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PubMed2004

Suppression of atopic-like dermatitis by treatment with antibody to lymphocyte function-associated antigen-1 in NC/Nga mouse.

The effect of a blocking-antibody specific for lymphocyte function-associated antigen-1 (LFA-1) was studied in an atopic-like dermatitis model, which was induced by the repeated application of picrylchloride in NC/Nga mice. Prophylactic treatment with anti-LFA-1 monoclonal antibody (mAb), not therapeutic treatment, significantly inhibited the skin severity score and the acanthosis with ulceration and infiltration of mast cells. Furthermore, the serum immunoglobulin E levels and cytokine production (interleukin-4 and interferon-gamma) by splenocytes stimulated with anti-CD3 antibody were also inhibited by treatment with anti-LFA-1 mAb. Our results suggest that LFA-1 plays an important role in the induction phase of the atopic-like dermatitis model.

Animals↗

PubMed2005

Mechanisms of insulin resistance caused by nutrient toxicity.

Insulin resistance, the impaired action of insulin, has been linked to many important consequences, including Type 2 diabetes, hypertension, dyslipidemia, acanthosis nigricans and polycystic ovarian syndrome. Although there are some genetic causes for insulin resistance, the most common cause is an excess of nutrition a condition called "Nutrient Toxicity". Both excess glucose and excess fat can cause insulin resistance in muscle and fat tissues and excess fat can cause insulin resistance in the liver. High fat feeding and fat infusion rapidly lead to the development of insulin resistance caused by impairment in glucose transport. Other studies have shown defects in insulin signaling possibly secondary to activation of Protein Kinase C resulting from the accumulation of active fatty acyl CoA's. Glucose toxicity has been studied both in vivo and in vitro. In vivo it has been shown that rats over-expressing the gluconeogenic enzyme Phosphoenol Pyruvate Carboxykinase (PEPCK) develop insulin resistance in fat and muscle tissues and some features of the metabolic syndrome including mild obesity and dyslipidemia. Excess glucose entry in fat cells results in increased flux through the hexosamine biosynthesis pathway leading to activation of protein kinase C and impairment of glucose transport. Obesity resulting from excess nutrient intake can also cause insulin resistance by an increase in the production of agents that impair insulin action such as TNFalpha and resistin and a decrease in the production of an insulin sensitizing compound adiponectin. Both glucose and free fatty acids acutely stimulate insulin secretion but chronic exposure to high levels of either nutrient leads to impairment of beta cell function. The combination of insulin resistance and beta cell failure leads to diabetes. Nutrient toxicity is thus the driving cause of the diabetes epidemic that is being recorded around the world.

Journal Article↗

PubMed2005

Insulin resistance and clinical aspects of non-alcoholic steatohepatitis (NASH).

Non-alcoholic steatohepatitis (NASH) is one of the most common liver disorders. This is highly prevalent in obese and diabetic subjects. Persons with central obesity are at particular risk. Other clinical predictors are age more than 40-50 years and hyperlipidemias, but none of these factors is invariable for causation of NASH. Other reported associations are, celiac disease, Wilson's Disease and few other metabolic diseases. Drugs, particularly amiodarone, tamoxifen, nucleoside analogues and methotrxate have also been linked to NASH. The disease is evenly distributed in both sexes but advanced disease is more common in women. Ethnic variation exists and African Americans are less affected than Hispanic Americans. Specific clinical features of NASH are infrequent. Patients usually come to clinical attention by elevated liver enzymes found on routine evaluation but on history, about two third of patients will admit to have mild fatigue and about half will report right upper quadrant pain. Rarely, patient may present with a complication of cirrhosis. Physical examination may reveal hepatomegaly and splenomegaly. Research in last few years has stressed that development of steatosis, stetohepatitis, fibrosis with subsequent cirrhosis are most probably the result of insulin resistance. Therefore, clinical features may reflect existence of insulin resistance. Obesity, particularly central obesity is most important of these. Patients may have sleep apnea syndrome. Hypertension and manifestations of diabetes mellitus like polyuria, polydypsia, and neurological deficits may occur. Patients may have varying combination of obesity, diabetes, hyperlipidemia, hypertension and impaired fibrinolysis (syndrome X). Children with insulin resistance may show acanthosis nigricance. Patients with polycystic ovary syndrome, which consists of insulin resistance, diabetes, obesity, hirsutism, oligo or polymenorrha and hyperlipidemia may have NASH. Other rare manifestations of insulin resistance, which can be seen in patients of NASH are lipomatosis, lipoatrophy/lipodystrophy and panniculitis. Most other rare conditions known to cause NASH like peroxisomal diseases, mitochondialpathies, Weber-Christian disease, Mauriac syndrome, Madelung's lipomatosis and abetaliopprotenemia also have insulin resistance. This is believed that primary defect underlying insulin resistance is impairment in postreceptor pathways (through tyrosine kinase activity) of insulin action. Primary defect in insulin receptors appear uncommon. This results in down regulation of insulin receptor substance 1 (IRS-1) signaling by excess free fatty acids. In muscle, activated IRS-1 promotes translocation of glucose transporter protein 4 (GLUT4) to cell membrane. As a result, monocyte glucose uptake by GLUT4 increases glucose disposal from blood and reduced need for insulin. PKC-0 is a likely candidate as serine kinase in muscle regulated by fatty acids that can impair the activation of IRS-1. Insulin resistance is usually evaluated by fasting insulin levels, Quantitative Insulin Check Index (QUICKI) and Homeostasis Model Assessment of Insulin Resistance (HOMA), C-peptid/insulin ratio oral glucose tolerance test and hyper insulinemic euglycemic clamp. The clamp technique is considered the gold standard.

