiocytopathy" is proposed. Rheumatoid factor (RF) positivity and active arthritis were common in this group, with anti-Ro and anticardiolipin antibodies being co-factors contributing to vascular injury in some cases. Immunofluorescent testing in three patients revealed dominant vascular IgA deposition. In nine patients, the main pattern was one of neutrophilic dermal and/or subcuticular infiltrates manifested clinically as urticarial plaques, pyoderma gangrenosum and panniculitis. CONCLUSIONS: The cutaneous manifestations of RA are varied and encompass a number of entities, some of which define the dominant clinical features, such as the rheumatoid papule or subcutaneous cords, while others allude to the histopathology, i.e. rheumatoid neutrophilic dermatosis. We propose a more simplified classification scheme using the adjectival modifiers of "rheumatoid-associated" and then further categorizing the lesion according to the dominant reaction pattern. Three principal reaction patterns are recognized, namely extravascular palisading granulomatous inflammation, interstitial and/or subcuticular neutrophilia and active vasculopathy encompassing lymphocyte-dominant, neutrophil-rich and granulomatous vasculitis. In most cases, an overlap of the three reaction patterns is seen. Co-factors for the vascular injury that we believe are integral to the skin lesions of RA include RF, anti-endothelial antibodies of IgA class, anti-Ro and anticardiolipin antibodies.
Adult↗
Atrophying tinea versicolor: a clinical and histological study of 12 patients.
BACKGROUND: We describe 12 patients with an atrophying dermatitis in whom the biopsy findings were compatible with tinea versicolor. DESIGN: We encountered 12 skin biopsies from 12 patients in whom a clinically atrophying dermatosis was associated with light microscopic (LM) evidence of atrophy and epidermal colonization by Pityrosporum sp. Formalin-fixed, paraffin-embedded tissue sections were cut at 5 microns and stained with H&E, alcian blue-PAS and PAS-diastase preparations. RESULTS: Five men and seven women aged 17-73 years in whom lesions characterized as atrophic plaques, patches or macules prompted clinical differential diagnoses including parapsoriasis or mycosis fungoides (MF), anetoderma, lupus erythematosus, and steroid atrophy. A LM examination showed epidermal colonization with pityrosporum hyphae and spores accompanied by variable epidermal and dermal atrophy characterized by rete-ridge effacement, subepidermal fibroplasia, pigment incontinence and elastolysis. CONCLUSIONS: Atrophying cutaneous lesions comprise part of the clinical spectrum of tinea versicolor for which we propose the term 'atrophying tinea versicolor'. The pathogenetic basis is unclear but could be the sequela of delayed type hypersensitivity and the release by T-helper lymphocytes of leukotrienes which perturb collagen metabolism and/or keratinocyte growth. Lesions may be mistaken clinically for MF or other atrophying dermatoses.
Adolescent↗
Lupus profundus, indeterminate lymphocytic lobular panniculitis and subcutaneous T-cell lymphoma: a spectrum of subcuticular T-cell lymphoid dyscrasia.
INTRODUCTION: The diagnosis and classification of lymphocytic lobular panniculitis (LLP) has historically proven to be a difficult challenge. We encountered 32 cases of primary LLP which could be categorized as: 1) lupus erythematosus profundus (LEP) (19 patients); 2) an indeterminate group termed indeterminate lymphocytic lobular panniculitis (ILLP) (6 patients); and 3) subcutaneous T-cell lymphoma (SCTCL) (7 patients). OBJECTIVE: We attempted to better define the subtypes of LLP by morphologic, phenotypic and genotypic features and to correlate those features to clinical presentation and outcome. METHOD: Skin biopsy material was studied by conventional light microscopy, through immunophenotyping performed on sections from paraffin-embedded, formalin-fixed tissue and in some cases on sections of tissue frozen after receipt in physiological (Michel's) medium, and by polymerase chain reaction single-stranded conformational polymorphism analysis to assess for clonality of T-lymphocytes. Clinical features were correlated to histologic, phenotypic, and genotypic analyses. RESULTS: Patients with LEP had a prior diagnosis of LE or overlying skin changes which light microscopically were characteristic of LE. Patients with ILLP had no concurrent or prior history of LE, no systemic symptoms or cytopenias, and a clinical course not suggestive of lymphoma. Cases of SCTCL showed hemophagocytic syndrome