Factors associated with pruritic papular eruption of human immunodeficiency virus infection in the antiretroviral therapy era.

BACKGROUND: Pruritic papular eruption (PPE) of HIV is common in HIV-infected populations living in the tropics. Its aetiology has been attributed to insect bite reactions and it is reported to improve with antiretroviral therapy (ART). Its presence after at least 6 months of ART has been proposed as one of several markers of treatment failure. OBJECTIVES: To determine factors associated with PPE in HIV-infected persons receiving ART. METHODS: A case-control study nested within a 500-person cohort from a teaching hospital in Mbarara, Uganda. Forty-five cases and 90 controls were enrolled. Cases had received ART for ≥ 15 months and had an itchy papular rash for at least 1 month with microscopic correlation by skin biopsy. Each case was individually matched with two controls for age, sex and ART duration. RESULTS: Twenty-five of 45 cases (56%) had microscopic findings consistent with PPE. At skin examination and biopsy (study enrolment), a similar proportion of PPE cases and matched controls had plasma HIV RNA < 400 copies mL(-1) (96% vs. 85%, P = 0·31). The odds of having PPE increased fourfold with every log increase in viral load at ART initiation (P = 0·02) but not at study enrolment. CD4 counts at ART initiation and study enrolment, and CD4 gains and CD8(+) T-cell activation measured 6 and 12 months after ART commencement were not associated with PPE. Study participants who reported daily insect bites had greater odds of being cases [odds ratio (OR) 8·3, P < 0·001] or PPE cases (OR 8·6, P = 0·01). CONCLUSIONS: Pruritic papular eruption in HIV-infected persons receiving ART for ≥ 15 months was associated with greater HIV viraemia at ART commencement, independent of CD4 count. Skin biopsies are important to distinguish between PPE and other itchy papular eruptions.

Differential expression of PHLDA1 (TDAG51) in basal cell carcinoma and trichoepithelioma.

BACKGROUND: A recent small series demonstrated perfect sensitivity and specificity utilizing immunostaining for PHLDA1, a marker of follicular stem cells, in the distinction of desmoplastic trichoepithelioma and morphoeiform basal cell carcinoma (BCC) in small biopsy specimens. OBJECTIVES: To assess this result more broadly. METHODS: We performed immunoperoxidase staining of BCCs (superficial n = 16, nodular n = 15, micronodular n = 15, infiltrative n = 17, morphoeiform n = 16, infundibulocystic n = 14) and trichoepitheliomas (conventional n = 19, desmoplastic n = 16) with PHLDA1. RESULTS: Morphoeiform BCCs typically lacked PHLDA1 staining (88% demonstrated no staining and 12% of cases had staining in < 25% of the tumour), while in contrast 74% of classical and 88% of desmoplastic trichoepitheliomas demonstrated strong PHLDA1 staining in over half of the tumour. However, micronodular BCCs demonstrated focal to diffuse positive staining in a third of the cases. CONCLUSIONS: Based upon our staining results, we discuss the biological significance of PHLDA1 expression and the limits in its diagnostic utility.

Bacillary angiomatosis masquerading as Kaposi's sarcoma in East Africa.

BACKGROUND: Bacillary angiomatosis (BA) is a rare manifestation of infection caused by Bartonella species, which leads to vasoproliferative lesions of skin and other organs. Bacillary angiomatosis affects individuals with advanced HIV disease or other immunocompromised individuals. In sub-Saharan Africa, despite the high prevalence of HIV infection and documentation of the causative Bartonella species in humans, mammalian hosts, and arthropod vectors, BA has only rarely been described. METHODS: Three adult patients from Uganda and Kenya with deep purple dome-shaped papules or nodules of the skin underwent punch biopsies for histopathologic diagnosis. The biopsies of all 3 patients were sent to a local pathologist as well as to a dermatopathologist at the University of California, San Francisco. RESULTS: All 3 patients were clinically suspected to have Kaposi's sarcoma (KS), and local pathologists had interpreted the lesions as KS in 2 of the cases and nonspecific inflammation in the third. Histologic examination by dermatopathologists in the United States revealed nodular dermal proliferations of irregular capillaries lined by spindled to epithelioid endothelial cells. The surrounding stroma contained a mixed inflammatory infiltrate with lymphocytes, eosinophils, and neutrophils. Extracellular deposits of pale amphophilic granular material were noted in the surrounding stroma. A Warthin-Starry stain highlighted clumps of bacilli, confirming the diagnosis of BA. CONCLUSIONS: These 3 cases, to our knowledge, are the first reports of BA in East Africa in the biomedical literature. Each had been originally incorrectly diagnosed as KS. We speculate BA is underdiagnosed and underreported in resource-poor regions, such as sub-Saharan Africa, that have high endemic rates of HIV infection.

