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B R Smoller

Publications and source records attributed to B R Smoller.

At least 145 records · Page 8Linked to original sources
PubMed1990

Immunohistochemical demonstration of factor XIIIa expression in neurofibromas. A practical means of differentiating these tumors from neurotized melanocytic nevi and schwannomas.

Neurofibromas, schwannomas, and neurotized melanocytic nevi may closely resemble one another at the light microscopic level. We studied 10 neurofibromas, 10 schwannomas, and 10 partially neurotized melanocytic nevi immunohistochemically using an antibody directed against factor XIIIa to determine if this antibody might provide a useful method of differentiating these lesions. The cases were also stained with S100 protein. All of the neurofibromas stained intensely for factor XIIIa. The proportion of cells staining within the tumors varied from 30% to 70%. In contrast, none of the schwannomas and neurotized nevi studied demonstrated staining of tumor cells with this antibody. S100 protein was expressed by 100% of neurofibromas, schwannomas, and melanocytic nevi. Our findings suggest that factor XIIIa may provide a reliable and practical means of differentiating cutaneous neurofibromas from neurotized nevi and cutaneous schwannomas. Distinguishing between these different tumor types may be important in some clinical situations, particularly with respect to rendering a diagnosis of von Recklinghausen's neurofibromatosis. The differences in the immunohistochemical profiles of neurofibromas and neurotized nevi support the concept that these tumors are histogenetically distinct, despite their similar histologic appearances.

Antigens, Neoplasm↗
PubMed1990

"Activated" keratinocyte phenotype is unifying feature in conditions which predispose to squamous cell carcinoma of the skin.

While some cutaneous squamous cell carcinomas (SCC) arise from predisposing conditions such as burn scars, draining sinuses, and chronic, nonhealing wounds, the vast majority of these tumors arise from actinically damaged epidermis. It has been shown previously that keratinocytes within healing wounds show an "activated" immunophenotype when stained with antibodies to psi-3, involucrin, filaggrin, and cytokeratins. A similar pattern has been seen in keratinocytes from patients with recessive dystrophic epidermolysis bullosa (RDEB), in whom the incidence of cutaneous SCC is markedly increased. We tested the hypothesis that actinic keratoses (AK), recognized as precursors in the development of the majority of SCC, would show a similar activated immunophenotype when stained with the antibody panel described above. We examined 10 AK, biopsied from the facies and extremities of ten patients, ages 60 to 80, with antibodies to psi-3, involucrin, filaggrin, and AE1. All lesions examined had an immunostaining pattern indistinguishable from that seen in keratinocytes from patients with RDEB or within healing wounds. There was suprabasilar staining of keratinocytes with antibodies to psi-3 and AE1. Involucrin and filaggrin was expressed by all keratinocytes above the midstratum spinosum. Within the acrosyringia and acrotrichia, the staining pattern was that of the normal epidermis, i.e., AE1 staining of basal keratinocytes, granular layer staining of involucrin and filaggrin, and absence of psi-3 expression. These data suggest that an activated keratinocyte phenotype is a unifying feature in conditions which predispose to development of cutaneous SCC.

Aged↗
PubMed1990

Detection of the interferon-gamma-induced protein 10 in psoriasiform dermatitis of acquired immunodeficiency syndrome.

Interferon-gamma-induced protein 10 is a 10-kd protein produced by human keratinocytes following an exposure to interferon gamma. Keratinocytes within psoriatic plaques and within delayed-type hypersensitivity reactions have been shown to stain strongly with an affinity-purified rabbit antibody prepared against interferon-gamma-induced protein 10, suggesting a possible role for interferon gamma in the production of the lesions. A psoriasiform eruption has been seen in patients with acquired immunodeficiency syndrome (AIDS). Its severity appears to correlate with the degree of immunodeficiency in the early stages of AIDS. We stained 10 lesions of psoriasiform dermatitis of AIDS with the anti-interferon-gamma-induced protein 10 antibody using immunoperoxidase techniques. As controls, we studied 10 lesions of non-AIDS psoriasis, six lesions of seborrheic dermatitis with psoriasiform hyperplasia, one lesion of lichen simplex chronicus, and four biopsy specimens of normal skin from patients with AIDS. In addition, normal skin specimens taken from patients with AIDS and human immunodeficiency virus-negative patients at time of autopsy were examined. An identical, strong and diffuse staining pattern was seen in all cases of psoriasiform dermatitis of AIDS, non-AIDS psoriasis, seborrheic dermatitis, and lichen simplex chronicus. The specimens of normal skin showed only weak basal layer staining with anti-interferon-gamma-induced protein 10. Thus, the presence of interferon-gamma-induced protein 10 in keratinocytes was associated with psoriasiform hyperplasia and could be detected in both AIDS-associated and classic psoriasis.

