Disseminated extrafacial rosacea with papulonecrotic lesions.

In paediatric rosacea, ocular symptoms are often predominant. Literature about systemic therapy of paediatric ocular rosacea is sparse, though. Analysis of children with ocular rosacea treated systemically, particularly addressing remission and recurrence rates. Retrospective study reviewing the medical records of children with ocular rosacea treated with systemic antibiotic therapy. Nine of 19 patients were chosen for detailed analysis. To our knowledge, this is the first study in paediatric ocular rosacea requiring systemic therapy with a larger patient group and a longer follow-up (mean follow-up = 30.2 months). 17 patients (89.5%) suffered from blepharitis, 15 patients (78.9%) from conjunctivitis, twelve patients (63.2%) from chalazia/styes and nine female patients (47.4%) from corneal involvement. We used erythromycin (n = 9) or roxithromycin (n = 1) in patients younger than 8 years and doxycycline (n = 8) or minocycline (n = 1) in patients older than 8 years. Seven of nine patients treated with erythromycin, one of eight patients treated with doxycycline and the patient treated with minocycline achieved a complete remission of ocular and cutaneous symptoms. Two of nine patients treated with erythromycin, seven of eight patients treated with doxycycline and the patient treated with roxithromycin achieved a partial remission. Relapses occurred in the patient treated with minocycline (cutaneous), two of eight patients treated with doxycycline (ocular and cutaneous) and one of nine patients treated with erythromycin (cutaneous). To achieve a complete remission of cutaneous and ocular rosacea, a long-term anti-inflammatory treatment of at least 6 months is necessary. The relapse rates seem to be lower than in adults especially in the patients treated with erythromycin.

Ocular rosacea is a special manifestation of rosacea with unknown etiology. Eye involvement in rosacea patients is surprisingly common; however, it is often underdiagnosed, resulting in inappropriate treatment. We aimed to provide an updated epidemiologic perspective on ocular rosacea in Germany to improve patient care. Data of 777 rosacea patients were assessed using a detailed online questionnaire regarding ocular and skin symptoms, previous dermatological and ophthalmological consults, presence of type 1 hypersensitivities, and Demodex testing. All data were statistically analyzed. Most patients reported ocular symptoms (399/777, 51.4%), including red eyes (179/399, 44.9%), itching (187/399, 46.9%), sty or chalazion (309/399, 77.4%), and dryness (108/399, 27.1%). Ocular rosacea was confirmed in 149/309 cases who consulted an ophthalmologist (45.3%). A total of 159/399 (39.8%) had no pre-existing allergies. Eye involvement was significantly associated with the presence of skin symptoms (P < 0.05), impacting patients' general well-being and overall treatment satisfaction. About half of Demodex-positive patients (21/45, 46.7%) showed ocular symptoms. Eye involvement in rosacea patients was common, often presenting with unspecific symptoms.

Keratoacanthomas associated with sorafenib therapy

Tetracycline derivatives provide moderate benefit in the treatment of ocular rosacea. Recently, azithromycin has been found to be an effective alternative in the treatment of cutaneous papulopustular rosacea. We planned a study to evaluate the effects of azithromycin on ocular symptoms, signs and tear function tests of papulopustular rosacea patients. An open-labelled study was performed in a population of 20 papulopustular rosacea patients. Eighteen subjects completed the trial. Significant improvement was seen in ocular symptoms, eyelid findings and conjunctival hyperaemia scores (P = 0.002, P < 0.0001, and P = 0.005, respectively). Therapeutic benefit was not observed in ocular surface staining scores. Baseline values of Schirmer test results were within normal limits. No significant side-effects were observed. Limitations The study population is limited to dermatology patients who had been referred to the ophthalmology clinic. Azithromycin may be a new promising therapeutic alternative in ocular rosacea.

