FIZIOLOGIA
physiology
FOUNDING EDITORCHIEF EDITOR
CO-CHIEF EDITORSASSOCIATE EDITORSEXECUTIVE EDITORSFRANCISC SCHNEIDERCARMEN PANAITESCUCARMEN TATUFLORINA BOJINMIHAI NECHIFORSORIN RIGAGABRIELA TANASIEDACIANA NISTORCALIN MUNTEANEDITORIAL BOARD
ARDELEAN AURELBĂDĂRĂU ANCA
BENEDEK GYORGYBENGA GHEORGHECOJOCARU MANOLEGĂLUȘCAN ATENAIANCAU MARIAMIHALAŞ GEORGETA
MUNTEAN DANINAMUREŞAN ADRIANANESTIANU VALERIUOPREA TUDORPANAITESCU CARMEN(Arad)(Bucureşti)(Szeged)(Cluj)(Bucureşti)(Timișoara)(Craiova)(Timişoara)(Timişoara)(Cluj)(Craiova)(New Mexico)(Timişoara)PĂUNESCU VIRGILPETROIU ANAPODARIU ANGELA CODRUTA
RÂCZ OLIVERRIGA DANSABĂU MARIUS
SAULEA I. AURELSIMIONESCU MAIASWYNGHEDAUW BERNARDTANGUAY M. ROBERTTATU ROMULUS FABIANVLAD AURELIANVOICU VICTORZĂGREAN LEON

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Fiziologia - Physiology • 2017.27.1(93)CONTENTS
1. Clinico-Pathological Evaluation of Pregnancy Induced Hypertension ................................................. 4
Zaha DC, Vesa C, Cismas-Pruteanu P, Daina LG

2. Hyperuricemia – The New Cardiovascular Risk Factor - Consequences and Effects ......................... 9
Moisi MI, Vesa CM, Ardelean AI, Zaha D, Cismaş-Pruteanu P, Magyar I, Popescu MI

3. Implication of Distress and Emotional Intelligence in Forensic Practice ........................................... 14
Cojocaru A, Ageu L

4. Associated Congenital Anomalies in New-Borns Diagnosed with Congenital
Diaphragmatic Hernia ............................................................................................................................ 17
Vesa C, Zaha D, Cismas-Pruteanu P, Moisi M, Mekeres F, Jurca C

5. Depressive Pathology and Bipolar Disorder: Particularities of the Theory of Mind .......................... 20
Homorogan C, Barboianu R, Rivis I, Tulbure BT, Giurgi-Oncu C, Bredicean C

6. Pulmonary Aspergilloma in an Immunocompetent Patient. A Case Report ....................................... 24
Cioboata R, Bazavan I, Georgescu M, Chaudrey S, Gaman AE

CUPRINS
1. Evaluarea clinico-patologică a hipertensiunii induse de sarcină .......................................................... 4
Zaha DC, Vesa C, Pruteanu Cismas P, Daina LG

2. Hiperuricemia asimptomatica - noul factor de risc cardiovascular? - Consecințe și efecte .............. 9
Moisi MI, Vesa CM, Ardelean AI, Zaha D, Cismaş Pruteanu P, Magyar I, Popescu MI

3. Implicațiile distresului și ale inteligenței emoționale în activitatea medicilor legiști ........................ 14
Cojocaru A, Ageu L

4. Anomalii congenitale asociate la nou-născuții cu hernie diafragmatică congenitală ........................ 17
Vesa C, Zaha D, Cismas-Pruteanu P, Moisi M, Mekeres F, Jurca C

5. Patologia depresivă și tulburările bipolare: particularități ale teoriei minții ....................................... 20
Homorogan C, Barboianu R, Rivis I, Tulbure BT, Giurgi-Oncu C, Bredicean C

6. Aspergilom pulmonar la un pacient immunocompetent. Prezentare de caz ...................................... 24
Cioboata R, Bazavan I, Georgescu M, Chaudrey S, Gaman AE

Fiziologia - Physiology • 2017.27.1(93)3CLINICO-PATHOLOGICAL EVALUATIONOF PREGNANCY INDUCED HYPERTENSIONDANA CARMEN ZAHA, COSMIN VESA, PETRISOR PRUTEANU CISMAS,
LUCIA GEORGETA DAINA
University of Oradea, Faculty of Medicine and Pharmacy of Oradea

ABSTRACTIntroduction. ecause the clinical manifestation of preeclampsia can be heterogeneous, laboratory tests can be very useful forearly preeclampsia diagnosis in pregnancy induced hypertension patients.
Method. A total 110 patients with clinical diagnosis of pregnancy induced hypertension (PIH) were included in the study.
Complete blood count, urine examination, biochemical tests (ALT, AST, LDH, T-bilirubin, uric acid) and coagulation tests weredone in all patients. The urinary test checked the usual parameters and proteinuria (24-hour urine collection). In addition, proteincreatinine ratio was evaluated in urinary specimen with a rapid test
Results. In our study, 66 patients had mild PIH and 44 severe PIH. Headache was the predominant symptom followed bygiddiness. Pathological changes of the biochemical, hematological and coagulation parameters were observed mainly in severe
PIH.
Conclusion. Patients significantly younger, low parity had significantly increased systolic and diastolic pressure and changesof values of liver enzymes, uric acid, urine protein, and LDH levels. Abnormalities (qualitative and quantitative abnormalities) of
red blood cells and platelets are frequently seen in PIH. Spot urinary P/C ratio in pregnancy induced hypertension patients canbe used as a screening test as a good predictor for significant proteinuria and could not be used for diagnostic tests to replace24-h urine protein measurements.
Keywords: pregnancy, hypertension, preeclampsia, diagnostic.

INTRODUCTION
Pregnancy-induced hypertension (PIH) remains a major
cause of perinatal and maternal morbidity and mortality,
occurring in 6-10% of all pregnancies [1]. It is defined as
systolic blood pressure (SBP) >140 mmHg and diastolicblood pressure (DBP) >90 mmHg and classified as mild
(SBP 140-149 and DBP 90-99 mmHg), moderate (SBP 150159 and DBP 100-109 mmHg) and severe (SBP ≥160 and
DBP ≥110 mmHg).
To a certain extent, mothers suffer from major complications like development of disseminated intravascular
coagulation (DIC), cerebrovascular accidents, renal failure,
retinal detachment, pulmonary edema, liver rupture,
abruptio placentae, and death. In the case of the fetus,
intrauterine growth retardation, prematurity and intrauterine
death may occur, all being the consequences of placental
insufficiency. Preeclampsia is characterized by theappearance of hypertension and proteinuria, usually after 20
weeks of gestation. There are many tests or methods
reported in the literature for predicting the development ofpreeclampsia, but none of them had shown sufficient
predictive value.

HELLP syndrome, a severe form of pre-eclampsia
develops in 4-12% of women with pre-eclampsia oreclampsia and it is characterized by microangiopathic
hemolytic anemia associated with liver and kidney damage[2]. Based on the maternal platelet count, HELLP syndrome
is classified into three classes:‐ Class 1 - PLT <50,000/mm3,‐ Class 2 – PLT >50,000/mm3 and <100,000/mm3, and‐ Class 3 - PLT >100,000/mm3 and <150,000/mm3.
Thrombocytopenia is the most common hematologic
abnormality and its detection is important because it is oneof the preventable factors that contribute to a great
proportion of life threatening cerebral and hepatic
hemorrhages.
Proteinuria is an important sign of preeclampsia.
According to the International Society for the Study ofHypertension in Pregnancy proteinuria is diagnosed basedon the following criteria: spot urine protein/creatinine >30
mg/mmol or > 300 mg/day or at least 1 g/l (2+) on dipstick
testing [3]. The gold standard for detecting significant
proteinuria is 24-hour urine collection, but 24-hour urine
collection is associated with delayed diagnosis and therapy.

Received 15th of May 2017. Accepted 10th of June 2017. Address for correspondence: Dana Carmen Zaha, Lecturer, Department of Preclinical
Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 10 of 1 December Square, 410068 Oradea, Romania; phone +40723–
604 496, e-mail: danaczaha@gmail.com

4

Fiziologia - Physiology • 2017.27.1(93)Various methods have been used to shorten the time todiagnosis of preeclampsia.
Reagent strip tests for detecting proteinuria fail to detect
minimal elevation in urinary excretion of albumin that may
be present before other clinical signs and symptoms ofpreeclampsia appear. Microalbuminuria refers to subclinicalelevation of urinary albumin excretion and it has been shown
to precede the development of chronic renal failure inpatients with insulin-dependent diabetes mellitus, and may
be an evidence of renal involvement in hypertension.
In order to predict significant proteinuria random urinary
protein-creatinine ratio has been suggested as a rapid test
in recent years. A good correlation between random urinary
protein/creatinine ratio and 24-hour protein excretion has
been demonstrated by many studies, while others havefound it to be of limited use [4].
Our study purpose is to evaluate hematological,
coagulation and biochemical abnormalities associated withurinary excretion of protein in a cohort of women presenting
pregnancy induced hypertension.

MATERIAL AND METHODSThis retrospective study was done on 110 pregnant
women admitted in the department of Obstetrics andGynecology Oradea Hospital between January 2015 andOctober 2017. Clinical examination, complete hemogram,urine examination, coagulation tests and biochemical tests
were done on selected patients.
Paired samples for measurement of urinary protein:creatinine ratio, 24-h protein excretion were collected. Spoturine specimens for measuring protein: creatinine ratio wascollected before 24-hour urine collection. Architect automatic
analyzer method was used to measure 24-h protein excretionand biochemical parameters. We consider proteinuria asurine protein excretion greater than or equal to 300 mg/24 h.
Protein-creatinine ratio was evaluated in a random urinary
specimen with a rapid test. Patients with urinary tract
infections, preexisting chronic renal disease, diabetes,
chronic hypertension, were removed from the study.
Quantitative data were presented as mean (SD) or
median (range) while qualitative data were presented as n(%). Student`s t-test and the chi-squared test were used tocompare groups. For all these tests, the level of significance(P-value) is below 0.05.