and/or lesional progression with demise attributable to the disease. Lesions in all groups showed proximal extremity predilection. Females predominated in the LEP group. The average age of onset was 38, 40 and 55 years in the LEP, ILLP and SCTCL groups, respectively. Cytopenia was seen in 4 LEP patients; 1 also developed fever. In LEP and ILLP, lesions resolved with hydroxychloroquine and/or steroid therapy, with recurrences following cessation of therapy. In the SCTCL group 4 developed hemophagocytic syndrome, 4 died within 2 years of diagnosis, and 3 went into remission following chemotherapy. The LEP and SCTCL groups manifested histological similarities: dense perieccrine and lobular lymphocytic infiltration, lymphoid atypia, histiocytes with ingested debris, eosinophilic necrosis of the fat lobule and thrombosis. The atypical lymphocytes although pleomorphic did not have a cerebriform morphology. The infiltrate in ILLP had a similar cytomorphology and distribution with variable angioinvasion which in all save one case was of lesser intensity and was not associated with significant fat necrosis or vasculitis. Germinal centers, dermal/subcuticular mucin deposition and an atrophying interface dermatitis with hyperkeratosis and follicular plugging were largely confined to the LEP group. Erythrophagocytosis, characteristic of SCTCL, usually indicated a supervening subcuticular lymphoid dyscrasia when encountered in ILLP and LEP. SCTCL showed a selective loss of CD5 expression with or without diminution in CD7 and monoclonal CD3 expression. Of 4 cases studied, 3 showed a CD8 dominant infiltrate while 2 others exhibited CD56 and CD30 positivity, respectively. All cases of SCTCL with amplifiable DNA showed T-cell clonality. Similar molecular and phenotypic features indicative of subcuticular lymphoid dyscrasia were encountered in cases of LEP and ILLP including a reduction in CD5, CD7, and/or monoclonal CD3 expression, a preponderance of CD8 lymphocytes within the subcutaneous fat and T-cell clonality. These cases showed lymphoid atypia with variable erythrophagocytosis. Cases of phenotypically abnormal and/or clonal LEP showed one or more of local destruction, lesional size progression, fever, and cytopenias, but lesions responded to hydroxychloroquine and/or prednisone therapy and death attributable to panniculitis could not be documented. Cases that were phenotypically normal and without clonality had none of the aforesaid atypical clinical features. CONCLUSION: Lymphoid atypia, erythrophagocytosis, loss of certain pan T-cell markers, a reduced CD4/8 ratio and TCR rearrangement define subcuticular T-cell lymphoid dyscrasia, including a subset of LEP and ILLP. The subcuticular lymphoid infiltrates represent a spectrum of histologic, immunophenotypic, and molecular abnormalities which range from those which are clearly benign to those which are clearly neoplastic, and also encompasses those cases which defy precise classification into the two aforesaid poles.
Adult↗
Sweet's syndrome in the setting of CD34-positive acute myelogenous leukemia treated with granulocyte colony stimulating factor: evidence for a clonal neutrophilic dermatosis.
BACKGROUND: Sweet's syndrome in the setting of hematologic dyscrasias can be categorized into paraneoplastic-associated SS, drug-induced SS, and SS with leukemia cutis. Apart from those cases demonstrating concomitant leukemic infiltrates, it has been surmised that SS is a reactive phenomenon induced by a specific cytokine milieu. METHODS: The authors present a patient with CD34+ acute myelogenous leukemia (AAML) who developed SS in the setting granulocyte colony stimulating factor (GCSF) therapy. Routine light microscopy and molecular studies were carried on the patient's skin biopsy specimen and post-treatment marrow. An X inactivation assay for clonality was employed. RESULTS: Routine light microscopic examination revealed differentiated myeloid precursors including myelocytes and metamyelocytes within the subcutis; myeloblasts were not identified. In addition, in the overlying skin, features typical of SS were observed. The neutrophils demonstrated dysplastic features including hypolobation compatible with a Pseudo Pelger-Huet anomaly. X inactivation studies showed clonality both within her post-treatment marrow and skin biopsy specimen. CONCLUSIONS: Sweet's syndrome developing in CD34+ AML patients following GCSF therapy likely reflects therapy induced differentiation of sequestered leukemic cells, hence indicative of a clonal neutrophilic dermatosis.
