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Hyperkeratosis
Kinds of Hyperkeratosis Selected AbstractsEuropean Standard Series patch test results from a contact dermatitis clinic in Israel during the 7-year period from 1998 to 2004CONTACT DERMATITIS, Issue 2 2006Aneta Lazarov The results of a 7-year retrospective study (1998,2004) from patch testing with the European Standard Series (ESS) establishing the frequency of sensitization in a contact dermatitis clinic in Israel are presented. 23 allergens were patch tested on 2156 patients, 1462 females (67.8%) and 694 males (32.2%). Atopy and asthma were present in 21.9% of the patients. One or more allergic reactions were observed in 937 patients (43.5%). The highest yield of patch test positives from the 1076 positive reactions were obtained from nickel sulfate (13.9%), fragrance mix (7.1%), potassium dichromate (3.8%), Balsam of Peru (3.6%), CL + Me-isothiazolinone (3.4%) and cobalt chloride (3.4%). Allergens which produced the least amount of positive results were primin and clioquinol. Allergic contact dermatitis (ACD) was established in 32.8%, whereas occupationally related allergic (8.0) and irritant contact dermatitis (5.6%) affected a total of 13.6% of the cases studied. The most common clinical forms of dermatitis were chronic dermatitis (47.7%) followed by acute dermatitis (22.8%), and lichenification and hyperkeratosis (7.9%). The hands (30.7%), face and neck (23.9%) and extremities (11.3%) were the most frequently affected areas. Four allergens in our study differed from the top 10 allergens in Europe namely: Cl + Me-isothiazolinone, formaldehyde, 4-tert-butylphenol formaldehyde resin and sesquiterpene lactone mix reflecting an existing difference in environmental exposure. Our study is the first to provide data on the frequency of sensitization and important allergens in the aetiology of ACD in Israel. In spite of the existing differences with Europe, we conclude that ESS is an appropriate screening system for the diagnosis of ACD in Israel. [source] P43 Acute urticaria to infliximabCONTACT DERMATITIS, Issue 3 2004Ana Giménez-Arnau Infliximab is a chimeric antitumor necrosis factor-alpha monoclonal antibody used to treat Crohn's disease and rheumatoid arthritis. Acute infusion reactions, headache, fever, chills, urticaria and chest pain were seen in 17% of patients with infliximab compared with 7% of those receiving placebo. Other adverse cutaneous reactions are fungal dermatitis, eczema, seborrhoea, hordeolum, bullous eruption, furunculosis, periorbital oedema, hyperkeratosis, rosacea, verruca, skin pigmentation, alopecia, leukocytoclastic vasculitis, lichenoid drug eruption, erythema multiforme, perniosis-like eruption, granuloma annulare and acute folliculitis. Any pathogenic mechanism has been suggested. Patch test with infliximab can induce flare-up of lesions, nausea and malaise and suggest a percutaneous absortion. A sixty years-old man with atopy background and rheumatoid arthritis treated with Remicare®, infliximab who developed a severe acute urticaria with angioedema is presented. The lesions appearance after previous endovenous administrations and the worsening spreading wheals days after the injection clinically suggested an hypersensitivity mechanism. The protocolized study drug hypersensitivity performed showed only the Prick Test positivity with infliximab at 30/60 minutes. Patch test with infliximab was negative and any adverse event was reported. Actually the patient is treated with etanercept and this drug is well tolerated. This result suggested a type I hypersensitivity mediated reaction. Urticaria could be induced as immunologic reaction of the host against the murine part of infliximab, just as it hapens with other antichimeric antibodies. [source] P58 Multisensitization to plants: clinical caseCONTACT DERMATITIS, Issue 3 2004António Luís Santos We observed a 65 years old male patient with pruritus, scaling erythema and liquenification areas on the face, neck, forearms and hands. For six years he had a story of episodic crisis of exsudative erythema associated with farm work. The skin biopsy showed irregular acantosis with slight hyperkeratosis and a mild multifocal lymphohistiocytic infiltrate, with many eosinophils. The patch tests with the Contact Dermatitis Portuguese Group of Study standard tray were positive for colophony, perfume mix and lactone mix. The patch tests with plant series were positive to atranorin, usnic acid, alantolactone, Parthenolide, lichen mix, Frulania dilatata, Achillea millefolium and Tanacetum extracts. Treatment was started with oral prednisone and hydroxyzine plus topical hydrocortisone and emollient cream with great improvement. The patient was advised about the avoidance of possible allergens sources. This kind of multisensitization to plants is an uncommon finding and poses diagnostic and therapeutic problems. This patient had a sustained recovery by avoiding farm work and by removal of in house plants. [source] Does Imiquimod Histologically Rejuvenate Ultraviolet Radiation,Damaged Skin?DERMATOLOGIC SURGERY, Issue 12 2007KATHLEEN SMITH MD BACKGROUND Imiquimod (IMI) 5% is believed by some to result in an improved cosmetic appearance of chronically ultraviolet radiation (UV)-damaged skin. OBJECTIVE The objective was to determine what histologic and immunohistologic changes were present in actinically damaged skin after treatment with IMI. METHODS AND MATERIALS Pre- and posttherapy biopsies of 12 patients with histories of actinic keratoses were evaluated with routine histology and immunohistochemical stains including p53, p63, proliferating cell nuclear antigen (PCNA), c-kit, and Factor XIIIa. RESULTS After IMI therapy there was less compact hyperkeratosis, a more uniform rete ridge pattern with a more ordered proliferation of the epidermis, and a decrease in sun-damaged melanocytes. The papillary dermis showed a more uniform cellularity, and there was increased cellularity within the area of solar elastosis. After therapy, staining for p53, p63, and PCNA was decreased within the epidermis; staining for c-kit was decreased but more uniform in the basal cell; and Factor XIIIa expression was increased within the papillary dermis with a more ordered pattern of staining. CONCLUSION These morphologic and immunohistochemical patterns may explain some of the improvement in overall skin appearance after IMI therapy and may be related to the spectrum of signaling pathways induced by the imidazoquinolines. [source] Treatment of Nevoid Hyperkeratosis of the Nipple and Areola Using a Radiofrequency Surgical UnitDERMATOLOGIC SURGERY, Issue 6 2005Irfan Özyazgan MD Background. Nevoid hyperkeratosis of the nipple and areola (NHNA) is a rare condition of unknown etiology. Verrucous thickening and pigmentation of the nipple and areola are the main features of the condition. Different therapeutic options, both medical and surgical, have been described. Objective. To use a radiofrequency surgical unit to treat an NHNA case, which was unresponsive to keratolytic therapy. Materials and Methods. The lesions of the nipple and areolas