Cutaneous melanoma with myxoid features: twelve cases with differential diagnosis.

Substantial myxoid change can occur in malignant melanoma, but its importance in primary disease has not been systematically evaluated. This report describes the clinical, microscopic, histochemical, and immunohistochemical findings in 12 patients with primary cutaneous malignant melanoma with myxoid features. The tumors presented as solitary lesions situated on the limbs (six lesions), trunk (four lesions), and head and neck (two lesions). The patients included six women and six men, whose ages ranged from 26 to 95 years, with a mean of 63 years. Breslow thickness varied from 0.48 mm to more than 12 mm, with a mean of more than 3.2 mm. Clinical follow-up for an average of 22 months showed one local recurrence, but no evidence of metastases yet. In all cases, there was a combination of myxoid and nonmyxoid areas. A minimum of 15% myxoid cross-sectional area was required for inclusion in the study, and up to 80% was observed. The pale blue mucin identified on hematoxylin and eosin staining was sensitive to hyaluronidase and positive for alcian blue in the 10 cases stained. Immunohistochemical staining was positive for S-100 in all 9 cases stained, positive for HMB-45 in 9 (90%) of 10, and negative for cytokeratin in all 9 cases in which myxoid melanoma remained in the block after previous sections. The presence of myxoid stroma did not define a biologically significant subgroup of melanoma. Only in cases with extensive (>50%) myxoid stromal effacement of the melanoma was there a major diagnostic hurdle. The diagnosis of primary cutaneous melanoma with myxoid features was seldom as problematic as metastatic myxoid melanoma. Positive S-100 stains, negative cytokeratin immunohistochemical stains, and hyaluronidase-sensitive alcian blue staining assisted in the diagnosis of this entity.

Efficacy of RS-61443 in reversing acute rejection in a rat model of hindlimb allotransplantation.

The requirement for effective, minimally toxic immunosuppression remains a major obstacle to performing human composite tissue allotransplantation. The skin component of composite tissue (e.g., limb) allografts is especially antigenic, necessitating toxic immunosuppressant doses to prevent or reverse acute rejection. In previous experiments, RS-61443, an experimental mycophenolic acid ester that inhibits lymphocyte proliferation with minimal toxicity, prevented acute limb allograft rejection in rats for more than 8 months when started on the day of transplantation. In this study, the ability of RS-61443 to reverse established acute rejection was tested in a rat model of hindlimb allotransplantation. Brown-Norway donors and Fischer 344 recipients provided a MHC mismatch for orthotopic midfemur limb transplants that were performed with microsurgical repair of femoral vessels and sciatic nerve. Three groups were studied: untreated allografts (n = 6); allografts receiving RS-61443 at 30 mg/kg/day, started on postoperative day 7 (n = 11); and allografts receiving RS-61443 at 30 mg/kg/day, started on postoperative day 9 (n = 9). Skin and soft tissues were biopsied periodically to assess rejection. Untreated allografts had complete acute rejection within 12-13 days. Animals in both the 7- and 9-day groups developed moderate to severe rejection clinically and histologically before initiation of immunosuppressive therapy. In both groups, RS-61443 was able to reverse rejection completely in all animals from which biopsies were obtained at the time of death at 9-16 weeks after transplantation (P < 0.007). RS-61443 was highly effective as a primary immunosuppressant for reversing established acute rejection in rat hindlimb allografts.