RESULTS
The median maternal age was 28.9±6.67 years (range
15–46 years), and the mean body mass index (BMI) was
30.6±5.3 kg/m2 (range 20–53 kg/m2). The mediangestational age was 33.8±4.3 weeks (range 20–39 weeks).
In total, 43.11% of patients were under 34 weeks ofFiziologia - Physiology • 2017.27.1(93)gestation, while 56.89% of patients were after 34 weeks ofgestation at diagnosis. Of the 110 cases 68.8% of patientswere nulliparous.
In our study, 66 (60%) had mild PIH and 44 cases (40%)
had severe PIH. The mean age in the mild PIH was
29.54±6.67 years (range 15-46 years) and 28.57±6.6 years(range 16-45 years) in severe PIH. Table I shows age
distribution of cases.
Table I. Age distribution
Age (years)
15 - 20
21 - 25
26 - 30
31 - 35
36 - 40
41 – 45
46 - 50

Number of cases (%)
Severe PIH
Mild PIH
7
8
11
6
12
21
9
18
3
9
2
2
0
2

Cases with mild PIH were asymptomatic, whereas allcases of severe PIH were symptomatic with headache being
the predominant symptom present in 22 cases (50%)
followed by blurred vision in 3 cases (6.8%), dizziness in 6
cases (13.6%), vomiting in 5 cases (11.3%), reduced urine
output in 4 cases (9%), and epigastric pain in 4 cases (9%).
Mean serum creatinine level was 0.65±0.12 mg/dL(range 0.46–1.24 m/dL); 3 (2.7%) of these patients had ablood creatinine level of 1 mg/dL or higher. Mean uric acidlevel was 5.2±1.38 mg/dL (range 2.8–9.1 mg/dL) higher
levels appearing in severe PIH. Serum bilirubin levels wereraised only in 4 cases of severe PIH and were normal in theremaining cases. Aspartate aminotransferase (AST) levels
ranged between 10-393 IU/L (mean 32.57±52 IU/L), withhigher values being present in cases of severe PIH. Meanalanine aminotransferase levels was 30.6± 62.8 IU/L (range
7-543 IU/L), markedly elevated (>70 IU/L) in the same 4cases of severe PIH. Higher levels of serum LDH
corresponds to cases with higher values of BP as we cansee in Table II.
Table II. Biochemical evaluation results.
Parameter
Mean
Serum
Severe PIH
0.85±0.11
creatinine
Mild PIH
0.66± 0.14
(mg/dL)
Severe PIH
5.7±1.4
Uric acid(mg/dL)
Mild PIH
4.28 ±1.2
Severe PIH
0.67±0.12
T-bilirubin(mg/dL)
Mild PIH
0.32± 0.06
Severe PIH
36.75±77.3
ALT (IU/L)
Mild PIH
19.76 ± 15.85
Severe PIH
37.78± 64.91
AST (IU/L)
Mild PIH
23.38 ± 11.67
Severe PIH
421±201.4
LDH (IU/l)
Mild PIH
356±122.8

Range
0.56 -1.4
0.32 - 1
3.8 – 9.1
2.8 – 6.2
0.27 – 1.6
0.20 – 0.7
7 - 543
8 - 68
10 - 393
11 - 6198 - 921
101 - 452

5

Hemoglobin levels of all patients varied from 7.4 to 14.35
g%, the mean value being 11.57 g%. The mean corpuscularvolume (MCV) and mean corpuscular hemoglobin (MCH) in
mild PIH and in severe PIH had close average values. Platelet
count was between 61.080 – 466.000/mm3 in cases of severe
PIH and 123.000 – 544.000/mm3 in mild PIH. The otherhematological parameters did not differ significantly fromthose expressed in normal pregnancy that is why they were
not statistically processed.
Table III. Hematological parameters
Parameter
Mean
Severe PIH
11.68 ± 1.6
HGB (g%)Mild PIH
11.43±1.53
Severe PIH
83.06±6.25
MCVMild PIH
83.38±6.01
Severe PIH
27.25±2.75
MCH
Mild PIH
27.5±2.48
Severe PIH
249±80.34
PLT
Mild PIH
269±105.65

Range
7.4 – 12.35
8.57 – 14.11
62.3 - 94
70 - 99
18 – 33.5
22 - 32
61.08 - 466
152 - 544

Concerning the coagulation tests, fibrinogen wasincreased in all cases, mean value 676.29±200.67mg/dL.
APTT was normal in all cases of mild PIH and most cases ofsevere PIH but prolonged (>29 s) in 6 cases of the last one.
The PT was significantly prolonged only in 4 cases of severe
PIH.
Table IV. Coagulation tests results
Parameter
Mean
Severe662.79Fibrinogen
PIH±197.19(mg/dl)Mild PIH
700.2±208.3
Severe24.7±2.75
PIH
APTT (sec)Mild PIH
25.78±3.2
Severe8.79±1.13
PIH
PT (sec)
Mild PIH
9.16±0.75

Range
198 - 1388
256 - 1228
18.9 – 32.5
18.1 – 32.2
5.4 – 13.5
7.8 – 11.3

The mean protein level was 3.94 g (range 0.1–13 g) in
24-hour protein excretion test for 110 patients. Values werehigher in the severe PIH group. The mean P/C ratio was
3.16 mg/g (range 0.12–69.6 mg/g). Urine examination
revealed 1+ and 2+ proteinuria in 48 cases (72.72%) of mild
PIH, while majority (41 cases, 93.18%) of those with severe
PIH had 2+ and 3+ proteinuria.
Table V. Urinary results
Parameter
Urinary
protein(mg/24h)
Spot urine protein(mg/dL)
Spot urine creatinine(mg/dL)
Protein/creatinine
ratio (mg/mg)

6

Severe PIH
Mild PIH
Severe PIH
Mild PIH
Severe PIH
Mild PIH
Severe PIH
Mild PIH

2866.28±3328.81
886.67±525.6
314.68± 257.73
145.90±107.79
92.03± 68.87
85.09±49.65
3.17±0.79
2.92± 0.48

DISCUSSION
In the present study, the mean age in the mild PIH groupwas 29.49 ± 6.66 years and, in the severe PIH group it was
28±6.67 years, being in concordance with the observation
made by O’Brien et al. that PIH is mainly a disease of young
nulliparous [5]. Headache was the predominant symptom
seen in 50% of severe PIH patients followed by dizziness in
13.6% of patients, the results being similar with the one
reported in other studies.
Abnormal serum bilirubin levels were detected as result of
liver damage, including because of pre-eclampsia, its risesignifying the severity of the condition. On the other hand,bilirubin is described as an anti-oxidant and levels in the upper
end of the normal range are associated with reduced
cardiovascular and respiratory morbidity [6]. It has beensuggested that a higher oxidative stress response means amore severe form of pre-eclampsia, therefore consumption of
more anti-oxidants e.g. bilirubin. Many studies reported meanbilirubin concentration in severe PIH to be significantly higher
than in mild PIH. In our study, there was no significant
difference in mean bilirubin concentration between the mildand severe PIH groups; levels have been raised only in 4
cases of severe PIH.
Serum LDH levels has signiﬁcant associations withvarious disorders, therefore total serum LDH is a sensitive
but a nonspecific test. In preeclampsia also LDH may beelevated and can indicate the prognosis for both mother andfetus [7]. Because levels of LDH < 600 IU/L are common innormal pregnancy only levels > 800 IU/L were reported to
be associated with complicated pre-eclampsia [8]. In thepresent study the LDH levels raised proportionally with theincrease of the values of DP and BP, but only 4 cases
showed values over 800 IU/l, in the severe PIH group.
The mean AST, ALT values were higher than normal(>70 IU/L) in severe PIH group, four cases presented values
greater than 100 IU/L. Liver enzymes may contribute to thediagnosis of HELLP syndrome in addition with the otherbiochemical and hematological parameters.
During early pregnancy serum uric acid level decreases,
related to the effects of estrogen and the increase in renal
blood flow. Uric acid levels then increase during the third
trimester, reaching levels of 4–5 mg/dL by term. It is known
that subjects who develop preeclampsia show slightly higher
serum uric acid levels during the first trimester in association
with a relative reduction in urinary urate excretion and thedegree of elevation correlates with the severity of thematernal and fetal complications [9]. In our study, 30 patientsover 20 weeks of pregnancy had elevated uric acid levels(>8 mg/dL), 21 belonging to severe PIH group, with values
between 6 and 9.1 mg/dL. The remaining cases withelevated uric acid, between 6-8.2 mg/dL belonged to themild PIH group.
Women with pre-eclampsia develop a variety ofhematologic dysfunctions such as platelet abnormalities, redcells abnormalities with impact on the maternal and neonatal
Fiziologia - Physiology • 2017.27.1(93)morbidity and mortality. Patients with severe pre-eclampsia
have a microangiopathic hemolytic anemia. The meanvalues of hemoglobin, MCV and MCH were close in the
two PIH groups. Patients with anemia were included in theiron deficiency cause of microscopic hypochromic anemia(25 from 110 cases). Hemolytic peripheral blood picture
was present in only four cases of severe PIH, confirmedby findings on peripheral smear (burr cells, schistocytes,
polychromasia). All these four cases had thrombocytopenia
and elevated liver enzymes.
The platelet count decreases in normal pregnancy
possibly due to haemodilution, with a maximal decrease in
the third trimester. On the other hand, thrombocytopenia is
a common hemostatic abnormality of preeclampsia,
present in approximately 50% of patients according to a
recent study done by Donimath et al. [10] In our study, 10%
patients had thrombocytopenia and they were part of thesevere PIH group. There is a significant relationshipbetween thrombocytopenia and the severity of the PIH.
Pregnancy is associated with changes in hemostasis,an increase in the level of clotting factors, a decrease in
the quantity of natural anticoagulants and a reduction in
ﬁbrinolytic activity. Pregnancy leads to a state of
hypercoagulability, likely due to hormonal changes andincreases the risk of thromboembolism. Coagulation
profile is an important parameter for detecting effects of
PIH or pre-eclampsia, patients could have a significant
abnormality in platelet function as well as number.
Coagulation studies were done in all the patients included
in our study. The mean PT was significantly prolonged incases with severe PIH, according with similar observation
made by others [11] The mean APTT in severe PIH wassignificantly prolonged in the study done by Thomas et al.
and Jambhulkar et al. [11,12]. There were no significant
differences between the mean APTT of mild and severe
PIH patients in our study.
Proteinuria is a diagnostic test of pre-eclampsia. In ourstudy, proteinuria was present in all the cases (100%). Using
24-hour protein collection, Jambhulkar et al. observed
proteinuria in only 68% cases of mild PIH and 92% cases ofsevere PIH [12]. The P/C ratio in spot urine was introduced
as an alternative test. Many studies reported potential errors
in determining protein in a spot urine sample due to the daily
variation of protein elimination. Evaluation of spot urine P/Cratio in pregnant women with suspected preeclampsia has
been found to be closely correlated with the 24-hour urine
protein measurement, but there is no reliable evidence
about the optimal cut-off value for defining it. The mostrecent study stated that the optimum threshold for P/C ratio
to determine proteinuria is between 0.30 and 0.35, withdetermining sensitivity and specificity values above 75%;
when the sensitivity and specificity above 80% was
accepted, there was no cut-off found [13]. In our study, urine
parameters examined have shown higher values in thesevere PIH group.