were excised tangentially with a diamond-shaped electrode of a radiofrequency surgical unit under local anesthesia. Results. The patient had a good cosmetic appearance after the treatment, and there was no recurrence at the ninth postoperative month. Conclusion. Radiofrequency for tangential excision in the treatment of NHNA lesions that have not responded to medical therapy can be an alternative surgical method. [source] THERAPEUTIC HOTLINE: Alefacept in the treatment of hyperkeratotic palmoplantar psoriasisDERMATOLOGIC THERAPY, Issue 5 2010Sagi Lior ABSTRACT Plaque-type palmoplantar psoriasis (PPP) is associated with marked morbidity and frequently resistant to conventional therapies. Patients with long-standing plaque-type PPP failing previous treatments were included and treated with a 12-week intramuscular alefacept. The biweekly evaluation included hyperkeratosis, itching, and pain grading. In all of the seven treated patients significant to complete improvement in hyperkeratosis, pruritus and pain were observed, along with dose reduction or complete discontinuation of additional systemic treatments and without any recorded side effects. Alefacept should be considered as a therapeutic option for plaque-type PPP. [source] Clinical pathologic correlations for diagnosis and treatment of nail disordersDERMATOLOGIC THERAPY, Issue 1 2007Olympia I. Kovich ABSTRACT:, Clinicopathologic correlation is crucial to the correct diagnosis of disorders of the nail unit. This chapter will explore four common clinical scenarios and how pathology can help differentiate between their various etiologies. These include: dark spot on the nail plate (melanin versus heme), subungual hyperkeratosis (onychomycosis versus psoriasis), longitudinal melanonychia (benign versus malignant), and verrucous papule (verruca versus squamous cell carcinoma). Consideration must be given to both when to perform a biopsy and the location of the biopsy site, which must be based on an understanding of the origin of the changes. An overarching principle is that lesions within the same differential diagnosis may be present concomitantly, such as malignant melanoma of the nail unit associated with hemorrhage. Therefore, even with a biopsy-proven diagnosis, the clinician must always monitor lesions of the nail unit for appropriate response to treatment and consider an additional biopsy for recalcitrant lesions. [source] New developments in our understanding of acne pathogenesis and treatmentEXPERIMENTAL DERMATOLOGY, Issue 10 2009Ichiro Kurokawa Abstract:, Interest in sebaceous gland physiology and its diseases is rapidly increasing. We provide a summarized update of the current knowledge of the pathobiology of acne vulgaris and new treatment concepts that have emerged in the last 3 years (2005,2008). We have tried to answer questions arising from the exploration of sebaceous gland biology, hormonal factors, hyperkeratinization, role of bacteria, sebum, nutrition, cytokines and toll-like receptors (TLRs). Sebaceous glands play an important role as active participants in the innate immunity of the skin. They produce neuropeptides, excrete antimicrobial peptides and exhibit characteristics of stem cells. Androgens affect sebocytes and infundibular keratinocytes in a complex manner influencing cellular differentiation, proliferation, lipogenesis and comedogenesis. Retention hyperkeratosis in closed comedones and inflammatory papules is attributable to a disorder of terminal keratinocyte differentiation. Propionibacterium acnes, by acting on TLR-2, may stimulate the secretion of cytokines, such as interleukin (IL)-6 and IL-8 by follicular keratinocytes and IL-8 and -12 in macrophages, giving rise to inflammation. Certain P. acnes species may induce an immunological reaction by stimulating the production of sebocyte and keratinocyte antimicrobial peptides, which play an important role in the innate immunity of the follicle. Qualitative changes of sebum lipids induce alteration of keratinocyte differentiation and induce IL-1 secretion, contributing to the development of follicular hyperkeratosis. High glycemic load food and milk may induce increased tissue levels of 5,-dihydrotestosterone. These new aspects of acne pathogenesis lead to the considerations of possible customized therapeutic regimens. Current research is expected to lead to innovative treatments in the near future. [source] Surgical treatment options for hidradenitis suppurativa and critical review of own experienceEXPERIMENTAL DERMATOLOGY, Issue 6 2006Wolfgang Christian Marsch HS (acne inversa) is a chronic, progressive, initially inflammatory, ultimately a fistulating and scarring disease affecting apocrine gland-bearing skin areas. Late phases afford a broad surgical removal of affected skin areas including subcutaneous fatty tissue, with secondary mesh grafting after a period of granulation tissue formation. Fifty-three patients have been treated surgically at our Dermatology Department. Long-term results are excellent concerning satisfaction of the patients and functional objectives. Local recurrences or development of new lesions in formerly unaffected areas were noticed only in some patients who did not stop smoking. Patient details were as follows: gender distribution: male (M) 20 (38%), female (F) 33 (62%), age: M 19,62 (average 40.7), F 15,56 (average 35.4), onset: M 16,57 (32.2), F 8,50 (25.5), duration: 3 months to 37 years (8.0), F 6 months to 37 years (9.9). Sites mainly affected: axillary and perigenital. Specific regions for men: perineum and rima ani, for women: inguinal, submammary and abdominal. Multiple anatomical regions involved: men 40%, women 91%. Familiarity 0.4%. Associated acne papulo-pustulosa or nodulo-cystica (=conglobata): 19%. Cigarette smokers: men 100%, women 67%. Excised material from each operation was carefully examined histologically. The results endorse the concept of ,acne inversa' by recognizing a perifollicular accumulation of lymphocytes simultaneously at different infrainfundibula of terminal hair follicles. However, a follicular hyperkeratosis seems secondary to this, follicular perforation, and a combination of sinus, abscess and scar formation are most obviously tertiary events. Therefore, HS seems to be an inflammatory, probably an immunological disease with an initially strictly dermal target, even followed by an intradermal horizontal propagation. Laser flux imaging could visualize the subclinical peripheral extension of the basically dermal perifollicular inflammation. Biologics may have a beneficial effect on these early or perpetuating inflammatory events; however, thus far surgery remains the first-line therapy in late phases of the disease. [source] Surgical treatment of acne inversa (hidradenitis suppurativa): a 20-year experienceEXPERIMENTAL DERMATOLOGY, Issue 6 2006Wolfgang Hartschuh Acne inversa (AI) is caused by follicular hyperkeratosis in intertriginous areas rich in apocrine glands followed by occlusion and rupture of the follicle and inflammation. Sinus tracts, scarring and often contraction with limitation in mobility may occur. There is a world-wide