Acquired Immunodeficiency Syndrome↗
PubMed1990

An unusual cutaneous manifestation of Crohn's disease.

Crohn's disease is a multisystem disease that involves the skin in approximately 20% of afflicted individuals. Most often, it is characterized by an erythema nodosum-like reaction or by a fistulous tract in skin adjacent to mucosal membranes. We recently saw a patient who presented with crusted malar plaques and a long-standing history of Crohn's disease. The skin lesions relapsed and recurred in concert with exacerbations of the gastrointestinal disorder. On biopsy, the sections showed a diffuse neutrophilic inflammatory infiltrate. There was no evidence of a granulomatous infiltrate on step sections through the block. We believe this to be a previously unrecognized pattern of Crohn's disease involving the skin.

Acute Disease↗
PubMed1990

The natural history of vasculitis. What the histology tells us about pathogenesis.

While histopathologic analysis may offer some clues as to the pathogenesis of vasculitis, observations must be interpreted with caution, as there is considerable overlap in the histologic pattern. In most cases, a predominantly neutrophilic vasculitis affecting small dermal venules suggests a relatively acute, immune complex-mediated reaction. Less commonly, this histologic pattern may be seen in non-immunologically mediated processes, such as in the presence of bacterial toxins or malignant hypertension, or in more chronic disease states, such as granuloma faciale or erythema elevatum diutinum. A predominantly lymphocytic vasculitis may represent several pathogenetic mechanisms. In lesions more than 24 to 48 hours old, a lymphocytic vasculitis may represent a resolving phase of an immune complex-mediated neutrophilic vasculitis. Alternatively, this histologic pattern may be seen de novo in conditions with a presumed cell-mediated immunologic pathogenesis. Lymphocytic vasculitis may also be seen in rickettsial infections such as Rocky Mountain spotted fever. The pathogenesis of granulomatous vasculitis remains poorly understood and is thought to be induced by a combination of circulating immune complexes and a cell-mediated immune response.

Granuloma↗
PubMed1989

Keratinocyte protein expression in rapidly regenerating epidermis following laser-induced thermal injury.

We examined 20 punch biopsies taken from five patients at varying intervals following CO2 laser-induced thermal injury. The regenerating epidermis was studied with monoclonal antibodies AE1 and AE3 (directed against low and high molecular weight keratins), and involucrin, a protein found within the cellular envelope of the most mature keratinocytes. Twenty-four hours following thermal damage, there was extensive spillage of keratins and involucrin into the papillary dermis and disarray of all constituents of the necrotic keratinocytes. Early ingrowth of basaloid keratinocytes weakly expressed AE1. By 1 week, keratinocytes expressed AE1 in varying intensities throughout the epidermis. AE3 was present in its normal distribution, staining all but the most basaloid keratinocytes. Involucrin stained cells deep within the epidermis. Six weeks following the initial injury, the staining pattern within the epidermis had returned to normal. Thus, it appears that the regenerating epidermis produces low molecular weight keratins in cells at all levels and forms premature cellular envelopes, perhaps as a protective measure, before expression of these constituents reverts to the normal pattern. These findings suggest that keratinocyte differentiation in wound-healing following laser-induced thermal injury is similar to that seen in other types of injury. Observed clinical differences may be attributable to differences in keratinocyte proliferative or migratory capabilities.

Adult↗
PubMed1989

Reducing adult phlebotomy blood loss with the use of pediatric-sized blood collection tubes.

The feasibility of collecting smaller blood volumes during phlebotomy for diagnostic laboratory testing was evaluated by substituting pediatric-size for adult-size blood collection tubes. The volume of blood drawn with the use of pediatric-size tubes from 41 patients in an intensive care unit (120.2 mL total; 32.2 mL/day) was 46.8% lower than in that of a control population for which adult-size tubes were used (226.1 mL total; 55.6 mL/day). Sufficient blood was available for performance of all laboratory tests ordered at the time of the phlebotomy. Although substituting pediatric-size tubes does not address the problem of excessive use of laboratory tests, smaller tubes may reduce the severity of phlebotomy-induced anemia in adults without compromising laboratory test procedures.

Blood Specimen Collection↗
PubMed1989

HMB-45 staining of dysplastic nevi. Support for a spectrum of progression toward melanoma.

