Perivascular Neutrophilic Infiltrate Research Articles

Ethylene Glycol Poisoning with Acute Liver Injury Due to Delayed Diagnosis: An Autopsy Case Report and Literature Review

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Neutrophilic urticarial dermatosis without systemic disease: case report

Neutrophilic urticarial dermatosis (NUD) is an uncommon and not well understood disease. We report a 24-year-old female with persistent present with pruritic and painful urticarial plaques unresponsive to convential treatment. Histopathologically, it demonstrates a perivascular and interstitial neutrophilic infiltrate with leukocytoclasia without evidence of vasculitis or dermal edema consistent with neutrophilic urticarial dermatosis. Further investigations to rule out underlying autoimmune, autoinflammatory and gentic systemic disease were negative. Furthermore, the cutaneous eruption was resistant to multiple therapeutic interventions including colchicine and dapsone treatment, and show significant response to treatment with anakinra, interleukin-1 receptor antagonist. Based on literature review, the case reported here is the second case with clinical and pathologic features of NUD without systemic disease and the first case of NUD that showed resistant to colchicine and dapsone treatment, with adequate response to anakinra.

Diascopy and histopathological evaluation of nonblanching erythematous dermatoses in dogs.

Diascopy is a point-of-care diagnostic test used to differentiate skin erythema due to vascular dilation from haemorrhage. In the veterinary literature, only a handful of diseases have been described to be associated with a negative (nonblanching) diascopy result, and histological investigation of haemorrhage has been inconsistent. Retrospective study to undertake a histopathological investigation of canine, nonblanching erythematous dermatoses for the presence or absence of haemorrhage and vascular changes. Skin biopsies from dogs presented with moderate-to-severe nonblanching erythema were evaluated histologically. Additionally, clinical data about each patient were analysed. Twenty cases were identified with nonblanching erythema. Diagnoses included vasculopathy (n = 6), canine eosinophilic dermatitis (n = 3), cutaneous epitheliotropic T-cell lymphoma (n = 2), and one case each of sterile granuloma and pyogranuloma syndrome, German shepherd dog pyoderma, multiple mast cell tumours, haemangiosarcoma, exfoliative cutaneous lupus erythematosus, canine leishmaniosis with sebaceous adenitis, sebaceous adenitis with concurrent dermatophytosis, calcinosis cutis and canine atopic dermatitis with insect-bite reaction. One or more vascular changes were present in all 20 cases and included perivascular oedema, endothelial swelling and neutrophilic infiltration of vessel walls. Haemorrhage was identified in 17 of 20 cases (85%). Three cases without dermal haemorrhage were calcinosis cutis, sebaceous adenitis with dermatophytosis and canine atopic dermatitis with insect-bite reaction. Negative diascopy was associated with haemorrhage and vascular pathological findings in the majority of cases, yet not all. Haemorrhage was identified histologically in all diseases previously reported as nonblanching as well as in a few additional diseases.

Epidermal growth factor receptor inhibitor Geftinib-induced erosive pustular dermatosis of the scalp – A report with a brief review of the literature

Gefitinib is an epidermal growth factor receptor inhibitor used in the treatment of non-small cell carcinoma of the lungs, adenocarcinoma of the lungs, and solid malignancies of the head and neck region. A 65-year-old female patient with non-small cell carcinoma lung with bone metastasis was started on gefitinib monotherapy after which the patient noticed papulo-pustular lesions on the scalp, later leading to loss of hair. Dermatological examination revealed erythema, pustules with crusting, along with matting of the hair on the frontoparietal area with some areas of hair loss. Trichoscopic examination showed the absence of follicular openings indicating scarring alopecia. Skin biopsy showed perivascular mixed infiltrate of lymphocytes and neutrophils and absent hair follicles, consistent with gefitinib-induced erosive pustular dermatosis of the scalp, a rare entity.

A case of hypocomplementemic urticarial vasculitis syndrome complicated by eosinophilic pneumonia: a case report and review of the literature.