consensus that in chronic disease surgical removal of all involved tissue as early as possible is the most effective treatment modality. The aim of this study is to demonstrate our operative strategy, including postoperative wound care and prevention, the results and pitfalls in the treatment of AI. The operations are increasingly performed in tumescence anaesthesia, followed by secondary healing. Only removal of extended skin areas in the inguino-genital and ano-perineal regions demand general anaesthesia. In axillary regions, all hair-bearing skin including the sweat glands is removed to obtain a hair-free, dry skin area. In the other regions with ill-defined hair and apocrine gland areas, only involved indurated skin is excised. For early limited disease with fluctuant abscesses, unroofing instead of mere incision and drainage is a good first option. Professional wound care with shaving and stretching of the wound margins is very important to avoid premature wound closure. Locally applied disinfectant soaps and 2% triclosane ointments are effective in pre- and postoperative skin care. Follow-up evaluation and collaboration among surgeons and dermatologists and an improved insight in the pathogenesis of AI are mandatory for the successful long-term management of patients afflicted with this complex and debilitating disease. [source] De novo mutations in monilethrixEXPERIMENTAL DERMATOLOGY, Issue 6 2003Liran Horev Abstract: Mutations in the hair keratins hHb1 and hHb6 have been recently reported to cause monilethrix, an autosomal dominant hair shaft disorder, characterized by variable degrees of hair fragility and follicular hyperkeratosis. We found 10 families with monilethrix in which the parents were not clinically affected, and sequenced the hair keratin hHb1, hHb3 and hHb6 genes in seven patients. In five patients no mutations were found, while in two patients we identified de novo germline missense mutations at the helix termination motif: E402K (hHb6) and E413K (hHb1). [source] Identification of a novel mutation in keratin 1 in a family with epidermolytic hyperkeratosisEXPERIMENTAL DERMATOLOGY, Issue 1 2000M. J. Arin Abstract: Epidermolytic hyperkeratosis (EHK) is a hereditary skin disorder typified by blistering due to cytolysis. One in 100,000 individuals is affected by this autosomal-dominant disease. The onset of the disease phenotype is typically at birth. Histological and ultrastructural examination of the epidermis shows a thickened stratum corneum and tonofilament clumping around the nucleus of suprabasal keratinocytes. Linkage studies localized the disease genes on chromosomes 12q and 17q which contain the type II and type I keratin gene clusters. Recently, several point mutations in the genes encoding the suprabasal keratins, K1 and K10, have been reported in EHK patients. We have investigated a large kindred affected by EHK and identified a new point mutation in the 2B region of keratin 1 (I107T), resulting from a T to C transition in codon 478. [source] Biochemical and mutational analyses of the cathepsin c gene (CTSC) in three North American families with Papillon Lefèvre syndromeHUMAN MUTATION, Issue 1 2002Y. Zhang Abstract Papillon Lefèvre syndrome (PLS) is an autosomal recessive disorder characterized by palmoplantar hyperkeratosis and severe periodontitis. The disease is caused by mutations in the cathepsin C gene (CTSC) that maps to chromosome 11q14. CTSC gene mutations associated with PLS have been correlated with significantly decreased enzyme activity. Mutational analysis of the CTSC gene in three North American families segregating PLS identified four mutations, including a novel mutation p.G139R. All mutations were associated with dramatically reduced CTSC protease enzyme activity. A homozygous c.96T>G transversion resulting in a p.Y32X change was present in a Mexican PLS proband, while one Caucasian PLS proband was a compound heterozygote for the p.Y32X and p.R272P (c.815G>C) mutations. The other Caucasian PLS proband was a compound heterozygote for c.415G>A transition and c.1141delC mutations that resulted in a p.G139R and a frameshift and premature termination (p.L381fsX393), respectively. The c.415G>A was not present in more than 300 controls, suggesting it is not a CTSC polymorphism. Biochemical analysis demonstrated almost no detectable CTSC activity in leukocytes of all three probands. These mutations altered restriction enzyme sites in the highly conserved CTSC gene. Sequence analysis of CTSC exon 3 confirmed the previously reported p.T153I polymorphism in 4 of the 5 ethnically diverse populations studied. © 2002 Wiley-Liss, Inc. [source] Nonmutilating palmoplantar and periorificial kertoderma: a variant of Olmsted syndrome or a distinct entity?INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 6 2010Ahmad Nofal MD Background, Olmsted syndrome is a rare keratinization disorder characterized by mutilating palmoplantar and periorificial keratoderma as the two major diagnostic features. Some authors believe that atypical cases without this standard combination may not really belong to Olmsted syndrome. Herein, we describe two familial cases with congenital nonmutilating palmoplantar and periorificial keratoderma, and discuss their similarities and differences with Olmsted syndrome. Patients, The study included two sisters who presented with focal and punctate nonmutilating palmoplantar keratoderma (PPK), periorificial hyperkeratotic plaques, and widely distributed keratotic lesions. Fragile denuded areas of the skin were found in sites exposed to trauma. Fingernails showed a characteristic form of leukonychia. Results, Histopathology of plantar keratoderma showed psoriasiform hyperplasia with marked compact hyperkeratosis, while vicinity of denuded skin revealed thin parakeratotic zone and dissolution of the granular cell layer. Immunohistochemistry demonstrated suprabasal staining pattern for acidic keratin (AE1) and uniform positivity, starting four to six layers above the basal layer, for cytokeratin 10. Electron microscopy showed defective keratinization. Cytogenetic studies revealed normal karyotype and no chromosomal breakage. Conclusion, Our cases share Olmsted syndrome in the early onset, and the presence of symmetrical PPK, periorificial keratoderma and keratotic lesions. However, the striking nonmutilating nature of PPK and the presence of unique features in our patients suggest a newly described keratinization disorder. [source] Sporadic dystrophic epidermolysis bullosa with albopapuloid and prurigo- and folliculitis-like lesionsINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 8 2009Yi-Ming Fan MD A case of sporadic dystrophic epidermolysis bullosa (DEB) with albopapuloid and prurigo- and folliculitis-like lesions is reported. Histopathology of the scalp biopsy showed hyperkeratosis, a subepidermal cleft near the orifice of a hair follicle, dermal fibrosis, and a moderate perivascular and perifollicular lymphohistiocytic inflammatory cell infiltrate in the papillary dermis, without neutrophilic infiltrate in the orifice of the hair follicle. It is uncertain whether