Biomedical subjects

Suada Heljić

Publications and source records attributed to Suada Heljić.

6 recordsLinked to original sources

PubMed2006

[Fryns syndrome].

Fryns syndrome is an extremely rare developmental disorder associated with deletion of long arm of chromosome 16. Characteristics of the Fyns syndrome are: craniofacial dysmorfism, diaphragmatic defects with lung hypoplasia, distal digital hypoplasia, brain and urogenital abnormalities and other developmental disturbances. After the first description in two stillborn sisters by Fryns (1971), new reports appeared with descriptions included disorders which have not described previously. We described a case of female live born with deletion of long arm of chromosome 16. Our patient had a typical craniofacial dysmorfism, brain abnormalities (Dandy Walker malformation), cardiac defects (artial septal defect and persistent ductus arteriosus), renal hypoplasia, gastrointestinal problems, hypotonia and feeding difficulties. Our patient had no diaphragmatic hernia and he survived neonatal period with severe neurological impairment.

Abnormalities, Multiple↗

PubMed2005

[Fungal colonization of newborn in neonatal intensive care unit: a prospective study].

Invasive candidiasis in neonates has become an increasing problem over the past decade in Neonatal Intensive Care Units (NICUs) in the world; it is a relatively common cause of late onset sepsis associated with a high mortality. Prior colonization is the major risk factor for candidemia. To determine the rate of colonization, risk factors and the possible modes of acquisition of Candida spp. in neonates in NICU of Pediatric University Hospital, Sarajevo, during 3 months. Samples (mucocutaneous swabs, urine, stool, blood) were obtained weekly until the time of discharge or death (one infant enrolled in the study exited). Care health worker hands were cultured weekly (55 samples). Candida spp. from various body sites samples were isolated in 7 patients (rate of colonisation 14,8%) while 7 samples of haelth workers hands were positive for C. spp (14,5%). Patients colonizated or infected by Candida spp. in our study were or very preterm newborns (3/7) or compromised term newboms (4/7), with congenital abnormalities (2/7) or gastrointestinal surgical interventions (2/7). Two very preterm neonates were colonized early from the birth, which indicates possible vertical transmission. In other 5 patients, colonization occurred more lately, after at laest 15 days stay in NICU, which indicates nosocomial transmission as a predominant mode of acquisition. Among 10 positive patterns from different body sites, Candida albicans was isolated in 6 cases; other 4 cases were C. glabrata (2/10), C. krusei (1/10) and C. famata (1/10). Rather than focusing on methods of identifying of pregnant women with vaginal Candida colonization, attention should be directed to high risk neonates and infection control maesures including hands washing by health care workers.

Candida↗

PubMed2004

[Wolf-Hirschhorn syndrome].

Wolf-Hirschhorn syndrome (WHS) is a rare developmental disorder associated with hemizygous deletion of short arm of chromosome 4. Main phenotype characteristics of WHS are: intrauterine growth retardation, mental retardation, typical facial dysmorphism ("Greek warrior helmet"), microcephaly and midline fusion defects (cleft lip or palate, cardiac septal defects). Other abnormalities, like agenesis of corpus callosum, dysplastic kidneys, coloboma iris, skeletal abnormalities have been described occasionally. We described female newborn baby with 4p deletion, who had most of the phenotype characteristics of Wolf-Hirschhorn syndrome: intrauterine growth retardation, microcephaly, facial dysmorphism, congenital hypotonia and seizures in neonatal period. Other abnormalities included: hypoplastic cervical vertebra C4-C5, renal cyst and partial agenesis of corpus callosum. Patient had not cardiac septal defect. Due to a broad spectrum of possible morphologic abnormalities followed by mental retardation, prenatal diagnosis is very important. Postnatal recognition of the syndrome requires genetic counseling of parents and supportive multidisciplinary treatment.

Abnormalities, Multiple↗

PubMed2003

[Intraventricular hemorrhage in premature neonates: etiopathogenesis, detection and prevention].

