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At least 1,621 records · Page 90Linked to original sources
PubMed1999

Cutaneous lymphocyte-associated antigen expression in children with atopic dermatitis and non-atopic healthy children.

Cutaneous lymphocyte-associated antigen (CLA) is a cell surface glycoprotein which has been implicated in the homing of lymphocytes to cutaneous sites. It is postulated to play an important role in T-cell migration to skin in atopic dermatitis; however, the expression of CLA in both normal children and children with atopic dermatitis has not been extensively studied. If CLA expression on T cells were important in the traffic of lymphocytes to atopic dermatitis skin lesions, it might be expected that the proportion of CLA+ T cells in unstimulated peripheral blood from children with atopic dermatitis would be elevated. We have examined the proportion of CLA+ T cells in children with atopic dermatitis and non-atopic age-matched controls. The proportion of CLA+ T cells in non-atopic children was highly associated with and increased with increasing age (r = 0.88, p < 0.001). There was no difference between the proportion of T cells expressing CLA in the unstimulated peripheral blood mononuclear cells from children with severe (p = 0.18) or with mild/moderate (p = 0.3) atopic dermatitis and age-matched non-atopic controls. Despite this, children with atopic dermatitis did show evidence of perturbation of CLA expression, as unlike the non-atopic children the proportion of CLA+ T cells in the atopic children did not correlate with age. These findings suggest that while CLA expression may play a role in atopic dermatitis, other as yet undefined surface markers are likely to principally determine the migration of T cells to skin in atopic dermatitis.

Adult↗
PubMed2004

Using stable hydrogen and oxygen isotope measurements of feathers to infer geographical origins of migrating European birds.

Successful application of stable-hydrogen isotope measurements (deltaDf) of feathers to track origins of migratory birds and other wildlife requires a fundamental understanding of the correlation between deltaDf and deuterium patterns in rainfall (deltaDp) over continental scales. A strong correlation between deltaDp and deltaDf has been confirmed for birds and insects in North America, but not yet for other continents. Here, we compare deltaDf data from resident European birds to new deltaDp basemaps for Europe. Three maps, representing growing-season and mean annual deltaDp estimates from an elevation-explicit, detrended interpolation model and growing-season deltaDp estimates from simple Kriging, all indicate that strong isotope gradients occur across Europe with a general depletion occurring in a northeast direction. The feather data, representing 141 individuals of 25 avian species from 38 sites, ranged from -131 to -38 per thousand. Regression analysis showed that strong correlations existed between both mean annual and growing-season deltaDp estimated by detrended interpolation and deltaDf of non-aquatic and non-corvid birds (r2=0.66 and 0.65, respectively). We also examined mean annual and growing-season delta18Op vs. delta18Of for our samples. Both oxygen regressions were similar (r2=0.56 and 0.57, respectively) but poorer than for deuterium. Our study reveals that deltaD measurements of feathers from migratory birds in Europe may be used to track their origin and movements, and so provide a powerful investigative tool for avian migration research in Europe.

Animals↗
PubMed2005

Critical role of macrophage migration inhibitory factor activity in experimental autoimmune diabetes.

Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that plays a pivotal role in several immunoinflammatory and autoimmune diseases. In this study we examined the role of MIF in the development of immunoinflammatory diabetes induced in susceptible strains of mice by multiple low doses of streptozotocin. We found that MIF protein was significantly elevated in islet cells during the development of diabetes, and that targeting MIF activity with either neutralizing antibody or the pharmacological inhibitor (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester, markedly reduced clinical and histopathological features of the disease, such as hyperglycemia and insulitis. Lymphocytes from mice treated with the MIF inhibitors exhibited reduction of both islet antigen-specific proliferative responses and adhesive cell-cell interactions. Neutralization of MIF also down-regulated the ex vivo secretion of the proinflammatory mediators, TNF-alpha, interferon-gamma, and nitric oxide, while augmenting that of the antiinflammatory cytokine, IL-10. This study provides the first in vivo evidence for a critical role for MIF in the immune-mediated beta-cell destruction in an animal model of human type 1 diabetes mellitus and identifies a new therapeutic strategy for the prevention and treatment of this disease in humans that is based on the selective inhibition of MIF activity.

Animals↗
PubMed1999

Endothelial expression of VCAM-1 in experimental crescentic nephritis and effect of antibodies to very late antigen-4 or VCAM-1 on glomerular injury.