the present case should be classified as DEB pruriginosa or represents a new subtype of DEB. [source] A novel mutation in the ATP2C1 gene is associated with Hailey,Hailey disease in a Chinese familyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2009Zhou Jiang Liu MD Background, A three-generation Chinese family with Hailey,Hailey disease (HHD) was identified and characterized. The proband developed HHD with severe recurrent blisters and crusted erosions involving the body folds. Skin biopsy studies showed epidermal hyperkeratosis and defects in cell-to-cell adhesion. Three other members in the family were also affected with HHD and had the same clinical manifestations. The purpose of this study was to identify the pathogenic gene or mutation in the family. Methods, All exons and exon,intron boundaries of ATP2C1 were polymerase chain reaction (PCR) amplified and sequenced with DNA samples from the proband. Restriction fragment length polymorphism (RFLP) analysis for the intron 23,exon 24 boundary of ATP2C1 was performed in all family members and in 100 normal control subjects. Results, A novel 2-bp deletion (c.2251delGT) was detected in exon 24 of the ATP2C1 gene. The mutation was present in the three other affected family members and in two asymptomatic young carriers, but not in the other normal family members or the 100 normal controls. The mutation resulted in a frameshift change and led to the formation of a premature termination codon (PTC) four amino acid residues downstream from the sixth transmembrane domain. Conclusions, Our results indicate that the novel c.2251delGT (p.V751fs) mutation in the ATP2C1 gene is responsible for HHD in this Chinese family. This study expands the spectrum of ATP2C1 mutations associated with HHD. [source] Late-onset Papillon,Lefevre syndrome with pyogenic liver abscesses: report of one caseINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2009Ameneh Yazdanfar MD A 25-year-old woman living in Hamedan, Iran, presented originally at 7 years of age with erythematous, hyperkeratotic lesions on the palms and soles with extension to the dorsal side of the hands and feet. Involvement of the elbows and knees was also seen. From 12 years of age, she started to lose her teeth. At the same age, she experienced fever, chills, malaise, myalgia, and right upper quadrant abdominal pain. With a diagnosis of pyogenic liver abscesses, the patient underwent successful surgical treatment. ,Examination revealed erythematous, hyperkeratotic, scaling plaques on the palms and soles, dorsal side of the hands and feet (Fig. 1), elbows and knees. All the teeth were missing from the mouth (Fig. 2), and she used a dental prosthesis. A surgical scar was observed on the right upper quadrant of the abdomen (Fig. 3). Skull X-ray and computed tomography scan were normal. Skin biopsy of the dorsal right hand demonstrated hyperkeratosis, focal parakeratosis, hypergranulosis, and acanthosis with a mild inflammatory infiltrate around the vessels (Fig. 4). Figure 1. Hyperkeratotic plaques on the hands and feet Figure 2. Loss of permanent teeth Figure 3. Surgical scar on the right upper quadrant of the abdomen and hyperkeratotic plaques on the hand Figure 4. Hyperkeratosis, focal parakeratosis, hypergranulosis, and acanthosis (hematoxylin and eosin, ×40) [source] Pseudoepitheliomatous hyperplasia , an unusual reaction following tattoo: report of a case and review of the literatureINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2007Wei Cui MD A 59-year-old woman presented with an itchy and uncomfortable raised lesion at a tattoo site (Fig. 1) on the lateral aspect of the left leg, just above the ankle. The tattoo had been placed 2 years before her presentation and the tattoo site was sun exposed. Immediately after she had the tattoo, she noticed redness of the skin. After a week, a pruritic and red scaly nodule developed that continued to gradually enlarge until her presentation. The patient had tried topical vitamin A and D ointment with no relief. The patient also had tattoos on the arms without any noticeable skin changes. The patient reported that the tattoo procedure on her leg was more painful than that on her arms, and was performed by a different (and perhaps inexperienced) tattoo artist. The original tattoo contained red, green, and yellow pigments. Figure 1. Raised nodular lesion with irregular margins A diagnosis of tattoo granuloma was considered; squamous cell carcinoma and fungal infection were included in the differential diagnosis. A punch biopsy was performed, followed by complete surgical excision of the lesion with a split-thickness skin graft from the right thigh. The skin excision specimen showed a 3 × 2.5-cm granular and pitted pink lesion with well-demarcated, somewhat irregular borders. The lesion was raised 0.5 cm above the skin surface. The lesion was present in the center of the original tattoo. Portions of the original tattoo with green and blue,green pigmentation were visible on either side of the lesion. No satellite lesions were identified. Microscopically, the raised lesion demonstrated striking pseudoepitheliomatous hyperplasia, with irregular acanthosis of the epidermis and follicular infundibula, hyperkeratosis, and parakeratosis (Fig. 2). Follicular plugging was present with keratin-filled cystic spaces. There was a brisk mononuclear inflammatory infiltrate in the dermis, composed primarily of lymphocytes, with admixed plasma cells and histiocytes. Giant cells were occasionally identified. Dermal pigment deposition was noted both within the lesion and in the surrounding skin, corresponding to the original tattoo. Variable dermal fibrosis was noted, with thick collagen bundles in some areas. There was no evidence of epidermal keratinocytic atypia, dyskeratosis, or increased suprabasal mitotic activity. Special stains (periodic acid,Schiff and acid-fast) for microorganisms were negative. Figure 2. (a) Raised lesion with marked pseudoepitheliomatous hyperplasia and follicular plugging (hematoxylin and eosin; magnification, ×2.5). (b) Irregularly elongated and thickened rete pegs with blunt ends associated with dermal chronic inflammation (hematoxylin and eosin; magnification, ×5). (c) Follicular dilation and plugging with keratin-filled cystic spaces (hematoxylin and eosin; magnification, ×5). (d) Dermal pigment and fibrosis (hematoxylin and eosin; magnification, ×10) [source] Annular atrophic lichen planusINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 5 2007Rosa María Ponce-Olivera MD A 30-year-old woman presented with a 1-year history of a pruritic eruption on the extremities, characterized by several annular plaques. The patient had been treated unsuccessfully with medium-potency topical steroids. The lesions had an erythematous papular border with an atrophic center (width, 1,4 cm) (Fig. 1). No oral, genital, or nail lesions were observed. Figure 1. Annular lesion with an infiltrated border and atrophic center A skin biopsy from one of the plaques was performed. Histopathologic examination of the raised border showed hyperkeratosis of the stratum corneum, focal thickening