Faculty of Medicine

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PLUCNA EMBOLIJA U BOLESNIKA S LEIDENOVOM TROMBOFILIJOM FAKTORA V I PSORIJAZOL: PRIKAZ SLUCAJ.
(Association of pulmologists from Republika Srpska, 2023-05)
Baloski Marjan
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Bushev Jane
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Brishkoska-Boshkovski Vesna
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Hasan Taner
Cilj: Genetski faktori rizika pove!avaju rizik venske tromboembolije. Poremecaji u sintezi ili aktivnosti faktora koagulacije. Faktor V Leiden, protrombin (20210-A), antitrombinski deficit, deficit proteina C i proteina S i hiperhomocisteinemija najcesce su mutacije gena povezanih sa venskim tromboembolijom . Uvod : Psorijaza i prisutvo mutacije trombofilnih gena povecava rizik venske tromboembolije. Prethodna venska tromboembolija je jedan od najjacih faktora rizika, cak i kod pacijenata koji su aktivno leceni antikoagulansom. Psorijaza je kompleksna imuno posredovana bolest, povezana sa kardiovaskularnim rizikom, markerima hiperkoagulabilnosti i povisenim homocisteinom. Mnogo izvjestaja o opservacijama sugerira povecanu ucestalost venskih trombembolickih dogadaja kod pacijenata sa psorijazom. Nalazi: Prikazujemo bolesnika s nasljednom trombofilijom i kronicnom difuznom psorijazom kompliciranom plu!nom embolijom. Analiza DNK ukazuje na prisutnost homozigoze za mutaciju faktora V Leidena. Dermatoloska anamneza je pozitivna na psorijazu. Zaklju!ak: Prikaz ovog slucaja ukazuje na povezanost venske tromboembolije i psorijaze. Pacijenti sa naslednom trombofilijom, psorijazom I plucnim tromboembolizmom, imaju visoki rizik od razvoj venske tromboembolije.
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LUNG CANCER AS A COMORBIDITY OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
(2023-01)
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Buklioska Adriana
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Mickovski Ivana
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Trajkova Vesna
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COPD is a risk factor for lung cancer development independent of smoking status, with three to six times more likely to develop lung cancer at a rate of 0.8–1.7%/year. This may be associated with genetic susceptibility to cigarettes, chronic inflammation caused by toxic gases. Inflammatory mediators may promote the growth of bronchioalveolar stem cells, and activation of nuclear factor-κB and signal transducer and activator of transcription 3 play crucial roles in the development of lung cancer from COPD. The aim of the study is to evaluate the prevalence of lung cancer in patients with COPD. We performed a retrospective study, from 2012 to 2022, among patients with pathologically confirmed diagnosis of lung cancer, aged 40-75 years. Patients with lung cancer that had COPD diagnosed >= 10 years before lung cancer diagnosis, were investigated group. Histological subtypes of lung cancer were determined based on histopathology reports and were categorized as squamous carcinoma, adenocarcinoma, small cell lung cancer (SCLC), large cell lung cancer (LCLC; including large cell neuroendocrine carcinoma), and other histological types according to 2015 WHO classification of lung tumors. At the time of registration, sex, age, BMI, smoking status, treatment history, and symptoms, including the CAT score, were recorded. In addition, at the time of registration, spirometry was performed both before and after inhalation of a bronchodilator, and a blood test and chest CT were also performed. The GOLD criteria was used to diagnose and assign severity of COPD: patients with a postbronchodilator FEV1/FVC <0.70 were classified as having COPD; FEV1 ≥0.8 was defined as mild, 0.5≤ FEV1 <0.8 as moderate, 0.3≤ FEV1 <0.5 as severe, and FEV1 ≤0.3 as extremely severe. Patients were excluded if they presented with simultaneous or sequential second primary cancers or had a history of asthma, bronchiectasis, tuberculosis, pulmonary fibrosis, or other confounding diseases. The middle age of lung cancer diagnosis was 61.1±8.5 years. Of the total number of patients with COPD and lung cancer (260), 195 (75.0%) were male and 65 (25.0%) female. 190 (73.07%) were current smokers or ex-smokers. The histological subtypes identified were as follows: squamous carcinoma (96 [36.9%]), adenocarcinoma (115 [44.2%]), SCLC ( 26 [10.0%]), LCLC (13 [5.0%]), and other histologic types (including adenosquamous, carcinoma carcinoid tumors, sarcomatoid carcinoma; 16 [6.15%]). The proportion of squamous carcinoma was higher in smokers/ex smokers with COPD, while adenocarcinoma was more frequently observed in COPD non-smokers. Emphysema predominant phenotype was an independent prognostic risk factor for squamous carcinoma. The prevalence of COPD in lung cancer patients was 35.5%. Compared with lung cancer patients with non-COPD, those with COPD were older (P<0.001), had a lower BMI (P<0.001), and majority were male (P<0.001) and smokers (P<0.001). Annual low-dose computed tomography (LDCT) is an effective procedure for the early detection of lung cancer in high-risk patients like patients with COPD.