The migration of leukocytes into glomeruli in crescentic glomerulonephritis is fundamental to pathogenesis, and offers important therapeutic opportunities. We addressed the importance of VCAM-1, and its leukocyte ligand very late antigen-4 (VLA-4), in such leukocyte migration. In a rat model of nephrotoxic nephritis, glomerular expression of VCAM-1, studied by immunohistochemistry, was up-regulated by day 6 of nephritis. To quantify kidney endothelial VCAM-1 expression, a differential radiolabeled mAb technique was used, which demonstrated that protein expression was not up-regulated by day 2 of nephritis, but rose threefold between days 2 and 5, and remained elevated until at least day 28. An in vivo study was then performed, using blocking mAbs to either VCAM-1 or VLA-4, starting mAb treatment on the day prior to disease induction, and continuing until animals were sacrificed at day 7. mAbs to VLA-4 significantly attenuated renal injury (albuminuria, glomerular fibrinoid necrosis, and crescent formation), but mAbs to VCAM-1 had no significant effect. Surprisingly, the number of leukocytes within glomeruli was unaffected by anti-VLA-4 mAb therapy, despite the reduction in renal injury. Paradoxically, classical markers of macrophage activation were increased in the anti-VLA-4- and anti-VCAM-1-treated animals. This study demonstrates that kidney endothelial VCAM-1, in contrast to ICAM-1, is not up-regulated by day 2 of nephrotoxic nephritis, and plays little part in early leukocyte influx into glomeruli. However, VLA-4 is an important mediator of glomerular injury, operating after transendothelial leukocyte migration, and presumably binding to alternate ligands within the kidney.

Albuminuria↗
PubMed2005

A role for TLRs in the regulation of immune cell migration by first trimester trophoblast cells.

Normal pregnancy is characterized by the presence of innate immune cells at the maternal-fetal interface. Originally, it was postulated that the presence of these leukocytes was due to an immune response toward paternal Ags expressed by the invading trophoblasts. Instead, we and others postulate that these innate immune cells are necessary for successful implantation and pregnancy. However, elevated leukocyte infiltration may be an underlying cause of pregnancy complications, such as preterm labor or preeclampsia. Furthermore, such conditions have been attributed to an intrauterine infection. Therefore, we hypothesize that first trimester trophoblast cells, upon recognition of microbes through TLRs, may coordinate an immune response by recruiting cells of the innate immune system to the maternal-fetal interface. In this study, we have demonstrated that human first trimester trophoblast cells constitutively secrete the chemokines growth-related oncogene, growth-related oncogene alpha, IL-8, and MCP-1 and are able to recruit monocytes and NK cells, and to a lesser degree, neutrophils. Following the ligation of TLR-3 by the viral ligand, poly(I:C), or TLR-4 by bacterial LPS, trophoblast secretion of chemokines is significantly increased and this in turn results in elevated monocyte and neutrophil chemotaxis. In addition, TLR-3 stimulation also induces trophoblast cells to secrete RANTES. These results suggest a novel mechanism by which first trimester trophoblast cells may differentially modulate the maternal immune system during normal pregnancy and in the presence of an intrauterine infection. Such altered trophoblast cell responses might contribute to the pathogenesis of certain pregnancy complications.

Chemokines↗
PubMed1994

Reversible binding of tolmetin, zomepirac, and their glucuronide conjugates to human serum albumin and plasma.

Acyl glucuronides of drugs and bilirubin have been shown in the past decade to be reactive metabolites undergoing acyl migration and irreversible binding. The latter reaction has been hypothesized to be facilitated by or to proceed through the formation of a reversible complex. Furthermore, it has been suggested that the decreased binding seen in patients with compromised excretory function may be due to competition by elevated plasma concentrations of the glucuronides. In these reversible binding studies, we characterized the extent and the "site" of binding of tolmetin, zomepirac, their glucuronides and isomeric conjugates. We also examined the displacement between the parent drugs and their glucuronide conjugates using a rapid ultrafiltration method. Tolmetin exhibited three classes of binding sites with a primary association constant of 1.7 x 10(6) M-1 (Kd1 = 0.60 microM). The primary association constant of zomepirac (1.16 x 10(6) M-1, Kd1 = 0.86 microM) is similar to that of tolmetin. The beta 1 and alpha/beta 3 glucuronides of both compounds bind to a lesser extent than their parent aglycones. The isomeric glucuronide conjugates of both compounds showed much stronger binding than the beta/1 conjugates. Of the four glucuronides investigated, tolmetin glucuronide-alpha/beta 3 isomer was bound by fatty acid free human serum albumin with the highest affinity (4.6 x 10(5) M-1, Kd = 2.22 microM). Protein binding of the parent drugs and conjugates were decreased significantly at pH 5.0. In displacement studies, except for salicylate and acetylsalicylate, drugs known to bind to Sites I and II as well as the digitoxin and tamoxifen binding sites had little inhibitory effect on the binding of tolmetin, zomepirac, and their glucuronide conjugates.