PILOMATRICOMA: A CASE REPORT AND INTRAORAL SURGICAL APPROACH

Ocular rosacea (OR) is a rosacea subtype, typically presenting as dry eye, foreign body sensation, and photophobia. Prevalence estimates of OR in cutaneous rosacea (CR) range from 0.03% to 65%. This systematic review and meta-analysis consolidate the prevalence of diagnosed OR within CR and ocular involvement of CR. Primary research studies reporting the prevalence of OR in adults with CR were eligible for inclusion. Embase, MEDLINE, Web of Science, ProQuest, and Cochrane Central Register of Controlled Trials (CENTRAL) were searched. The Joanna Briggs Institute Critical Appraisal tool for Prevalence Studies and a Peters' regression test assessed risk of bias. Results were analyzed through random intercept logistic regression models using R. Studies reporting diagnosed OR were analyzed separately from those reporting ocular involvement. 28 studies were identified, 11 reported on diagnosed OR, and 17 reported on ocular involvement in CR. Prevalence of diagnosed OR (N = 124 093) was 10.3%, whereas the prevalence of ocular involvement in CR (N = 1 747) was 44.3%. In diagnosed OR, publication year significantly contributed to variations in reported OR prevalence, with more recent studies reporting a lower prevalence of diagnosed OR compared to older studies. This study highlights the variability in reported prevalences of OR and ocular involvement in CR. This might be explained by a lack of clear guidelines on how to diagnose and refer patients with CR and co-occurring ocular signs and symptoms. Greater clinician awareness and clear referral guidelines are warranted.