of the granular layer, basal liquefaction degeneration of the epidermis, and a band-like subepidermal infiltration with numerous Civatte bodies. In the center of the lesion, the epidermis became thinner (Fig. 2). Elastic fibers were reduced or absent in the papillary dermis. Figure 2. (a) Biopsy of the border of a plaque with the typical changes of lichen planus (hematoxylin and eosin, ×10), with flattened epidermis in the center of the plaque; (b) medium power of the border of the plaque with details of the changes of lichen planus (hematoxylin and eosin, ×40) The patient was treated with high-potency topical steroids for 2 months with clinical improvement. [source] Tuberculosis verrucosa cutis: antitubercular therapy, a well-conceived diagnostic criterionINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2005Virendra N. Sehgal MD A 39-year-old housewife sustained inadvertent trauma to the right index finger about 6 years ago, whilst stitching clothes. A couple of weeks later, the site of trauma became hard and gritty. Ever since, it has progressed slowly, without any appreciable outward sign. It was not associated with any discomfort/pain. Consequent on an opinion from a surgeon, it was decided to operate on the right index finger. During the operation, under local anesthesia, a hard and gritty material was removed. The material was subjected to histopathologic study. Several stitches were applied to the wound. It failed to respond to antimicrobial therapy over a 4-week period, prompting the patient to seek another opinion. Examination of the skin surface revealed a plaque with an irregular configuration on and around the distal interphalangeal joint of the right index finger. It was erythematous and pigmented. The top of the plaque was irregular and had alternating elevations and depressions (Fig. 1). Diascopy was negative for apple jelly nodule. A bacillus Calmette,Guérin (BCG) vaccination scar was identified on the left deltoid. There was no regional lymphadenopathy or systemic abnormality. Mantoux test with intradermal injection of 0.1 mL SPAN's tuberculin (purified protein derivative/5 tuberculin units/0.1 mL) (Span Diagnostic Ltd., Murat, India) was negative after 72 h. Investigations, including total and differential leukocyte count, erythrocyte sedimentation rate, serum biochemistry, and renal and liver function tests, were within the normal range, as was a chest X-ray. Figure 1. Tuberculosis verrucosa cutis before (a) and after (b) antitubercular therapy (ATT) Hematoxylin and eosin-stained sections prepared from the biopsy taken from the lesion revealed noteworthy changes in the epidermis and the dermis. The former was marked by the presence of hyperkeratosis, acanthosis, and papillomatosis, whilst the latter contained tubercle granulomas. Each of the granulomas was well formed and consisted of large numbers of lymphocytes, histiocytes, and foreign body (Langerhans') giant cells (Fig. 2). Caseation necrosis and acid-fast bacilli could not be demonstrated. The preceding revelations were fairly conducive to the diagnosis. Accordingly, antitubercular therapy (ATT), comprising 450 mg of rifampicin, 300 mg of isonicotinic acid hydrazide, and 800 mg of ethambutol, was recommended for oral administration each day for 60 days. The outcome of the treatment was satisfactory, resulting in perceptible regression of the skin lesion (Fig. 1b). The patient was advised to continue the treatment for another 30 days, after which 450 mg of rifampicin and 300 mg of isonicotinic acid hydrazide were to be continued for another 6 months. Figure 2. Tuberculosis verrucosa cutis depicting well-formed tubercle(s) comprising lymphocytes, histiocytes, neutrophils, and a few giant cells (hematoxylin and eosin, × 100) [source] Epidermolytic hyperkeratosis: a keratin 1 or 10 mutational eventINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2005Nicole L. Lacz MD Epidermolytic hyperkeratosis is an unusual type of ichthyosis. This inherited keratinization disorder is characterized clinically by erythema, blistering, and peeling shortly after birth. It may resolve and be replaced with thick scaling. It can lead to life-threatening complications, such as sepsis. Histologically, there is a hyperkeratosis and vacuolar degeneration. Genetically, this is an autosomal dominant disease with complete penetrance; however, 50% are spontaneous mutations. The clinical phenotype is a result of alterations in the gene(s) for keratin 1 and/or 10. We review this disorder and its therapy, which is mainly symptomatic with emollients and retinoids. [source] Axillary intertriginous granular parakeratosis responsive to topical calcipotriene and ammonium lactateINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 5 2003Michael E. Contreras MD A 70-year-old white man presented to our clinic with a 6,8-month history of a pruritic, occasionally burning eruption in both axillae. He had been using the same deodorant for more than 1 year and denied any changes in laundry detergent, soaps, or shampoos. He also denied application of other topical products. On physical examination, there were slightly erythematous, lichenified plaques in both axillae, with more extensive involvement of the left side (Fig. 1). Histologic examination of a punch biopsy specimen from a left axillary plaque revealed hyperkeratosis with retention of nuclei and keratohyaline granules in the stratum corneum (Fig. 2). The stratum granulosum was slightly thickened, and the epidermis was mildly acanthotic. Patch tests of the patient's deodorant and shampoo were negative. The patient was advised to discontinue use of his deodorant. His right axilla was treated with topical calcipotriene, applied twice daily, and his left axilla was treated with topical 12% ammonium lactate, applied twice daily. One month later, the lesions in the right axilla had completely resolved. The left axilla was slightly improved, but still exhibited dusky erythematous plaques. After one additional month of treatment with ammonium lactate, the left axillary lesions completely resolved. A follow-up examination 9 months later revealed no recurrence of the lesions in either axilla. Figure 1. Erythematous, lichenified plaques in the axilla Figure 2. Photomicrograph of biopsy specimen showing keratohyaline granules in the stratum corneum (hematoxylin and eosin, × 200) [source] An interesting case of colocalization of segmental lichen planus and vitiligo in a 14-year-old boyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 8 2002Kabir Sardana MD A 14-year-old boy had segmental vitiligo (L3,4) on the right thigh and leg for 4 years, and was advised to apply topical clobetasol propionate, 0.05%, in the night, with daily sun exposure for 10 min, as he refused to comply with topical psoralens. As there was no response to therapy even after 3 months, the patient stopped the steroid cream but continued with the sun exposure. Subsequently, the patient noticed gradual-onset, itchy, violaceous, pigmented, raised lesions superimposed on the vitiligo macules. Cutaneous examination revealed violaceous, polygonal papules, 0.5 × 0.5 cm in