Journal Article↗

PubMed2005

Clinical and histopathological findings in Bannayan-Riley-Ruvalcaba syndrome.

Bannayan-Riley-Ruvalcaba syndrome is a rare autosomal dominant genodermatosis with the classical triad of macrocephaly, genital lentiginosis, and intestinal polyposis. Characteristic mucocutaneous manifestations include vascular malformations, lipomatosis, speckled lentiginosis of the penis or vulva, facial verrucae-like or acanthosis nigricans-like lesions, and multiple acrochordons of the neck, axilla, and groin. We present a case of Bannayan-Riley-Ruvalcaba syndrome with macrocephaly, abnormal facies, lipoma, tender and painful arteriovenous hemangiomas, lymphangiokeratomas, musculoskeletal abnormalities, and localized myopathy. We also describe previously unreported findings, including peripheral neuropathy, punctate cystic changes in acral tubular bones, and enostosis of talus. Bannayan-Riley-Ruvalcaba syndrome needs recognition by dermatologists because affected patients may present with mucocutaneous and subcutaneous lesions that may simulate other dermatological disorders.

Abnormalities, Multiple↗

PubMed2006

Imiquimod as an antiaging agent.

BACKGROUND: Topical imiquimod therapy has proven to be effective for a variety of infectious, neoplastic, and inflammatory dermatologic diseases. Several published reports have validated the benefit of imiquimod therapy for actinic keratoses and superficial melanoma and nonmelanoma skin cancers. There is, however, limited evidence demonstrating the use of topical imiquimod application as an antiaging treatment. OBJECTIVES: We examined the effectiveness of imiquimod 5% cream in the treatment of photoaging by evaluating pretreatment and posttreatment biopsy specimens and documenting the histologic changes. METHODS: This study represents an extension of an earlier project in our department in which patients with biopsy-proven lesions of lentigo maligna (LM) were recruited from a university dermatology service, a hospital, and referrals from private practitioners for an open-labeled efficacy trial with daily topical application of 5% imiquimod for 3 months. Biopsy of clinically affected skin was carried out on all patients before and after treatment. Using a semiquantitative method, biopsy specimens were analyzed for changes in the dermal collagen table (solar elastosis vs papillary dermal fibroplasia). Additional parameters analyzed included epidermal changes (atrophy vs acanthosis, melanin content, and hypergranulosis) and inflammatory effects (epidermal and dermal cell populations along with presence of pigment incontinence). Variables were compared using paired Wilcoxan rank sums. RESULTS: Of 26 evaluable patients who completed 3 months of daily application, 24 (>92.3%) showed a significant increase in papillary dermal fibroplasia (P < .0001) with associated reduction in solar elastosis (P = .0036). Other noteworthy findings were restoration of normal epidermal thickness (P = .0073) and melanization (P < .0001). LIMITATIONS: This study only evaluates the effect of imiquimod in the lesional skin of LM. It is not known whether the results are applicable to nonlesional, photoaged skin. CONCLUSION: Topical imiquimod appears to induce reparative changes to the epidermis and the dermal collagen table in chronically sun-damaged skin associated with LM, indicating its potential use as an antiaging treatment. These findings need to be confirmed in photodamaged skin not associated with LM.