Dysplastic nevi are melanocytic tumors that occupy intermediate positions in the spectrum of melanocytic proliferations. Although they are invariably cured if completely excised, their biologic potential if left untreated is unknown. We examined a series of such lesions with HMB-45, a melanocyte-specific antibody, in order to explore protein expression within these borderline lesions. HMB-45 has previously been shown to label intraepidermal melanocytes within melanomas and within all nevi. Intradermal melanoma cells also label with HMB-45, but dermal nevus cells within common melanocytic nevi do not normally stain. In contrast, we found mild to moderate staining of nevus cells within the papillary dermis of dysplastic nevi and within residual nevus cells adjacent to malignant melanomas. In the same lesions, we demonstrated strong staining of intraepidermal melanocytes. Thus, dermal nevus cells within dysplastic nevi and within residual nevus cells adjacent to malignant melanomas are expressing low-level amounts of a protein expressed by melanoma cells, but not by dermal nevus cells within wholly benign melanocytic tumors. This lends support to the concept of these lesions as precursor lesions with undetermined biologic potential.

Antibodies, Neoplasm↗
PubMed1989

HMB-45 recognizes stimulated melanocytes.

A monoclonal antibody (HMB-45) was previously reported to bind to melanoma cells, and the junctional component of nevus cells, but not to normal adult melanocytes. We have tested HMB-45 binding in several conditions under which melanocyte stimulation might be expected in adults, i.e. 3 simple lentigines, 2 solar lentigines, 7 recent surgical scars (from re-excision of non-melanocytic tumors), 2 surgical scars from re-excisions of melanomas (after complete primary excisions), 9 hemangiomas from non-sun-exposed skin, 1 basal cell carcinoma, 1 acute ecchymosis, 1 keloid, and 1 dermatofibroma. Positive controls included 6 malignant melanomas and 1 fetal skin sample. Melanocytes were strongly positively stained overlying hemangiomas, within or near recent surgical scars of melanocytic and non-melanocytic tumor re-excisions, near basal cell carcinoma, and in fetal skin. Melanocytes either were not stained or were stained only focally for trace amounts in the normal skin near the new margins of the wide re-excision specimens for melanoma, i.e., at a distance from the scar, in the simple lentigines and in the fibrotic lesions. Thus, HMB-45 is staining an antigen which appears in adult melanocytes during stimulation and in fetal skin, as well as in melanomas. This stimulation is associated with conditions that would have increased vascularity, suggesting a melanocyte response to a plasma factor, or other endothelial cell derived factor. HMB-45 would not be a useful marker for residual melanoma cells in melanoma re-excision specimens.

Antibodies, Monoclonal↗
PubMed1989

Xanthomatous infiltrate of the face.

We report 2 cases which shared an unusual histopathologic pattern of a xanthomatous infiltrate occurring on the nose. Both patients were women in their fifth decade. Each presented to the dermatology clinic with multiple soft, flesh-colored papules, up to 1 cm, in diameter on the lateral aspects of the nose. The lesions had been present for several years. Both patients were otherwise completely well, and asymptomatic. In one case, focal telangiectasia and central umbilication was noted, and the clinical differential diagnoses included basal cell carcinomas and appendageal tumors. In each case, a biopsy was performed. The lesions appeared histologically quite similar. The epidermis was unremarkable. Within the dermis, there was a mid-reticular dermal infiltrate of macrophages with unilocular and multilocular fat laden cytoplasm, and scalloped nuclei. Only a scant inflammatory infiltrate of lymphocytes and histiocytes was present. Minimal dermal fibrosis was also present. We believe that xanthomatous infiltrate of the face is a distinct clinical entity which presents as multiple flesh-colored papules on the nose, which have a characteristic histologic appearance of abundant lipid-laden macrophages within the dermis.

Diagnosis, Differential↗
PubMed1988

Low-fluence carbon dioxide laser irradiation of lentigines.

Low-fluence carbon dioxide (CO2) laser irradiation of skin has previously been shown to induce damage limited primarily to the epidermis. To evaluate whether this technique was therapeutically effective for pigmented epidermal lesions, ten lentigines caused by methoxsalen and ultraviolet light therapy were treated in one patient using the CO2 laser at fluences ranging from 3.0 to 7.7 J/cm2 for 0.1-s exposures with 4.5-mm spot size. Based on substantial clearing in seven of ten lesions treated, 146 solar lentigines were treated in five patients at fluences of 3.0, 3.7, or 4.4 J/cm2. Biopsies were performed on a total of 30 lesions immediately and 24 hours, seven days, and six weeks after irradiation. Of 125 lesions followed up clinically for six weeks, 12 cleared completely, 81 lightened substantially, and 28 remained unchanged. Only two demonstrated atrophic change. Hyperpigmentation or hypopigmentation did not occur. All lesions that improved had been treated at 3.7 or 4.4 J/cm2. Immediate histologic injury consisted of vacuolar and spindly change and subsequent vesiculation limited to the basilar epidermis. Twenty-four hours later there was epidermal necrosis with regeneration, 0.1 mm of dermal basophilia and stromal condensation, and a mild inflammatory infiltrate. These alterations were dose-dependent, with near complete epidermal necrosis and superficial dermal involvement at the highest fluence, and only focal epidermal necrosis at the lowest. At seven days, epidermal regeneration was complete with traces of melanin remaining in keratinocytes. Melanophages first appeared at seven days and persisted at six weeks, by which time the inflammatory infiltrate had cleared. No lentiginous proliferation was evident and epidermal pigmentation had become normal. Low-fluence CO2 laser irradiation is an effective means of damaging the epidermis with only minimal dermal change. This mode of therapy is an effective way to lighten the pigmentation of lentigines without substantial scarring.