The primary symptom of urticarial vasculitis (UV), which is a histopathological leukocytoclastic vasculitis disease, is an eruption that resembles urticaria. Other organs may also experience accompanying symptoms. Lung lesions with UV are mostly obstructive pulmonary disease with smoking. However, the coexistence of eosinophilic pneumonia (EP) and complicated UV remains unclear. We report a man in his 70s with chronic obstructive pulmonary disease who attended our department with ring-shaped erythema, marginal edema, and pigmentation. Additionally, a skin histological analysis showed nuclear dust and perivascular neutrophil infiltration, while a blood sample showed a decrease in C3 and C1q concentrations. Administration of prednisone temporarily improved the eruption. However, he developed a cough and a new UV eruption 1 year later. Computed tomography revealed infiltration in the right upper lobe of the lungs, and a blood sample showed a high eosinophil count. He was finally diagnosed with hypocomplementemic urticarial vasculitis syndrome and idiopathic chronic EP. A previous study showed that serum C1q concentrations in patients with EP were lower when this disease was active. Whether a decline in C1q concentrations can cause EP is unclear. However, our case is unique owing to the co-onset of EP with low complement concentrations and recurrence of UV.

A RED HERRING? PAINFUL URTICARIA FOLLOWING AMPICILLIN CONTACT EXPOSURE

<h3>Introduction</h3> Acute painful urticaria is often caused by an underlying systemic illness or exposure to a drug or vaccine. Occasionally, no cause is found which prompts consideration of other etiologies. <h3>Case Description</h3> A 22-year-old male nurse with a history of Amoxicillin allergy (delayed-onset exanthematous rash) presented to the ED with an urticarial rash, 48 hours following an accidental ampicillin exposure to his right hand at work. Initial symptoms started 24 hours later with painful swelling of bilateral hands. Despite treatment with prednisone and diphenhydramine, a painful, pruritic urticarial rash developed on his arms, trunk, gluteal cleft, and knees. New onset arthralgias and angioedema prompted presentation to the ED, where he was treated for anaphylaxis and started on intravenous steroids and antihistamines. Initial labs showed a neutrophilic leukocytosis and a mild elevation in CRP. Workup revealed normal complement with negative infectious and rheumatologic evaluations. A punch biopsy showed "perivascular and interstitial neutrophilic infiltrate with few eosinophils," concerning for neutrophilic urticarial dermatosis (NUD) or a serum sickness like drug reaction (SSLR). Seven days after exposure, symptoms began to improve leading to discharge. <h3>Discussion</h3> NUD often occurs in the setting of an underlying systemic disease such as SLE or adult-onset Still's disease. Recently, SSLRs have also been identified as a cause of NUD. SSLRs are not well understood and have not previously been described as systemic contact reactions. Although, ampicillin exposure was thought to be a red herring in this case, further investigation is needed to better understand a potential relationship when another etiology cannot be identified.

Surto de intoxicação sistêmica com dermatite de contato irritante devido à cipermetrina em vacas leiteiras - relato de caso

ABSTRACT Pyrethroids are ectoparasiticides safe for mammals and widely used in farm animals. An outbreak of systemic intoxication with irritant contact dermatitis resulting from the use of cypermethrin pour on in dairy cows is reported in the state of Pernambuco. Eight adult animals were affected, three died on the property and five were referred to the Clínica de Bovinos, Universidade Federal Rural de Pernambuco, Campus Garanhuns. These received 100 mL of pour on Cypermethrin (Ectonil ®, Cipermetrina, Labgard, Brasil). Apathy, hyperexcitability, muscle tremors, sialorrhea, bradycardia and crusted lesions were observed on the dorsum of the neck, scapula, ears and ulcerations in the oral and vaginal mucosa. There was hyperfibrinogenemia and leukocytosis due to neutrophilia with a regenerative left shift. Histopathology showed areas of erosion and ulceration of the epidermis and perivascular lymphohistiocytic and neutrophilic infiltrate in the superficial dermis. Supportive treatment was done with improvement of systemic signs and skin lesions, however, in one animal (with 19 days hospitalized), there was no complete regression of neurological alterations of bradycardia and muscle tremors, even so, it was possible to return to productive activity. High doses of pour on cypermethrin may cause systemic intoxication in cattle and result in bradycardia, hyperexcitability, muscle tremors and sialorrhea with irritant contact dermatitis, and death in severe cases.

Effects of Chronic Secondhand Smoke (SHS) Exposure on Cognitive Performance and Metabolic Pathways in the Hippocampus of Wild-Type and Human Tau Mice.

