Fuat Erel

The role of ace gene polymorphism in the development of angioedema secondary to angiotensin converting enzyme inhibitors and angiotensin II receptor blockers

BACKGROUND Angiotensin Converting Enzyme inhibitors (ACEi) may cause angioedema, with an incidence of 0.1 % to 1 %, which may be life-threatening. ACEi induce angioedema by increasing the levels of bradykinin. Angiotensin II receptor blockers (ATRB), have a pharmacological profile similar to ACEi. The polymorphism of the ACE gene is based on the presence or absence of a 287-bp element on intron 16 on chromosome 17. The plasma level of ACE is related to gene polymorphism. ACE level in genotype DD is double that in genotype II. OBJECTIVE The aim of this study was to investigate whether the relationship between ACE gene polymorphism and ACEi induced angioedema is present or not. METHODS ACE gene polymorphism was investigated in patients with angioedema due to the use of ACEi or ATRB (n:32, group 1), in patients receiving ACEi or ATRB without angioedema (n:46, group 2), and healthy controls (n:96, group 3). RESULTS ID polymorphism was the most frequent genotype in all groups, without any significant difference among the groups (p:0.868). ACE gene polymorphism was not related with the drugs used (ACEi or ATRB), localisation of angioedema, and female sex, in group 1. CONCLUSION Our results showed that ACE gene polymorphism has no effect on ACEi or ATRB induced angioedema.

Serum Leptin Levels and Lipid Profiles in Patients with Allergic Rhinitis and Mild Asthma

BACKGROUND Despite improved understanding of the pathophysiology of allergic rhinitis and asthma, the effect of serum leptin level is still controversial. Only a few studies have been performed to investigate the serum leptin levels in allergic rhinitis and asthma, and contradictory results have been observed. OBJECTIVE We aimed to investigate the association between leptin, lipid profiles and allergic rhinitis and mild asthma, and to determine whether inhaled and/or intranasal steroids affect the leptin levels. PATIENTS AND METHODS We studied 43 patients with allergic rhinitis (10 of with mild asthma) (mean age 29.81, range 18-45 yr) and 32 volunteers as a control group (mean age 30.53, range 20-45 yr). RESULTS Serum leptin levels in patients were 8.49 +/- 10.76 microg/ml, and did not differ from volunteers 5.42 +/- 6.63 microg/ml. (p > 0.05). We found a direct link between increased body mass index (BMI) and serum leptin levels (p = 0.008). No association was seen between leptin and triglyceride, HDL-cholesterol, VLDL-cholesterol, eosinophil, total IgE (p > 0.05); except for total cholesterol and LDL-cholesterol (p < 0.05). Although, no correlation between allergic rhinitis and mild asthma and serum level of leptin was shown, these parameters and age correlations were stronger in female than in male (p = 0.39 for male and p = 0.011 for female), and also found direct link between increased BMI and sex and patients group (p = 0.008 for male and p = 0.0001 for female). We also determined that there was no effect of inhaled and/or intranasal steroids statistically on serum leptin levels. CONCLUSION Our data demonstrate that the serum levels of leptin and lipid profiles on allergic rhinitis and mild asthma were not different than those in controls.

A successful pregnancy and uncomplicated labor with C1INH concentrate prophylaxis in a patient with hereditary angioedema

Patients with hereditary angioedema (HAE) need a special concern during pregnancy. Although, the disease has a relatively benign course during pregnancy, maternal mortality has been reported. We present a HAE patient with recurrent attacks during pregnancy, but uncomplicated labor under C1INH concentrate prophylaxis.

Atopy is a Risk Factor for Acute Appendicitis? A Prospective Clinical Study

PurposeThe purpose of the study was to assess the role of atopy on the development of appendicitis. Acute appendicitis is the most common indication for emergent laparotomy especially in the late teens and early 20s. The pathogenesis generally begins with luminal obstruction caused by fecal mass, seeds, stricture, and bacterial, parasitic, or viral infections. The present study was designed to evaluate whether allergic reaction is indeed an undefined leading factor for luminal obstruction.Material and MethodsMix inhalant and food prick tests were performed in 111 patients who underwent appendectomy for acute appendicitis and in 100 control patients. The material of appendectomy was examined, acute appendicitis was verified and graded according to the severity of inflammation and eosinophilic infiltration rate in the wall of appendix by a pathologist. Demographic data were recorded, and peripheral eosinophil count was also performed.ResultsMix prick test of 33 patients (29.7%) and food prick test of 14 patients (12.6%) were positive in study group when compared with 7 patients (7%) and 1 patient (1%) in control group (p < 0.001). A total of 38 patients (34.2%) in the study group were reactive with mix or food prick test when compared with 8 patients (8%) in control group. There was no significant difference between eosinophilic infiltration rate, peripheral eosinophil count, severity of inflammation, and Alvarado score of mix prick test positive and negative patients in study group.ConclusionAtopy incidence in patients with acute appendicitis was significantly higher when compared with control group. However, eosinophilic infiltration rate, inflammation grade, and peripheral eosinophil count were not able to explain the relationship between the two conditions. Atopy is a risk factor for acute appendicitis.

Is allergenic similarity predictable in respiratory allergies

BACKGROUND First degree relatives of patients with allergic diseases are at increased risk of having the disorder. However, it is not clear whether two such related patients with allergic diseases are sensitive to the same antigens or not. OBJECTIVE The aim of this study to determine whether or not first degree relatives with respiratory allergies are more likely to be skin test positive to the same allergen extracts as unrelated patients. PATIENTS AND METHODS Skin test results for 35 common aeroallergens were compared in 264 pairs of genetically related subjects and 264 pairs of age and sex matched, but unrelated, subjects. We calculate the percentages of the concordant and discordant results in each group. Results are compared by using chi2 test. RESULTS For all related and unrelated groups combined, there were significant differences with mites (der. pteronyssinus, der. farinae) and some moulds (aspergillus mix and rhizopus nigricans) (p<0.05); When the groups were subdivided into parent-child pairs and same or different sibling pairs, and the same comparisons were made, a significant difference was only found in both sibling pairs (p<0.05), not in parent-child pairs (p>0.05). Since there was no both positivity with aspergillus mix and rhizopus nigricans in the two groups, these two allergens were excluded from the study. CONCLUSION It is concluded that we could not say that if one or both of parents are atopic to any allergens, their child will be atopic to the same allergens. Besides, when a respiratory allergy occurs in siblings, only the one who has house dust mite allergy sensitivity can possess the similar antigen sensitivity.

Not all ACE inhibitor related angioedema is always evident: A case which is misdiagnosed as panic attack and speech disorder

Angiotensin-converting enzyme (ACE) inhibitors are the most common medications responsible for angioedema. Angioedema is a potentially life threatening conditions especially in geriatric age patients that they have take a several medications include ACE inhibitors and non steroidal anti inflammatory drugs. We present a case an ACE inhibitor induced angioedema that confused many clinical events.