Adult↗
PubMed1987

Port-wine stains: a new hypothesis.

Port-wine stains have been shown to be derived from a progressive ectasia of the superficial vascular plexus. Recent studies have documented a marked decrease in nerves associated with these abnormal vessels. It is suggested that this nerve loss is primarily of autonomic origin (sympathetic) and the failure to regulate blood flow is the basis for the progressive vascular ectasia that characterizes these lesions.

Adrenergic Fibers↗
PubMed1987

Unexpected vascular response to epinephrine in port wine stains.

Success of argon laser therapy as a therapeutic modality for port wine stains has been correlated with the degree of vascular congestion within the lesions. Epinephrine causes vasoconstriction and erythrocyte stasis within normally innervated vessels. We tested the hypothesis that subcutaneous injection of epinephrine would cause vasoconstriction, altered hemodynamics, and increased red cell mass in port wine stains and thus allow more directed and less nonspecific damage and a better cosmetic result. Two clinically similar and adjacent areas within port wine stains were biopsied from 10 patients following subcutaneous injection of either Xylocaine or Xylocaine with epinephrine. Erythrocytes within vessels of the superficial cutaneous vascular plexus were increased in areas pretreated with Xylocaine plus epinephrine (55.3 versus 45.9 percent; p less than 0.09). This increase was seen in 9 of 10 patients studied (p less than 0.05). Epinephrine appears to increase erythrocytes within ectatic vessels of port wine stains and thus would likely improve laser energy absorption and cosmetic results.

Adolescent↗
PubMed1986

Phlebotomy for diagnostic laboratory tests in adults. Pattern of use and effect on transfusion requirements.

Although anemia is a frequently observed complication of phlebotomies for laboratory tests in neonates, this problem has received little attention in adult populations. We analyzed the phlebotomy records of 100 hospitalized patients and found that 50 patients who spent all of their hospitalization in general wards had blood samples drawn an average of 1.1 times a day. A mean volume of 12.4 ml a day was drawn, and the total volume drawn during their entire hospitalization was 175.0 ml. In contrast, 50 patients who spent part or all of their hospitalization in an intensive care unit were phlebotomized a mean of 3.4 times a day, for a mean volume of 41.5 ml of blood drawn a day and a total volume of 762.2 ml. Patients in the intensive care unit who had arterial lines had more blood drawn (944.0 ml), more often (4.0 times a day), than patients in the intensive care unit who did not have such lines (300.9 ml; 1.9 times a day). Of 36 patients who received transfusions, 17 (47 percent) had large losses from phlebotomy (greater than 180 ml of red cells) that contributed to their transfusion requirements. We propose the use of sample tubes of the size used in pediatrics, batching of requests for laboratory tests, and review of the cumulative volume of blood removed from individual patients as approaches to reducing blood loss from phlebotomy.

Adult↗
PubMed1986

Port-wine stains. A disease of altered neural modulation of blood vessels?

Port-wine stains result from a progressive ectasia of the cutaneous superficial vascular plexus. One hypothesis for the pathogenesis of this lesion is an abnormal neural regulation of blood flow. Biopsy specimens of 11 port-wine stains, seven hemangiomas, and 17 benign lesions were stained for S100 protein using immunoperoxidase techniques. All specimens were of facial biopsies or excisions and were evaluated for vessels per square millimeter, nerves per square millimeter, vessel-to-nerve ratio, and frequency of vessels coursing within 0.03 mm of nerves. These variables were evaluated in the superficial 0.8 mm of dermis, a zone that includes almost all abnormal port-wine-stain vessels. Controls showed 18.3 +/- 2.8 vessels/sq mm (+/- SD), 21.1 +/- 9.2 nerves/sq mm, 0.9 +/- 0.3 vessels to nerves, and 75% +/- 11% of vessels coursing within 0.03 mm of nerves, values that did not alter with age. Port-wine stains had a significant decrease in nerve density and increase in vessel-to-nerve ratio when compared with normal skin; only 17% +/- 3% of vessels were associated with nerves in port-wine stains. These findings document a deficit in the number of perivascular nerves in port-wine stains and raise the possibility that a lack of neural modulation of vascular flow may be involved in the pathogenesis of port-wine stains.

Adolescent↗