Although the incidence of intra-periventricular hemorrhage has reduced in recent years, the increasing survival rates for the very low birth babies indicates that the lesion remains to be a big problem. Neuropathologic base of IVH-PVH is subependimal bleeding into germinal matrix, with consecutive dilatation of lateral ventricles and possible development of germinal matrix destruction, posthemorrhagic hydrocephalus and periventricular hemorrhagic infarction. Pathogenesis of IVH-PVH is multifactorial with participation of intravascular, vascular and extravascular factors. Detection of IVH-PVH and its neuropathologic consequences has been facilitated greatly by the introduction of real-time cranial ultrasonography. Long-time prognosis relates to the mechanisms of brain injury, i.e. presence of hypoxic-ischemic injury, posthemorrhagic hydrocephalus and periventricular hemorrhagic infarction. Extensive parenchymal lesions are associated with frequent subsequent motor, less frequent cognitive deficits. Prevention of IVH-PVH remains the most important goal. That includes prenatal interventions, such as prevention of premature birth, transportation of the premature infant "in utero", prenatal administration of phenobarbital and K-vitamin and optimal management of labor and delivery. Postnatal interventions include careful newborn resuscitation, correction of fluctuating cerebral blood velocity, correction of hemodynamic disturbances and pharmacologic interventions. Postnatal administration of different medicaments (phenobarbital, indomethacin, ethamsylate and vitamin E), have showed inconsistent results in reduction of IVH-PVH, thus there is no pharmacologic agent yet to be recommended for routine use in premature infants.

Cerebral Hemorrhage↗

PubMed2002

[Neural tube dysraphism: meningomyelocele and related disorders].

Neural tube disorders develop as a result of failure of neural tube closure between 3rd and 5th gestational weeks. This failure can cause soft structure anomalies (spina bifida, lumbal meningocela) or possible can contain neural tissue (meningomyeloccla, encephaloccla). Etiology of this disorder is not clear enough, and probably has multifactorial roots. Besides genetic factors, there are impact of some nutritional causes like folic acid. 28 cases with neural tube dysraphism hospitalized during period August 1999 till August 2002. at the Pediatric Clinic KCU Sarajevo were analyzed through retrospective study. 19/28 (67.8%) of newborn were from controlled pregnancy but without folic acid supplementation, 4 of them (14.2%) had prenatal diagnosis. Dysraphic disorder was the most often accompanied by paraplegia 16/28 (57.1%), hydrocephalus 17/28 (60.7%), from which 6/17 (35.2%) with Arnold Chiary malformation. 13/28 (46.4%) had skeletal deformities. Active preoperative treatment was conducted in 20/28 (71.4%) cases, and the rest of them were treated with home palliative care because of parent's rejection of surgery or major accompanied anomalies presence. In order to decrease the incidence of dysraphic disorders it is necessary to conduct periconceptional folic acid prevention, and provide early prenatal diagnosis. Long term treatment of children with meningomyclocele requires multidisciplinary approach that includes surgeons, orthopedists, pediatricians, physical therapists, in order to improve life quality of survived children.

Abnormalities, Multiple↗

PubMed2002

[Neonatal hyperbilirubinemia: evaluation and treatment].

We have analyzed 132 newborns with hyperbilirubinemia (BW < 2500 g, GW > 37 weeks) hospitalized in Neonatal Unit of Paediatric Hospital during 2001. In 78 out of 132 (59.1%) newborns, causal diagnosis were established. Rh isoimmunization caused hyperbilirubinaemia in 2.8% (3/132) cases, ABO isoimmunization in 15.95% (21/32), infections in 9.15% (12/32) and other (polycitaemia, kephalhaematoma, loss of weight > 8%, jaundice related to the brestafeeding) in 31.8% (42/132). Maximal serum bilirubin level was reached between fourth and seventh day of life. In 47/132 newborns (40.9%) non-specific hyperbilirubinaemia were diagnosed. All babies were successfully treated by fototherapy. Blood exchange transfusion was performed in only 2 cases. Rh isoimmunisation was not significant factor in etiology of hyperbilirubinemia because of global prevention of Rh negative mothers. Hyperbilirubinemia of "healthy full-term newborn" was most often seen in 40.9% cases. Diagnostic criteria for hyperbilirubinemia were revised, and fottherapy, as safe, non-invasive method, replaced blood exchange transfusion, as an expansive procedure with low but constant mortality.

Humans↗