A 44-year-old woman with a history of cocaine and heroin abuse presented with a painful, necrotic rash. Five weeks before presentation, the patient had experienced a cough and mild dyspnea. She was diagnosed with pneumonia, completed a 7-day course of ciprofloxacin and doxycycline, and her respiratory symptoms resolved. Three weeks before presentation, the patient had reported fevers, chills, diaphoresis, arthralgias, and myalgias, and developed a small erythematous lesion on her left breast. The lesion subsequently enlarged and became hemorrhagic. She simultaneously developed additional lesions on her chest, abdomen, arms, and back. The largest of these, located on her left arm, was 15 cm in diameter. All of the lesions were exquisitely tender. She was hospitalized at an outside hospital for 5 days and given a diagnosis of cocaine-induced vasculitis. Upon discharge, she was instructed to abstain from cocaine and was prescribed trimethoprim/sulfamethoxazole for a possible cellulitis involving the skin lesions. Ten days after discharge from the outside hospital, the patient presented to our institution for pain management and further evaluation. The rash had progressed since her earlier discharge. She had continued to use cocaine, heroin, and prescription opioids. She had last smoked cocaine 3 days before presentation and last used intranasal heroin 1 week before admission. She reported acquiring cocaine from a new supplier 2 weeks before her rash had begun. The patient had a history of nephrolithiasis and had undergone a cholecystectomy for gallstones. She had had 5 normal pregnancies. The patient had received ciprofloxacin, doxycycline, and trimethoprim/sulfamethoxazole in the weeks before her presentation. She also took combined oxycodone and acetaminophen for pain. She had no known drug allergies. Her youngest son had developed idiopathic thrombocytopenia at age 3 years. A paternal aunt had breast cancer and a nephew had cystinosis. She was unmarried, unemployed, and homeless. Three of her children were grown; the youngest two were in state custody. The patient had smoked 1 pack of cigarettes/day since age 15 years. She denied injection drug use and did not drink alcohol, but smoked cocaine and used intranasal heroin. The patient reported headache and fatigue secondary to poor pain control and disrupted sleep. She denied visual changes, sicca symptoms, jaw pain, oral ulcers, and dysphagia. She denied shortness of breath, cough, chest pain, palpitations, gastrointestinal symptoms, and abdominal pain. She had no genitourinary symptoms, arthritic pain, or musculoskeletal tenderness. She reported new upper extremity edema in her hands and arms bilaterally, more significant on the left than on the right, and equal bilateral lower extremity swelling. She had no sick contacts or recent travel. The patient was an obese woman in significant pain from her skin lesions. She was afebrile but had a pulse of 108/minute. Her blood pressure was 163/86 mm Hg, her respiratory rate was 22/minute, and her oxygen saturation was 97% on room air. She had a rash distributed in a symmetric pattern overlying fatty areas on the breasts, abdomen, upper arms, back, and flanks. The lesions consisted of stellate, purpuric plaques ranging in size from 5 cm to 15 cm (Figure 1A). The largest lesion was located on the left upper extremity (Figure 1B). The lesional borders were well demarcated and contained a reticular pattern surrounded by a 5-mm rim of erythema (Figure 1C). Small 1–2-cm lesions were also located on the earlobes bilaterally (Figure 1D). Many of the lesions were associated with flaccid bullae and exquisite tenderness to palpation. An additional dermatologic finding was a livedo pattern on her back and extremities. There was pitting edema in the upper and lower extremities bilaterally. Picture of the patient's necrotic rash. A, Multiple purpuric plagues were distributed symmetrically over the patient's back and flanks. Each lesion had reticulated borders consistent with a vasculopathic process. B, The largest lesion on the left arm had a necrotic appearance and contained central bullae. C, Borders were well demarcated and surrounded by a rim of erythema. D, Purpuric and necrotic lesions, 1–2 cm in diameter, were located on the earlobes. Color figure can be viewed in the online issue, which is available at http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2151-4658. Examination of the head and neck was unremarkable, and there was no lymphadenopathy. The cardiovascular examination demonstrated a regular rate and rhythm, normal heart sounds, and no murmurs. The lungs were clear to auscultation. The abdomen was soft, nondistended, nontender, and without palpable masses. A neurologic examination showed intact cranial nerves and normal sensation and strength. Cerebellar signs were absent, and the gait was normal. The complete blood cell count, coagulation times, electrolytes, bilirubin levels, liver enzymes, cardiac biomarkers, and urinalysis were within normal limits. The patient had a mild normochromic anemia with a hematocrit of 35% and a mean corpuscular volume of 82 femtoliters (normal range 80–100). The serum iron saturation level was 4.5% and the ferritin was mildly elevated at 217 ng/ml (normal range 10–200). The erythrocyte sedimentation rate was 33 mm/hour (normal range 0–17). The patient's D-dimers were significantly elevated at 5,541 ng/ml (normal value <500), but the fibrinogen concentration was normal. Blood and urine cultures showed no growth. Assays for syphilis, hepatitis B and C, and the human immunodeficiency virus were nonreactive. An antinuclear antibody assay was positive at a titer of 1:160 (speckled). Assays for antibodies to both double-stranded DNA and histones were positive at titers of 1:20 (normal titer <1:10) and 2.2 units (normal value <1.5), respectively. Assays for antibodies to the Ro, La, Sm, and RNP antigens were negative. The serum C3 and C4 levels were 137 mg/dl (normal range 86–184) and 10 mg/dl (normal range 20–58), respectively; cryoglobulins were not detected. An IgM anticardiolipin antibody (aCL) assay was strongly positive at 150 IgM phospholipid units (normal range 0–15), but the IgG aCL assay was negative at 4.2 IgG phospholipid units (normal range 0–15). Assays for a lupus anticoagulant and antibodies to β2-glycoprotein I were negative. The serum antithrombin IIIA level was 66% (range 80–130%). Because of the resemblance of the skin lesions to warfarin necrosis, a serum warfarin level was assayed and found to be normal. An immunofluorescence assay for antineutrophil cytoplasmic antibodies (ANCAs) was positive in a perinuclear ANCA (pANCA) pattern of staining. Enzyme-linked immunosorbent assays (ELISAs) confirmed the presence of antibodies to myeloperoxidase (MPO ANCA). Antibody activity was measured at 1,050 units (normal value ≤2.8). An ELISA for antibodies to proteinase 3 (PR3) was negative. A serum parathyroid hormone (PTH) was normal, and assays for PTH-related peptide and plasma activated inhibitor 1 were negative. A serum protein electrophoresis with immunofixation studies was normal. Cocaine, oxycodone, and opiates were identified in a urine toxicology screen. A chest radiograph was normal, and ultrasound studies of the lower extremities and left arm showed no deep venous thromboses. A diagnostic test was performed. The patient is a 44-year-old woman with active cocaine and heroin use who presented with a painful, bullous, necrotic rash that developed after receiving a short course of antibiotics. The skin lesions have persisted despite conservative management for 5 weeks. The physical examination is otherwise remarkable for bilateral upper and lower extremity swelling. Laboratory studies are significant for an IgM aCL and MPO ANCA. Here we discuss the differential diagnosis of the patient's necrotic rash in the context of her laboratory abnormalities. A primary concern on admission was a hypercoagulable state. Heritable disorders of coagulation typically are considered in patients with a history of venous or arterial thrombi or pregnancy loss, or a family history of such events. Our patient had no such history. Laboratory testing confirmed the absence of mutations in the prothrombin, antithrombin III, and factor V Leiden genes. Protein C and S activities and the homocysteine level were normal. Acquired hypercoagulable states were considered early in the management of this patient. The patient had no history of recent surgery, immobilization, cancer, pregnancy, or hormonal therapy. All of these risk factors are associated more strongly with venous thrombi than with arterial clots, and ultrasonography excluded evidence of venous thrombosis. In any event, the distribution and necrotic appearance of the rash were more consistent with an arterial process. One common hypercoagulable state that leads to arterial or venous thrombi (or both) is the antiphospholipid syndrome (APS). The APS can develop at any age, is more common among women, and has a diverse range of clinical manifestations (1). The APS is characterized by the detection within serum of antiphospholipid antibodies (aPL); specifically, aCL, antibodies to β2-glycoprotein I, or a lupus anticoagulant. By the Sapporo criteria, the diagnosis of APS is entertained in the setting of a typical rash (e.g., livedo racemosa) and the presence of aPL within the serum (2, 3). To fulfill the laboratory criteria, aPL must be detected on at least two occasions separated by more than 12 weeks. Overall, we had a high suspicion of APS, given the clinical manifestations and laboratory findings of IgM aCL. Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis of medium-sized arteries that can affect any organ system. Skin involvement is common. The characteristic skin findings include livedo reticularis (racemosa), tender erythematous nodules, bullae or vesicular eruptions, and ulcers (4). Palpable purpura can be present to a minor degree and when found, represents concomitant small-vessel involvement. Skin lesions can result in infarction and gangrene of the distal extremities or deep ulcerations that extend into the subcutaneous tissue. In PAN, the cutaneous involvement is often accompanied by renal disease (e.g., renin-mediated hypertension, kidney infarctions), an axonal sensorimotor mononeuritis multiplex, and mesenteric vasculitis. None of these other features was present in our patient. A form of PAN limited to the skin exists, but that condition is more subacute in its presentation and seldom leads to such dramatic bulla formation (5). PAN is a “seronegative” condition, i.e., one that is not associated with known autoantibodies. This fact poses a significant challenge in diagnosis compared with, for example, systemic lupus erythematosus and the ANCA-associated vasculitides (AAVs). A minority of PAN patients have been infected recently by the hepatitis B virus and have serologies consistent with that condition. Our patient had no history of hepatitis B exposure, and the titers of aCL and MPO ANCAs suggested alternative diagnoses. Cryoglobulinemia was considered in the differential diagnosis because the patient had palpable purpura and bilateral earlobe lesions. Both of these physical findings suggest small vessel involvement. Nonetheless, the absence of lymphadenopathy, hepatosplenomegaly, peripheral neuropathy, and renal insufficiency made cryoglobulinemia less likely. Secondary causes of type I cryoglobulinemia were considered. Electrophoresis studies of the serum and urine were negative, appearing to exclude a paraproteinemia. Mixed cryoglobulinemia (types II and III) can occur secondary to hepatitis C or human immunodeficiency virus infections, but testing for our patient was negative. Most importantly, careful attempts to isolate cryoglobulins from the serum were unsuccessful. The necrotic rash and positive ANCA assay are consistent with an AAV. There are two major ANCA immunofluorescence patterns: cytoplasmic ANCA (cANCA) describes diffuse staining throughout the cytoplasm and pANCA refers to perinuclear staining. In patients with systemic vasculitis, the preponderance of cANCA staining is caused by antibodies directed against serine PR3. In contrast, in a patient who has a primary vasculitic syndrome, the pANCA pattern is generally caused by antibodies to MPO. In our patient, the high-titer MPO ANCA suggested several possibilities: Wegener's granulomatosis (WG), microscopic polyangiitis (MPA), Churg-Strauss syndrome (CSS), and drug-induced AAV. The clinical presentations of WG and MPA are difficult to distinguish in some cases. In WG, skin lesions can range from mild erythematous purpura to severe ulcerations (6). Skin manifestations are reported in 40% of patients with WG and generally correspond to the presence of generalized disease (7). However, vasculitic involvement of the skin in WG is unlikely to involve the trunk and upper extremities in the absence of lower extremity disease. In addition, our patient had no sign of the classic extracutaneous disease manifestations that typify WG: specifically, upper respiratory tract dysfunction, pulmonary disease, and glomerulonephritis. The MPO ANCA detected in our patient is more typical of either MPA or CSS than of WG. In MPA, skin findings usually consist of purpura or livedo racemosa rather than bullae and extensive necrosis (8). Approximately 50% of CSS patients are ANCA positive, and in such cases, the antibody specificity is directed against MPO. However, the diagnosis of CSS is unlikely in the absence of renal or pulmonary involvement and eosinophilia. In summary, the diagnosis of an idiopathic form of AAV is tenuous without some sign of extracutaneous disease. The constitutional symptoms, necrotic rash, and high MPO ANCA titer are consistent with both drug-induced AAV and drug-induced lupus. The two entities, which have been described both together and separately in the literature, may represent a spectrum of the same disease process. Both syndromes are associated with arthralgia, myalgia, and rash at disease onset (9). Dramatically elevated MPO ANCA titers are more strongly associated with drug-induced AAV than with idiopathic AAV (10). In addition, antihistone and aPL antibodies (both present in this case) are observed more commonly in drug-induced processes than in idiopathic AAV (11, 12). In both drug-induced ANCA vasculitis and lupus, the syndromes occur after exposure to a drug over a prolonged period of time. This contrasts with the short exposures to medications usually linked to hypersensitivity vasculitis syndromes, of which antibiotics are the most common offenders (13). Numerous medications have been implicated in both drug-induced AAV and drug-induced lupus (Table 1). However, the strongest correlations are with medications used to treat hyperthyroidism (particularly propylthiouracil) and with hydralazine, D-penicillamine, and minocycline (10, 14, 15). Our patient had no exposure to any of these agents. She had been treated previously with a short course of doxycycline, but tetracyclines other than minocycline have not been associated with drug-induced AAV (15). Ciprofloxacin has been implicated in vasculitis case reports (16, 17). In the 5 most recent reports, ciprofloxacin exposure ranged from 3–14 days, similar to our patient's 7-day course. However, the skin findings in ciprofloxacin-induced cutaneous vasculitis are generally mild in comparison to our patient's lesions, and those patients do not develop ANCAs or antinuclear antibodies (17). In both drug-induced AAV and drug-induced lupus, early withdrawal of the offending agent usually leads to resolution of the clinical syndrome (9). Prolonged cases of AAV can occur if exposure to the medication has been lengthy, as in some cases of propylthiouracil-associated disease. In our patient's case, her doxycycline and ciprofloxacin had been stopped even before the onset of the rash. In summary, the likelihood that the antibiotics to which she had been exposed had caused her severe skin rash appeared low. Case reports correlating cocaine use with skin lesions emerged first in the 1980s (18, 19). Since that time, palpable purpura; violaceous papules, bullae, and blisters; livedo racemosa with cutaneous necrosis; and multifocal necrotic lesions of the skin and muscle have been associated with cocaine use (4, 20-22). Skin biopsy samples in such patients often demonstrated vasculopathic patterns rather than frank vasculitis (21, 22). Cocaine use is well known to trigger a disorder known as midline destructive lesion that mimics limited WG closely, even including the finding of cANCA positivity on immunofluorescence testing (21-23). In such cases, ELISA testing demonstrates ANCA directed against PR3 and/or human neutrophil elastase (HNE). It is not clear if ANCA contributes to the pathogenesis of these lesions. HNE and PR3 are both serine proteinases that share gene localization as well as structural and functional characteristics. It has been speculated that the true antigen in cases of cocaine-induced midline destructive lesion is HNE, and that the PR3 ANCA results from cross-reactivity with HNE (21, 24). However, investigators recently demonstrated the coexistence of distinct antigen-specific antibodies that recognize unique epitopes (25). Cocaine use is also associated with the APS. One prospective study showed a higher percentage of aCL positivity in