A long-term study of allogeneic rat hindlimb transplants immunosuppressed with RS-61443.

Although technically possible, limb allotransplantation has not been applied clinically. The skin component is especially antigenic, requiring high immunosuppressant doses with an unacceptable toxicity profile. RS-61443, an experimental mycophenolic acid ester that inhibits lymphocyte proliferation without major systemic toxicity, was tested as an immunosuppressant to prevent rejection of rat hindlimb allotransplants. Utilizing Brown-Norway donors and F344 recipients to provide a major mismatch at the MHC, midfemur orthotopic limb transfer was performed with microsurgical repair of femoral vessels and sciatic nerve. Four primary groups were studied: autografts (n = 4); untreated allografts (n = 6); allografts receiving CsA 10 mg/kg for 20 days, then twice per week (n = 6); and allografts receiving RS-61443 30 mg/kg/day (n = 6). Skin and soft tissues were biopsied to assess rejection. Autografts had indefinite limb survival, while untreated allografts had complete acute rejection within 10-12 days. Five of the six CsA rats developed delayed mild-moderate acute rejection within 6 months. In contrast, 5 of the 6 RS-61443 rats had no rejection after at least 32 weeks, while the sixth rat developed only slight rejection on skin biopsy. All animals regained full sensation and partial functional return. RS-61443 is highly effective as a primary immunosuppressant for hindlimb allotransplantation. The disturbing moderate rejection observed in CsA animals, which was absent with RS-61443, may significantly hamper function of transplanted limbs.

Mixed allogeneic chimerism as a reliable model for composite tissue allograft tolerance induction across major and minor histocompatibility barriers.

BACKGROUND: Although prolonged composite tissue allograft (CTA) survival is achievable in animals using immunosuppressive drugs, long-term immunosuppression of CTAs in the clinical setting may be unacceptable for most patients. The purpose of this study was to develop a model for reliable CTA tolerance induction in the adult rat across a major MHC mismatch without the need for long-term immunosuppression. METHODS: Mixed allogeneic chimeras were prepared by using rat strains with strong MHC incompatibility [WF (RT1Au), ACI (RT1Aa)] WF + ACI-->WF, n=23. The bone marrow (BM) of recipient animals was pretreated with low-dose irradiation (500-700 cGy), followed by reconstitution with a mixture of T cell-depleted syngeneic (WF) and allogeneic (ACI) cells. Additionally, the recipient animals received a single dose of anti-lymphocyte serum (10 mg) 5 days before bone marrow transplantation (BMT) and tacrolimus (1 mg/kg/day) from the day before BMT to 10 days post-BMT. Hindlimb transplants were performed 12 months after BMT. Five animals received a limb allograft irradiated (1000 cGy) just before transplantation. Rat chimeras were characterized (percentage of donor cells present within the bloodstream) by flow cytometry at 3 and 12 months after BM reconstitution and after hindlimb transplantation. RESULTS: Peripheral blood lymphocyte chimerism (WF/ACI) remained stable >12 months after BM reconstitution in 18/23 animals. Multi-lineage chimerism of both lymphoid and myeloid lineages was present, suggesting that engraftment of the pluripotent rat stem cell had occurred. In animals with donor chimerism >60% (n=18) no sign of limb rejection was present for the duration of the study. All animals with chimerism <20% (n=5) developed moderate signs of rejection clinically and histologically. Gross motor and sensory reinnervation (weight bearing, toe spread) developed at >60 days in 14/21 rats. Postoperative flow cytometry studies demonstrated stable chimerism in all animals studied (n=10). Five out of five animals with irradiated limb transplants showed no sign of GVHD at >100 days. CONCLUSIONS: Stable mixed allogeneic chimerism can be achieved in a rat hindlimb model of composite tissue allotransplantation. Hindlimb allografts to mixed allogeneic chimeras exhibit prolonged, rejection-free survival. Partial functional return should be expected. The BM transplanted as part of the hindlimb allograft plays a role in the etiology of GVHD. Manipulating that BM before transplantation may influence the incidence of GVHD. This represents the first reliable rat hindlimb model demonstrating rejection-free CTA survival in an adult animal across a major MHC mismatch without the long-term need for immunosuppressive agents.