Fiziologia - Physiology • 2017.27.1(93)CONCLUSION
Younger patients with lower parity grade had significantly
increased systolic and diastolic blood pressure values andelevations of values of liver enzymes, uric acid, urine protein,and LDH levels. Abnormalities (qualitative and quantitative
abnormalities) of red blood cells and platelets are frequently
seen in PIH. Coagulation tests can be changed because ofthrombocytopenia, as increased platelet consumption is anearly feature of this disorder. We conclude that spot urinary P/Cratio in hospitalized women with suspected preeclampsia canbe used as a screening test and a good predictor for significant
proteinuria but cannot be used as diagnostic tests to replace 24h urine protein measurements.

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Hemat Blood Trans 1998; 16:7-11.
12. Jambhulkar S, Shrivastava R, Shrikhande A, Deshmukh K.
Coagulation profile in pregnancy induced hypertension,
Indian Journal of Hematology and Blood Transfusion 2001;
19(1):3-5.

7

13. Demirci O, Kumru P, Arınkan A, et al. Spot
Protein/Creatinine Ratio in Preeclampsia as an

Alternative for 24-Hour Urine Protein. Balkan Med J 2015;
32:51-5.

EVALUAREA CLINICO-PATOLOGICĂ A HIPERTENSIUNII INDUSE DE SARCINĂREZUMAT
Introducere. Deoarece manifestările clinice ale preeclampsiei pot fi heterogene, testele de laborator sunt foarte utile în
diagnosticul precoce al preeclampsiei la pacientele cu hipertensiune indusă de sarcină.
Metode. În acest studiu au fost incluse 110 paciente cu diagnostic clinic de hipertensiune arterială indusă de sarcină (PIH). S-au
efectuat următoarele analize la toate pacientele: hemoleucogramă, examen sumar de urină, teste biochimice (ALT, AST, LDH,
bilitubina totală, acid uric) și teste de coagulare. Testele urinare au inclus parametrii uzuali și determinarea proteinuriei (în urina
colectată 24h). În plus, a fost determinat și raportul proteine/creatinină (P/C) în probele de urină cu ajutorul unui test rapid.
Rezultate. În acest studiu, 66 de paciente au prezentat PIH ușoară și 44 de paciente au avut PIH severă. Cefaleea a fost
simptomul predominant, urmat de amețeli. Modificările patologice ale parametrilor hematologici, biochimici și de coagulare au
fost observate mai ales la pacientele cu PIH severă.
Concluzii. Pacientele semnificativ mai tinere, cu paritate scăzută au prezentat valori semnificativ crescute ale tensiunii sistoliceși diastolice și modificări ale valorilor enzimelor hepatice, acidului uric, proteinelor urinare și LDH. Anomalii (calitative și
cantitative) ale eritrocitelor și trombocitelor sunt întâlnite frecvent în PIH. Testul rapid de determinare a raportului P/C din urină
la pacientele cu hipertensiune indusă de sarcină poate fi folosit ca test de screening în predicția proteinuriei semnificative și nu
poate fi utilizat ca test diagnostic în locul evaluării proteinuriei/24 h.
Cuvinte cheie: sarcină, hipertensiune, preeclampsie, diagnostic.

8

Fiziologia - Physiology • 2017.27.1(93)HYPERURICEMIA – THE NEW CARDIOVASCULARRISK FACTOR - CONSEQUENCES AND EFFECTSMĂDĂLINA IOANA MOISI1, COSMIN MIHAI VESA1, ADRIANA IOANA ARDELEAN2, DANAZAHA2, CISMAŞ PETRIŞOR PRUTEANU2, IOAN MAGYAR2, MIRCEA IOACHIM POPESCU2
1Emergency County Hospital Oradea
2Faculty of Medicine and Pharmacy, University of Oradea

ABSTRACTIntroduction: The concept of correlation between serum uric acid high levels and cardiovascular disease is strongly debatedlately and remains controversial. Different authors believe that uricemia is a risk factor, prediction factor or even causal factor.
Interpretation of data is difficult because of strong interrelations between serum uric acid and all CV risk factors, especially whenmetabolic syndrome is associated.
Material and Methods: We gathered the documents of patients dispensed from the cardiology department of the County
Emergency Clinical Hospital from Oradea, from 2016, and we formed a study lot consisting of 25 patients. The study lot was
divided in two gruops, so the subjects with normal serum level of uric acid represented the control group (C.G), and the patientswith hyperuricemia were included in the refference group (R.G). Clinical examination, laboratory tests , electocardiography and
2D echocardiography were also performed.
Results: The C.G. developped especially grade I and II hypertension, stable angina pectoris and heart failure NYHA I and II.
This fact reflects the correlation of hyperuricemia with high blood pressure ( grade III) in 33.33% of the R.G. , unstable angina
pectoris in 26,66% of the R.G., and heart failure NYHA III and IV was discovered in 40% and 20 % of the subjects fromthe R.G. Acute myocardial infarction was detected only in the R.G. The explanation reflects that uric acid under ischemic
conditios will generate oxidative stress reactive species (peroxynitrite) promoting endothelial disfunction, inflammation,oxidized LDL synthese which will be storaged in the foamy cells from the initmal layers of the vessels, so the atheroma plaquewill be intiated.
Conclusions: Even if the quality of risk factor isn’t well defined, it is mandatory that a regular laboratory examination include
the uric acid serum levels. In the global assessment of cardiovascular risk factors , uric acid determination may be helpful,providing dates for estabilishing a long therm prognosis and future therapeutic intervention. In patients with cardiovascularpathology who have a high CV risk, the detection and management of hyperuricemia has become essential. European
guidelines regarding the heart failure and coronary artery disease recommends treatment with allopurinol in patients withhyperuricemia.
Keywords: Hiperuricemie, endothelial disfunction, reactive species of oxygen, inflammation

INTRODUCTION
Important epidemiological studies have demonstrated
the association of serum uric acid high levels withhypertension, cerebrovascular disease, coronary arterydisease, preeclampsia and renal disease [1].
Analyzing the data of numerous prospective studies
investigating the association of serum uric levels in different
subjects, most authors concluded that in the general population
at low CV risk, if the traditional risk factors are eliminated, uricacid becomes a poor morbidity predictor. In hypertensive andespecially in high and high risk CV categories (in diabetics, inthe case of a history of stroke, in those with coronary
angiographic disease or in patients with heart failure), uric acidhas been shown to be a major CV risk predictor [2].

The release of adenosine is increased under hypoxia
conditions and its vasodilating action will restore local bloodflow thus preventing tissue ischemia. The final adenosine
catabolism product is uric acid, thus hyperuricemia became
an important marker for detecting subclinical ischemia.
Xanthine oxidoreductase represents the enzyme
responsible for degradation of the adeosine to uric acid andpossess two isoforms, who are operating in different
conditions. Xanthine dehydrogenase, the form that operates
predominantly under physiological conditions, uses theoxidized form of nicotinamide adenine dinucleotide (NAD +)as an electron acceptor [3]. In case of ischemia, xanthine
dehydrogenase is converted to xanthine oxidase, whichuses molecular oxygen as an electron acceptor andproduces, in addition to uric acid, free oxygen radicals.

Received 22nd of April 2017. Accepted 13th of May 2017. Address for correspondence: Madalina Moisi, Emergency County Hospital Oradea,
Republicii Street 37, Oradea 410167, Romania; phone: 0259 437 750; e-mail: mada_vidican@yahoo.ro

Fiziologia - Physiology • 2017.27.1(93)9MATERIAL AND METHODS
We gathered the documents of patients dispensed fromthe cardiology department of the County Emergency Clinical
Hospital from Oradea, from 2016, and we formed a study lot
consisting of 25 patients. The study lot was divided in two
gruops, so the subjects with normal serum level of uric acidrepresented the control group (C.G), and the patients withhyperuricemia were included in the refference group (R.G).
Clinical examination, paraclinic assessment including thefollowing tests: serum uric acid level, LDL-c, HDL-c, total
serum cholesterol, triglycerides, urea, creatinine, glomerular
filtration rate and fasting blood glucose, along withelectocardiography and 2D echocardiography were
performed.

RESULTS
Fig. 1. Xanthin oxidoreductase isoforms

The high uric acid will promote oxidized LDL particles
synthesis through these oxygen stress reactive species(peroxynitrite) [4]. These molecules will be stored in the
foamy cells in the intimal layers of the vessels, consisting
the first step in developing the atheroma plaque.
Another source of production for foam cells is smoothmuscle cells from medium layer of the vessels. Unlike
macrophages, smooth muscle cells have a higher
expression of LDL receptors on their surface. Both cell types
have frenzied mechanisms that prevent excessive
incorporation of cholesterol, but accumulation of cholesterol
is more pronounced in atherosclerotic areas. It is assumed
that apo-E with increased affinity for LDL favors
macrophage metamorphosis [5].
Modified LDL stored in the intimal layers inhibits NO
production and stimulates ET1 synthesis, inhibits therelease of prostacyclin favoring thromboxane production,
augmenting vasoconstriction and platelets aggregation.
Another consequence of high uric acid and oxidative
reactive species production is the release of NF-IB (nuclear
transcription factor) which is responsible for inflammation
through increased cytokines synthesis [6].
The family of adhesion molecules can be divided into
three categories: selectins (L-selectin, E-selectin, P-selectin),
integrins and immunoglobulins (VCAM, ICAM, PECAM-1) [4].
Adhesion of endothelial monocytes, platelets and neutrophils
leads to so-called endothelial activation with various
consequences: synthesis of pro-inflammatory cytokines byactivated macrophages, T lymphocytes, endothelial cells,smooth muscle cells; surface receptor production, enzymes,
growth factors. Inflammatory cytokines are interleukins, TNF,
MCP-1, MCP-4, COX-2 [4]. Inflammation is responsible forcellular apoptosis and uric acid production.

10

Fig. 2. Paraclinical characteristics of the study group.

The analyses of the cases with angina pectoris
revealed the fact that stable angina pectoris wascharacteristic for 50% of the C.G. and 70% of the R.G.,
whereas unstable angina pectoris and myocardial infarction
were found only in the R.G. in 26.66 % of subjects,
respectively 21.40 % of patients. These made us
determinate the relatioship between uric acid levels andappearance of unstable angina in the hole study lot. It iseasy to see that only values situated between 12-14 mg/dl
was associated unstable AP.

Fiziologia - Physiology • 2017.27.1(93)40% of patients were included in NYHA class III;
20% of patients were enrolled in NYHA IV class.
The conclusion is that severe heart failure is seen inpatients with hyperuricemia whereas light heart failure wascharacteristic for patients with normal uric acid levels.
The relationship of interdependence between
hyperuricemia and heart failure incidence in the R.G. reveals
that values between 8-12 mg / dL included NYHA class II and
III subjects, values between 13-15 mg / dL corresponded to
NYHA classes II, III and IV patients with congestive heart
failure. Most cases of NYHA IV heart failure coincided with thehighest uricemic values, respectively 14 and 15 mg / dl.
‐‐

Fig. 3. Uric acid values correlation with unstable AP

Fig. 5. Relationship of interdependence between uric acid levels(mg/dl) and congestive heart failure degree (NYHA class) in the R.G.