cocaine users compared with controls (26). Whether this was an incidental finding or has broader clinical implications for the occurrence of APS in the setting of cocaine use remains unknown. Some cocaine users who have experienced acute strokes or myocardial infarctions have been reported to have aPL, suggesting the possibility of a synergistic effect between cocaine and aPL that propagates thromboembolic phenomena (27, 28). Based on the patient's clinic findings and serologic abnormalities, the two most likely causes of the patient's presentation appeared to be either drug-induced AAV or drug-induced APS, either of which might have been induced by cocaine. Skin biopsy was essential to distinguish between these two conditions, which require different approaches to treatment (in addition to cocaine cessation). Skin biopsy samples were obtained from the right proximal and distal forearm. Histologic examination revealed fibrin thrombi within small and medium-sized blood vessels in the superficial and deep dermis and the subcutaneous tissue (Figures 2A and B). There was no evidence of endothelial swelling, leukocytoclasis, or fibrinoid necrosis within blood vessel walls. The histopathology was thought to be highly consistent with APS. Skin pathology. A, Small and medium-sized vessels (arrows) occluded by fibrin thrombi in the superficial dermis, deep dermis, and subcutaneous tissue (original magnification × 40). Inset: medium-sized artery with the lumen almost completely occluded by an organizing fibrin thrombus (original magnification × 200). B, Multiple small arteries (arrows) with luminal fibrin thrombi (original magnification × 200). The most striking features of this case were the rapid appearance of the patient's bullous, necrotic rash and the high titers of both aPL and MPO ANCA in her blood. Although we believe that both autoantibodies were induced by her cocaine use, the histopathology of her skin lesions suggests that aPL were responsible for her skin rash. This conclusion is consistent with the current knowledge regarding drug-induced ANCA positivity. In several cross-sectional and prospective studies of propylthiouracil, between 20% and 60% of patients treated with this medication on a long-term basis developed ANCA, usually in high titers (29, 30). However, only a minority of patients who developed ANCA demonstrate clinical manifestations of drug-induced AAV. In one study (31), 8 (26.7%) of 30 patients receiving long-term antithyroid medication became ANCA positive. Among those, none developed frank AAV but 3 experienced myalgia and arthralgias after the appearance of ANCAs. Patients with idiopathic AAV are known to have a predisposition to venous thrombotic events (32, 33). Variable degrees of thrombosis can also be observed on lesional biopsy samples from patients with AAV, but such findings are accompanied by more classic patterns of injury to the blood vessel wall: endothelial swelling, leukocytoclasis, and fibrinoid necrosis. Although it is impossible to exclude an interaction between the patient's aPL and MPO ANCA that heightened the intensity of her cutaneous reaction, the major histopathologic findings implicate aPL as the primary etiology of the patient's skin disease. One theory of APS pathogenesis proposes that aPL develop in genetically susceptible individuals after exposure to an unknown infectious agent. Clinical manifestations subsequently occur after a “second hit” such as smoking, prolonged immobilization, pregnancy, hormone use, or cancer. Various medications are suspected triggers of APS (Table 1). IgM aCL in particular have been linked to drug-induced APS cases. Cocaine has also been implicated in the pathogenesis of APS. Although our patient was a chronic cocaine user, it is of interest that prior to the onset of her rash she had found a new cocaine supplier, perhaps leading to exposure to new contaminants in the cocaine. One commonly recognized contaminant in cocaine is levamisole. Levamisole, an alkaline phosphatase inhibitor, appears to potentiate the action of cocaine on dopaminergic pathways. Levamisole is widely available because it is used in agriculture worldwide as an antihelminthic drug. In humans, levamisole has been studied in various clinical settings for the treatment of autoimmune and malignant diseases (34). The compound has established efficacy in relapsing nephrotic syndrome in children. Most recently, levamisole has been reported to cause agranulocytosis in cocaine users (35, 36). Approximately 70% of seized cocaine entering the US contains levamisole (35). We conducted a literature search on levamisole-induced vasculitis and vasculopathies. Levamisole-induced vasculitis has only been reported in 4 adult cases (37-39). The histopathology reported in these describes vasculitis, but the results of ANCA or aPL testing were not In the literature, there are case reports of cutaneous vasculitis secondary to levamisole Five cases were characterized by earlobe purpura and necrosis, as in our case In 4 of the skin biopsy samples demonstrated a thrombotic ANCA serologies were reported in 4 pANCA patterns in 3 cases and a cANCA pattern in 1 aPL antibodies were detected in 3 We that levamisole is the active compound in cases of cocaine-induced vasculitis or cocaine-induced This further associated with antiphospholipid her was with a and was to warfarin prior to discharge. was for the diagnosis of APS. the high ANCA there was among the the patient from her acute presentation and the of the skin lesions, the patient was on and this her skin lesions and her was after 3 after her she had from cocaine and had no of her rash. She has developed of her necrotic skin rash. All were in the or it for and the to be for had to of the in the study and for the of the and the of the and of and of