Aminoquinolines↗

PubMed2004

Reduced dermal infiltration of cytokine-expressing inflammatory cells in atopic dermatitis after short-term topical tacrolimus treatment.

BACKGROUND: In several clinical studies, topical calcineurin inhibitors have been shown to be effective in the treatment of atopic dermatitis (AD). They target signaling pathways that control gene expression, particularly the expression of cytokines. OBJECTIVE: We examined the cellular infiltrate in skin lesions of 10 patients with AD and characterized the cytokine pattern expressed by the infiltrating cells before and after short-term topical therapy with tacrolimus 1% ointment. METHODS: Skin biopsies were examined for histologic alterations (hematoxylin and eosin staining), composition of the cellular inflammatory infiltrate (immunofluorescence), and cytokine expression (ribonuclease protection assay, ELISA, immunofluorescence) before as well as 1 and 3 weeks after initiation of tacrolimus therapy. For comparison, biopsies from nonlesional AD and normal skin were analyzed. Systemic immunologic effects were assessed by analyzing peripheral blood leukocytes (immunofluorescence) as well as in vitro stimulated pan-T-cell cytokine production (ELISA). RESULTS: All patients showed a significant improvement of their skin lesions associated with a marked regression of spongiosis, acanthosis, and density of the cellular infiltrate in the dermis. The last was a result of reduced infiltration of T cells, B cells, and eosinophils. In contrast, the numbers of mast cells did not change. Moreover, the expression of the T H 2 cytokines IL-5, IL-10, and IL-13 in CD4 + T cells was reduced after therapy. Interestingly, tacrolimus therapy was also associated with a reduction of CD8 + T cells expressing the T H 1 cytokine IFN-gamma. Furthermore, the numbers of epidermal CD1a + dendritic cells increased after treatment. In the peripheral blood, a decrease of granulocytes (eosinophils and neutrophils) but no changes in the distribution of lymphocyte subpopulations were noticed. CONCLUSION: Topical tacrolimus treatment has anti-inflammatory effects on AD skin as indicated by reduced infiltration of cytokine expressing inflammatory cells. No evidence for drug-induced systemic immunosuppression was obtained.

Administration, Topical↗

PubMed2005

FGFR3 dimer stabilization due to a single amino acid pathogenic mutation.

Mutations in the transmembrane (TM) domains of receptor tyrosine kinases (RTKs) have been implicated in the induction of pathological phenotypes. These mutations are believed to stabilize the RTK dimers, and thus promote unregulated signaling. However, the energetics behind the pathology induction has not been determined. An example of a TM domain pathogenic mutation is the Ala391-->Glu mutation in fibroblast growth factor receptor 3 (FGFR3), linked to Crouzon syndrome with acanthosis nigricans, as well as to bladder cancer. Here, we determine the free energy of dimerization of wild-type and mutant FGFR3 TM domain in lipid bilayers using Förster resonance energy transfer, and we show that hydrogen bonding between Glu391 and the adjacent helix in the dimer is a feasible mechanism for dimer stabilization. The measured change in the free energy of dimerization due to the Ala391-->Glu pathogenic mutation is -1.3 kcal/mol, consistent with previous reports of hydrogen bond strengths in proteins. This is the first quantitative measurement of mutant RTK stabilization in a membrane environment. We show that this seemingly modest value can lead to a large increase in dimer fraction and thus profoundly affect RTK-mediated signal transduction.

Alanine↗

PubMed2005

Adiponectin levels in women with polycystic ovary syndrome and severe insulin resistance.