Cutaneous manifestations of maternal engraftment in patients with severe combined immunodeficiency: a clinicopathologic study.

SCID is a heterogeneous group of disorders characterized by defective T cell and B cell function. Eczematous and morbilliform eruptions are common, and graft-versus-host disease (GVHD) due to maternal engraftment has been documented. We sought to better characterize SCID-related cutaneous disease observed prior to BMT and to compare the eruption to conventional GVHD. Medical records of 51 patients with SCID treated between 1982 and 1999 were reviewed. Ten of 51 (20%) had rash and evidence of maternal engraftment prior to BMT (study group). Eleven of 51 (22%) had no rash or evidence of engraftment pre-BMT but developed GVHD following transplant (control group). Skin biopsies were available for review for 8/10 of the study group and for 8/11 of the control group. Cutaneous findings consisted of a scaling, erythematous maculopapular eruption spread widely over the trunk and extremities, with near-erythroderma in some patients. Microscopically, biopsies from the study group differed significantly from controls. Key differences included parakeratosis (P < or = 0.01), psoriasiform hyperplasia (P < or = 0.04) and spongiosis (P < or = 0.04). The dermatopathologic findings of transplacental GVHD differ from the pattern of post-transplant GVHD. A 'psoriasiform-lichenoid-spongiotic' pattern with necrotic keratinocytes should trigger consideration of SCID and maternal engraftment in the dermatopathologic evaluation of eruptions of infancy.

Cytologic diagnosis of aspergillosis in cardiac transplantation.

Fine-needle aspiration of the lung is now widely utilized to diagnose pulmonary neoplasms, but often serologic techniques or open-lung biopsy is relied on for the diagnosis of infectious pulmonary processes. We report a series of four patients in whom the fine-needle aspiration technique was used to make the rapid cytologic diagnosis of pulmonary aspergillosis. Culture confirmation was also obtained on the aspirated material. A discussion of the available techniques for the laboratory diagnosis of pulmonary aspergillosis is presented and the advantages of fine-needle aspiration cytology are stressed. Our favorable results support expanded use of fine-needle aspiration cytology in the evaluation of lung nodules appearing in immunosuppressed populations.

Kaposiform hemangioendothelioma. An aggressive, locally invasive vascular tumor that can mimic hemangioma of infancy.

BACKGROUND: Kaposiform hemangioendothelioma is a rare, aggressive vascular proliferation in children that is clinically and histologically distinct from hemangioma of infancy. It often manifests later than infantile hemangioma, and complication by Kasabach-Merritt syndrome is common. OBSERVATIONS: We examined 3 children with kaposiform hemangioendothelioma, all of whom were initially misdiagnosed as having infantile hemangioma. All 3 children developed Kasabach-Merritt syndrome, in association with a rapidly growing cutaneous vascular mass. Treatment with systemic corticosteroids, interferon alfa, vincristine, and radiation therapy appeared to halt progression of the disease. None had evidence of human herpesvirus 8 infection. CONCLUSIONS: Cutaneous kaposiform hemangioendothelioma may appear in early infancy but often appears months to years later. It is frequently complicated by Kasabach-Merritt syndrome, has no known association with Kaposi sarcoma related to human immunodeficiency virus infection, and demonstrates aggressive local behavior with invasion but not distant metastasis. Awareness of this entity is important to prevent a mistaken diagnosis of common hemangioma of infancy.

p53 oncoprotein expression and proliferation index in keratoacanthoma and squamous cell carcinoma.