Background:Exposure to secondhand smoke (SHS) is a risk factor for developing sporadic forms of sporadic dementia. A human tau (htau) mouse model is available that exhibits age-dependent tau dysregulation, neurofibrillary tangles, neuronal loss, neuroinflammation, and oxidative stress starting at an early age (3–4 months) and in which tau dysregulation and neuronal loss correlate with synaptic dysfunction and cognitive decline.Objective:The goal of this study was to assess the effects of chronic SHS exposure (10 months’ exposure to ) on behavioral and cognitive function, metabolism, and neuropathology in mice.Methods:Wild-type (WT) and htau female and male mice were exposed to SHS (90% side stream, 10% main stream) using the SCIREQ® inExpose™ system or air control for 168 min per day, for 312 d, 7 d per week. The exposures continued during the days of behavioral and cognitive testing. In addition to behavioral and cognitive performance and neuropathology, the lungs of mice were examined for pathology and alterations in gene expression.Results:Mice exposed to chronic SHS exposure showed the following genotype-dependent responses: a) lower body weights in WT, but not htau, mice; b) less spontaneous alternation in WT, but not htau, mice in the Y maze; c) faster swim speeds of WT, but not htau, mice in the water maze; d) lower activity levels of WT and htau mice in the open field; e) lower expression of brain PHF1, TTCM1, , and HSP90 protein levels in WT male, but not female, mice; and f) more profound effects on hippocampal metabolic pathways in WT male than female mice and more profound effects in WT than htau mice.Discussion:The brain of WT mice, in particular WT male mice, might be especially susceptible to the effects of chronic SHS exposure. In WT males, independent pathways involving ascorbate, flavin adenine dinucleotide, or palmitoleic acid might contribute to the hippocampal injury following chronic SHS exposure. https://doi.org/10.1289/EHP8428

Histopathology of brain AVMs part I: microhemorrhages and changes in the nidal vessels

BackgroundArteriovenous malformations of the brain (bAVM) may rupture from aneurysms or ectasias of the feeding, draining, or nidal vessels. Moreover, they may rupture from the immature, fragile nidal vessels that are characteristic to bAVMs. How the histopathological changes of the nidal vessels associate with clinical presentation and hemorrhage of the lesion is not well known.Materials and methodsWe investigated tissue samples from surgically treated bAVMs (n = 85) using standard histological and immunohistochemical stainings. Histological features were compared with the clinical presentation of the patient.ResultsMicrohemorrhages from nidal vessels were found both in bAVMs with a history of clinically evident rupture and in bAVMs considered unruptured. These microhemorrhages were associated with presence of immature, pathological nidal vessels (p = 0.010) and perivascular inflammation of these vessels (p = 0.001), especially with adhesion of neutrophils (p < 0.001). In multivariate analysis, perivascular inflammation (OR = 19, 95% CI 1.6 to 230), neutrophil infiltration of the vessel wall (OR = 13, 95% CI 1.9 to 94), and rupture status (OR = 0.13, 95% CI 0.017 to 0.92) were significantly associated with microhemorrhages.ConclusionsClinically silent microhemorrhages from nidal vessels seem to be very common in bAVMs, and associate with perivascular inflammation and neutrophil infiltration. Further studies on the role of perivascular inflammation in the clinical course of bAVMs are indicated.

Three Patterns of Cutaneous Involvement in Granulomatosis with Polyangiitis

BackgroundSkin involvement in granulomatosis with polyangiitis (GPA) is common and can appear as an initial presentation of the disease or more commonly through its course. Case presentationWe report a case of a 24-year-old male patient, previously diagnosed as having GPA, admitted with fever, hemoptysis, generalized hemorrhagic blisters associated with arthralgia, fatigue, myalgia, nasal crusting, and vertigo. Three weeks prior to admission, he developed erythematous papules on both elbows, and purpuric papules on both lower limbs. Histopathological examination revealed: interstitial granulomatous dermatitis (elbows) and foci of dermal hemorrhage, foci of interstitial histiocytes and zones of altered necrobiotic collagen (lower limbs) consistent with cutaneous lesions of GPA. Two weeks later, his rash progressed to widespread purpura associated with hemorrhagic blisters. Another biopsy revealed leukocytoclastic vasculitis with fibrinoid necrosis of the vessel walls associated with perivascular infiltrate of neutrophils, nuclear dust and extravasated erythrocytes without an associated granulomatous inflammation or necrobiosis. The constellation of the results of the three biopsies together with clinical correlation pointed to a flare of GPA. ConclusionSkin involvement in GPA is quite common, and it can manifest in different forms in the same patient. Our patient developed three different skin pathologies within a short period of time.

Symmetrical drug-related intertriginous and flexural exanthema: A little-known drug allergy

Symmetrical drug-related intertriginous and flexural exanthema: A little-known drug allergy

Stabilization of Perivascular Mast Cells by Endothelial CNP (C-Type Natriuretic Peptide).