OBJECTIVE: Adiponectin is an adipokine that is decreased in obesity and type 2 diabetes. Women with polycystic ovarian syndrome (PCOS) are obese and are at risk for type 2 diabetes. The objective of the current study was to investigate the relationship of adiponectin to obesity and insulin resistance in women with PCOS and severe insulin resistance. METHODS: Thirty women with PCOS and acanthosis nigricans indicating severe insulin resistance were included in the study. Eleven body mass index (BMI)-matched women with normal ovulatory cycles served as controls. Fasting glucose, insulin, and adiponectin levels were measured, and a standard oral glucose tolerance test (OGTT) with insulin levels was performed. To further investigate the role of insulin sensitivity on adiponectin levels, 10 women with PCOS were treated with 4 mg rosiglitazone daily for 6 months and adiponectin levels were measured before and after treatment. RESULTS: Fasting insulin levels (33.5 +/- 3.8 microU/mL; P <.001) and insulin area under the curve (AUC) during OGTT (536.2 +/- 70.5 microU/mL; P <.01) were higher in women with PCOS, while glucose levels were similar to controls. Adiponectin levels were lower (P <.01) in women with PCOS (5.6 +/- 2.6 microg/mL) compared with controls (8.5 +/- 3.9 microg/mL). There was a significant negative correlation between adiponectin levels and fasting insulin levels (r = -0.40, P = .02), insulin AUC during OGTT (r = -0.47, P = .008), fasting glucose levels (r = -0.45, P = .01), and glucose AUC during OGTT (r = -0.51, P = .003). There was no correlation between BMI and serum adiponectin (r = -0.12, P = .508) in women with PCOS, while there was a negative correlation (r = -0.746, P = .013) in controls. There was a significant (P <.01) increase in adiponectin levels when treated with rosiglitazone, despite unchanged BMI. CONCLUSION: These results indicate that in women with PCOS and severe insulin resistance, insulin sensitivity appears to be the major determinant of adiponectin levels rather than adiposity. Low adiponectin levels may predict women with PCOS who are at high risk for developing type 2 diabetes.

Adiponectin↗

PubMedDate not supplied

Evidence for identifying children at risk for being overweight, cardiovascular disease, and type 2 diabetes in primary care.

INTRODUCTION: Practitioners have noted the escalating risk for children being overweight and having cardiovascular disease and type 2 diabetes. The purpose of this study was to apply current recommendations in examining children and to test an expanded model of assessment to predict risk. METHOD: A nonexperimental descriptive design was applied at an academic nurse-managed clinic. Children who consented to participate (n = 118) were examined for height/weight (and calculated body mass index), blood pressure, family history, smoking exposure, acanthosis nigricans, and point-of-care nonfasting blood analysis of glucose, hemoglobin A(1C), total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. Children with a body mass index greater than the 85th percentile were invited to return for fasting venipuncture, testing glucose, insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides (n = 23). RESULTS: High rates of being overweight and additional risk factors were identified. Point-of-care machines had limited usefulness beyond usual measurements in identifying childhood risk. DISCUSSION: Recommendations are made for nurses to take careful family histories and complete analysis of physical measurement to identify children needing further intervention to prevent and treat being overweight and disease risks.

Adolescent↗

PubMed2005

[Monogenic severe insulin resistance syndromes].

PURPOSE: To make a point about monogenic insulin resistance syndromes. CURRENT KNOWLEDGE AND KEY POINTS: Extreme insulin resistance syndromes are rare entities. The clinical and biological presentation is similar to that one of metabolic syndrome. Polycystic ovaries syndrome, non-alcoholic liver steatosis, acanthosis nigricans and overall, lipo-atrophic syndrome must be sought. Genetically determined forms are mainly linked to mutations of the insulin receptor gene and to lipoatrophic syndrome-linked mutations. The three syndromes related to mutations of the insulin receptor gene are Type A syndrome, first described by Kahn in young women, whereas leprechaunism and Rabson-Mendenhall syndromes are of neonatal onset. Main insulin resistance syndromes associated with lipo-atrophy are 1) Berardinelli-Seip or congenital generalized lipo-atrophic syndrome linked to mutations of seipin or AGPAT2 gene, 2) Dunnigan or partial familial lipoatrophic syndrome linked to mutations of lamin A/C, or sometimes PPAR gamma gene, and 3) acro-mandibular dysplasia and Köbberling syndrome. FUTURE PROSPECTS AND PROJECTS: In conclusion, an early onset of insulin resistance, especially in association with lipodystrophy must suggest a monogenic insulin resistance syndrome. Outstanding advances in insulin resistance pheno- and genotype identification, despite incomplete yet, offers a better understanding of insulin resistance, atherosclerosis and ageing mechanisms, that should lead to therapeutic improvement.

Diagnosis, Differential↗

PubMed2005

Papillon-Lefèvre syndrome with albinism: a review of the literature and report of 2 brothers.