As most of severe pahological conditions were discoveredin the R.G. we considered usefull to detect the variations of
LDL and HDL cholesterol in the refference study lot. We
discovered that high uric acid levels situated between 8-12
mg/dl associated normal LDL and HDL values. High uric acidlevels ranging from 13 to 15 mg/dl included high LDL values
and decreased HDL.
Fig. 4. Repartition of NYHA heart failure classes in the study lot

We tried to determinate the incidence of heart failure in
the study lot. We concluded the following results: 40% ofcases with heart failure were discovered in the C.G. and thefollowing repartition was characteristic:‐ 10% of patients were included in NYHA class I;‐ 20% of patients were included in NYHA class II;‐ 10% of patients were included in NYHA class III;No cases with NYHA class IV heart failure have been
detected in this batch
The R.G. reveals a different incidence of heart failure.
From the total amount of 80% of cases detected with heart
failure in this group no NYHA I subjects were identified andthe repartition was the following:‐ 20% of patients were included in NYHA class II;
Fiziologia - Physiology • 2017.27.1(93)Fig. 6. Relationship of interdependence between uric acid levels
and LDL and HDL values in the R.G.
11

Finally we considered usefull to determinate if differtents
paraclinical parametrs have pathoogical values in patientswith hyperuricemia.
We have synthesized a summary of changes in thevarious parameters previously analyzed in relation to thesame common variable, namely uricemia.
The conclusions obtained supported the data from theliterature of speculation and outlined that a progressive
increase in uricemia attracts the following:‐ Proportional increase in LDL;
‐ Proportional increase of SBP;
‐ Proportional increase in abdominal circumference;‐ Proportional increase of DBP;
‐ Proportional increase of BMI;
‐ Proportional HDL reduction.
250

240

240

240

230

BMI

230

CONCLUSIONS
Even if the quality of risk factor isn’t well defined, it ismandatory that a regular laboratory examination include theuric acid serum levels. In the global assessment ofcardiovascular risk factors, uric acid determination may be
helpful, providing dates for estabilishing a long therm
prognosis and future therapeutic interventio, as loweringhigh uric acid levels may be beneficial for cardiovasculardisease outocme. In patients with cardiovascular pathology
who have a high CV risk, the detection and management ofhyperuricemia has become essential. Sometimes uric acidhigh level is the only condition found in patients withessential hypertension. European guidelines regarding theheart failure and coronary artery disease recommends
treatment with allopurinol or oxipurinol in patients withhyperuricemia. Also the Hypertension European Guideline
reclaims determination of uric acid serum levels in patientswith high blood pressure.

220
210

200

200
193

200
200

190

180

180
160
160

170

Axis Title

170

166

187 185

180

SBP
127

125

120

120

110

115

100
90

90
90

95

100

97

124

112
105

110

102
100
99 115
110
108
105

110
93

105 92
100

100

99

100

LDL

60
50

30

DBP

93

70

40

Abdominal
circumf
erence

165

160

156

130

80

170

190

150

140

100

180

175

173

160
150

170 170

168

167
170

180

40

35

35

39

37

35

40

37

38

40

40

40

29

28

40

40

30
35

32

30

20

27
20

10

30

26

23

20

25
19

27

HDL

19

REFERENCES
1. Waring WS, Web DJ, Maxwell SRJ. Uric acid as a risk factor
for cardiovascular disease. QJM 2000; 93(11): 707-713.
2. So A, Thorens B. Uric acid transport and disease. J Clin
Invest 2010; 120 (6): 1791-97.
3. Wu LL, Wu JT. Serum uric acid is a marker of inflammation
and a marker predicting the risk of developing CVD, stroke,
renal failure and cancer. J Biomed Lab Sci 2008; 20 (1-2):
1-5.
4. Kanellis J, Watanabe S, Li JH, Kang DH, Li P, Nakagawa T,
et al. Uric Acid Stimulates Monocyte Chemoattractant
Protein-1 Production in Vascular Smooth Muscle Cells Via
Mitogen-Activated Protein Kinase and Cyclooxygenase-2.
Hypertension 2003; 41: 1287-1293.
5. Strazzullo P, Puig JG. Uric acid and oxidative stresss:
relative impact on CV disease? Nutr Metab Cardiovasc Dis
2007; 17: 409-414.
6. Iliesiu A, Campeanu A, Dusceac D. Serum uric acid andcardiovascular disease. J Clin Med 2010; 5(3): 186-190.

0
8

8

8

9

10

11

11

12

13

13

13

14

14

14

15

Fig. 7. Variations of different parameters with uric acid serum
levels in the R.G.

12

Fiziologia - Physiology • 2017.27.1(93)HIPERURICEMIA ASIMPTOMATICA - NOUL FACTOR DE RISC
CARDIOVASCULAR? - CONSECINȚE ȘI EFECTEREZUMAT
Introducere: Conceptul de corelație între valorile ridicate ale acidului uric seric și bolile cardiovasculare este dezbătut în ultimul
timp și rămâne controversat. Diferiți autori confirmă faptul că hiperuricemia constituie un factor de risc, un factor de predicție
sau chiar un factor cauzal. Interpretarea datelor este dificilă datorită interacțiunilor puternice dintre acidul uric seric și toți factorii
de risc CV, mai ales când se asociază si sindromul metabolic.
Material și Metode: Am selectat documentele pacienților externaţi din departamentul de cardiologie al Spitalului Clinic Județean
de Urgență din Oradea, din anul 2016, și am format un lot de studiu format din 25 de pacienți. Lotul de studiu a fost împărțit îndouă grupe, subiecții cu un nivel normal al acidului uric în serul seric au reprezentat grupul de control (C.G), iar pacienții cu
hiperuricemie au fost incluși în grupul de referință (R.G). Au fost de asemenea efectuate examinări clinice, rezultate de laborator,
electrocardiografie și ecocardiografie 2D.
Rezultate: C.G. au dezvoltat în special hipertensiune arterială grad I şi II, angină pectorală stabilă și insuficiență cardiacă NYHAI și II. Acest fapt reflectă corelarea hiperuricemiei cu tensiunea arterială ridicată (gradul III) în 33,33% din cazuri din R.G., angina
pectorală instabilă în 26,66% din cazuri, de la R.G., și insuficiența cardiacă NYHA III și IV la 40% , respectiv 20% din pacienții
din RG. Infarctul miocardic acut a fost detectat detectat numai în RG Explicația reflectă faptul că acidul uric ,în conditii ischemice,va genera specii reactive de stres oxidativ (peroxinitrit) care promovează disfuncția endotelială, inflamația, sinteza particulelor
LDL oxidate care vor fi depozitate la nivelul celulelor spumoase din itraturile intimale ale vaselor, formându-se astfel placa deaterom.
Concluzii: Chiar dacă rolul de factor de risc nu este bine definit, este obligatoriu ca un examen de laborator să includă și
detectarea nivelurile serice ale acidului uric. În evaluarea globală a factorilor de risc cardiovasculari, determinarea acidului uricpoate fi utilă, oferind date pentru stabilirea unui prognostic şi viitoarele ţinte terapeutice. În cazul pacienților cu patologie
cardiovasculară și risc crescut CV, detectarea și gestionarea hiperuricemiei au devenit esențiale. Ghidurile europene deinsuficiența cardiacă și boala coronariană recomandă tratamentul cu alopurinol la pacienții cu hiperuricemie.
Cuvinte cheie: Hiperuricemie, disfuncție endoteliala, specii reactive ale oxigenului, inflamație

Fiziologia - Physiology • 2017.27.1(93)13IMPLICATION OF DISTRESS AND EMOTIONALINTELLIGENCE IN FORENSIC PRACTICEADRIANA COJOCARU, LUMINIȚA AGEU
Center of Mental Health for Children and Adolescents, Timisoara, Romania

ABSTRACTThe present paper aims to investigate the relationship between empathy and distress, as well as their implications in the activityof the forensic practitioners. The study was conducted on a group of 30 doctors. Emotional distress was measured using theProfile of Affective Distress (PDA), and the Emotional Intelligence Scale (SEI) was used to evaluate the level of empathy andthe way subjects manage emotions.
The results showed that both women and men are equally emphatic, with no differences when it comes to regulating theemotions of others and emotions evaluation.
Keywords: emotional intelligence, forensic, distress.

INTRODUCTION
The medical-forensic clinic and pathology are the two
cutting-edge medical disciplines where doctors often receive
information that is agonizing and traumatically from a
psychological point of view, first-hand information, in the formof historical results, of examination and investigation. They do
not receive the information in an ad-hoc manner (as is thecase with the emergency department physicians), but in adaily continuous way, throughout their active career [1, 2].
Their short and long term implications on the physician's
psychological health as well as the defence mechanisms in the
medic's way of thinking and the implications on their personality
and behaviour have been very poorly researched [3-5].
If the doctor does not use his wisdom and the experienceobtained over the years in order to cope with the distress, hemay be overwhelmed by the situation and his opinion may
become subjective, biased. The emotional lability of a doctor
may lead him on some unprofessional ways.

negative emotions, and positive emotions. The Emotional
intelligence scale comprises 4 subscales: Emotion
Assessment; adjusting one's personal emotions; adjusting
the emotions of others and the utilisation of emotions [6].
The average age of the subject group is 48 years, of which
12 are female, with the remaining 18 subjects being male.

RESULTS
Figure 1 shows that there is a weak link between the twovariables; only 7.7 percent of positive emotions have an
influence on the regulation of personal emotions.

MATERIAL AND METHODS
A group of 30 people aged between 36 and 60, having
a work experience between 10 and 40 years, forensic
experts were asked to complete two questionnaires
regarding emotional distress and emotional intelligence. The
questionnaires used were: Profile of Affective Distress (PDA)
and Emotional Intelligence (SEI), each scale containing
several other subscales. The affective distress scale is a tool
developed for the purpose of assessing the subjective
dimension of negative functional emotions, dysfunctional

Fig. 1. Influence of positive emotions on the ability to regulate
personal emotions

Received 10th of March 2017. Accepted 12th of April 2017. Address for correspondence: Luminița Ageu, PhD, Center of Mental Health forChildren and Adolescents, Corbului Street no. 7, Timisoara, Romania; phone: +0723056089; e-mail: lumiageu@yahoo.com

14

Fiziologia - Physiology • 2017.27.1(93)From the graphical representation below (Figure 2) it
appears that between the two variables, a weak link exists,
namely 4% of the positive emotions influence the regulationof the emotions of the others.