Activated perivascular mast cells (MCs) participate in different cardiovascular diseases. Many factors provoking MC degranulation have been described, while physiological counterregulators are barely known. Endothelial CNP (C-type natriuretic peptide) participates in the maintenance of vascular barrier integrity, but the target cells and mechanisms are unclear. Here, we studied whether MCs are regulated by CNP. Approach and Results: In cultured human and murine MCs, CNP activated its specific GC (guanylyl cyclase)-B receptor and cyclic GMP signaling. This enhanced cyclic GMP-dependent phosphorylation of the cytoskeleton-associated VASP (vasodilator-stimulated phosphoprotein) and inhibited ATP-evoked degranulation. To elucidate the relevance in vivo, mice with a floxed GC-B (Npr2) gene were interbred with a Mcpt5-CreTG line to generate mice lacking GC-B in connective tissue MCs (MC GC-B knockout). In anesthetized mice, acute ischemia-reperfusion of the cremaster muscle microcirculation provoked extensive MC degranulation and macromolecule extravasation. Superfusion of CNP markedly prevented MC activation and endothelial barrier disruption in control but not in MC GC-B knockout mice. Notably, already under resting conditions, such knockout mice had increased numbers of degranulated MCs in different tissues, together with elevated plasma chymase levels. After transient coronary occlusion, their myocardial areas at risk and with infarction were enlarged. Moreover, MC GC-B knockout mice showed augmented perivascular neutrophil infiltration and deep vein thrombosis in a model of inferior vena cava ligation. CNP, via GC-B/cyclic GMP signaling, stabilizes resident perivascular MCs at baseline and prevents their excessive activation under pathological conditions. Thereby CNP contributes to the maintenance of vascular integrity in physiology and disease.

Cutaneous dermatophyte invasion below the stratum corneum in an immunocompetent patient: To blame mixed creams or not?

Dermatophytes are pathogenic fungi that infect human skin, nails, and hair. Dermatophytes very rarely invade the epidermis below the stratum corneum in an immunocompetent host. Herein, we report a case of invasive cutaneous dermatophytosis in a 30-year-old immunocompetent male who had a history of intermittent mixed cream application on the lesion. Biopsy from the plaque showed neutrophilic spongiosis with superficial perivascular infiltrate of neutrophils, eosinophils, and lymphocytes. On periodic acid–Schiff staining, multiple branched septate hyphae in the stratum corneum were seen. Some of them were seen invading the stratum granulosum and upper spinous layer. On culture, Trichophyton schoenleinii species was isolated.

Drug Induced Autoimmunity Related Neutrophilic Dermatosis by Calcium Channel Blockers

Autoimmunity Related Neutrophilic Dermatoses (ARND) is a recently described entity characterized by urticarial papules and plaques with histology showing a neutrophilic perivascular and interstitial infiltrates with leukocytoclasis, along with variable vacuolar interface dermatitis. We report a 38 year old Caucasian female with a ten year history of lupus who presented with pruritic urticarial papules and plaques on the face, trunk, upper extremities and thighs. The onset occurred 10 days after she started a calcium channel blocker (CCB), diltiazem. Histopathology revealed scattered dyskeratotic keratinocytes, vacuolar interface dermatitis, and a sparse perivascular and interstitial mixed infiltrate of neutrophils within the dermis. There was focal leukocytoclasis, dermal edema, and rare eosinophils. The patient initially improved with prednisone taper, but flared again upon starting a different CCB, verapamil. Exposure to certain medications such as CCB in the setting of autoimmune connective tissue disorder may be the inciting trigger for a neutrophilic dermatoses. Future studies may provide further information on the pathogenesis of ARND and cutaneous drug eruption in the setting of SLE.

Neutrophilic urticarial dermatosis: an entity bridging monogenic and polygenic autoinflammatory disorders, and beyond.

Neutrophilic urticarial dermatosis (NUD) has been described in 2009. Clinically, it is an eruption of rose or red macules or slightly elevated plaques, vanishing within 24h. It occurs mostly on the trunk and the limbs. Extracutaneous signs such as fever or joint pain can be associated. The histopathological findings are a dense perivascular and interstitial infiltrate of neutrophils with leucocytoclasia but without vasculitis. It is often associated with other systemic diseases such as Schnitzler syndrome, adult-onset Still disease (AOSD), cryopyrin-associated periodic syndrome (CAPS) and Lupus erythematosus (LE). The pathogenesis of NUD is not well established but its association with CAPS and AOSD suggests that NUD is linked to autoinflammation. The management of NUD depends on the clinical findings and the potential associated systemic condition. Neutrophil migration inhibitors, such as dapsone or colchicine, and IL-1 antagonists, in particular, anakinra, are the main therapeutic options for the treatment of NUD. The prognostic value of NUD, especially when occurring in the setting of LE is not known and needs to be further investigated.

