İnsu Yılmaz

Invasive pulmonary aspergillosis in patients with chronic obstructive pulmonary disease.

BackgroundInvasive pulmonary aspergillosis (IPA) is an infection often occurring in neutropenic patients and has high mortality rates. In recent years, it has been reported that the incidence of IPA has also increased in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study is to investigate the clinical and demographic characteristics and treatment responses of IPA in patients with COPD.MethodsSeventy-one patients with a positive culture of Aspergillus from lower respiratory tract samples were examined retrospectively. Eleven (15.4%) of these patients, affected with grade 3 or 4 COPD, had IPA.ResultsAspergillus hyphae were detected in lung biopsy in three (27.3%) out of 11 patients and defined as proven IPA; a pathological sample was not taken in the other eight (72.7%) patients, and these were defined as probable IPA. Aspergillus isolates were identified as six cases of Aspergillusfumigatus and three of Aspergillusniger in nine patients, while two isolates were not identified at species level. While five patients required intensive care unit admission, four of them received mechanical ventilation. The most common finding on chest X-ray and computed tomography (CT) (respectively 63.6%, 72.7%) was infiltration. Amphotericin B was the initial drug of choice in all patients and five patients were discharged with oral voriconazole after amphotericin B therapy. Six patients (54.5%) died before treatment was completed.ConclusionsIPA should be taken into account in the differential diagnosis particularly in patients with severe and very severe COPD presenting with dyspnea exacerbation, poor clinical status, and a new pulmonary infiltrate under treatment with broad-spectrum antibiotics and steroids.

Learning curve of conventional transbronchial needle aspiration

Intrathoracic lymphadenopathy usually occurs as a result of neoplasm, granulomatous diseases, infections or reactive hyperplasia. Conventional transbronchial needle aspiration (C‐TBNA) is a cheap and safe procedure for diagnosing intrathoracic lymphadenopathy. The aim of this study was to assess the learning curve and diagnostic accuracy of C‐TBNA after an observational education programme.

Biphasic anaphylaxis to gemifloxacin.

Anaphylaxis have been documented as adverse effects of ciprofloxacin, ofloxacin, norfloxacin, levofloxacin, and moxifloxacin. However resistant and biphasic anaphlylactic reactions to gemifloxacin have not been reported to date. Management of severe anaphylaxis in the elderly can be complicated by concurrent medications such as beta (β) adrenergic, alpha (α) adrenergic blockers and angiotensin-converting enzyme (ACE) inhibitors. We report here in the case of a 60-year-old male who was taking on ACE inhibitor, α and β blockers and experienced a severe, resistant and biphasic anaphlylactic reaction to gemifloxacin mesylate.

Combination of omalizumab and bee venom immunotherapy: does it work?

Bee venom immunotherapy (b-VIT) can be combined with omalizumab therapy in order to suppress systemic reactions developing due to b-VIT itself. Omalizumab acts as a premedication and gains time for the immunotherapy to develop its immunomodulatory effects. However, the combination of omalizumab and b-VIT is not always effective enough. Herein we present a patient in whom successful immunotherapy cannot be achieved with combination of omalizumab to b-VIT.

Clinical and Serological Features of Eosinophilic and Vasculitic Phases of Eosinophilic Granulomatosis with Poliangiitis: a Case Series of 15 Patients