BACKGROUND: Papillon-Lefèvre syndrome (PLS) is a very rare autosomal recessive disorder characterized by palmoplantar hyperkeratosis and severe early onset of destructive periodontitis leading to premature loss of both primary and permanent dentitions. The etiopathogenesis of the condition suggests that there is a genetic basis for susceptibility to specific virulent pathogens. Variation in the clinical presentation of PLS has recently been observed. OBJECTIVE: The objective was to present the first report, which describes the concurrence of PLS and albinism. The etiology, pathology, and management of the condition were reviewed and genetic analysis was performed. SUBJECTS AND CLINICAL PRESENTATION: The probands are Jordanian brothers aged 13 and 20 years on their initial presentation. The parents were second cousins and not affected. The patients exhibited the typical clinical features of PLS with type 1 oculocutaneous albinism (OCA1). They also had increased susceptibility to infection manifested in recurrent tonsillitis, respiratory tract infection, pyoderma, onychogryphosis, and other pathosis. Skin biopsy demonstrated hyperkeratosis, focal parakeratosis, hypergranulosis, and acanthosis. Ectopic calcification of the dura was noticed in one of the probands. Hematological parameters tested were within the normal limits. The probands were tested for mutations in the causative genes of PLS and OCA1, cathepsin C (CTSC), and tyrosinase, respectively. Independent mutations (c.318-1G>A and c.817G>C/p.W272C) were identified in CTSC and tyrosinase, respectively. The probands were homozygous and their sister who had only PLS was homozygous for the same (CTSC) mutation but heterozygous for tyrosinase gene. CONCLUSION: We hope that this report of coinheritance PLS and albinism will initiate further investigations to disclose other possible variations that may enhance our knowledge on gene mutations of this intriguing syndrome.

Adolescent↗

PubMed2006

White sponge nevus: report of a three-generation family.

OBJECTIVE: White sponge nevus (WSN) is a rare autosomal dominant disorder that results in soft, white, and spongy plaques in the oral mucosa. The aim of this study was to describe the clinical, histopathologic, and genetic features of a family, spanning 3 generations, affected by WSN. STUDY DESIGN: This study was performed using a cross-sectional layout analyzing a family with WSN. RESULTS: Clinical examination of family members revealed that of 23 descendants, 8 (34.78%) had WSN features. Unaffected and affected members transmitted the disease to their offspring. The offspring recurrence risk was 0.34, and an incomplete level of penetrance was observed. The lesions showed many clinical and histopathologic similarities to cases previously reported. The most affected sites were buccal and labial mucosa, with a rare appearance in the palate. No extraoral lesion was found. Histological examination showed intense acanthosis and hyperparakeratosis-induced epithelial hyperplasia. Within the spinous layer, cells showing perinuclear eosinophilic condensation of the cytokeratin (CK) filaments were frequent. CONCLUSION: The disease was transmitted by an autosomal dominant mode of inheritance, appearing mainly in the buccal and labial mucosa.

Cross-Sectional Studies↗

PubMed2006

Rare case of recurrent angiokeratoma of Fordyce on penile shaft.

Angiokeratomas are benign cutaneous vascular lesions characterized by dilated thin-walled blood vessels lying in the upper part of the dermis, mostly associated with an epidermal reaction such as acanthosis and/or hyperkeratosis. Angiokeratomas of Fordyce are predominantly located on the scrotum and are only rarely found on the penis and then usually on the glans penis. We report a rare case of angiokeratoma of Fordyce located on the shaft of the penis and associated with two recurrences after appropriate surgical excision.

Adult↗

PubMed2006

Seasonal allergic dermatitis in sheep in southern Brazil caused by Culicoides insignis (Diptera: Ceratopogonidae).

The incidence of seasonal dermatitis was studied in a Hampshire Down flock on a farm in southern Brazil. Epidemiological data, clinical signs and macroscopic pathology were obtained by visiting the farm. Histological lesions were studied in skin biopsies of affected sheep. Biting insects were collected from January to April 2005 in an attempt to identify the etiological agent of the disease. Disease prevalence was 40%; the age of the affected animals was variable. Disease occurred from December to March, some animals had lesions for the entire year. Clinical signs include pruritus on the ears, around the eyes and ventral abdomen. Initially erythema and small red papules were seen, followed by alopecia and crust formation. Histologically the lesions were characterized by perivascular eosinophilic dermatitis. Hyperkeratosis and acanthosis were observed in the chronic lesions. Both Anopheles albitarsis and Culicoides insignis were captured during the study. C. insignis bites caused pruritus in sheep. Both types of insects were caught when they approached the sheep baits approximately 30min after sunset. Results suggested that the disease occurred as a result of an immediate hypersensitivity reaction to C. insignis.