MACROLIDE BEFORE A BETA-LACTAM DECREASES DISEASE SEVERITY IN A MURINE PNEUMOCOCCAL PNEUMONIA MODEL

SESSION TITLE: Chest Infections 1 SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/10/2018 01:00 PM - 02:00 PM PURPOSE: Streptococcus pneumoniae is the leading bacterial cause of community-acquired pneumonia (CAP) and an important cause of morbidity and mortality. Clinical practice guidelines recommend against the use of macrolide monotherapy among hospitalized patients with CAP. We evaluated the hypothesis that combination therapy with Mac plus a beta-lactam (Mac/BL) compared to Mac monotherapy improves survival, decrease bacterial burden and lower disease severity in a murine pneumococcal pneumonia model. METHODS: Mice were infected intratracheally with 10ˆ5 CFU of S. pneumoniae and challenged intraperitoneally with one or two antibiotics: Ampicillin (BL) at a dose of 80mg/kg and/or Azithromycin (Mac) at 50mg/kg, respectively. After 30 hours, mice were randomized in 2 groups (Mac/BL [n=6] vs. Mac alone [n=6]). Three sets of outcomes were assessed: 1) Survival study: all groups were followed 7 days post infection; 2) Disease severity was tested by the validated lung pathology score (scored 0-5 based on peribronchial and perivascular inflammation, neutrophil infiltration and alveolar consolidation); 3) Bacterial burden: measured by daily bacteremia using colony forming units/ml. RESULTS: The 7-day survival for the Mac/BL group was 50% compared to 17% for the Mac group. After 18 hours of treatment bacteremia in the Mac/BL group had cleared (median= 0 log CFU/ml) compared to the Mac group (median=6.3 log CFU/ml). The lung pathology score was lowest among the Mac/BL group (median of 2) vs. Mac (median of 3.5). CONCLUSIONS: Our results suggest that the combination of a macrolide with a BL compared to Mac monotherapy may lower disease severity, bacterial load and survival. Translation of these findings in humans may potentially impact the use of antibiotics in pneumococcal pneumonia. CLINICAL IMPLICATIONS: This pre-clinical data supports the clinical practice guidelines regarding the use of Mac/BL combination therapy for patients with pneumococcal pneumonia. DISCLOSURES: No relevant relationships by Antonio Anzueto, source=Web Response No relevant relationships by Bettina Babu, source=Web Response No relevant relationships by Cecilia Hinojosa, source=Web Response I own stock relationship with nektar Please note: $20001 - $100000 Added 03/04/2018 by Mark Metersky, source=Web Response, value=Nothing was received No relevant relationships by Jay Peters, source=Web Response No relevant relationships by Marcos Restrepo, source=Web Response No relevant relationships by Alexander Shaffer, source=Web Response No relevant relationships by Grant Waterer, source=Web Response

Pirfenidone alleviates lung ischemia-reperfusion injury in a rat model

ObjectiveLung ischemia-reperfusion injury is among the complications seen after lung transplantation, resulting in morbidity and mortality. Pirfenidone, an antifibrotic agent for the treatment of idiopathic pulmonary fibrosis, is reported to have cytoprotective properties in various disease models. The purpose of this study was to investigate the effect of pirfenidone on lung ischemia-reperfusion injury. MethodsMale Lewis rats (260-290 g) were divided into 3 groups: sham group (n = 5), warm ischemia (WI) group (n = 10), and WI plus pirfenidone (WI+PFD) group (n = 10). The sham group underwent 210 minutes of perfusion without ischemia. The WI and WI+PFD groups underwent 90 minutes of warm ischemia and 120 minutes of reperfusion. In the WI+PFD group, pirfenidone (300 mg/kg) was administered orally by gavage 30 minutes before ischemia. After reperfusion, arterial blood gas analysis, lung mechanics, lung wet-to-dry weight ratio, and histologic findings were obtained. The gene expressions of proinflammatory cytokines in lung tissue were measured by quantitative reverse transcription polymerase chain reaction. ResultsCompared with the WI group, the WI+PFD group had significantly better dynamic pulmonary compliance (P < .01) and oxygenation levels (P < .05). The wet-to-dry ratio was lower in the WI+PFD group (P < .05). Histologic analysis showed that the WI+PFD group had reduced perivascular edema and neutrophil infiltration. The expression of tumor necrosis factor-α messenger RNA was decreased in the WI+PFD group (P < .05). ConclusionsOur results revealed that in a rat hilar clamp model, pirfenidone alleviated lung ischemia-reperfusion through anti-inflammatory effects.