OBJECTIVES Eosinophilic granulomatosis with poliangiitis (EGPA) which was previously called Churg-Strauss Syndrome, is classified into eosinophilic and vasculitic phases. To characterize the eosinophilic and vasculitic phases of the disease in terms of clinical findings, serology, and treatment. MATERIALS AND METHODS We included 15 EGPA patients in the study. The clinical, serological, and therapeutic characteristics and the treatment responses of the patients were recorded. RESULTS Thirteen patients were classified as being in the eosinophilic phase and two were classified as being in the vasculitic phase of EGPA. Initial symptoms were worsening asthma in all patients (n=15; 100%). All patients had rhinosinusitis, and 66.6% had hypersensitivity to nonsteroidal anti-inflammatory drugs. The two patients in the vasculitic phase did not have nasal polyposis. Pulmonary and nervous system involvement were the most common symptoms. The erythrocyte sedimentation rates (ESRs) of the two patients in the vasculitic phase were 65 mm/h and 55 mm/h, while ESR was normal in eosinophilic-phase patients. Antineutrophil cytoplasmic antibodies (ANCA) was detected in one patient (6.6%) who was in the vasculitic phase (Case 15). The disease was under control with higher doses of methylprednisolone in the vasculitic phase (Case 14: 12 mg/day, Case 15: 10 mg/day) than in the eosinophilic phase. Relapse was detected in the two patients in the vasculitic phase. Oral corticosteroid was not discontinued in any case, and no mortality was reported. CONCLUSION Patients with eosinophilic phase or vasculitic phase EGPA had similar clinical onset. However, higher ESR, ANCA positivity, and extrapulmonary organ involvement were only found in patients in the vasculitic phase. Corticosteroid responsiveness was very good in all patients in the eosinophilic phase, and the disease could be controlled with a very low maintenance dose of a corticosteroid.

Comment on: “Targeting the PGD2/CRTH2/DP1 Signaling Pathway in Asthma and Allergic Disease: Current Status and Future Perspectives”

We read with great interest the report of Kupczyk and Kuna [1], in which they outline the PGD2/CRTH2/DP1 signaling pathway and its role in asthma/allergic disorders, and preclinical evidence indicating that blocking prostaglandin D2 (PGD2) signaling via receptor antagonists may offer a therapeutic benefit. We especially want to thank the authors for their comprehensive work. They report the results of 13 key clinical studies on molecules targeting the PGD2/CRTH2/DP1 signaling pathway in asthma and allergic diseases. The patients in these studies have either allergic rhinitis or atopic, eosinophilic asthma. However, studies on chronic rhinosinusitis with nasal polyposis (CRSwNP), aspirin-exacerbated respiratory diseases (AERD) and eosinophilic asthma with CRSwNP phenotypes are needed. We believe that these drugs may be more effective in patients with AERD. AERD is a distinct clinical syndrome characterized by chronic eosinophilic inflammation of the upper and lower airways with symptoms that are exacerbated by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) [2]. This group, previously called Samter’s triad or aspirin intolerant asthma, was named AERD by Stevenson et al. [3]. In time, upper and lower airway symptoms were found to be related to not only aspirin, but also all cyclooxygenase (COX)-1 inhibitors in AERD patients [3, 4]. It is estimated that only approximately 10% of patients with nasal polyps and approximately 9% of patients with chronic rhinosinusitis have AERD [5]. In contrast, only approximately 7–10% of patients with asthma have AERD [4]. The prevalence of AERD can increase to approximately 15% among patients with severe asthma and a significant association between severe asthma and enhanced sinonasal inflammation has been reported [4, 6]. In AERD pathogenesis, the arachidonic acid pathway produces increased amounts of leucotrienes LTC4, LTD4 and LTE, which result in bronchoconstriction, airway mucus production and eosinophil migration. PGD2 levels, responsible for bronchoconstriction and eosinophil chemotaxis, also increase. Conversely, levels of PGE2— which lowers 5-lipoxygenase (5-LO) activity, leucotriene production and eosinophil migration—decrease [7]. Compared with aspirin-tolerant asthma, patients with AERD have higher eosinophil levels both in tissue and in blood, as well as increased tissue mast cell levels. Due to prostaglandin E2 receptor (EP2) deficiency, PGE2-mediated blockage of the 5-LO pathway occurs to a lesser extent, ensuring already high levels of leucotriene. When COX-1 is inhibited by NSAIDs (in the absence of COX-2), the production of PGE2, the anti-inflammatory prostanoid, decreases even more and together with PGD2 derived from mast cells, leucotriene production from eosinophils, mast cells and other cells increase dramatically [8–10]. Also, as thromboxane A2 (TxA2) decreases, LTC4 synthetase upregulates, resulting in more leucotriene production [7]. This letter refers to the original article available at doi:10.1007/ s40265-017-0777-2.