Animals↗

PubMed1995

Cutaneous paraneoplastic syndromes in solid tumors.

OBJECTIVE: To provide an overview of the clinical manifestations, pathophysiology, and oncologic implications of the cutaneous paraneoplastic syndromes that occur predominantly in patients with solid tumors. METHODS: A review was performed of the literature identified by a comprehensive MEDLINE search. RESULTS: Diverse cutaneous paraneoplastic syndromes may be associated with underlying tumors. They include musculoskeletal disorders (clubbing, hypertrophic osteoarthropathy, dermatomyositis, and multicentric reticulohistiocytosis), reactive erythemas (erythema gyratum repens and necrolytic migratory erythema), vascular dermatoses (Trousseau's syndrome), papulosquamous disorders (acanthosis nigricans, tripe palms, palmar hyperkeratosis, acquired ichthyosis, pityriasis rotunda, Bazex's syndrome, florid cutaneous papillomatosis, the sign of Leser-Trélat, and extramammary Paget's disease), and disorders of hair growth (hypertrichosis lanuginosa acquisita). The clinical manifestations of these dermatoses may precede, coincide with, or follow the diagnosis of cancer. The presence of a cutaneous paraneoplastic syndrome is often associated with a poor prognosis. CONCLUSIONS: Cutaneous paraneoplastic syndromes are specific constellations of mucous membrane and/or skin abnormalities that are caused by an underlying tumor. Since they may be the presenting sign of an occult cancer, cognizance of their features and clinical implications are of considerable importance. Individuals with these syndromes should have a thorough workup for an associated malignancy.

Female↗

PubMed1994

Syringocystadenoma papilliferum of the eyelid.

Syringocystadenoma papilliferum is a benign adnexal tumor of the scalp and face. We treated syringocystadenoma papilliferum in a 31-year-old man who had a circumscribed cup-shaped lesion of the left upper eyelid with a central crater. On histologic examination, the epidermal edge showed hyperkeratosis and invasive acanthosis with papillary projections that filled the central crater. The deeper portions of the projections resembled ductal structures lined by an inner columnar epithelium, which demonstrated luminal apical decapitation secretions, and an outer layer of smaller cuboidal cells. The fibrovascular dermal tissue exhibited prominent plasmacytic infiltration underlying the papillary epithelium. Although rare, syringocystadenoma papilliferum should be considered in the differential diagnosis of umbilicated squamous or basal cell tumors, especially if noted in a young individual.

Adenoma, Sweat Gland↗

PubMed1990

Subepidermal calcified nodules of the eyelid.

Two children had subepidermal calcified nodules of the upper eyelid. The first patient was a 13-year-old girl who noted painless increase in size of a lesion involving her right upper eyelid over four months. The clinical diagnosis was "warty papilloma." The second patient was a 13-year-old boy who had a slowly growing, keratinized lesion involving his left upper eyelid. The clinical diagnosis was "cutaneous horn." On histopathologic examination, the nodules demonstrated the characteristic changes associated with subepidermal calcified nodules, including the presence of calcified material in the uppermost dermis, occasional foreign body giant cells around the calcific masses, acanthosis of the overlying epithelium, and calcium granules in the epidermis.

Adolescent↗

PubMed1978

Conjunctival resection treatment and ultrastructural histopathology of superior limbic keratoconjunctivitis.

Four patients with symptomatic superior limbic keratoconjunctivitis underwent resection of the superior bulbar conjunctiva. One of these patients also underwent a tarsal conjunctival resection in the other eye. Three of the patients had previously been treated by various regimens without resolution; the fourth had had no prior treatment. All four patients had immediate and continued relief of the ocular symptoms after the superior bulbar conjunctiva was excised. The patient who underwent tarsal conjunctival resection experienced only short-term relief. We studied the conjunctival tissue by light and transmission electron microscopy. Both techniques revealed abnormalities related to the bulbar conjunctival surface with keratinization of the epithelium, acanthosis, degeneration of the nuclei, and intracellular accumulation of glycogen. Inflammatory cells were minimally present. The tarsal conjunctiva appeared essentially normal.

Adult↗