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Alpha-1 antitrypsin deficiency (AATD) in a young female patient
(General Hospital Tešanj, 2022-11-12)
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Mickovski Ivana
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Baloski Marjan
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Bushev Jane
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Buklioska Adriana
Introduction The alpha-1 antitrypsin deficiency (AATD) is a hereditary autosomal codominant disease. The phenotype Pi ZZ is associated more frequently with pulmonary disease and is responsible for the presence of emphysema early in life, particularly in smokers. Generally, AATD is suspected in young patients with pulmonary emphysema or chronic obstructive pulmonary disease (COPD). Patients often suffer from diagnostic gaps and are misdiagnosed with chronic obstructive pulmonary disease (COPD), asthma, and airway hyper-reactivity (AHR), as AATD may present with nonspecific respiratory symptoms. AATD is most common in white people, and it most frequently affects the lungs and liver. In the lungs, the most common manifestation is early-onset (patients in their 30s and 40s) pan acinar emphysema most pronounced in the lung bases. However, diffuse or upper lobe emphysema can occur, as can bronchiectasis. The most frequently described symptoms include dyspnea, wheezing and cough. Pulmonary function testing shows findings consistent with COPD; however, bronchodilator responsiveness may be seen and may be labelled as asthma. Case presentation We describe a case of a 40-year-old Caucasian female patient, admitted to hospital because of dyspnea, malaise, cough. Symptoms started one year ago, after mild SARS-COV 2 infection. Chest X-ray during the acute illness described emphysema, with flattened diaphragm, and no signs of consolidation. According to history she was a non-smoker, office worker, with negative family history of respiratory or liver illness. She never used any regular therapy before, no comorbid diseases and denied frequent respiratory infections during childhood. Chest computer tomography (CT) presented pan acinar emphysema most pronounced in the lung bases. Post bronchodilator spirometry revealed forced expiratory volume in 1st second (FEV1) 54%, and forced vital capacity (FVC) 84%, with FEV1/FVC=0.64. Routine biochemistry laboratory was normal. Gas analyses noted respiratory failure type 1 (partial) with hypoxemia partial oxygen pressure 8.1kPa, hypocapnia because of hyperventilation with partial carbo dioxide pressure 4.1kPa, and oxygen saturation 92%. Echocardiography without any findings of right heart failure, normal systolic pulmonary arterial pressure (sPAP). Abdominal ultrasound without pathological findings, no liver disease detected. According to CT finding the patient was sent to the Institute for clinical immunology and genetic disorders where the serum value of alpha-1 antitrypsin was measured. The value was 0,2 micromoles /L (reference value 5-6 micromole /L). The patient was prescribed inhaled therapy of long acting anticholinergic, short acting beta-2 agonist. She was also suggested therapy with intravenous human alpha 1-proteinase inhibitor (AAT augmentation therapy). Conclusion It is never too late to suspect AATD, especially in a patient with an unusual medical history. In recent years, evidence is beginning to emerge that there may be value in identifying and treating patients who do not already have deterioration of functional parameters. The Alpha-1 Foundation recommendations for the diagnosis and management of AATD in adult patients indicate that treatment should be provided for patients with FEV1 between 30 and 65%. It may be useful to evaluate and treat patients based on clinical symptoms, even outside the established parameters, in particular cases.