Last station in the eosinophilic asthma with chronic rhinosinusitis and/or nasal polyposis march: Eosinophilic asthma with radiological findings associated with blood eosinophilia

ABSTRACT Objective: Eosinophilic asthma with chronic rhinosinusitis and/or nasal polyposis (EA-CRS/NP) is a subphenotype of adult-onset eosinophilic asthma. Blood eosinophil levels are shown to be highly elevated in patients with EA-CRS/NP and have potential for tissue infiltration. We aimed to demonstrate the clinical features of the patients who have a blood eosinophil level above 10% and have thorax computed tomography findings due to blood eosinophilia. Methods: Patients who were followed up in our clinic between 2012 and 2017 were retrospectively evaluated. Inclusion criteria were as follows: 1) Eosinophilic severe asthma, 2) eosinophilia >10%, 3) chronic sinusitis and/or nasal polyps, 4) patients with pathologic findings on thorax computed tomography, 5) regular follow-up for at least 1 year. Results: We identified 36 patients who met the above criteria. We defined this group as “Eosinophilic Asthma with chronic Rhinosinusitis and/or nasal polyposis with Radiological findings related to blood eosinophilia” (EARR). The mean age was 44.9 ± 11 years and 64% were females. Nasal polyps, aspirin exacerbated respiratory disease, and atopy, were present in 81%, 47%, and 25% of the patients, respectively. The mean blood eosinophil count was 1828.6 cells/mm3 (19%). The majority of EARR patients had upper lobe dominant ground-glass opacities. The mean follow-up period was 3.2 ± 2.5 years. EARR patients did not evolve into eosinophilic granulomatous polyangiitis in the follow-up. Conclusions: This phenotype is the first eosinophilic asthma sub-phenotype reported in the literature. EARR is the final stage of the allergic march of EA-CRS/NP.

Ranitidine-Induced Anaphylaxis in a Patient with Acute COPD Exacerbation

Ranitidine is a well-tolerated H2-receptor antagonist commonly used in peptic ulcer treatment and stress ulcer prophylaxis. Anaphylaxis is rarely observed with ranitidine. We report the case of a patient who developed anaphylaxis after intravenous injection of ranitidine for acute COPD exacerbation. This article underlines the importance of awareness that in COPD acute exacerbation treatment, ranitidine, which is usually administered with methylprednisolone, also has anaphylaxis potential.

Deri Yama Testi ile Doğrulanan Tenoksikamın Neden Olduğu Fiks İlaç Erüpsiyonu

Fixed drug eruption (FDE) with oxicams is very rare. FDE due to tenoxicam has been reported in several case reports. Skin patch test with the suspected or responsible drug is applied on sites of previous lesions developing with FDE. Recently, the test has been used quite often for diagnosis of FDE although results are variable. Our case was a 63-year-old woman who had developed itching and erythematous lesions 3-5 cm in size localized on her hands and elbows 3-4 hours after the intake of tenoxicam and ranitidine. The lesion became vesiculobullous a few days later. After two weeks, it resolved with hyperpigmentation. The diagnosis of tenoxicaminduced FDE was confirmed after applying patch and provocation tests. Here we described a case of bullous fixed drug eruption due to tenoxicam and we demonstrated the contribution of skin patch tests to the FDE diagnosis.

Is nonhomogeneous expression of tissue mast cells or allergen specific IgEs bound to tissue mast cells possible

Skin prick tests (SPTs) are widely used to demonstrate an IgE-mediated hypersensitivity reaction to a specific allergen. However, local allergic conditions cannot be diagnosed with SPTs. Local specific IgE production was only presented before in mucosal tissues. We present a patient with house dust mite sensitization that had variable SPTs results in different body regions.