Fig. 4. Influence of negative emotions on the emotions of others

DISCUSSION
Fig. 2. Influence of positive emotions on the emotions of others

By testing the relationship of negative emotionsadjusting personal emotions we can observe that a weaklink exists, only 6.6% of negative emotions are affecting theregulation of personal emotions (Figure 3).

Fig. 3. Influence of negative emotions on the ability to regulate
personal emotions

As in the case above, it has been demonstrated thatnegative emotions have only a slight influence regarding theregulation of the emotions of others, expressed by apercentage of 1% (Figure 4).

Fiziologia - Physiology • 2017.27.1(93)Studies show that the burnout syndrome is present at
more than half of the physicians. This affects theprofessional efficiency and well-being of the doctor, whichleads to the development of dysfunctional defense
mechanisms, such as the distancing from professional tasks
and the negative attitude towards his work [7-9].
In most experimental studies, distress and the burnout
syndrome correlate negatively with emotional intelligence
respectively empathy, which suggests that patholigists witha high level of burnout are less able to appreciate andconstructively express their own emotional feelings and therelationing with others; this proves inefficiency in the
management and proactive use of emotions in the solvingof the problematic situations [10-15].
A consideration of the association between empathy,
distress, and burnout syndrome is that the ability to control
powerful emotions such as work-related frustration oranxiety or the inability to give patients the necessary
attention can improve the quality of interpersonal
relationship, a thing that may reduce the source of stress, aswell as burnout syndrome. The ability to adequately
understand, express and regulate emotions can lead topositive feelings of competence, achievement, andconfidence in one's own abilities [16-18].
Psychologists who have tried to make a correlation
between distress-burnout have concluded that from all the
distress factors (workload, reduced time, poorly motivatedcolleagues), one of the most serious factors is the lack ofstaff [19-21].

15

CONCLUSION
Analysing the scientific literature as well as the resultsof the current study, it was concluded that age positively
influences the emotional intelligence, respectively empathy,
and adversely distress.
The current study may provide useful data for some future
experimental work. A future perspective may represent theanalysis of the correlations between the many variables
existing in the paper.

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2. Nilsson P. Empathy and Emotions. On The Notion of
Empathy as Emotional Sharing. Ůmea Studies in
Philosophy 7, Gunnar Andersson, Ingvar Johansson andSten Lindstrom eds., Department of Philosophy and
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Puiu M, Todica A. The Prognostic and Clinical Significanceof Neuroimagistic and Neurobiological Vulnerability Markers
in Correlation with the Molecular Pharmacogenetic Testingin Psychoses and Ultra High-Risk Categories. Rom J
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4. Nussbaum L, Gradinaru R, Andreescu N, Dumitrascu V,
Tudor A, Suciu L, Stefanescu R, Puiu M. The Response to
Atypical Antipsychotic Drugs in Correlation with the CYP2D6
Genotype: Clinical Implications and Perspectives. Farmacia
2014, 62(6): 1191-1201.
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R, Ștefănescu R, Puiu M. Modern Treatment Approaches in
Psychoses. Pharmacogenetic, Neuroimagistic and ClinicalImplications. Farmacia 2017, 65(1), 75-81.
6. Dymond R. A scale for the measurement of empathic ability.
J Consult Psychol 1949, 13:127-133.
7. Battin D. Book reviw on ”Psychoanalytic Empathy”, by
Stefano Bolognini. In: JAPA 2005; 53: 1010-1014.
8. Maibom HL. Empathy: Philosophical and Psychological
Perspectives, edited by Amy Coplan and Peter Goldie,
2014, 123-491.
9. Shirom A. Job-related burnout: A review, In Quick JC, Tetrick
LE (eds.), Handbook of Occupational Health Psychology,
American Psychological Association, Washigton, DC, 2009.

10. Timar B, Popescu S, Timar R, Baderca F, Duica B, Vlad M,
Levai C, Balinisteanu B, Simu M. The usefulness ofquantifying intraepidermal nerve fibers density in the
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The impact of diabetic neuropathy on balance and on therisk of falls in patients with type 2 diabetes mellitus: a crosssectional study. PLoS One 2016, 11(4): e0154654.
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N, Puiu M. Molecular Study of Weight Gain Related to Atypical
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Rom J Morphol Embryol 2014, 55(3): 877-884.
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R, Puiu M. Pharmacological and Clinical Aspects of Efficacy,
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Muntean C, Ștefănescu R, Puiu M. Antipsychotic Treatment
Emergent Adverse Events in Correlation with thePharmacogenetic Testing and Drug Interactions in Children
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Farmacia 2016, 64(5): 736-744.
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Moreira P, et al. Cross-cultural Measurement Invariance of
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for the romanian population. Journal of Cognitive andBehavioral Psychotherapies 2007; 8: 139- 158.
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mental health of the forensic medical service officials inChile. 2015: 427-34.
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IMPLICAȚIILE DISTRESULUI ȘI ALE INTELIGENȚEI EMOȚIONALE
ÎN ACTIVITATEA MEDICILOR LEGIȘTIREZUMAT
Lucrarea de față are drept scop cercetarea relației dintre empatie și distres, precum și implicațiile acestora în activitatea
medicilor legiști. Studiul a fost efectuat pe un lot de 30 de medici legiști. Distresul emoțional a fost măsurat folosind
Profile of Affective Distress (PDA), iar pentru a evalua nivelul empatiei si a modului in care subiectii gestioneaza emotiile s-a
folosit Scala Inteligenței Emoționale (SEI).
Rezultatele au arătat că atât femeile cât și bărbații sunt la fel de empatici, neexistând diferențe atunci când vine vorba dereglarea emoțiilor celorlalți și evaluarea emoțiilor.
Cuvinte cheie: inteligență emoțională, medicină legală, distres.
16

Fiziologia - Physiology • 2017.27.1(93)ASSOCIATED CONGENITAL ANOMALIESIN NEW-BORNS DIAGNOSED WITH CONGENITAL
DIAPHRAGMATIC HERNIACOSMIN VESA1, DANA ZAHA3,PETRIȘOR CISMAȘ- PRUTEANU3, MĂDĂLINA MOISI1,FLORICA MEKEREȘ2, CLAUDIA JURCA3
1Clinical County Emergency Hospital Oradea
2University of Oradea, Faculty of Medicine and Pharmacy, Department of Morphological Disciplines
3University of Oradea, Faculty of Medicine and Pharmacy, Preclinical Department

ABSTRACT
Congenital diaphragmatic hernia is an anomaly that appears as a result of abnormal embryological development of thediaphragmatic muscle. The mortality is high reaching 40-62% because of respiratory failure secondary to pulmonary hypoplasia.
Between 2005 and 2015 there were recorded 12 cases of congenital diaphragmatic hernia in Bihor County. All the recorded
cases presented left congenital diaphragmatic hernia. The cases that had additional congenital malformations were classified
as complex congenital diaphragmatic hernias and the other ones were isolated congenital diaphragmatic hernias. All thepatients that had another congenital anomaly died soon after birth. The incidence of congenital diaphragmatic hernia was lower
than expected. The disease appeared manly in male new-borns. Survival was 50%, none of the new-borns with complex
congenital diaphragmatic hernia survived the first week of life. Associated anomalies were diverse: ranging from left pulmonary
hypoplasia to transposition of the great vessels, patents ductus arteriosus or patent foramen ovale.
Key words: dismorphology, congenital malformations, diaphragmatic hernia

INTRODUCTIONRESULTS

Congenital diaphragmatic hernia is an anomaly thatappears as a result of abnormal embryological developmentof the diaphragmatic muscle. It shows up early and has anincidence of 1 in every 2000-3000 live births. It is frequently
associated with other congenital anomalies. The mortality ishigh reaching 40-62% because of respiratory failure
secondary to pulmonary hypoplasia. Of current interest is therole that retinoic acid plays in different biological processes,
including embryogenesis and pulmonary development.
Retinoic acid signalling pathway was identified as animportant factor in the diaphragmatic muscle development.

Between 2005 and 2015 there were recorded 12 casesof congenital diaphragmatic hernia, less than expectedconsidering the mean annual natality in Bihor County of
approximately 6000 and the incidence of congenital
diaphragmatic hernia. 11 cases appeared in male newborns. All cases had left congenital diaphragmatic defect. 6of the 12 analysed cases had complex congenital
diaphragmatic hernia meaning that they presented othercongenital anomalies. The diversity of the other congenital
anomalies consisted in: left pulmonary hypoplasia (4 cases),left pulmonary agenesia with right pulmonary hypoplasia (2cases), persistence of the ductus arteriosus (1 case),transposition of the great vessels (2 cases), patent foramen
ovale (1 case), dextrocardia (2 cases), and common
mesentery (2 cases). There were a number of 14 congenital
anomalies distributed among 6 cases, most new-borns
having 2 or more congenital anomalies. All the patients withcomplex congenital diaphragmatic hernia died in the
neonatal period, while all the others survived with surgicaltreatment.

MATERIAL AND METHOD
We studied the records of new-borns diagnosed withcongenital diaphragmatic hernia taken in evidence by the
Regional Medical Genetics Centre of Bihor County from theClinical City Hospital „Dr. Gavril Curteanu” Oradea spanningon 11 years (2005-2015).

Received 10th of March 2017. Accepted 12th of April 2017. Address for correspondence: Cosmin Vesa, Emergency County Hospital Oradea,
Republicii Street 37, Oradea 410167, Romania; phone: 0259 437 750; e-mail: v_cosmin_15@yahoo.com

Fiziologia - Physiology • 2017.27.1(93)17Case 2 –isolated diaphragmatic hernia: male born in 2009
with left congenital diaphragmatic hernia, managed
surgically, favourable evolution, X-ray and further clinicaland paraclinical exam did not show any additional
congenital malformations.
Case 3 – complex diaphragmatic hernia: male born in 2006
with left congenital diaphragmatic hernia, died at 4 hours
after birth. Autopsy findings: left CDH, common mesentery,
dextrocardia.

Fig. 1. Sex distribution

Case 4 – isolated diaphragmatic hernia: male born in 2010
with left congenital diaphragmatic hernia, favourable
evolution, managed surgically, interestingly had a brotherwho died 8 years before after being diagnosed withcongenital diaphragmatic hernia.

Fig. 2. Classification of congenital diaphragmatic hernia cases

Fig. 4. Apgar score variation according to phenotype, CDH is
isolated CDH, CDH+ is complex CDH

Case 5 – isolated diaphragmatic hernia: female born in
2006, left congenital diaphragmatic hernia, treatedsurgically, favourable evolution, no other congenital
anomalies detected during clinical and paraclinicalexamination
Case 6 – complex diaphragmatic hernia: male born in 2009,
left congenital diaphragmatic hernia, deteriorated rapidly,
died 1 hour after birth. Autopsy findings: left CDH,
dextrocardia.