size, some of which coalesced to form discrete violaceous plaques, confined to areas of vitiligo, with a clear-cut demarcation from normal skin (Fig. 1). The scalp, palms, soles, nails, and mucosa were normal. Histopathology of the polygonal papules revealed hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis with saw toothing of the rete ridges, basal cell liquefaction, and a band-like lymphocytic infiltrate (Fig. 2), consistent with lichen planus. The patient was subsequently prescribed fluticasone propionate (0.05%) ointment once daily for the lesions of lichen planus. There was a marked improvement in the lesions of lichen planus after 1 month. Figure 1. Violaceous papules of lichen planus colocalized on vitiligo macules with associated leukotrichia seen on the right leg Figure 2. Histopathology reveals hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis with saw toothing of the rete ridges, basal cell liquefaction, and a band-like lymphocytic infiltrate (hematoxylin and eosin, × 40) [source] Lichen planopilaris [cicatricial (scarring) alopecia] in a childINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 7 2001FNASC, FRAS (Lond.), Virendra N. Sehgal MD A mother of a 12-year-old boy, 2 years ago, noticed that he showed patchy loss of hair on the vertex of the scalp. It was asymptomatic and progressive. Subsequently, similar patches appeared elsewhere on the scalp. Some of these patches joined to form a large bald patch. This was accompanied by dusky blue eruptions over the left upper lip and eyebrows. Later, there was localized loss of hair. A family history of a similar ailment was absent. Examination of the scalp revealed plaques of alopecia with mild to moderate erythema. The skin was smooth, shiny, and atrophic (Fig. 1). Atrophy was apparent by the presence of wrinkles in places, and by holding the skin between the thumb and the index finger. The periphery of the lesions was well demarcated and was occupied by erythematous, scaly, follicular papules. Lesions were also located on the patches of alopecia. In addition, flat-topped, dusky blue, papules/plaques were present over the upper lip. Figure 1. Lichen planopilaris: plaques of alopecia showing smooth, shiny, atrophic skin with erythema A study of hematoxylin and eosin-stained microsections prepared from the upper lip and vertex of the scalp was undertaken. The former revealed hyperkeratosis, hypergranulosis, sawtooth irregular acanthosis, and destruction of the basal cell layer which, in turn, was embraced by a lymphohistiocytic infiltrate disposed in a band-like fashion. A few cells were seen invading the epidermis. Pigment-laden histiocytes were found intermingled with the infiltrate. In the scalp skin, on the other hand, atrophy of the epidermis with punctuation of keratin plugs, together with fibrosis of the dermis, was prominent. The walls of the hair follicles were hyperkeratotic, while their lumina were conspicuous by their dilatation and contained keratotic plugs (Fig. 2a,b). Sebaceous and sweat glands were absent. Figure 2. Lichen planopilaris showing atrophy of the epidermis, fibrosis of the dermis, dilatation of the hair follicle lumina containing keratotic plug(s), and hyperkeratosis of the wall of the follicle (hematoxylin and eosin: a , ×,40; b , ×,100) Response to treatment, comprising ultramicronized griseofulvin (Gris O.D.) 375 mg/day (Sehgal VN, Abraham GJS, Malik GB. Griseofulvin therapy in lichen planus ,- a double blind controlled trial. Br J Dermatol 1972; 86: 383,385; Sehgal VN, Bikhchandani R, Koranne RV et al. Histopathological evaluation of griseofulvin therapy in lichen planus. A double blind controlled study. Dermatologica 1980; 161: 22,27) and prednisolone 20 mg/day for 6 months, was excellent (Fig. 3). Topical betamethasone dipropionate (Diprovate) lotion was used as a supplement. Figure 3. Perceptible decline in band-like lymphohistiocytic inflammatory infiltrate (hematoxylin and eosin, a, × 40; b, ×,100) [source] Erythema dyschromicum perstans and hepatitis C virus infectionINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 5 2001George J. Kontochristopoulos MD A 48-year-old woman with a 10-month history of widespread, hyperpigmented, slightly pruritic macules, with a red border, involving the trunk and the proximal limbs (Fig. 1) was referred to our outpatient department. The oral mucosa, palms, soles, scalp, and nails were normal. Figure 1. Multiple hyperpigmented macules with an active border on the trunk Laboratory tests showed elevated liver enzymes [alanine aminotransferase (ALT), 68 IU/L (normal value, <,40 IU/L); aspartate aminotransferase (AST), 41 IU/L (normal value, <,40 IU/L)], the presence of antibodies to hepatitis C virus (anti-HCV) and HCV RNA (Amplicor Roche). In addition, cryoglobulinemia type III (IgM,,,, IgG,,,) was detected with a high cryocrit value, and there was detectable C-reactive protein, rheumatoid factor, and a low titer of antinuclear antibodies (1 : 80). A percutaneous liver biopsy showed changes compatible with mild chronic hepatitis (grade, 6; stage, 0). The possible source of infection was unknown, as the patient had no history of parenteral transmission (e.g. blood transfusions, intravenous illicit drug use). A skin biopsy specimen from the active border of a lesion showed hyperkeratosis, parakeratosis, and hydropic degeneration of the basal cell layer, with the formation of colloid bodies in the epidermis. A moderate perivascular lymphohistiocytic infiltrate with melanophages and free melanin granules was observed in the upper dermis (Fig. 2). Immunostaining of paraffin-embedded tissue sections with the TORDJT-22 IgG1 mouse monoclonal antibody to HCV (Biogenex, Son Ramon, USA), which is specific for the nonstructural region of HCV (NS3-NSH, C100 antigen) using the avidin,biotin,peroxidase complex (ABC) as well as the alkaline phosphatase antialkaline phosphatase (APAAP) methods, failed to detect HCV in the lesion of erythema dyschromicum perstans (EDP) (Nakopoulou L, Manolaki N, Lazaris A et al. Tissue immunodetection of C100 hepatitis C virus antigen in major thalassemic patients. Hepato-Gastroenterol 1999; 46: 2515,2520). Direct immunofluorescence showed IgG, IgM, IgA, and fibrinogen deposits on colloid bodies. EDP was diagnosed on the basis of these clinical and laboratory findings. Figure 2. Hydropic degeneration of the basal cell layer with colloid bodies in the epidermis. Moderate perivascular lymphohistiocytic infiltrate with melanophages and free melanin granules in the upper dermis (hematoxylin and eosin, ×,200) The patient was treated with interferon-,2b (Intron-A, Schering Plough Athens, Greece), 3 MU thrice weekly subcutaneously for 12 months, with additional topical steroid application. There was no response to this treatment with new lesions appearing in previously unaffected areas of the trunk and extremities. HCV RNA remained persistently positive. Thus, a modified regimen with interferon-,2b, 6 MU thrice weekly for 6 months, was tried. At the end of the treatment course, the eruption of EDP had greatly improved. Liver enzymes were normal (ALT, 22 IU/L; AST, 24 IU/L) and