Investigation of ACE genome insertion/deletion correlation with immunohistochemical profile in pituitary adenomas.

AIM: The deletion polymorphism of the angiotensin-converting enzyme (ACE) genome causes neoplastic development in several organs by increasing the angiotensin 2 (A2) formation. In this study, we aimed to identify the ACE genome insertion/deletion polymorphism in pituitary adenomas and to compare it with the control group. MATERIAL AND METHODS: Patients operated for pituitary adenomas were included in the study. Genomic DNA was extracted from tumoral tissues and peripheral blood samples of the patients by using the Miller method. Primary sequence was selected via targeting the polymorphic region of intron 16 of ACE genome 17q23. DNA samples were multiplied by PCR using HACE3s and HACE3as primers. RESULTS: Twenty-one operated cases were studied. In the study group; 44 % of the patients were identified as D/D, 33% of them as I/D and 23% of them as I/I. In 60%, D allele was identified. According to immunohistochemical investigation, we found that 100% of the patients with Cushing adenoma were D/D alleles. CONCLUSION: Presence of high rate of ACE genome deletion in patients with pituitary adenoma and grade 3-4 patients suggest that ACE genome polymorphism can be a risk factor for the development of pituitary adenomas.

Diagnosis and management of pituitary abscess: a case series and review of the literature.

AIM: Pituitary abscess is a disorder characterized with central nervous system (CNS) infection, mass effect, and endocrine dysfunction. These abscesses generally occur due to hematogenous spread in conditions such as paranasal sinusitis, sepsis, and where the blood brain barrier breaks down. This paper aims to discuss four cases of preoperatively diagnosed pituitary abscess in the light of the literature. MATERIAL AND METHODS: Following detailed clinical and hormonal examinations and imaging tests, 210 cases of pituitary adenoma and other sellar pathologies were operated on at the Neurosurgery clinic of Göztepe Training and Research Hospital. RESULTS: All the patients showed fever, systemic signs of toxemia and endocrine dysfunction at the time of diagnosis. In these cases, a preoperative diagnosis of the disease was made thanks to characteristic MRI findings. The four cases were operated by the transnasal transsphenoidal approach and histopathological and microbiological studies were performed for surgical specimens. CONCLUSION: Pituitary abscesses are rare disorders responsible for a high mortality risk. Mortality and morbidity can be reduced by early surgical drainage and appropriate antibiotic treatments. Additionally, these cases should be closely followed-up in terms of pituitary insufficiency, surgical complications and infection.

Neuroprotective effects of caffeic acid phenethyl ester on experimental traumatic brain injury in rats.

The aim of this study was to evaluate the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) with an experimental traumatic brain injury (TBI) model in rats. Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups of 8 rats each: control, TBI, and TBI + CAPE treatment. In TBI and TBI + CAPE treatment groups, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 4 h after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. To date, no biochemical and histopathological changes of neurodegeneration in the frontal cortex after TBI in rats by CAPE treatment have been reported. The TBI significantly increased tissue malondialdehyde (MDA) levels, and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of CAPE (10 µmol/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels and also significantly increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the TBI group, severe degenerative changes, shrunken cytoplasma and extensively dark picnotic nuclei in neurons, as well as vacuolization indicating tissue edema formation. The morphology of neurons in the CAPE treatment group was well protected. The number of neurons in the trauma alone group was significantly less than that of both the control and TBI +CAPE treatment groups. The caspase 3 immunopositivity was increased in degenerating neurons of the traumatic brain tissue. Treatment of CAPE markedly reduced the immunoreactivity of degenerating neurons. TBI caused severe degenerative changes, shrunken cytoplasma, severely dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the frontal cortex. In conclusion, the CAPE treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications. We believe that further preclinical research into the utility of CAPE may indicate its usefulness as a potential treatment on neurodegeneration after TBI in rats.

The effect of polymorphisms in the promoter region of the MMP-1 gene on the occurrence and invasiveness of hypophyseal adenoma.

BACKGROUND: The matrix metalloproteinase-1 enzyme (MMP-1, also called collagenase 1) plays a key role in turnover of collagen fibers in the intercellular matrix. Insertion of a guanine residue was found within the promoter region of the MMP-1 gene. We found that MMP-1 levels increased approximately twofold over normal when this insertion was present, enabling MMP-1 to facilitate tumor invasion and metastasis. MMP-1 is also believed to play a role in tumor development. The aim of our study is to investigate the effect of polymorphisms in the promoter region of the MMP-1 gene on the development of benign and invasive hypophyseal adenomas. PATIENTS AND METHODS: Thirty patients with hypophyseal adenomas diagnosed by radiological examination underwent surgical removal, and the diagnosis was confirmed using immunohistochemical staining of the pathology specimens. We found that ten of these patients had invasive adenomas confirmed by radiological examination and immunohistochemical staining. DNA isolation was performed on all specimens, and 5-cc venous blood samples were obtained from all patients as well as 30 volunteers using the Qiagen QIAquick kit. Promoter regions of MMP-1 genes from the DNA samples were amplified using polymerase chain reaction (PCR) and primers designed for the site-directed mutation method. Following PCR, a guanine residue within the promoter region of the MMP-1 gene was identified using the restriction fragment length polymorphism method and the ALU I restriction enzyme. Three genotypes were detected in a genotyping assay: 2G/2G, 1G/2G, and 1G/1G. RESULTS: Of the surgically treated patients, 36.6% had the 2G/2G genotype, 46.6% had the 1G/2G genotype, and 16.6% had the 1G/1G genotype. The 2G allele frequency was found to be 83.4%. In 90% of cases of invasive adenoma, a homozygous 2G/2G genotype was detected. DISCUSSION: The risk for development of hypophyseal adenoma may be greater in patients with the 2G allele. In cases of existing hypophyseal adenoma, those with the homozygous 2G allele tend to be invasive.