Ultrasound-guided synovial biopsy improves diagnosis of septic arthritis in acute arthritis without enough analyzable synovial fluid: a retrospective analysis of 176 arthritis from a French rheumatology department.

To assess the diagnostic value of ultrasound-guided (US-guided) synovial biopsy in routine clinical practice in cases of acute and chronic arthritis. A retrospective, single-center study of US-guided synovial biopsies between 2003 and 2013. The clinical, laboratory, radiographic, synovial fluid, and histological and bacteriological results of synovial biopsies were analyzed. Arthritis was classified according to disease duration < 6weeks (AA) or ≥ 6weeks (CA). Synovial biopsy success rate was defined by the rate of capsular and/or synovial tissue analyzed. The diagnostic efficiency was defined by synovial biopsy success rate multiplied by the clinical utility (validation of a diagnostic hypothesis leading to a specific therapy). One hundred seventy-six US-guided synovial biopsies (51 AA and 125 CA) were analyzed. Synovial biopsy success rate was 82.4%. The diagnostic efficiency was 19.9%. Among the acute arthritis cases, 11 were septic. Only three patients had a positive biopsy culture while the synovial fluid puncture was of insufficient quantity to allow bacteriological analysis. The perivascular infiltration of neutrophils (PMN) had a sensitivity of 81.8%, a specificity of 84.2%, and a positive likelihood ratio of 5.2 for the septic arthritis diagnosis. Among the chronic arthritis cases, no case of pyogenic septic arthritis was found. No histological lesions, examined separately, were specific to a type of chronic inflammatory joint disease. US-guided synovial biopsies remain relevant for the diagnosis of septic arthritis, in cases of acute arthritis when joint aspiration is not possible.

Histologic characterization of cellular infiltration in autoimmune subepidermal bullous diseases in a tertiary hospital in Saudi Arabia.

BackgroundAutoimmune subepidermal bullous dermatoses have similar clinical features to those of a spectrum of immune reactants at the dermoepidermal junction (DEJ). It is difficult to obtain a precise diagnosis without an immunofluorescence assay because of their similar clinical presentations. The aim of this study was to describe the cellular cutaneous infiltration among autoimmune subepidermal bullous dermatoses.Materials and methodsThis retrospective analysis was conducted at a hospital in Riyadh, Saudi Arabia using biopsy-based data collected from 65 patients.ResultsSpongiotic changes, neutrophils, and lymphocyte infiltrations in the epidermis differed among the subepidermal bullous diseases. The DEJ showed a difference in the extent of neutrophil infiltration. The dermis showed differences in perivascular lymphocytic infiltration, neutrophilic infiltration, eosinophilic infiltration, and dermal edema.ConclusionThe dermal and DEJ showed most of the histopathologic changes in subepidermal autoimmune bullous dermatoses.

The Histopathology of Urticaria Revisited-Clinical Pathological Study.

The classic histopathological findings of urticaria include dermal edema and a sparse perivascular infiltrate of neutrophils, eosinophils, macrophages, and lymphocytes. However, this pattern is inconsistently described. To describe the histological and immunofluorescence characteristics of urticaria and to identify distinctive patterns. A retrospective study was performed in which the medical files and biopsy specimens of 58 patients with acute and chronic classical urticaria were reviewed. Pathological parameters were quantified. We recognized 2 distinctive patterns of urticaria: lymphocyte and neutrophil predominant; the former was characterized by a perivascular location, whereas the latter was associated with an interstitial location and a denser infiltrate. Mast cells were relatively sparse, better demonstrated with special stains. Tryptase stain demonstrated more mast cells than Giemsa stain. Extravasated erythrocytes were present in 50% of the cases, but vasculitis was not observed. Histological findings in classical urticaria show a spectrum of findings from a sparse superficial perivascular to a deep perivascular and interstitial infiltrate. Distinctive groups based on the dominant cell type can be identified, accounting for the similarity to neutrophilic urticarial dermatosis. Lesions may have a purpuric appearance, but leukocytoclastic vasculitis is never present.