Acute Disease↗
Giant cells in pyoderma gangrenosum.
It has been claimed that pyoderma gangrenosum (PG) lesions may contain granulomatous foci when associated with Crohn's disease. To test this assertion, we obtained clinical histories and archived cutaneous biopsies from 34 PG patients. Thirteen of these patients had inflammatory bowel disease (IBD). Immunostaining with PGM1, a macrophage marker, revealed well-formed giant cells with three or more nuclei in biopsies from 6 of 13 patients with IBD. Five of the 6 biopsies came from patients with Crohn's disease and one from a patient with ulcerative colitis. Two were peristomal. In the 21 patients who had PG without IBD, no giant cells were seen. Thus, PGM1+ histiocytic giant cells within a PG lesion may be indicative of associated IBD (p = 0.006), particularly Crohn's disease.
Crohn Disease↗
The cutaneous neutrophilic vascular injury syndromes: a review.
The skin manifestations of vasculitis reflect injury by all of the classic immune reactions of Gell and Coombs. As the skin affords a window of opportunity for the clinician to obtain tissue for diagnostic purposes in patients with systemic vasculitic syndromes, a thorough understanding of the dermatopathologic manifestations of those systemic diseases is a considerable asset to the practicing pathologist. This review focuses on those systemic diseases that can provoke a small vessel neutrophilic injury pattern in the skin and provides clues by which these diseases can be separated from each other and from their innocuous mimics in which cutaneous vascular injury is the only significant consequence.
Humans↗
A causal role for parvovirus B19 infection in adult dermatomyositis and other autoimmune syndromes.
BACKGROUND: Infection with parvovirus B19 (B19) has been associated with connective tissue disease (CTD) stigmata, namely, a systemic lupus erythematosus (SLE)-like illness, seronegative polyarthritis resembling rheumatoid arthritis, and vasculitis. The dermatopathology and pathogenetic basis of such B19-associated CTD-like syndromes have not been elucidated. OBJECTIVE: We attempted to document persistence of the B19 genome in skin lesions of 7 patients with CTD-like symptomatology following B19 infection and to correlate systemic manifestations to dermatopathological findings. METHOD: In 7 prospectively encountered patients in whom history, clinical signs and/or serology supported a diagnosis of CTD in the setting of B19 infection, dermatopathological and clinical features were correlated. Parvovirus B19 viral genome was sought in skin tissue using the polymerase chain reaction (PCR). RESULTS: Two patients had clinical features diagnostic of myopathic dermatomyositis (DM), 1 of whom is still symptomatic 1.5 years after the onset of her illness, and the other has had typical clinical features of DM for a duration of 3.5 years. A 3rd patient with SLE remains symptomatic 4 years after the onset of her illness. A 4th patient has persistent seronegative symmetrical polyarthritis of 6 years' duration and cutaneous lesions of granuloma annulare (GA). The 5th patient has a 1.5-year history of debilitating polyarthritis and cutaneous lesions with overlap features of DM and subacute cutaneous LE (SCLE). The 6th patient has had a persistent folliculocentric necrotizing vasculitis for 3 years. The 7th patient has a 1-year history of microscopic polyarteritis nodosa (PAN) with cutaneous vasculitis and persistent active renal disease. In 4 patients, exposure to children with fifth disease immediately preceded the onset of their CTD. Parvovirus B19 infection was documented serologically in 6 patients with antibodies of IgG subclass in 6 and of IgM subclass in 1. Four of 6 patients questioned had a history of atopy. Skin biopsies from patients with clinical features of SLE or DM demonstrated an interface dermatitis with dermal mucinosis. A necrotizing vasculitis with epithelial pustulation was seen in 2 patients. Interstitial GA-like infiltrates were seen in 5 cases. Immunofluorescent (IF) testing revealed a positive lupus band test (LBT) and epidermal nuclear and vascular staining for IgG and C5b-9 in the SLE patient. One DM patient had a negative LBT in concert with C5b-9 deposition along the dermoepidermal junction (DEJ) and within blood vessels while the other showed endomysial vascular Cs5b-9 deposition. In all patients, skin biopsy material contained B19 genome, which was absent in the serum of 4 patients analyzed. Symptomatic relief followed immunosuppressive and immunomodulatory therapy with agents including prednisone, cyclophosphamide, hydroxychloroquine, non-steroidal anti-inflammatory drugs and etanercept, but no patient has had complete symptom resolution. CONCLUSIONS: Persistent B19 infection may be of pathogenetic importance in certain prototypic CTD syndromes, to which underlying immune dysregulation associated with a blunted IgM response to viral antigen may predispose. Anti-viral therapy might be worthy of consideration since traditional immunosuppressive therapy was unsuccessful in our cases.