HCV RNA had become negative. Four months later, however, cutaneous lesions reappeared and hepatitis C relapsed. At this time point, combination therapy of interferon-,2b, 3 MU thrice weekly, with ribavirin, 1000 mg daily, was given. Six months later, liver enzymes were normal (ALT, 42 IU/L; AST, 39 IU/L), HCV RNA was negative, and the lesions of EDP had resolved. [source] A unique variant of Darier's diseaseINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 4 2001Christopher M. Peterson MD A 45-year-old black woman presented with a chief complaint of an increasing number of ,,light spots'' on her face, upper trunk, and legs. She had a 4-year history of a pruritic eruption on the dorsum of her hands. The eruption was particularly pruritic in the summer months. Other family members, including her sister and her daughters, reportedly had a similar dermatologic problem. The patient had been previously evaluated and biopsied by another dermatologist. The earlier biopsy was nondiagnostic, however, and she presented for further evaluation of this problem. On physical examination, the patient had hypopigmented macules along her jawline (Fig. 1), lateral neck, and upper chest. She had similar hypopigmented macules on her thighs. She had hyperkeratosis of the palmoplantar surface of her hands and feet. The dorsum of her hands had numerous coalescing, shiny, flat-topped, hypopigmented papules (Fig. 2), and several of her fingernails had distal, V-shaped notching. Figure 1. Hypopigmented macules on the cheek and along the jawline Figure 2. Coalescing, hypopigmented papules on the dorsal aspect of the fingers and hand, with distal notching of the fingernails A punch biopsy from a papule on the dorsum of her hand was obtained. The epidermis had corps ronds present with focal areas of acantholysis above the basal layer (Fig. 3). The dermis had sparse, superficial, perivascular infiltrates composed of lymphocytes and histiocytes. These changes were consistent with our clinical diagnosis of Darier's disease (keratosis follicularis). Figure 3. Corps ronds (large arrow) and focal acantholysis with suprabasal clefts (small arrow) are present in the epidermis (hematoxylin and eosin; original magnification, ×,40) [source] Hereditary palmoplantar keratoderma (four cases in three generations)INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2001Virendra N. Sehgal MD A 39-year-old man reported with progressive thickening of the skin of the hands and feet and an inability to flex his hand. It was largely asymptomatic; however, brisk walking caused excessive sweating, pain, and widening of the fissures on the soles of the feet. He was unable to walk barefooted. According to his mother, the first episode presented with blistering at 7 days of age. Ever since, the condition has steadily worsened to acquire the current status. He was married at the age of 18 years, and had a stillborn child 18 months afterwards. Presently, he has three children, two girls aged 14 and 12 years and a son aged 10 years. Both the daughters are similarly affected. While cataloguing the details of the pattern of inheritance, the mother of the index case was also found to be affected (Fig. 1). The natural history of the disease was identical. Figure 1. Palmoplantar keratoderma: pattern of inheritance; black indicates affected individuals Examination of the palms was marked by pronounced thickening of the skin resulting in the masking of palmar creases. The thickening was well demarcated and its margins were prominent and surrounded by an erythematous halo. The color of the skin was yellow and waxy (Fig. 2a). Contractures were present on all the fingers; nevertheless, the deformity of the middle and distal interphalangeal joints of the little finger was prominent. The soles of the feet had a similar morphology. In addition, marked fissuring was obvious (Fig. 2b). His daughters had an identical affliction of the palms and soles. The texture and morphology of the nails were normal. Light microscopy performed on scrapings from the fissures, mounted on 10% potassium hydroxide, revealed mycelia (hyphae) and spores. Figure 2. Well-demarcated hyperkeratosis depicting the yellow, waxy color of the palms, with masking of creases (a). Marked fissuring on the soles was prominent (b) Hematoxylin and eosin-stained microsections from the palms and soles showed exquisite changes in the epidermis characterized by considerable uniform orthohyperkeratosis. Hypergranulosis and acanthosis were other associated changes. In addition, perinuclear vacuolization and keratohyalin granules of varying sizes and shapes were located at the periphery of the cells. A sparse mononuclear infiltrate was located at the dermo-epidermal junction. Hyphae and spores of fungi were also identified in the stratum corneum (Fig. 3). Figure 3. Orthohyperkeratosis, hypergranulosis, and acanthosis. Perinuclear vacuolization and keratohyalin granules at the periphery of the cells; a sparse mononuclear infiltrate was also present (hematoxylin and eosin, ×,40 (a), ×,400 (b)) Itraconazole, 400 mg/day in two equally divided doses, was administered with major meals for 7 days. In addition, high doses of vitamin A (100,000 IU) were given daily for 2 weeks, supplemented by 12% salicylic acid (Salicylix SF12) ointment for daytime application and an ointment containing 6% coal tar and 3% salicylic acid (Salytar) for night-time application. This treatment is useful in recalcitrant cases. [source] Dermatomyositis presenting as panniculitisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2000Yen-Yu Chao MD A 44-year-old obese woman was transferred to our clinic with a diagnosis of panniculitis. Examination showed multiple, indurated, erythematous, painful nodules and plaques distributed on the shoulders, back, forechest, abdomen, buttock, and bilateral thighs. These skin lesions appeared 2 months previously, measured 5,8 cm, and were tender on palpation. No obvious inducing factor was traced. The lesions seemed unresponsive to treatment with nonsteroidal anti-inflammatory drugs (ibuprofen, 400 mg three times a day) as similar lesions appeared in subsequent visits. Progressive proximal muscle weakness was found 1 month later. She was then admitted via the emergency room because of extensive painful skin plaques and abdominal pain. Diffuse erythematous to violaceous swelling of the face, neck, and shoulder was noted at about the same time ( Fig. 1). A skin biopsy specimen from the nodular lesion showed poikilomatous epidermal changes ( Fig. 2), and marked mononuclear cell infiltration in the dermis and subcutaneous fat ( Fig. 3). Dermatomyositis was considered as the diffuse violaceous facial erythema could be a form of heliotrope eruption, but Gottron's papule was not found. At admission, serum creatinine phosphokinase (CPK) was mildly elevated (436 IU/L; normal range, 20,170 IU/L), but serum asparagine transaminase (AST) and lactate dehydrogenase (LDH) levels were within normal limits (36 IU/L; normal, 11,47 IU/L; and 108 IU/L; normal, 90,280 IU/L, respectively). Antinuclear antibody was 1 : 80 positive with an atypical speckled