Adult↗
PubMed1979

Effects of thyroxine on postnatal cell acquisition in the rat brain.

The effects of treatment with L-thyroxine (3 micrograms by subcutaneous injection daily from birth) on cell acquisition in the rat brain were studied during the first 3 postnatal weeks. In the forebrain, thyroxine has no effect on cell proliferation in the first 6 days, but it causes decreased cell acquisition from 12 to 21 days so that cell number becomes significantly reduced. Estimates of cell proliferation kinetics and of cell death in the lateral ventricular subependymal layer show no apparent abnormality. In the cerebellum, treatment from birth leads to increased cell proliferation during the first week: in comparison with controls, the rate of [3H]thymidine incorporation into DNA, thymidine kinase activity, and the number of cells both in the major germinal site (external granular layer: EGL) and in the whole cerebellum are elevated. This initial effect of thyroxine appears by day 3 and is short-lived, being no longer evident after day 6. The build-up of cell numbers in the EGL at day 6 seems to be related to a preceding, transient retardation of cell migration from this layer rather than to an acceleration of cell replication, since cell cycle parameters are normal. From day 12 the rate of [3H]thymidine incorporation into DNA is severely reduced in treated rats. Advancement of cellular differentiation rather than increased cell death in the EGL appears to be involved in this phenomenon.

Aging↗
PubMed1983

Cigarette smoking stimulates lipoxygenase but not cyclooxygenase pathway in platelets.

Male rats were exposed to freshly generated cigarette smoke once daily for 4 to 8 weeks. Inhalation of smoke was verified by elevated level of carboxyhemoglobin. Arachidonate metabolism through lipoxygenase and cyclooxygenase pathways in platelets was determined. Cigarette smoking increased 12-lipoxygenase activity significantly without affecting the cyclooxygenase pathway. In view of platelet-leukocyte interactions and potent chemotactic activity of 12-HETE for aortic smooth muscle cell migration, increased 12-lipoxygenase activity may predispose individuals to atherosclerosis, thromboembolism and emphysema commonly found in smokers.

Animals↗
PubMed2004

A new method to account for the depth distribution of 137Cs in soils in the calculation of external radiation dose-rate.

This work reports a new method for calculating the external dose-rate as a function of height above land that has been contaminated with a surface deposition of (137)Cs. Unlike previous work this method accounts for vertical migration of (137)Cs using the Advection Dispersion Equation (ADE) with appropriate parameters. The results have been successfully verified with field measurements from the (137)Cs contaminated regions within the Republic of Belarus. The method also correctly predicts the observed variation of dose-rate with elevation above the soil surface and it is shown how this method can be used to predict the reduction in surface dose-rate after remediation measures such as deep ploughing have taken place.

Cesium Radioisotopes↗
PubMed2003

Cell proliferation in response to GABA in postnatal hippocampal slice culture.

Recent studies have implicated the inhibitory neurotransmitter GABA in the regulation of cell migration and proliferation in the embryonic brain. Herein, we examine the possibility that these effects are maintained postnatally. Using 5 days postnatal hippocampus, we tested GABA effects on growth into an incision made in CA1 and the possibility that this response to GABA is mediated via GABA(A)-receptor. Our data shows that GABA promotes neurite growth, cell proliferation and migration up to day 6 in vitro. GABA(A)-receptor is not involved in the trophic response to either exogenous or endogenous GABA. Moreover, GABA induced a 20% increase in NGF secretion to the growth medium, in a similar time frame to its effect on growth. Elevated NGF secretion was suppressed by the inhibition of cell proliferation. These results suggest that GABA can promote growth in postnatal hippocampal tissue. The effect involves cell proliferation and NGF secretion and does not depend on GABA(A)-receptor activation.