Adult↗
Hot spot mutations in keratin 2e suggest a correlation between genotype and phenotype in patients with ichthyosis bullosa of Siemens.
Ichthyosis bullosa of Siemens (IBS) is a rare disorder of cornification characterized by blister formation in the upper suprabasal layers of the epidermis. Molecular analysis of IBS has identified mutations in the keratin 2e (K2e) gene, which is located in the type II keratin gene cluster on chromosome 12q. We have studied two IBS families and have identified heterozygous point mutations in codon 493 of the K2e gene in both families. Whereas a non-conservative amino acid substitution at position 117 of the 2B region of K2e (E117K) was associated with a severe phenotype in family 1, family 2 showed mild clinical features as a result of a conservative substitution (E117D). These data suggest a phenotype-genotype correlation in these families.
Adult↗
Lichenoid and granulomatous dermatitis.
BACKGROUND: The prototypic lichenoid eruptions, lichen planus (LP), lichenoid drug eruptions, secondary syphilis, and collagen vascular disease, are defined histologically by a band-like lymphocytic infiltrate in close apposition to the epidermis. We describe a novel form of lichenoid dermatitis with a granulomatous component. DESIGN: Skin biopsies from 40 patients demonstrating a band-like lymphocytic infiltrate with concomitant granulomatous inflammation were encountered over 4 years. Clinicians were contacted to elucidate underlying triggers and medical illnesses. RESULTS: A lichenoid dermatitis, a linear eruption, vasculitis, annular erythema, and erythroderma were among the clinical presentations. A drug-based etiology was implicated in 14 cases: the drugs included antibiotics, lipid-lowering agents, anti-inflammatory drugs, antihistamines, hydroxychloroquine sulfate, and angiotensin-converting enzyme inhibitors. Over one-third of patients with drug-related eruptions had other medical illnesses associated with cutaneous granulomatous inflammation, namely rheumatoid arthritis (RA), Crohn's disease, hepatitis C, diabetes mellitus, and thyroiditis. A microbial trigger was implicated in 12 patients in the context of infective id reactions to herpes zoster, Epstein-Barr virus (EBV), or streptococci, or active infections by Mycobacterium tuberculosis, M. leprae, fungi, and spirochetes. The remainder had hepatobiliary disease and RA without obvious exogenous triggers, cutaneous T-cell lymphoma (CTCL), and idiopathic lichenoid eruptions (i.e. LP, lichen nitidus, and lichen striatus). One patient with LP had underlying multicentric reticulohistiocytosis. The histiocytic infiltrate assumed one or more of five light microscopic patterns: (i) superficially disposed loose histiocytic aggregates; (ii) cohesive granulomata within zones of band-like lymphocytic infiltration with or without deeper dermal extension; (iii) a diffuse interstitial pattern; (iv) scattered singly disposed giant cells; and (v) granulomatous vasculitis. Additional features included lymphocytic eccrine hidradenitis in those patients with drug reactions, hepatobiliary disease, and antecedent viral illnesses, tissue eosinophilia and erythrocyte extravasation in drug hypersensitivity, granulomatous vasculitis in patients with microbial triggers, drug hypersensitivity or RA, and lymphoid atypia in lesions of CTCL or drug hypersensitivity. CONCLUSIONS: The cutaneous lichenoid and granulomatous reaction may reflect hepatobiliary disease, endocrinopathy, RA, Crohn's disease, infection, or a drug reaction. One-fifth of cases represent idiopathic lichenoid disorders. Lymphoproliferative disease or pseudolymphomatous drug reactions must be considered in those cases showing lymphoid atypia.
Adolescent↗
Necrotizing eosinophilic folliculitis as a manifestation of the atopic diathesis.
