The Association between Plasma D-dimer Levels and Community-Acquired Pneumonia

BACKGROUND: Plasma D-dimer levels are directly related to the intra- and extra-vascular coagulation that occurs in acute and chronic lung damage in patients with community-acquired pneumonia (CAP). OBJECTIVES: This study examines the relationship between the severity of community-acquired pneumonia and D-dimer levels. In addition, the study examines the correlations among community-acquired pneumonia, the radiological extent of the disease and mortality. METHODS: The Pneumonia Severity Index was used to classify patients into five groups. Patients were treated at home or in the hospital according to the guidelines for community-acquired pneumonia. Blood samples were taken from the antecubital vein with an injector and placed into citrated tubes. After they were centrifuged, the samples were evaluated with the quantitative latex method. RESULTS: The study included 60 patients who had been diagnosed with community-acquired pneumonia (mean age 62.5 ± 11.7) and 24 healthy controls (mean age 59.63 ± 6.63). The average plasma D-dimer levels were 337.3 ± 195.1ng/mL in the outpatient treatment group, 691.0 ± 180.5 in the inpatient treatment group, 1363.2 ± 331.5 ng/mLin the intensive care treatment group and 161.3 ± 38.1ng/mL in the control group (p<0.001). The mean D-dimer plasma level was 776.1 ± 473.5ng/mL in patients with an accompanying disease and 494.2 ± 280.1 ng/mL in patients without an accompanying disease (p<0.05). CONCLUSIONS: Plasma D-dimer levels were increased even in community-acquired pneumonia patients who did not have an accompanying disease that would normally cause such an increase

The Prevalence of Hypersensitivity Reactions to Antirheumatic Biological Agents and Results of the Skin Tests: Experience of a Tertiary Referral Allergy Center in Turkey

WOS:000603358700003Objective: The use of biological agents (BAs) has increased dramatically for inflammatory diseases and this increase has led to a rise in hypersensitivity reactions (HSRs). The symptoms and diagnostic tools for HSRs are not standardized. We aimed to analyze the prevalence of HSRs to anti-rheumatic BAs and to evaluate the usefulness of skin tests (STs) as a diagnostic tool. Materials and Methods: Our study was conducted at the Ege University Medical Faculty, Department of Internal Medicine, Division of Allergy and Clinical Immunology and Division of Rheumatology, Izmir, Turkey. Four hundred sixty patients who received BAs between Jan 1st, 2015, and Jan 1st, 2016, were reviewed in this retrospective cross-sectional study. The prevalence of HSRs was retrospectively evaluated. Ten patients with HSRs were evaluated with STs containing commercially available culprit drugs. The data was collected from hospital records. The age, sex, atopic diseases, primary rheumatic diseases, and anti-rheumatic therapies of the patients were recorded. Results: Two hundred fifty patients were treated with rituximab (RTX), 45 with infliximab, 40 with tocilizumab (TOC), 36 with golimumab, 35 with etanercept, 34 with abatacept, 15 with certolizumab, and 5 with adalimumab. Fifty reactions with RTX and two reactions with TOC were infusion-related (IRRs). Ten HSRs were observed. Eight patients had immediate (7 immediate systemic reactions and 1 local injection site reactions), and 2 had late-onset cutaneous reactions. We detected the ratio of IRRs as 11.3%, immediate HSRs as 1.73%, IgE-mediated reactions as 1.08%, and anaphylaxis as 0.86%. STs were positive in 5 of 8 patients with immediate HSRs. Four of them had anaphylaxis, and remarkably, 3 of these had positive STs. None of the ten patients had high levels of specific IgE and only four had atopic diseases. Total IgE levels were not high and specific IgE levels were not positive in the presence of HSR to BAs (p=0.039). Conclusion: Five of the 8 (62.5%) patients with immediate reactions had positive STs, which suggested IgE-mediated reactions. The prevalence of HSRs to BAs was less than the ones mentioned in the literature

In Vitro Fertilization Using Luteinizing Hormone-Releasing Hormone Injections Resulted in Healthy Triplets without Increased Attack Rates in a Hereditary Angioedema Case

WOS: 000426177100001PubMed ID: 29666724Hereditary angioedema due to C1-inhibitor deficiency (C1-INH-HAE) is a rare, autosomal dominant disorder. The management of pregnant patients with C1-INH-HAE is a challenge for the physician. Intravenous plasma-derived nanofiltered C1-INH (pdC1INH) is the only recommended option throughout pregnancy, postpartum, and breast feeding period. In order to increase pregnancy rates, physicians use fertilization therapies increasing endogen levels of estrogens. Therefore, these techniques can provoke an increase in the number and severity of edema attacks in C1-INH-HAE. Our patient is a 32-year-old female, diagnosed with C1-INH-HAE type 1 since 2004. She had been taking danazol 50-200 mg/day for 9 years. Due to her pregnancy plans in 2013, danazol was discontinued. PdC1INH was prescribed regularly for prophylactic purpose. Triplet pregnancy occurred by in vitro fertilization using luteinizing hormone-releasing hormone (LHRH) injections. In our patient, LHRH injections were done four times without causing any severe attack during in vitro fertilization. Angioedema did not worsen during pregnancy and delivery due to the prophylactic use of intravenous pdC1INH in our patient. According to the attack frequency and severity, there was no difference between the three pregnancy trimesters. To our knowledge, this is the first published case of C1-INH-HAE receiving in vitro fertilization therapies without any angioedema attacks during pregnancy and delivery and eventually having healthy triplets with the prophylactic use of intravenous pdC1INH

Immediate and Late Onset Forms of Insulin Hypersensitivity Presenting with Glucose Dysregulation

WOS: 000452210500009We report the case of a 35-year-old woman allergic to detemir, neutral protamine Hagedorn, and glargine. Initially, local reactions to the insulin preparations occurred, which continued even after the types of insulin and the application areas were changed. When the use of insulin therapy was continued, the local reactions developed into systemic forms. Interestingly, blood glucose levels kept increasing to uncontrolled levels every time the cutaneous reactions occurred. The patient was referred to our clinic for further investigation. The results of the skin prick tests with insulin preparations were negative; however, the intradermal test results were positive with the following dilutions of the insulin preparations: 1/100 detemir, 1/100 glargine, 1/1.000 neutral protamine Hagedorn, and 1/1.000 regular insulin. The intradermal skin test results for glulisine, aspart, and lispro were negative. The levels of immunglobulin E specific to human insulin were high (194 kU/L; N 0-87 kU/L); whereas, the specific immunglobulin G4 levels were normal (35 mg/dL; N 0-125 mg/dL). We attempted to treat the patient with glulisine and aspart; however, similar reactions were observed with these insulin preparations as well. As we considered the levels of the anti-insulin antibodies and the late-onset local reactions, the insulin allergy in our patient was reckoned to be mediated by Type 1 and Type 4 hypersensitivity. The only insulin preparation that had never been used with this patient before was lispro, which also demonstrated negative intradermal skin test results. Therefore, we suggested the use of a continuous subcutaneous insulin infusion pump with lispro. Finally, the insulin hypersensitivity was successfully treated, and glycemic control was achieved