BACKGROUND AND DESIGN: Whether solitary keratoacanthoma (KA) is a malignant neoplasm despite its self-limited clinical behavior, and the distinction between KA and squamous cell carcinoma (SCC) are related aspects of a long-standing debate among dermatopathologists. Recent advances toward understanding the molecular basis of malignant transformation may allow this issue to be resolved. Mutant p53 tumor-suppressor protein has been shown to accumulate in cutaneous SCC and other tumors, and may be a relatively specific marker of malignancy. We studied 20SCCs, 20KAs, and an additional 10 regressing KAs (rKA) by immunohistochemistry for the expression of p53 protein. Since p53 is believed to play a pivotal role in the regulation of cell division, we also quantitated proliferation in the tumors by examining Ki-67 antigen expression. RESULTS: Sixteen (80%) of the KAs showed nuclear staining with anti-p53 antibody, distributed along the outermost layers of the aggregates of neoplastic cells, while 12 (60%) of the SCCs were p53 positive. Eight (80%) of the rKAs also showed p53 positivity. Mean Ki-67 proliferation fraction was higher for KA than for SCC (55% vs 46%), but this difference was not statistically significant. p53 Expression did not correlate with the grade of SCC. CONCLUSIONS: A majority of KA, rKA, and SCC contain stainable quantities of p53 protein, supporting the view that KA is a type of regressing SCC.

Overexpression of p53 tumor suppressor protein in porokeratosis.

BACKGROUND: p53 is a tumor suppressor nucleoprotein. Mutations of the p53 gene have been found in a variety of malignant neoplasms. Wild-type p53 has a short half-life, possibly only 20 to 30 minutes, and is not present in the nucleus at levels that are detectable with routine immunohistochemical techniques. Mutant p53 has a longer half-life, and is readily detectable with immunoperoxidase staining. RESULTS: We studied 17 specimens from patients with either porokeratosis of Mibelli or actinic porokeratosis, using immunoperoxidase staining with an antibody directed against the p53. There was staining of lesional keratinocyte nuclei in 16 of 17 specimens, limited in most cases to the zone between cornoid lamellae. Staining for proliferating cell nuclear antigen was increased above background levels in only six of 13 specimens. CONCLUSIONS: The finding of p53 immunoperoxidase staining in porokeratosis suggests genetic mutation, as occurs in other cutaneous keratinocytic neoplasms, and the lack of corresponding proliferating cell nuclear antigen expression in many specimens indicates that p53 overexpression is not simply a reflection of increased cellular proliferation.

Sweet's syndrome leading to acquired cutis laxa (Marshall's syndrome) in an infant with alpha 1-antitrypsin deficiency.

BACKGROUND: Marshall's syndrome is a rare pediatric skin disease that is characterized by acquired, localized neutrophilic dermatitis (Sweet's disease), followed by loss of elastic tissue in the dermis and cutis laxa. The cause of this syndrome is unknown. alpha 1-Antitrypsin (alpha 1-AT) deficiency is a codominantly inherited disorder of alpha 1-AT, the major serum antiprotease active against a number of serine-type proteases. OBSERVATIONS: The first patient with classic Marshall's syndrome who had coexisting alpha 1-AT deficiency and a review of other cases of Marshall's syndrome are presented, and pathogenic mechanisms are discussed. CONCLUSIONS: A deficiency of alpha 1-AT may allow proteases such as neutrophil elastase to destroy dermal elastin and, thus, produce cutis laxa in Marshall's syndrome. Other cases of acquired cutis laxa should be screened for alpha 1-AT deficiency to further evaluate this association and to enable patients and their families to be counseled about possible systemic complications of alpha 1-AT deficiency.

Rudimentary meningocele: remnant of a neural tube defect?