BACKGROUND: Eosinophilic folliculitis (EF) is an idiopathic eruption of sterile pustules and papules involving the trunk, face, and extremities, associated in many cases with human immunodeficiency virus (HIV) infection. The classic histopathology is one of follicular-based, eosinophilic spongiosis with variable microabscess formation. We describe nine HIV-negative patients who manifested a novel form of pustular EF in the setting of atopy. MATERIALS AND METHODS: Paraffin sections of skin biopsies from ten patients, stained with hematoxylin and eosin and special preparations to evaluate for microbial pathogens, were examined. Detailed clinical histories and serologic studies were obtained. RESULTS: Among the clinical presentations in seven men, two women, and one girl (age range, 11-62 years) were ulcerative and/or nodular plaques mainly on the face and/or extremities, sometimes in an annular configuration. The clinical considerations included deep mycotic infection, ulcerative herpes, systemic vasculitis, Mucha Haberman disease, and pyoderma gangrenosum. All patients had a personal and/or family history of atopy. Co-existent medical illnesses included psoriasis, lupus erythematosus, and lymphoproliferative disease. One patient was on a calcium channel blocker, one on multiple antidepressants, and two on antihistamines, all of which are associated with immune dysregulation. All skin biopsies showed variable intra- follicular eosinophilic microabscesses, follicular necrosis, folliculocentric necrotizing eosinophilic vasculitis, marked degeneration of connective tissue fiber elements, and striking tissue eosinophilia, including flame figure formation and dermal eosinophilic abscesses. Apart from commensals, such as Pityrosporum and Demodex, microbial pathogens were not identified. CONCLUSIONS: The presentations differed from conventional EF by virtue of a strong association with atopy and by the presence of ulceration, nodule formation, follicular and dermal necrosis, and eosinophilic vasculitis. We propose the term "necrotizing eosinophilic folliculitis," and suggest that the basis of this novel form of EF is an unrepressed T-helper lymphocyte type 2 (Th2)-dominant response to various epicutaneous stimuli in patients with atopy, the prototypic immune dysregulatory state associated with a Th2-dominant cytokine milieu.
Adult↗
The cutaneous manifestations of human parvovirus B19 infection.
The prototypical cutaneous manifestations of human parvovirus B19 (B19) infection include a petechial eruption in a glove and stocking distribution, reticular truncal erythema, and the "slapped cheek" sign. An association with connective tissue disease (CTD) stigmata has recently been made. The clinical and dermatopathologic findings in 14 patients whose skin lesions were accompanied by serological evidence of B19 infection or documentation of B19 genome in lesional skin are presented. The authors encountered skin biopsy specimens from 14 patients who presented with skin eruptions accompanied by clinical signs or serology suggestive of antecedent B19 infection. Clinical findings were correlated to the light microscopic appearance of the lesions and the presence of B19 genome in lesional skin. The study group comprised 9 women, 3 men, and 2 boys. Eruptions characteristic of fifth disease, including the slapped cheek sign, reticulated truncal erythema, and acral petechiae, were present in 3 patients, 1 of whom later developed granuloma annulare. The other patients had atypical clinical presentations comprising an asymptomatic papular eruption (2), an eruption clinically resembling Sweet's syndrome (3), myopathic dermatomyositis (DM) (2), lupus erythematosus (LE)-like syndromes (2), and lower-extremity palpable purpura (2). Skin biopsy specimens in 12 cases showed interstitial histiocytic infiltrates with piecemeal fragmentation of collagen and a mononuclear cell-predominant vascular injury pattern. Other features included an interface dermatitis, eczematous alterations, and papillary dermal edema. Lesions with features of DM or LE also showed mesenchymal mucinosis, whereas a biopsied lesion of palpable purpura showed leukocytoclastic vasculitis (LCV). Immunofluorescent testing showed a positive lupus band test (LBT) with epidermal IgG and C5b-9 decoration in 1 patient with a systemic LE-like illness, whereas the DM patients had negative LBTs and vascular C5b-9 deposition typical for DM. Skin biopsy specimens from 11 patients, including those whose presentations resembled LE and DM, were positive for B19 genome. The dermatopathology of B19 infection suggests tissue injury mediated by delayed-type hypersensitivity, by antibody-dependent cellular immunity directed at microbial antigenic targets in the epidermis and endothelium, and by circulating immune complexes in the setting of LCV. These mechanisms appear to generate a clinical and histopathological picture that recapitulates that of CTD.
Adult↗
Ectopic expression of the nude gene induces hyperproliferation and defects in differentiation: implications for the self-renewal of cutaneous epithelia.