Fig. 3. Associated anomalies in complex CDH

Case 1 – complex diaphragmatic hernia: male born in2009 with left congenital diaphragmatic hernia, withsymptoms that appeared immediately after birth, managed
surgically, died at 14 after birth. Autopsy findings: left CDH,
left pulmonary hypoplasia.
18

Case 7 – complex diaphragmatic hernia: male born in 2010,
left congenital diaphragmatic hernia, treated surgically, died
immediately after surgery. Autopsy findings: left CDH, left
pulmonary agenesia, transposition of great vessels,
persistence of the ductus arteriosus.
Case 8 – isolated diaphragmatic hernia: male born in 2012,
left congenital diaphragmatic hernia, symptoms appeared in
the first day of life, surgical management, favourable
evolution.
Fiziologia - Physiology • 2017.27.1(93)Case 9 – isolated diaphragmatic hernia : male born in 2005,
left congenital diaphragmatic hernia, symptoms appeared in
the first two hours after birth, surgical management,favourable evolution.

anomalies. Congenital diaphragmatic hernia is accompanied
frequently by pulmonary, cardiac and digestive
malformations which are responsible for the importantmortality.

Case 10 – complex diaphragmatic hernia: male born in
2006, symptoms appeared in the first day of life, surgicalmanagement, died after surgery. Autopsy findings: left CDH,
common mesentery.

REFERENCES

Case 11 – complex diaphragmatic hernia: male born in
2008, symptoms appeared in the first 10 minutes after birth,
surgical management, died immediately after surgery.
Autopsy findings: left CDH, right pulmonary hypoplasia,
patent foramen ovale.
Case 12 – isolated diaphragmatic hernia: male born in 2011,
left congenital diaphragmatic hernia, managed surgically,
favourable evolution.

CONCLUSION
In our study existed an equal proportion between casesof diaphragmatic hernia with and without associated1. Bembea M. Medical and Clinical Genetics, Oradea
University Ed., 2001.
2. Jones K. Smith's Recognizable Patterns of Human
Malformation, 5th edition, W.B. Saunders Company, 1997.
3. Kilby M, Johnson A, Oepkes D. Fetal Therapy: Scientific
Basis and Critical Appraisal of Clinical Benefits, Cambridge
Univerity Press, 2013.
4. Pober BR. Genetic aspects of human congenital
diaphragmatic hernia. Clinical Genetics 2008; 74 (1): 1-15.
5. Pober BR, Russell MK, Ackerman KG. Congenital
Diaphragmatic Hernia Overview, 1993.
6. Parikh DH, Crabbe D, Auldist A, Rothenberg S. PediatricThoracic Surgery, Springer, 2009: 483-493.
7. Turcios NL, Fink RJ. Pulmonary Manifestations of PediatricDiseases. W.B.Saunders, 2009: 302-305.
8. Tovar JA. Congenital Diaphragmatic Hernia, Orphanet
Journal of Rare Diseases, 2012.

ANOMALII CONGENITALE ASOCIATE LA NOU-NĂSCUȚIICU HERNIE DIAFRAGMATICĂ CONGENITALĂREZUMAT
Hernia diafragmatică congenitală este o anomalie care apare ca urmare a dezvoltării embriologice anormale a mușchiului
diafragmatic. Mortalitatea apare în 40-62% din cazuri din cauza insuficienței respiratorii secundare hipoplaziei pulmonare. Între
anii 2005 și 2015 au fost înregistrate 12 cazuri de hernie diafragmatică congenitală în județul Bihor. Toate cazurile au prezentat
hernie diafragmatică congenitală stângă. Cazurile care au avut malformații congenitale adiționale au fost clasificate ca hernii
diafragmatice congenitale complexe și celelalte au fost clasificate ca hernii diafragmatice izolate. Toți nou-născuții care aveau
o altă anomalie congenitală au decedat în perioada imediată nașterii. Incidența herniei diafragmatice congenitale a fost maiscăzută decât nivelul așteptat. Boala a apărut mai ales la nou-născuții de sex masculin. Supraviețuirea a fost de 50%, niciunul
din nou-născuții cu hernie diafragmatică congenitală complexă nu a supraviețuit după prima săptămână de viață. Anomaliile
asociate au fost diverse: au variat de la hipoplazie pulmonară stângă la transpoziția de vase mari, persistența ductului arterial
sau foramen ovale patent.
Cuvinte cheie: dismorfologie, malformații congenitale, hernie diafragmatică

Fiziologia - Physiology • 2017.27.1(93)19DEPRESSIVE PATHOLOGY AND BIPOLAR DISORDER:
PARTICULARITIES OF THE THEORY OF MIND
CLAUDIA HOMOROGAN1, RUXANDRA BARBOIANU1, IOANA RIVIS1,
BOGDAN TUDOR TULBURE2, CATALINA GIURGI-ONCU3, CRISTINA BREDICEAN3
1PhD student University of Medicine and Pharmacy Timisoara
2West University of Timisoara, Department of Psychology
3University of Medicine and Pharmacy Timisoara, Department Neuroscience.

ABSTRACTIntroduction: Theory of mind (ToM) is the cognitive ability to correctly determine the intentions and behavior of others, byreading other person’s emotions through the face or eyes. The ability is associated with deficits in affective disorders.
Aims: To compare particularities of Theory of Mind in Major Depressive Disorder to Bipolar Disorder, which may aid in thedevelopment of early psychiatric interventions among patients with these disorders.
Methods: We examined 34 subjects with major depressive disorder and 34 subjects with bipolar disorder, who were recruitedfrom the outpatient clinic and were included in the study based on inclusion and exclusion criteria. Socio-demographic data, theevolution of their clinical disorder (in years) and the number of relapses were collected from participants’ medical records. Also,
we applied the “Reading the Mind in the Eyes Test”. Data were statisticaly analyzed using SPSS Statistics.
Results: The application of Reading the Eyes in the Mind test revealed a total score of 16.11 (SD = 6.48) recognized emotions
for the depressive sample, and 17.05 (SD = 4.92) for the bipolar sample. These findings demonstrate deficits in experiencing
and recognizing emotions in MD and BD patients who underscore the relevance of these deficits in the psychosocial context.
Conclusions: There is a reduced capacity in recognizing emotions through the eyes in Major Depressive Disorder than in
Bipolar Disorder.
“Who are you going to believe, me or your own eyes?” – Groucho MarxINTRODUCTION
Mood disorders are described as changes in the way wefeel, and also changes on how we perceive ourselves andthe world around us. Previous research investigated theinteraction between clinical disorders and emotions inalmost all mental illnesses [1]. Mood disorders, including
here specifically Major Depressive Disorder (MDD) and
Bipolar Disorder (BD), are altered mental states during
which human physical and psychological functions aredramatically transformed and are associated with alterations
in multiple domains, including interpersonal functioning andsocial cognition e.g.theory of mind [2]. Depressive
symptoms are very variable. The patient experiences moodsfrom indifference to apathy, dejection, anhedonia anddespair. There is an inability to initiate thoughts and actions,to fulfill basic obligations which lead to the inability toachieve anything. Low self-esteem, and also self-blame,self-reproach, thoughts of guilt, are common symptoms
described by patients. This preoccupation with gloomythoughts impairs concentrations, memory and causes
feeling loss [3].

The bipolar disorder is characterized by opposite moodswing, from sadness to joy, from hopelessness tocheerfulness, despondency and despair to happiness andeuphoria. The mania can be manifest as grandiosity,
talkativeness, racing thoughts, and disinhibition. Mania canyield indiscriminate enthusiasm for interpersonal interactions,which can profoundly disrupt social function [3].
Theory of mind (ToM) is the cognitive ability to correctly
determine the intentions and behavior of others, using
information available in the immediate environment (e.g.,
facial expression, tone of voice, body posture) [4].
The emotions can be identified by following nonverbal
clues communicated both by the other person’s face andeyes. In 2001, W. G. Parrott had described the six basic
emotions: love, happiness, surprise, anger, sadness, fear [5].
These basic emotions are universal, and can be recognizedacross cultures, although there are specific culturaldifferences [6]. The ability to process and recognize theemotions through the eyes or face is important in social
interactions, having important effects on the affective stateand behavior. An accurate labeling the mental states ofReceived 15th of April 2017. Accepted 17th of May 2017. Address for correspondence: Claudia Homorogan, PhD student University of Medicine
and Pharmacy Timisoara, Eftimie Murgu Square No. 2A, RO-300041, Timișoara; e-mail: laviniahogea@yahoo.com

20

Fiziologia - Physiology • 2017.27.1(93)others is associated with ToM ability. Studies have showedthat ToM deficits appear in schizophrenia [7], autism [8], butalso in affective disorders [9,10]. Researches showed thatpatients with bipolar disorder displayed a pronounced deficit
in the cognitive domain of ToM(4), and were found with
impaired performance on theory of mind for both bipolardepressed and bipolar-manic patients [10]. A meta-analysisof studies comparing ToM abilities in MDD and healthy
controls included 18 studies comparing 613 patients with
MDD and 529 healthy controls. The results have shown that
MDD patients significantly underperformed healthy controlsin ToM (d=0.51-0.58). ToM impairment in MDD was evident
and was significantly related to severity of depressive
symptoms [11]. Another study showed that reduced ToM
ability in MDD was associated with poor psychosocial
functioning [12].
Therefore, the aim of this study was to compare
particularities of Theory of Mind in Major Depressive
Disorder and Bipolar Disorder, providing evidence for social
dysfunction, which may aid in the development of early
psychiatric interventions among patients with these
disorders.

METHODS
Participants
We examined a sample of 68 individuals (N=34 withmajor depressive disorder, N=34 with bipolar disorder) who
have been previously hospitalized in the Psychiatry Clinic of
Timisoara. Participants were recruited from the outpatient
clinic, where they come for regular psychiatric assessments.
All participants had a stable diagnosis of Major Depressive
Disorder or Bipolar Disorder, according to ICD-10 criteria.
Participants were tested while their symptoms wererelatively stable, although the clinical remission was notcomplete. In order to take part in this study, participants had
to fulfill the following inclusion criteria:
1. Current diagnostic of Major Depressive Disorder or
Bipolar Disorder according to ICD-10 criteria.
2. Had at least 5 years since the diagnostic was formallyregistered in their medical records.
We excluded participants who:
1. Were over 65 years old;
2. Had a serious cognitive impairment or mental
retardation;
3. Had a serious organic disorder.
All Participants have been inpatients at the Psychiatry
Clinic of Timisoara and are currently monitored in the outpatient clinic.
Procedure
Before the assessment, participants consented to takepart in the study by signing an informed consent. Each
Fiziologia - Physiology • 2017.27.1(93)participant was assessed individually. Socio-demographic
data, the evolution of their clinical disorder (in years) and thenumber of relapses were collected from participants’
medical records. Subsequently, participants were invited tocomplete a self-report scale that measures their ability torecognize emotions.
Measures
Reading the Mind in the Eyes Test (Baron-Cohen,
Jolliffe, Mortimore, & Robertson, 1997) consists of 36 greyscale photos displaying one of the six different basic
emotions in the area around the eyes: joy, love,
surprise, anger, sadness, fear. Each photo is surrounded byfour mental state terms and participants are instructed tochoose the word which best describes what the person in
the photo is thinking or feeling. Only one of the four items isdeemed correct (as judged by consensus from an
independent panel of judges in the initial psychometricstudy). Responses were coded as correct or incorrect, andone point is granted for each correct answer (total scorerage between 0 and 36).
Data analysis
Data were statisticaly analyzed using SPSS Statistics.
The two groups were compared using student t test (fortheir mean score) and chi square test χ2 (for the frequencyof recognized emotions). Also, associations between
variables was assessed using the Pearson correlation
coeficient r..
Hypothesis
1. Participants with bipolar disorder will display ahigher ability of reading the eyes in the mind thanthose with a major depressive disorder.
2. The number of relapses will be negatively
correlated with the ability of identifying emotions inboth groups.