Aging↗
PubMed2007

Rearrangement of 1,3-dipolar cycloadducts derived from bis(phenylazo)stilbene: a DFT level mechanistic investigation.

The 1,3-dipolar cycloaddition of bis(phenylazo)stilbene with activated ethene and ethyne derivatives and the subsequent rearrangement of the cycloadducts have been studied using model compounds at the B3LYP/6-31G(d) level of density functional theory (DFT). From the structural and electronic features, a five-membered zwitterionic ring system 9 (1,2,3-triazolium-1-imide system) formed from bis(phenylazo)ethylene is confirmed as the active 1,3-dipole species in the reaction. Formation of the 1,3-dipolar cycloadduct from the alkyne derivative is found to be 26.0 kcal/mol exergonic, and it requires an activation free energy of 19.4 kcal/mol. The 1,3-cycloadduct formed in the reaction undergoes a very facile migration of a nitrogen-bearing fragment, passing through a zwitterionic transition state. A small activation free energy of 8.2 kcal/mol is observed for this step of the reaction, and it is 19.6 kcal/mol exergonic. Further activation of the newly formed rearranged product is possible under elevated temperatures, again passing through a zwitterionic transition state and resulting in the formation of 2,5-dihydro-1,2,3-triazine derivatives. Such derivatives have been recently reported by Butler et al. (J. Org. Chem. 2006, 71, 5679). The charge separation in 9 and the zwitterionic transition states are stabilized through the pi-system of the phenyl rings and the carbonyl groups. Similar structural, electronic, and mechanistic features are obtained for the reaction of 9 with the ethylenic dipolarophile acrylonitrile. Molecular electrostatic potential analyses of the 1,3-dipole and the zwitterionic transitions states are found to be very useful for characterizing their electron delocalization features. The solvation effects can enhance the feasibility of these reactions as they stabilize the zwitterionic transition states to a great extent.

Cyclization↗
PubMed1999

Angiotensin converting enzyme inhibitors and vascular protection in hypertension.

Strategically located between the circulating blood and the vascular smooth muscle, endothelial cells release numerous vasoactive substances regulating the function of vascular smooth muscle and circulating blood cells. Endothelium-derived vasodilators include prostacyclin, nitric oxide and endothelium-derived hyperpolarizing factor. In particular, nitric oxide inhibits cellular growth and migration. In concert with prostacyclin, nitric oxide exerts potent antiatherogenic and thromboresistant properties by preventing platelet aggregation and cell adhesion. These effects are counterbalanced by vasoconstrictors, such as angiotensin II and endothelin (ET)-1, both of which exert prothrombotic and growth-promoting properties. In hypertension, elevated blood pressure causes vascular disease by inducing endothelial dysfunction. Hence, modern therapeutic strategies in human hypertension focus on preserving or restoring endothelial integrity. Beyond inhibiting the renin-angiotensin system, angiotensin-converting enzyme (ACE) inhibitors diminish the inactivation of bradykinin, thus leading to an augmentation of nitric oxide release. In addition, the compounds stabilize the B2-receptor, and reduce oxidative stress and tissue ET-1 levels. In patients with coronary artery disease, chronic ACE inhibition improves endothelial function. Further clinical studies are already under way which will prove whether these beneficial vascular effects of ACE inhibitors on endothelial dysfunction result in a clinical benefit for patients with hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Band 3 modulation and hypotonic-stimulated taurine efflux in skate erythrocytes.

Previous studies have shown that exposure of skate erythrocytes to hypotonic medium or isosmotic medium with permeant solutes such as ethylene glycol or ammonium chloride increases cell volume. Initial swelling is followed by a regulatory volume decrease accomplished by efflux of cell solutes, including the beta-amino acid taurine. Taurine efflux, as well as the cell volume recovery, is inhibited by stilbene disulfonates and other anion exchange inhibitors, suggesting involvement of the erythrocyte anion exchanger band 3. In the present study we show that binding of the stilbene dihydro 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (H2DIDS) to intact cells doubles after exposure to one-half hypotonic medium. Binding also increases after exposure of erythrocytes to medium of one-third hypotonic medium and ethylene glycol medium, but DIDS binding is not significantly elevated in ammonium chloride medium. To investigate possible mechanisms for modulation of band 3, cells were labeled with 32PO4 and levels of protein phosphorylation determined. Phosphorylation of three proteins of molecular masses of 99, 65, and 32 kDa increases with hypotonic stress. Because the anion exchanger migrates with molecular mass near 100 kDa, the anion exchanger was immunoprecipitated. Hypotonic stress induces a rapid and persistent increase in the 32PO4 phosphorylation of the exchanger. This modification may be responsible for the increased DIDS binding and could be related to stimulated taurine efflux.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Functional expression of HGF and its receptor in human colorectal cancer.