pattern. Muscle strength was weakest during the first 2 days, about grade 3 by the Medical Research Council (MRC) of Great Britain scale. Gower's sign was positive. An electromyogram showed myopathic changes and a nerve conduction velocity study was normal. Serum enzymes were elevated further on the third day: AST, 55 IU/L; CPK, 783 IU/L with 100% MM form. The diagnosis of dermatomyositis was established. As for the work-up result, anti-dsDNA antibody, anti-ENA antibody, and anti-Jo1 antibody were negative. Tumor marker screen (,-HCG, AFP, CEA, and CA-125), was negative, and rhinolaryngopharyngoscope examination and gynecologic sonography were normal. Figure 1. Diffuse erythematous swelling with subtle violaceous hue extending from the temporal area to the cheeks, neck, and shoulders. The crusted lip ulcers of herpes simplex were also noted Figure 2. Basketweave hyperkeratosis, mild acanthosis, subtle vacuolar degeneration of the basal cells, and melanin incontinence (hematoxylin and eosin, ×400) Figure 3. Heavy mononuclear cells infiltrated in the subcutaneous fat tissue (hematoxylin and eosin, ×100) Pancreatitis was initially suspected because of epigastric pain and tenderness, elevated serum lipase (382 U/L; normal, 23,200 U/L), and amylase (145 U/L; normal, 35,118 U/L). No evidence of pancreatitis could be found in abdominal sonography and abdominal computed tomography (CT), however. The epigastric pain and tenderness subsided soon after admission and the serum pancreatic enzyme level declined on the second day (amylase 69 U/L; lipase, 276 U/L). The patient was then diagnosed with dermatomyositis and treated with prednisolone (120 mg/day). CPK dropped dramatically from 3286 IU/L the day before treatment to 1197 IU/L 3 days after. Panniculitis lessened and the muscle power improved after 1 week of treatment. The disease activity fluctuated even with treatment with prednisolone and the patient often felt listless and weak. The muscle weakness sometimes deteriorated to affect the patient's mobility. Facial erythema and panniculitis-like lesions were found during the worse times. Methotrexate and azathioprine were then added (7.5 mg and 250 mg per week, respectively), but CPK was still mildly elevated (189 IU/L), and the patient still felt ill. Human immune globulin (5%, 500 mL per day, 5 days per month) intravenous infusion was initiated thereafter. There was a dramatic response. Full muscle strength was retained and CPK was within the normal range in the following 6 months with only immune globulin therapy. [source] Juvenile psoriatic arthritis with nail psoriasis in the absence of cutaneous lesionsINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 1 2000Carola Duran-McKinster MD A 4-year-old white boy without a significant family history had morning stiffness and painful swelling of his left knee and ankle, right elbow, and dorsolumbar region of 2 months' evolution. The following laboratory studies were within normal limits: complete blood cell count, C-reactive protein (CRP), latex, antistreptolysin, and antinuclear antibodies. Rheumatoid factor was negative and an increase in the erythrocyte sedimentation rate (ESR) was detected (56 mm/h). The pediatric department made an initial diagnosis of juvenile rheumatoid arthritis, and treatment with acetylsalicylic acid at 100 mg/kg/day and naproxen at 10 mg/kg/day was started. A thick, yellowish toenail was diagnosed as onychomycosis. No mycologic investigations were performed. Intermittent episodes of painful arthritis of different joints were present. The radiographic features of the peripheral joints included: narrow joint spaces, articular erosions, soft tissue swelling, and diffuse bony demineralization. Characteristic bilateral sacroiliitis and a swollen tendon sheath on the left ankle were detected. At 11 years of age the nail changes had extended to five other toenails and to four fingernails, were yellow,brown in color, and showed marked subungual hyperkeratosis ( Figs 1, 2). The rest of the nails showed significant nail pitting. Trials of griseofulvin alternated with itraconazole in an irregular form for five consecutive years resulted in no clinical improvement, which prompted a consultation to our dermatology department. On three different occasions, KOH nail specimens were negative for fungus, but the presence of parakeratotic cells aroused the suspicion of psoriasis. A complete physical examination was negative for psoriatic skin lesions. A nail bed biopsy specimen was characteristic of nail psoriasis ( Fig. 3). Figure 1. Thickened nails with severe subungual hyperkeratosis in five fingernails Figure 2. Secondary deformity of nail plate. No "sausage" fingers were observed Figure 3. Light microscopic appearance of a nail biopsy specimen showing parakeratotic hyperkeratosis, elongation of interpapillary processes, and Munroe abscess (arrow) (hematoxylin and eosin stain, ×40) The following human leukocyte antigens (HLAs) were positive: A9, A10, B12, B27, Cw1, Bw4, DR6, DR7, DQ1, DQ2, and DR53. A diagnosis of juvenile psoriatic arthritis associated with nail psoriasis was made. Toenail involvement became so painful that walking became very difficult. Occlusive 40% urea in vaseline applied to the affected toenails for 48 h resulted in significant improvement. Currently, the patient is 20 years old with nail involvement, but no psoriatic skin lesions have ever been observed. [source] FoxO1 , the key for the pathogenesis and therapy of acne?JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, Issue 2 2010Bodo C. Melnik Summary Five main factors play a pivotal role in the pathogenesis of acne: androgen dependence, follicular retention hyperkeratosis, increased sebaceous lipogenesis, increased colonization with P. acnes, and inflammatory events. This paper offers a solution for the pathogenesis of acne and explains all major pathogenic factors at the genomic level by a relative deficiency of the nuclear transcription factor FoxO1. Nuclear FoxO1 suppresses androgen receptor, other important nuclear receptors and key genes of cell proliferation, lipid biosynthesis and inflammatory cytokines. Elevated growth factors during puberty and persistent growth factor signals due to Western life style stimulate the export of FoxO1 out of the nucleus into the cytoplasm via activation of the phos-phoinositide-3-kinase (PI3K)/Akt pathway. By this mechanism, genes and nuclear receptors involved in acne are derepressed leading to increased androgen receptor-mediated signal transduction, increased cell proliferation of androgen-dependent cells, induction of sebaceous lipogenesis and upregulation of Toll-like-receptor-2-dependent inflammatory cytokines. All known acne-inducing factors exert their action by reduction of nuclear FoxO1 levels. In contrast, retinoids, antibiotics and dietary intervention will increase the nuclear content of FoxO1, thereby normalizing increased transcription of genes involved in acne. Various receptor-mediated growth factor signals are integrated at the level of PI3K/Akt activation which finally results in nuclear FoxO1 deficiency. [source] | |||||||||||||