RESULTS
Sample characteristics
The trial included 68 participants, divided into two equalgroups: Major Depressive Disorder (MDD), N=34 and
Bipolar Disorer (BD), N=34). In both groups mostparticipants were female (76% in MDD and 61% in BD).
Average age at the moment of assessment was 55.58 years(SD = 8.37) for MDD, and 40.52 years (SD = 9.13) for BD.
The average age at the onset of the disease was 43.73
years (SD = 9.38) for MDD, and 27.53 years (SD = 5.19) for
BD. The age at onset of the disease and the age at the
moment of assessment in both groups is significantly
different: t=8.81 (p<0.00) for age at onset, and t=7.08(p<0.00) for age at assessment. The level of education was

21

similar in both groups: an average of 11.85 years of schoolfor bipolar disorder and 11.14 years for depressive disorder.
Referring to professional status, in both groups, most participants were retired: 79% of depressive disorder and 68%
of bipolar disorder group. In terms of marital status 71% ofdepressive subjects were married but only 32% of bipolar
subjects were married. .The average duration of evolution
for the sample with MDD was 11.44 years, and 12.7 for BD.
The average numbers of relapses were 4.94 for MDD and5.52 for BD. No differences were found between the twogroups on these variables.
Reading the Eyes in the Mind test
The application of Reading the Eyes in the Mind test
revealed a total mean score of 16.11 (SD = 6.48) recognizedemotions for the depressive sample, and of 17.05 (SD =4.92) for the bipolar sample. Unfortunately no significant
differences emerged between the two groups in terms of
their ability to recognize emotions.
When we further compared the two groups, the only
difference that emerged was in terms of the frequency withwhich they recognized the emotion of Love χ2 (1) = 11.20 (p< 0.01) (see Table I). Most of the participants in the MDD
group seem to recognize one or two instances where love
was presented, while those in the BD group were moredisperse in this respect.
Table I. Frequency of recognized emotions (Love)
Love

Group

Total

0

1

2

3

Total

MDD

5

15

14

0

34

BD

10

12

6

6

34

15

27

20

6

68

Note:
0 points – no emotion identified, 1 point– 1 emotion identified,
2 points – 2 emotions identified, 3 points– 3 emotions identified(out of 3 possible total points.

For the total sample we found a negative correlation
between participants’ ability to recognize emotions and thenumber of years since their first diagnosis. More precisely, anegative correlations of r = -0.21 (p = 0.04) was foundbetween participants ability to recognize positive emotions
and the number of years since they got the first clinicaldiagnostic (see Fig. 1). This means that the longer they had
the clinical disorder the less able they were to correctly
recognize positive emotions. No relationship between
clinical history and participant’s ability to recognize negative
emotions was found. Finally, the number of relapses were
not significantly associated with participant’s ability ofrecognize emotions.

22Fig. 1. Correlation between participant’s clinical history (number ofyears of clinical evolution) and reading the mind in the eyes
(number of recognized positive emotions).

DISCUSSION
The fact that the numbers of relapses are negatively
correlated with the general ability of recognizing emotions
shows that the ability of recognizing emotions is maintained,that it is not influenced by the number of relapses over theyears. Depressive subjects performed worse than bipolar
subjects on the general score of emotions recognition of
fearful and disgusted faces. These results may in part explain
clinical behaviors observed in bipolar patients, that the ability
to perceive facial emotion may vary with the degree of mood
disturbance. These findings demonstrate deficits inrecognizing emotions in MD and BD patients, especially as
they advance in time and have a longer clinical history. The
demographic and the clinical disorder (MDD vs BD) seem tohave no influence on the emotion perception impairment.
These deficits appear to be moderate and stable, and might
contribute to social difficulties experienced by theseparticipants. Further studies are needed to characterizeinterpersonal functioning in mood-disorders and should be
integrated with findings from functional imaging studies of theprocessing of facial expression of emotions.

LIMITATIONS OF THE STUDY
The limitations of this study are represented by the small
sample (low statistical power) and by using only one selfreport measure for the dependent variable. Considering
these limitations, the obtained results should be regarded
with caution. Further investigations are needed to establish
the exact nature of the deficits experienced by MDD and BD
participants when it comes to their capacity to recognize
emotions (their theory of mind).

Fiziologia - Physiology • 2017.27.1(93)CONCLUSIONSNo differences were found between Major Depressive
Disorder (MDD) and the Bipolar Disorder (BD) groupregarding their ability to recognize emotions in others.
Participant’s clinical history (the number of years since
their first diagnostic) were negatively associated with theirgeneral ability of recognize positive emotions. So, the longer
they had the disorder the less able they were to recognize
positive emotions. This decrease in their ability to recognize
positive emotions as they have a longer clinical history could
have detrimental effects associated with their social
functioning. More well-designed studies are needed toclarify these complex relationships and shed light on theimpact of affective disorders on participant’s theory of mind.

REFERENCES
1. Wood SJ, Yung AR, Pantelis C. Cognitive precursors ofsevere mental disorders. Cogn Neuropsychiatry. 2013;
18(1-2): 1-8.
2. Sullivan S, Lewis G, Mohr C, Herzig D, Corcoran R, Drake
R, et al. The longitudinal association between social
functioning and theory of mind in first-episode psychosis.
Cogn Neuropsychiatry. 2014: 19(1): 58-80.

3. Oyebode F. Sims’ symptoms in the mind: Textbook of
descriptive psychopathology (5th ed.). Sims’ symptoms in themind: Textbook of descriptive psychopathology (5th ed.). 2015.
4. Montag C, Ehrlich A, Neuhaus K, Dziobek I, Heekeren HR,
Heinz A, et al. Theory of mind impairments in euthymic
bipolar patients. J Affect Disord 2010; 123(1-3): 264-9.
5. Parrott WG. Emotions in Social Psychology: Essential
Readings. Ann Arbor: Edwards. 2001. 378 pp.
6. Sauter DA, Eisner F, Ekman P, Scott SK. Cross-cultural
recognition of basic emotions through nonverbal emotional
vocalizations. Proc Natl Acad Sci 2010; 107(6): 2408-12.
7. Pentaraki AD, Stefanis NC, Stahl D, Theleritis C,
Toulopoulou T, Roukas D, et al. Theory of Mind as a potentialtrait marker of schizophrenia: A family study. Cogn
Neuropsychiatry. 2012; 17(1): 64-89.
8. Sabbagh MA. Understanding orbitofrontal contributions totheory-of-mind reasoning: Implications for autism. Brain andCognition. 2004; 55: 209-19.
9. Purcell AL, Phillips M, Gruber J. In your eyes: Does theoryof mind predict impaired life functioning in bipolar disorder?
J Affect Disord 2013; 151(3): 1113-9.
10. Kerr N, Dunbar RIM, Bentall RP. Theory of mind deficits inbipolar affective disorder. J Affect Disord. 2003; 73(3): 2539.
11. Bora E, Berk M. Theory of mind in major depressive disorder:
A meta-analysis. J Affect Disord. 2016; 191: 49-55.
12. Cusi AM, Nazarov A, Macqueen GM, McKinnon MC. Theoryof mind deficits in patients with mild symptoms of major
depressive disorder. Psychiatry Res. 2013; 210(2): 672-4.

PATOLOGIA DEPRESIVĂ ȘI TULBURĂRILE BIPOLARE:PARTICULARITĂȚI ALE TEORIEI MINȚIIREZUMAT
Introducere: Teoria minții (ToM) este capacitatea cognitive de a determina corect intențiile și comportamentul altora, prin citireaemoțiilor altor persoane la nivelul feței sau ochilor. Această abilitate este scăzută la subiecții cu tulburări afective.
Scop: Compararea particularităților teoriei minții în tulburarea depresivă majoră și tulburarea bipolară, care poate ajuta ladezvoltarea unor metode intervenționale psihiatrice precoce la pacienții cu aceste afecțiuni.
Metode: Am examinat 34 de subiecți cu tulburare depresivă majoră (MD) și 34 de subiecți cu tulburare bipolară (BD), care au
fost recrutați din ambulator și au fost incluși în studiu pe baza criteriilor de includere și excludere. Din fișa medicală a pacienților
au fost colectate date referitoare la caracteristicile socio-demografice, evoluția afecțiunii clinice (în timp) și numărul de recăderi.
De asemenea, am aplicat testul “Reading the Mind in the Eyes Test”. Datele au fost analizate statistic folosind SPSS Statistics.
Rezultate: Aplicarea testului ”Reading the Mind in the Eyes” a rezultat într-un scor total de 16.11 (SD = 6.48) pentru
recunoașterea emoțiilor la subiecții depresivi și de 17.05 (SD = 4.92) pentru subiecții bipolari. Aceste rezultate demonstrează
deficitul în trăirea și recunoașterea emoțiilor la pacienții cu MD și BD, care subliniază relevanța acestor deficite în contextul
psihosocial.
Concluzii: La subiecții cu depresie majoră există o capacitate mai redusă de recunoaștere a emoțiilor la nivelul ochilor decâtla subiecții cu tulburare bipolară.