BACKGROUND: Rudimentary meningocele, a malformation in which meningothelial elements are present in the skin and subcutaneous tissue, has been described in the past under a variety of different terms and has also been referred to as cutaneous meningioma. There has been debate as to whether rudimentary meningocele is an atretic form of meningocele or results from growth of meningeal cells displaced along cutaneous nerves OBJECTIVE: We reviewed the clinical, histological, and immunohistochemical characteristics of rudimentary meningocele in an attempt to assess the most likely pathologic mechanism for it. DESIGN: Retrospective study. SETTING: University hospitals. PATIENTS: Thirteen children with rudimentary meningocele. MAIN OUTCOME MEASURES: Medical records were reviewed and histopathologic examination as well as immunohistochemistry studies were performed for each case. A panel of immunoperoxidase reagents (EMA, CD31, CD34, CD57, S-100, and CAM 5.2) was used to assess lineage and to confirm the meningothelial nature of these lesions. RESULTS: Recent evidence indicating a multisite closure of the neural tube in humans suggests that classic meningocele and rudimentary meningocele are on a continuous spectrum. CONCLUSION: Rudimentary meningocele seems to be a remnant of a neural tube defect in which abnormal attachment of the developing neural tube to skin (comparable to that in classic meningocele) could explain the presence of ectopic meningeal tissue. In the majority of cases, no underlying bony defect or communication to the meninges could be detected. However, in light of the probable pathogenesis, imaging studies to exclude any communication to the central nervous system should precede any invasive evaluation or intervention.

Preoperative evaluation of the surgical patient.

Both the patient and the surgeon benefit from a complete and thorough preoperative evaluation. Such evaluation may permit the surgeon to identify surgical candidates at risk for problems, institute corrective measures, and thus reduce surgical complications. Time spent by the surgeon in preoperative patient education often yields increased patient confidence and enables patients to make informed decisions about their own care. The overall result is that surgical care becomes more efficient, more pleasant for the patient, and less stressful for the surgeon.

Fatal disseminated herpesvirus infection with hepatitis. A peritoneal fluid cytologic warning.

A 19-year-old man died of a disseminated herpesvirus infection. Microscopic examination of a peritoneal fluid specimen revealed cellular changes characteristic of a herpetic process, and an autopsy confirmed widespread herpes simplex virus type II infection. Viral infections may be diagnosed by cytologic examination of body fluid specimens.

Melanoma and melanoma in situ: build a better diagnosis through architecture.

Conventional microscopy has remained the gold standard for melanoma diagnosis for several decades, and a diagnosis of melanoma is optimally based on a summation of microscopic features (criteria) that are evaluated as objectively as possible by an experienced histopathologist. Most pathologists and dermatopathologists assess multiple criteria before arriving at a diagnosis of melanoma, but the diagnosis remains somewhat subjective as different interpreters employ similar criteria but assemble them in very different ways. Due to the subjective aspects of the microscopic diagnosis of melanoma, considerable interobserver variability exists, even among expert diagnosticians. This article includes a brief analysis of the reproducibility of a diagnosis of melanoma with a comparison of architectural and cytological criteria. There is evidence to suggest that architectural attributes hold greater reproducibility over cytological features in the diagnosis of melanocytic neoplasms. If architectural criteria outperform cytological criteria in terms of reproducibility, then architectural features should probably be given preference over cytopathological aberrations in daily diagnosis. The author forwards four steps that can be used in the evaluation of any melanocytic neoplasm as well as an approach to melanoma diagnosis in which architectural features are emphasized.

Eosinophilic and neutrophilic spongiosis: clues to the diagnosis of immunobullous diseases and other inflammatory disorders.

When eosinophils or neutrophils are found within the epidermis in concert with edema, the pattern is known as eosinophilic or neutrophilic spongiosis. Although eosinophilic spongiosis has been accepted as a clue to the diagnosis of blistering disorders for some time, the fact that either pattern can serve as a clue to the diagnosis of a variety of disorders, including immunobullous diseases, is less widely known. Herein, we review the types of inflammatory skin diseases, including spongiotic dermatitides, subepidermal vesicular dermatitides, intraepidermal vesicular dermatitides, and perivascular or diffuse dermatitides, that display intraepidermal eosinophils and neutrophils. We also review the known mechanisms that explain in part why intraepidermal granulocytes are commonly found in this diverse group of skin diseases.

Photosensitivity in HIV-infected individuals.