Nude mice are characterized by the absence of visible hair, epidermal defects, and the failure to develop a thymus. This phenotype results from loss-of-function mutations in Whn (Hfh11), a winged-helix transcription factor. In murine epidermis and hair follicles, endogenous whn expression is induced as epithelial cells initiate terminal differentiation. Using the promoter for the differentiation marker involucrin, transgenic mice that ectopically express whn in stratified squamous epithelia, hair follicles, and the transitional epithelium of the urinary tract were generated. Transgenic epidermis and hair follicles displayed impaired terminal differentiation and a subset of hair defects, such as delayed growth, a waved coat, and curly whiskers, correlated with decreased transforming growth factor (TGF)-alpha expression. The exogenous Whn protein also stimulated epithelial cell multiplication. In the epidermis, basal keratinocytes exhibited hyperproliferation, though transgene expression was restricted to suprabasal, postmitotic cells. Hair follicles failed to enter telogen (a resting period) and remained continuously in an abnormal anagen (the growth phase of the hair cycle). Ureter epithelium developed severe hyperplasia, leading to the obstruction of urine outflow and death from hydronephrosis. Though an immune infiltrate was present occasionally in transgenic skin, the infiltrate was not the primary cause of the epithelial hyperproliferation, as the immune reaction was not observed in all affected transgenics, and the transgene induced identical skin and urinary tract abnormalities in immunodeficient Rag1-null mice. Given the effects of the transgene on cell proliferation and TGFalpha expression, the results suggest that Whn modulates growth factor production by differentiating epithelial cells, thereby regulating the balance between proliferative and postmitotic populations in self-renewing epithelia.
Animals↗
Comparison of erbium:YAG and carbon dioxide lasers in resurfacing of facial rhytides.
OBJECTIVE: To compare the efficacy, adverse effects, and histological findings of erbium:YAG (Er:YAG) and carbon dioxide (CO2) laser treatment in removing facial rhytides. DESIGN: An intervention study of 21 subjects with facial rhytides. All participants were followed up for 6 months. The end points of the study were wrinkle improvement and duration of adverse effects. SETTING: Academic referral center. SUBJECTS: Nineteen female and 2 male volunteers with skin type I to III and wrinkle class I to III participated in the study. INTERVENTION: In all subjects, 1 side of the face was treated with a CO2 laser and other side with an Er:YAG laser. Skin biopsies were performed in 6 subjects before treatment and immediately, 1 day, 2 days, and 6 months after treatment. Observations were recorded by subjects, investigators, and a blinded panel of experts. MAIN OUTCOME MEASURES: Improvement in wrinkles and severity and duration of adverse effects. RESULTS: The CO2 laser-treated side had relatively better wrinkle improvement when evaluating all subjects (P<.03). However, in subjects receiving more than 5 passes of Er:YAG laser, improvement scores were not significantly different from those for 2 to 3 passes of CO2 laser treatment. Posttreatment erythema was noted at 2 weeks in 14 subjects (67%) on the Er:YAG laser-treated side and 20 subjects (95%) on the CO2 laser-treated side. The frequency of erythema was significantly less after Er:YAG laser treatment at 2 (P=.001) and 8 (P=.03) weeks. Hypopigmentation was seen in 1 Er:YAG-treated (5%) and 9 CO2-treated (43%) sides (chi2, P<.05). Histological evaluation showed residual thermal damage of up to 50 microm on the Er:YAG-treated side and up to 200 microm on the CO2-treated side. CONCLUSIONS: Erbium:YAG laser is safe and effective in removing facial rhytides. Subjects treated with Er:YAG laser recover more quickly from the procedure than those receiving CO2 laser treatment.
Adolescent↗
Malignant melanoma with prominent pigment synthesis: "animal type" melanoma--a clinical and histological study of six cases with a consideration of other melanocytic neoplasms with prominent pigment synthesis.