Fiziologia - Physiology • 2017.27.1(93)23

PULMONARY ASPERGILLOMA IN AN
IMMUNOCOMPETENT PATIENT. A CASE REPORTRAMONA CIOBOATA1, ILEANA BAZAVAN1, MARIUS GEORGESCU2,SAFRAN CHAUDREY1, ALICE ELENE GAMAN3
1 Internal Medicine-Pulmonology Department, University of Medicine and Pharmacy Craiova, Romania
2 Physiology Department, University of Medicine and Pharmacy “Victor Babes”, Timisoara, Romania
3 Microbiology Department, University of Medicine and Pharmacy of Craiova, Romania;

ABSTRACT
Aspergillosis is a severe pathologic condition caused by the Aspergillus organisms and is frequently seen in
immunocompromised patients. Aspergillus can cause a broad spectrum of diseases in the human host, ranging fromhypersensitivity reactions to direct angioinvasion. An aspergilloma is a fungus ball (mycetoma) that develops in a preexisting
cavity in the lung parenchyma. Computed tomography (CT) characteristic aspect for saprophytic aspergillosis (aspergilloma) is
a mass with soft-tissue attenuation within a lung cavity. The mass is typically separated from the cavity wall by airspace (“aircrescent” sign) and is often associated with the thickening of the wall and adjacent pleura.
The present case is an immunocompetent female patient aged 37 years, with no history of pulmonary pathology, who wasadmitted to our clinic with physical fatigue, fever, spontaneous micro-hemoptysis, weight loss. Following chest radiography andcomputed tomography the patient was diagnosed with pulmonary aspergilloma.
The particularity of the case consists in the appearance of a pulmonary aspergilloma in a patient without a history of pulmonary
pathology.
Key words: pulmonary aspergilloma, mycetoma, hemoptysis, computed tomography

INTRODUCTION
Pulmonary aspergillosis is a rare infectious disease,caused by contamination with the Aspergillus fungi,
especially the Aspergillus fumigatus and the Aspergillus
Niger, comprising several locations for the pathologicalprocess, the most common of which being chronic cavitary
pulmonary aspergillosis. Less common manifestations
include: Aspergillus nodule and single aspergilloma [1].
Aspergillosis develops more frequently in immunocompromised individuals. Pulmonary localization is the mostcommon, but the spectrum of fungal infections withAspergillus is much wider.
It appears that men are more frequently affected by thisinfection, the male:women ratio being 3:1. The infection isopportunistic (occurs especially when the immune system of
the host is affected) and is therefore more common in
immunocompromised patients. An aspergilloma is a fungus
ball (mycetoma) composed of Aspergillus hyphae, fibrin,mucus, and cellular debris which develops in pre-existinglung cavities that have become colonized with Aspergillus
spp [2,3]. The most common causes of pulmonary
aspergilloma are tuberculosis and sarcoidosis. Less

common causes include bronchogenic cyst and bullous
emphysema, while in HIV-positive patients, aspergilloma
can develop in cystic areas resulting from pneumonia with
Pneumocystis carinii [4].
While cavity walls are not invaded, in evolution
hemoptysis, coughing and fever can manifest. The mostcommon clinical manifestation of aspergilloma is hemoptysis,
however patients may remain asymptomatic.
Patients with a single Aspergillus nodule only require
antifungal therapy if it is not fully resected, but if multiple
nodules are present they can benefit from antifungal
treatment, while requiring a careful follow-up [1].
Surgical resection is necessary for patients with lifethreatening hemoptysis. Embolization of the bronchial arterycan also represent a very suitable therapeutic option,
especially for patients who cannot be subjected to moresophisticated surgical interventions [5].

CASE REPORTWe present the case of an immunocompetent female
patient, aged 37 years, with no history of pulmonary

Received 14th of March 2017. Accepted 10th of April 2017. Address for correspondence: Marius Georgescu, MD, PhD, Assistant Teaching
Professor, Department of Functional Sciences, Physiology, Eftimie Murgu Square No. 2A, RO-300041 Timișoara; phone: 0040765527318; email: mgeorgiu83@yahoo.com

24

Fiziologia - Physiology • 2017.27.1(93)pathology, who was admitted to our clinic for marked
physical asthenia, fever, spontaneous micro-hemoptysis,
weight loss.
She reported ongoing symptoms of spontaneous microhemoptysis and weight loss of about 5 kg over the preceding
4 weeks.
She is a current tobacco smoker with a 17-pack-years
history and denied drug usage or travel abroad in thepreceding year.
On examination, she was discovered to be underweight(IMC value of 20) with the following vital parameters values:
a body temperature of 38.1 Celsius degrees, a heart rate of
92 beats/minutes, respiratory rate was 17 /minute and bloodpressure was 130/80 mmHg.
Auscultation revealed sibilant wheeze on the upperareas of her left lung.
Routine blood examination showed normochromic
normocytic anaemia (haemoglobin 10.6 g/dL, red blood
cells 2.92×106/mmc, and mean corpuscular volume 100),platelets at 478000/mm3 and white cell blood count was
12,700/mm3 with 61% neutrophil, 33% lymphocyte, 4%monocyte, 1% eosinophil. The sputum smear and culture for
TB were negative, with no other pathogens found. TBinterferon γ release assay (TB-IGRA) result was also
negative.
Chest X-ray revealed the presence of a round, nonhomogeneous opacity, 3 cm in diameter, located on theupper half of her left lung.
Computerized tomography was performed and revealed
an excavated lesion of irregular shape (40 mm in diameter)in the dorsal segment of the left upper lobe with solid
vegetation inside, delimitated by a 3 mm thick wall and thesuggestive presence of the ‘halo sign’. No signs ofmediastinal adenopathy or pleural fluid are present (Figures
1, 2, 3).

Fig. 2. Thorax computed tomogram showing excavated lesion in
the dorsal segment of the left upper lobe with solid vegetation
inside, delimitated by a thick wall.

Fig. 3. CT scan revealed a soft tissue opacity with ‘air crescent’sign in the dorsal segment of the left upper lobe

DISCUSSION

Fig. 1. Computed tomography showing the mycetoma in the left
upper lobe excavated lesion.
Fiziologia - Physiology • 2017.27.1(93)Although the Aspergillus genus fungus is ubiquitous,
infection with these germs is rare, the vast majority of cases
being patients who are overwhelmed with antibiotics or with
low immunity. It also appears that men are more frequently
affected.
Aspergillosis is a serious pathological condition caused
by Aspergillus species and is more commonly seen in
immunocompromised patients [6].
Aspergilloma is generally diagnosed radiologicaly. The
disease rarely occurs independently and is often preceded by25

pulmonary tuberculosis or other cavitating lung diseases suchas bronchiectasis, necrotising pneumonia, lung neoplasia,
and sarcoidosis [7, 8]. In a survey of 544 patients with post
tuberculous cavities of at least 2.5 cm, with sputum negative
for tuberculous bacilli, it was reported that 25% of the patients
presented serum precipitins against Aspergillus, and 11% ofthem had radiographic evidence of aspergilloma [9].
In our case the patient was an immunocompetent female
with no history of pulmonary pathology or any other pathology.
Clinical, histological and radiological manifestations are
determined by the number and virulence of the Aspergillus
species as well as by the patient's immune response.
Although patients may remain asymptomatic, the mostcommon clinical manifestation of pulmonary aspergilloma ishemoptysis. Other uncommon symptoms include cough,weight loss and fever [10]. Our female patient presented
with spontaneous micro-hemoptysis.
Radiologically, the aspergilloma is characterized by thepresence of a solid, round-oval soft tissue mass. Typically,
the formation is separated from the cavity walls through avariable air-space of a semilunar shape. Occasionally, theformation can fully occupy the cavity taking its form [4].
In the case presented, the radiological examination
reveals revealed presence of a round, non-homogeneous
opacity, 3 cm diameter, located on the half upper part of her
left lung.
Differential diagnosis is done with: the image of an
abscess that does not have airway drainage or an air fluid
level and appears on the chest x-ray as a round image, with arelatively well-defined contour and intensely opaque;tuberculoma [4] which is an intraparenchymatous nodular
mass with dimensions ranging from 1 to 5 cm, however ourpatient sputum smear and culture for TB were negative as well
as TB-interferon γ release assay (TB-IGRA) result;bronchiectasis [11] is defined as a permanent dilation of thebronchi, however our patient did not demonstrate any
evidence of it on the CT scan; lung neoplasia, however her
age in combination with the imaging investigations and clinicalfindings was considered unlikely; and finally sarcoidosis [12]however our female patient had no evidence of pulmonaryor extrapulmonary features to sustain this diagnosis.
The appearance is more obvious in the CT examination.
CT plays a significant role in differentiating the aspergilloma
from other conditions like Wegener’s granulomatosis andcavitating lung carcinoma [13].
Computerized tomography in this case reveals an
excavated lesion of irregular shape (40 mm in diameter) in
the dorsal segment of the upper left lobe with solid
vegetation inside, delimitated by a 3 mm thick wall and thesuggestive presence of the ‘halo sign’.
The adequate treatment and optimal duration of therapy
for mycetoma has yet to be established since this uniquepresentation of pulmonary aspergilloma seen in
immunocompetent female patients is usually diagnosed
incidentally. Treatment options include amphotericin B,
voriconazole, itraconazole, caspofungin [14-16] and surgical26

resection which proved to be effective in preventing
recurrence of haemoptysis [17, 18].
In the present case we referred the patient to thethoracic surgery department for resection, however thepatient refused the surgical intervention.

CONCLUSION
Pulmonary aspergilloma is a fungal mass that develops
in pre-existing lung cavities resulting from a Koch bacillus
infection, sarcoidosis, and bronchiectasis and is morecommonly observed in immunocompromised patients.
The specificity of the case consists of the appearance ofa pulmonary aspergilloma in an immunocompetent female
with no history of pulmonary or any other pathology.
Radiology plays an essential role in the diagnosis of
pulmonary aspergillosis. When the radiological examination is
not conclusive, computed tomography allows the identificationof the intrapulmonary space replacement process.

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ASPERGILOM PULMONAR LA UN PACIENT IMMUNOCOMPETENT.
PREZENTARE DE CAZ
REZUMAT
Aspergiloza este o conditie patologică gravă cauzată de organismele din specia Aspergillus şi este mai frecvent observată lapacienţii imunocompromisi. Specia aspergillus poate cauza un spectru larg de afecţiuni variind de la reacţii de hipersensibilitatepană la angioinvazie. Aspergilomul este un ghem fungic (micetom) ce se dezvoltă în cavităţi pulmonare preexistente.
La examenul computer tomograf aspergiloamele se caracterizează prin prezenţa unei formaţiuni solid, rotund ovalare deintensitate submediastinală. Tipic formaţiunea este separată de pereţii cavitaţii printr-un spaţiu aerian de dimensiuni variabile
si de forma unei semilune.
Prezentăm cazul unei paciente in varstă de 37 de ani fără antecedente pulmonare patologice şi care se prezintă in clinica
noastră, pentru astenie fizica marcată, febra, microhemoptizii spontane, scădere ponderală. In urma investigatiilor imagistice in
special a tomografiei computerizate se stabileşte diagnosticul de aspergilom pulmonar. Particularitatea cazului constă in apariţia
unui aspergilom pulmonar la o pacientă fără antecedente pulmonare patologice.
Cuvinte cheie: aspergilom pulmonar,micetom, hemoptizie, tomografie computerizată

Fiziologia - Physiology • 2017.27.1(93)27