OBJECTIVE: To characterize photosensitivity in HIV-infected individuals using minimal erythema dosage (MED) UVA (ultraviolet A light) and UVB (ultraviolet B light) photoprovocation light testing. DESIGN: Prospective, controlled analytical study. SETTING: University of California, San Francisco, between March 1995 and January 1997. PATIENTS: 13 HIV-seropositive patients with clinical and pathological features consistent with photodermatitis, 13 HIV-seropositive patients with biopsy-proven eosinophilic foliculitis (EF), and 10 HIV-seropositive patients with CD4 (T helper cell) count below 200 cells/uL and no history of photosensitivity or EF. INTERVENTION: Each patient underwent MED testing for UVB. All 13 patients with suspected photodermatitis underwent full photochallenge testing with UVA and UVB for up to 10 consecutive week days. RESULTS: Mean MED to UVB in patients with clinical photosensitivity and EF was lower (p = 0.004 and p = 0.022 respectively) than that of patients without a clinical history of photodermatitis. There were no significant differences in mean CD4 count or Fitzpatrick skin type. Positive photochallenge tests (papular changes at site of provocative light testing) to UVB (9 of 13 patients) were much more common than reactions to UVA (3 of 13 patients) in the photodermatitis group. All patients with clinically active photodermatitis developed papular changes at the site of UVB photochallenge testing, but only 1 of 5 patients with photodermatitis in remission developed papular changes with UVB photochallenge testing. Seven of the 13 patients with photodermatitis had Native American ancestry. Photosensitive patients were commonly taking trimethoprim-sulfamethoxazole (TMP-SMX), but no more commonly than EF or control patients. CONCLUSIONS: Photosensitivity in HIV-infected individuals appears to be a manifestation of advanced disease. Most patients are sensitive to UVB. The most severely affected individuals are both UVB and UVA sensitive, and may show reactions to visible light. A significant Native American ancestry may be a risk factor for development of photodermatitis in patients with advanced HIV disease. Finally, patients with eosinophilic folliculitis may be subclinically photosensitive.

Vascular adhesion molecules in oral lichen planus.

OBJECTIVE: Because recruitment and retention of lymphoid cells appear to be critical components of the pathogenesis of lichen planus, we have compared the expression and distribution of a panel of vascular adhesion molecules (ELAM-1, P-selectin, ICAM-1, VCAM-1, PECAM-1, CD34) and leukocyte adhesion molecule ligands (LFA-1, Mac-1, VLA4, L-selectin) in biopsies of this disease. STUDY-DESIGN: Frozen sections of 12 clinically and histologically confirmed cases of lichen planus and 9 normal control tissues were evaluated immunohistochemically with a standard 1-day avidin-biotin peroxidase technique. Staining intensity of vascular endothelium was evaluated semiquantitatively. Three microvascular zones or compartments were defined and evaluated separately. RESULTS: Generally, different staining patterns were observed in association with the various endothelium-associated adhesion molecules. In normal controls, PECAM was intensely expressed and VCAM-1 was weakly expressed. Intermediate staining was associated with ELAM-1, P-selectin, ICAM-1, and CD34. Staining within the three microvascular compartments frequently showed variations in intensity. In lichen planus, increased staining for ELAM-1, P-selectin, ICAM-1, and VCAM-1 was evident in one or more of the microvascular compartments. In the subepithelial vascular compartment where the infiltrate was the most dense, VCAM-1 appeared to show the greatest positive change. Almost all cells in the lichen planus infiltrates stained positive for ICAM-1, L-selectin, LFA-1, and VLA4, and large numbers of cells also exhibited VCAM-1, PECAM-1, and Mac-1 immunoreactivity. CONCLUSIONS: It appears that upregulation of ELAM-1, ICAM-1, and VCAM-1 (especially by endothelial cells in the subepithelial vascular plexus) could play a role in the pathogenesis of lichen planus. The expression of leukocyte receptors L-selectin, LFA-1, and VLA4 by most of the cells in the lichen planus infiltrate suggest that these molecules may be responsible for recruitment as well as retention in the active lichen planus lesion.