Rare skin neoplasms in humans, comprising nodules of heavily melanized cells, mimic melanocytic neoplasms seen in horses and laboratory animals and thus are termed animal type melanomas. In part because of their rarity, behavior is unpredictable; many cases manifest a long indolent phase, and metastases are reportable. Over 6 years, the authors encountered nine skin and one lymph node biopsy specimens from six patients in whom light microscopy of formalin-fixed, paraffin-embedded tissue sections stained with hematoxylin and eosin showed melanocytic neoplasms with prominent pigment synthesis. Clinical follow-up was obtained by telephone contact with clinicians. There were three women, two men, and one boy, aged 9 to 85 years, whose lesions were described as blue-black nodules with irregular borders from 1.0 to 4.0 cm in size, located on the scalp, lower extremities, back, and sacrum. The dermatopathology comprised confluent dermal sheets of heavily melanized cells whose nuclei, where discernible, were large with irregularly thickened membranes, coarse chromatin, prominent, often spiculated nucleoli, and irregular parachromatinic clearing. Mitoses were infrequent. Four lesions had an epidermal component. One patient suffered metastases to regional lymph nodes, liver, and lungs with lethal effect, one experienced regional lymph node metastases but is still alive, one had local cutaneous metastases but was lost to follow-up, and one has a chest wall mass that has not yet been investigated. This rare dermal-based melanocytic neoplasm with prominent pigment synthesis, the animal type melanoma, has a biological behavior difficult to predict on morphological grounds. We advise complete excision with a 1.0- to 2.0-cm margin of normal skin and clinical investigation for regional or distant metastases.
Adolescent↗
Atypical pigmentary purpura: a clinical, histopathologic, and genotypic study.
BACKGROUND: The pigmentary purpuras (PPs) are a heterogeneous group of dermatoses defined by specific clinicopathologic features but sharing, at the light microscopic level, superficially disposed dermal lymphocytic infiltrates and hemorrhage. The term atypical pigmentary purpura (APP) is used by the authors in reference to cases of PP in which individual lesions, although clinically presenting as PP, show morphological features typically associated with mycosis fungoides (MF) including Sezary cells and epidermotropism. The integrated concept of lymphocyte atypia and PP is a confusing and enigmatic one to which reference in the literature has been previously made. Specifically, there are reports of PP presaging fully evolved MF, lymphoid atypia has been identified in lesions of routine PP and MF with purpuric features has been described. The clinical, light microscopic, and genomic features of biopsied lesions showing pathological features of APP and which clinically were consistent with PP is explored. DESIGN: The light microscopy of skin biopsy specimens from 34 patients with a pathological diagnosis of APP was correlated to medical and drug histories. In 14 cases, adequate tissue was present in the paraffin blocks to allow DNA extraction. The polymerase chain reaction (PCR) was used in these 14 cases to explore for rearrangement of the T-cell receptor. Fisher's exact test and pair wise exact tests were used to assess the significance of histological differences between cases determined by dinical features to be of MF- or drug-related origin, or to be idiopathic in nature. RESULTS: Of 34 patients, 7 were held to have MF related PP; specifically these patients had violaceous, infiltrative, variably purpuric plaques on trunk, buttocks, and thighs accompanied by typical PP lesions which occurred either concomitant to or preceded the MF lesions. In 10 cases, a diagnosis of idiopathic PP was made whereby the clinical presentation was characteristic of PP; there were no concomitant lesions suspicious for MF and a drug-based origin was excluded. A drug-based origin was established in 17 patients based on lesional onset related to initiation (5 patients) and/or resolution after discontinuation (12 patients) of drugs including calcium channel blockers, lipid-lowering agents, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, antihistamines, antidepressants, or analgesics. There was considerable overlap histologically between all 3 groups including the degree of lymphoid atypia in the dermis, the presence of dermal-based Sezary cells, the degree and pattern of epidermotropism, the paucity of other inflammatory cell elements, and the presence of laminated dermal sclerosis. Morphological features predictive of MF related APP over the other 2 groups were intraepidermal lymphocytes which were more atypical than the dermal-based infiltrate. Intraepidermal Sezary cells were less frequent in biopsies of drug-related APP relative to idiopathic PP (IPP) and MF related PP. PCR studies conducted in 14 cases (2 cases of MF, 6 cases of drug-related APP, and 6 cases of IPP) revealed clonality in 2 cases of drug-related APP and 2 cases of IPP; the 2 studied MF-related cases did nor show clonal restriction. CONCLUSION: APP should not be equated with purpuric MF; it is not necessarily a precursor lesion of MF, and may be of drug-based origin. Clinical features are critical to the final assessment because there is overlap pathologically in the 3 clinical subtypes of APP.
Adolescent↗