Efficacy of topical tacrolimus in the treatment of various cutaneous manifestations of lupus erythematosus

Necrobiotic xanthogranuloma with type 1 cryoglobulinemia mimicking necrobiosis lipoidica in a young woman with myeloma

Childhood granulomatous periorificial dermatitis (CGPD) is a self-limiting and well-recognized entity. A six-year-old male child, a known case of juvenile rheumatoid arthritis (JRA) presented with multiple red raised and yellowish lesions over the face, neck, trunk and upper extremities since one month with occasional itching. Cutaneous examination revealed multiple erythematous scaly papules of size up to 5 mm around the mouth, nose and periorbital areas, neck, trunk and upper extremities with few excoriations. Lesional skin biopsy was pathognomic of CGPD. We report a six-year-old Indian male child with extra-facial involvement and healing with small atrophic pigmented scars in a known case of JRA.

Le métronidazole, alternative thérapeutique des rosacées oculaires et cutanées de l’enfant

Background: The symptoms of ocular rosacea are often non-specific and there is no dependable diagnostic test for the disease, which may cause difficulties in diagnostics. The aim of this study was to examine the association between clinical findings of rosacea and self-reported ocular symptoms in a general population of middle-aged subjects. Methods: A clinical whole-body examination by a dermatologist was performed for 1,932 subjects belonging to the Northern Finland Birth Cohort 1966 Study. The presence of ocular symptoms was self-reported. The difference between rosacea and ocular symptoms was tested. Logistic regression analysis was used to identify associations between rosacea and ocular symptoms. Results: The prevalence of rosacea was 15.1% (n = 292); in the subjects with rosacea, erythematoteleangiectatic rosacea was found in 83.2% (n = 242), papulopustular in 15.4% (n = 45), ocular in 0.03% (n = 1), and phymatic in 0.1% (n = 3). Ocular symptoms in rosacea subjects were common, with dryness (32.3%), tearing (29.4%), foreign-body sensation (21.8%), and photophobia (20.5%) being the most common ones. Foreign-body sensation was reported significantly more often in those with rosacea compared to those without (p < 0.04). In logistic regression analyses, after adjusting, the subjects with rosacea had a 1.5-fold increased risk for decreased visual acuity in the dark (OR 1.48, 95% CI 1.01–2.14) compared to those without rosacea. Conclusion: Eye symptoms are common in subjects with rosacea. All patients with rosacea should be asked about ocular symptoms and both skin and eyelids should be examined even if the cutaneous findings are mild.

Innate lymphoid cells type 1 suffice to induce hallmarks of alopecia areata phenotype in organ-cultured human scalp hair follicles ex vivo and in human scalp skin xenotransplants in vivo, suggesting that these cells play a role in early AA pathogenesis.

Innate lymphoid cells type 1 suffice to induce hallmarks of alopecia areata phenotype in organ-cultured human scalp hair follicles ex vivo and in human scalp skin xenotransplants in vivo, suggesting that these cells play a role in early AA pathogenesis.

Perineural granulomas in cutaneous sarcoidosis have been rarely reported and their clinical significance has yet to be evaluated. Recently, a 27-year-old male presented with multiple pink papules on the flank and lower back, accompanied by a painful, burning sensation. Biopsies revealed well-defined granulomas, consistent with sarcoidosis, in the dermis and involving small cutaneous nerves. We hypothesized that perineural granulomas may be an under-recognized feature of cutaneous sarcoidosis and may be responsible for sensory disturbances. We reviewed cases from 29 consecutive patients with cutaneous sarcoidosis. Perineural granulomas were identified in 18/29 (62%) patients and in 22/40 (55%) biopsies. Perineural granulomas were identified in 7/9 biopsies from the proximal upper extremity, 1/3 from the distal upper extremity, 7/12 from the head and the neck, including 4/4 from the nose, 5/9 from the back, 1/2 from the flank and 1/1 from the proximal lower extremity and 0/4 from the distal lower extremity. The anatomical distribution is similar to sarcoidosis small-fiber neuropathy (SSFN), in which sarcoidosis patients without evident skin lesions experience sensory disturbances of unknown etiology involving the face, the proximal extremities and the trunk. Our results indicate perineural granulomas in cutaneous sarcoidosis are more common than previously appreciated, primarily involve the head, the proximal upper extremities and the back, and may be responsible for neurological manifestations.