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COPD as a risk factor for Coronary Artery Disease (CAD): Overview of 10-year atherosclerotic cardiovascular disease (ASCVD) risk assessment
(2022-12-01)
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Mickovski Ivana
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Baloski Marjan
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Doneva Daniela
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Neshovska Radmila
We aimed to investigate the association between COPD and CAD (overview of 10-year risk of fatal cardiovascularevent), and the relation to the severity of airflow limitation.Cross-sectional study including 220 patients with stable COPD as investigated group (IG), aged 40 to 75 yearsand 58 non-COPD subjects, matched by gender, age, BMI, smoking status, as control group (CG). All studysubjects underwent pulmonary, cardiological evaluation, lipid and glycemic status.The analysis compared the 10-year established ASCVD risk between COPD stages (according to GOLDclassification 1, 2, 3, 4) and between IG vs. CG. ASCVD score was classified as low (score <5%), borderline (5 to<7.5%), moderate (≥7.5 to <20) and high risk (score ≥20%). Results presented statistically significant differencebetween mean ASCVD value in IG 21,69±13,86% vs. CG 15,83±9,92% (p=0.0028). The median risk of ASCVDfor fatal cardiovascular events was high in IG and moderate in CG. The mean and median values of 10-yearASCVD risk in the IG subgroups were: GOLD1 16,79±8,04% (50% of the subjects with risk >15,7%), GOLD222,67±16,49% (50% of the subjects with risk >20,6%), GOLD3 26,81±14,15% (50% of the subjects with risk >27,6%) and GOLD4 20,70±13,52% (50% of the subjects with risk > 18,4%). The average ASCVD risk of fatalcardiovascular event was moderate in GOLD1 and GOLD4, and high in GOLD2 and GOLD3.We found higher risk for fatal cardiovascular outcome in patients with COPD, even in the early COPD stages(GOLD2), compared to non-COPD group. Our findings suggest that an urgent need to develop comprehensivestrategies for prevention, screening and early treatment are needed.
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Diabetes mellitus type 2 (T2D) as a comorbidity of Chronic Obstructive Pulmonary Disease (COPD)
(Publi Créations, 2022-01)
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Mickovski Ivana
We aimed to investigate the association between COPD and T2D and the relation to the severity of airflow limitation. Cross-sectional study including 120 patients with initially diagnosed COPD, aged 40 to 75 years and 60 nonCOPD subjects matched by age, smoking status, body mass index, as controls. All study participants underwent anthropometric measurements, fasting blood sugar (FBS), oral glucose tolerance test (OGTT) (performed in patients with fasting blood sugar level 5.6- 6.1mmol/L (measured two times), lipid profile, CRP, pulmonary evaluation (dyspnea severity assessment, baseline and post-bronchodilator spirometry, gas analyses, chest X-ray). Results presented statistically significant difference in presence of T2D in COPD patients compared to controls (45.0% vs 20.0%; P=0.0011). According to the GOLD classification, the frequencies of T2D in COPD patients were categorized in stages I, II, III, IV (25.0%, 43.3%, 52.5%, 58.3%, respectively), and according to combined assessment test in A, B, C, D (29.2%, 37.5%, 35.0%, 41.7% respectively). In GOLD 2 stage the risk for T2D was 2.3 times higher than GOLD1. COPD patients with T2D presented significant association with pulmonary function. FBS was higher in COPD than controls (8.4±1.1mmol/L vs 4.9±2.1mmol/L) with statistical significance (p<0.0001), but HDL was lower in COPD than controls (39.1±6.4mg/dl vs 49.6±3.9mg/dl) with statistical significance (p<0.0001).We found higher prevalence of T2D in patients with COPD even in early COPD stages compared to nonCOPD. Our findings suggest multidisciplinary approach in COPD patients for prevention, diagnosis and early start of treatment.

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