BACKGROUND: Hepatocyte growth factor (HGF) stimulates proliferation, migration and morphogenesis of epithelial cells by specific binding to its receptor c-met. Overexpression of HGF or c-met has been reported for human gastric or pancreatic cancer. In colorectal cancer overexpression of c-met but not HGF has been shown. However, elevated HGF serum levels have been detected in colorectal cancer patients. Therefore, the present study was performed to investigate expression patterns of both c-met and HGF in colorectal cancers and metastasis in comparison to normal mucosa. Furthermore, the mitogenic actions of HGF on colorectal cancer cells were studied in vitro. METHODS: Expression of c-met and HGF were analyzed by RT-PCR and Western blotting and localized in the tissues utilizing immunohistochemistry. Mitogenic effects of HGF were determined in four human colon cancer cell lines by (3)H-thymidine incorporation studies. RESULTS: C-met and HGF mRNA were detectable in 60% of the normal specimen, but in the majority of cancer samples, and in just 33% of the liver metastasis. In cancer samples a coexpression of c-met and HGF was detected in 77% of the specimens. The extent of protein expression of receptor and ligand correlated with the mRNA expression. Moreover, c-met protein expression was increased 2- to 3-fold in colorectal cancers. C-met was detected in cells of epithelial origin, whereas HGF was expressed by mesenchymal cells. In vitro, HGF significantly stimulated cell growth in all four cell lines. CONCLUSION: Overexpression of c-met protein in colorectal cancers is combined with an expression of HGF in the majority of cases suggesting a paracrine manner of growth enhancement, while only a weak expression of c-met or HGF was detected in metastatic tissues.

Adenocarcinoma↗
PubMed2002

An essential role for connexin43 gap junctions in mouse coronary artery development.

Connexin43 knockout mice die neonatally from conotruncal heart malformation and outflow obstruction. Previous studies have indicated the involvement of neural crest perturbations in these cardiac anomalies. We provide evidence for the involvement of another extracardiac cell population, the proepicardial cells. These cells give rise to the vascular smooth muscle cells of the coronary arteries and cardiac fibroblasts in the heart. We have observed the abnormal presence of fibroblast and vascular smooth muscle cells in the infundibular pouches of the connexin43 knockout mouse heart. In addition, the connexin43 knockout mice exhibit a variety of coronary artery patterning defects previously described for neural crest-ablated chick embryos, such as anomalous origin of the coronary arteries, absent left or right coronary artery, and accessory coronary arteries. However, we show that proepicardial cells also express connexin43 gap junctions abundantly. The proepicardial cells are functionally well coupled, and this coupling is significantly reduced with the loss of connexin43 function. Further analysis revealed an elevation in the speed of cell locomotion and cell proliferation rate in the connexin43-deficient proepicardial cells. A parallel analysis of proepicardial cells in transgenic mice with dominant negative inhibition of connexin43 targeted only to neural crest cells showed none of these coupling, proliferation or migration changes. These mice exhibit outflow obstruction, but no infundibular pouches. Together these findings indicate an important role for connexin43 in coronary artery patterning, a role that probably involves the proepicardial and cardiac neural crest cells. We discuss the potential involvement of connexin43 in human cardiovascular anomalies involving the coronary arteries.

Animals↗
PubMed2004

Upregulation of osteopontin by osteocytes deprived of mechanical loading or oxygen.

UNLABELLED: The pathway(s) by which disuse is transduced into locally mediated osteoclastic resorption remain unknown. We found that both acute disuse (in vivo) and direct hypoxia (in vitro) induced rapid upregulation of OPN expression by osteocytes. Within the context of OPN's role in osteoclast migration and attachment, hypoxia-induced osteocyte OPN expression may serve to mediate disuse-induced bone resorption. INTRODUCTION: We have recently reported that disuse induces osteocyte hypoxia. Because hypoxia upregulates osteopontin (OPN) in nonconnective tissue cells, we hypothesized that both disuse and hypoxia would rapidly elevate expression of OPN by osteocytes. MATERIALS AND METHODS: The response of osteocytes to 24 h of disuse was explored by isolating the left ulna diaphysis of adult male turkeys from loading (n = 5). Cortical osteocytes staining positive for OPN were determined using immunohistochemistry and confocal microscopy. In vitro experiments were performed to determine if OPN expression was altered in MLO-Y4 osteocytes by direct hypoxia (3, 6, 24, and 48 h) or hypoxia (3 and 24 h) followed by 24 h of reoxygenation. A final in vitro experiment explored the potential of protein kinase C (PKC) to regulate hypoxia-induced osteocyte OPN mRNA alterations. RESULTS: We found that 24 h of disuse significantly elevated osteocyte OPN expression in vivo (145% versus intact bones; p = 0.02). We confirmed this finding in vitro, by observing rapid and significant upregulation of OPN protein expression after 24 and 48 h of hypoxia. Whereas 24 h of reoxygenation after 3 h of hypoxia restored normal osteocyte OPN expression levels, 24 h of reoxygenation after 24 h of hypoxia did not mitigate elevated osteocyte OPN expression. Finally, preliminary inhibitor studies suggested that PKC serves as a potent upstream regulator of hypoxia-induced osteocyte OPN expression. CONCLUSIONS: Given the documented roles of OPN as a mediator of environmental stress (e.g., hypoxia), an osteoclast chemotaxant, and a modulator of osteoclastic attachment to bone, we speculate that hypoxia-induced osteocyte OPN expression may serve to mediate disuse-induced osteoclastic resorption. Furthermore, it seems that a brief window of time exists in which reoxygenation (as might be achieved by reloading bone) can serve to inhibit this pathway.

Animals↗
PubMed1998

Cytoskeletal actin reorganization in neutrophils from patients with localized juvenile periodontitis.

Localized juvenile periodontitis (LJP) is an early-onset periodontal disease associated with a polymorphonuclear neutrophil (PMN) defective migratory response. Kinetics of actin polymerization-depolymerization determine the shape changes occurring in the plasma membrane-associated cytoskeleton and provide the driving force for directed cell migration (chemotaxis). Therefore, we investigated the relation between an abnormality in LJP PMN chemotaxis and an altered reorganization of the actin filament network. PMNs isolated from peripheral blood of LJP patients (n=14) and matching control subjects (n=12) were evaluated for random and directed migration in a Boyden chamber assay, and the kinetics of actin polymerization were studied by flow cytometry. Three groups of LJP patients could be distinguished on the basis of their PMN-chemotactic response compared to their matched control: depressed (n=6), normal (n=4), and elevated (n=4). The abnormal (depressed or elevated) chemotaxis was generally not related to abnormal random migratory response, except for two patients. Since the kinetics of formyl-methionyl-leucyl-phenylalanine-induced F-actin response were highly variable from one subject to another, means were calculated at each timepoint with the values obtained from each group of subjects and compared by a general factorial design analysis. No statistically significant differences were detected between the control group and the LJP patient group. Furthermore, the data did not show a correlation between the kinetics of actin polymerization-depolymerization and the abnormal chemotactic response observed in LJP PMNs. Hence, the chemotaxis defect in LJP PMN appears to be mediated by signaling events that carry their effect independently of an intact cytoskeleton.

Actin Cytoskeleton↗
PubMedDate not supplied

Diagnostic challenge of glucagonoma: case report and literature review.

OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma. METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma. RESULTS: A 54-year-old-man, with no relevant history of endocrine disorders, presented to the hospital with a 5-year history of recurrent stomatitis and glossitis, a more recent weight loss of 11.5 kg, and recurrent pruritic maculae on the scalp in conjunction with raised erythematous maculae in the scrotal region and perineum that gradually migrated to the distal extremities, becoming bullous and painful. The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected. His blood glucose levels were in the normal range. Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures. Liver metastatic lesions were also excluded. After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously. The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma. Subsequently, all related symptoms resolved, and the glucagon levels normalized. CONCLUSION: The diagnosis of glucagonoma is often delayed. Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.

Erythema↗