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Objective To investigate the characteristics of radiation-induced optic neuropathy (RON) in patients with nasopharypgeal carcinoma after radiotherapy,and explore its risk factors.Methods A retrospective study was performed on the clinical data of 22 RON patients with nasopharyngeal carcinoma after radiotherapy,admitted to our hospital from January 1997 to January 2011.Their clinical manifestations,eye examinations and cranial MRI data were concluded.Results Visual deterioration,or even,blindness,was the most common manifestation.RON occurred after the initial radiotherapy in 18 cases,and during the initial radiotherapy in 2 cases.And 2 cases developed RON in re-irradiation for recurrences.Blindness developed in 8 eyes,and decreased vision occurred in 27 eyes; 14 patients displayed retinal optic nerve atrophy in the eye examinations.Typical radiological imaging of the skull showed optic nerve enlargement in 30 eyes,optic nerve atrophy in 5 eyes; and the incidence of optic neuropathy was high when radiation dose was over 70 Gy.Conclusion RON may occur in nasopharyngeal carcinoma patients following radiotherapy,having vision disorders,visual field changes,abnormal visual evoked potential and typical cranial imaging performances; the occurrence of RON may be correlated with radiation field and radiation dose; routine eye and imaging examination is of great significance.
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Objective To investigate the clinical characteristics and imaging features of radiation-induced hypopituitarism (RIH) in nasopharyngeal carcinoma (NPC) patients after radiotherapy.Methods Retrospective study was performed on the clinical data of 9 NPC patients (7 males and 2 females), diagnosed as RIH after radiotherapy in our hospital from 2000 to 2009; their clinical manifestations, anterior-pituitary hormone levels, cranial MRI features and follow-up results were analyzed. Results The interval between complications after radiotherapy and diagnoses of RIH varied from 10 months to 15 years.Multiple hormone deficits appeared in 5 patients; thyrotropin deficiency and hyperprolactinemia were the most common complications, followed by adrenocorticotropic hormone (ACTH) insufficiency.Typical radiological imaging of the pituitary gland displayed partially empty sella and atrophy of pituitaly gland,which was demonstrated in 2 patients.Five patients got improvement after hormone replacement therapy. Conclusion Radiation-induced hypopituitarism may occur in NPC patients; most patients are subclinical without typical radiological alterations in MRI for pituitary.Routine evaluation of adenohypophysis function is necessary for early detection of hormone deficiency and early hormone replacement treatment.
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Objective To investigate the effect of exogenous kallikrein on apoptosis of the neurons aroundthe cerebralinfarctareain rats. Methods Thirty rats wjth cerebral infarction induced by middle cerebral artery occlusion(MCAO)were assigned randomly into 3 groups(n=10),namely the blank control group,saline group,and pAdCMV-HTK group.In the pAdCMV-HTK group,kallikrein gene was delivered into the cerebral ischemie lesion via a replication-defective adenovims using stereotaetic injection technique, and the expression of exogenous kallikrein was detected immunohistoehemically.TUNEL staining was performed to evaluate the neuronal apoptosis around the infarct area,and RT-PCR used to detect the mRNA expressions ofbcl-2,bax and caspase-3 in the brain tissues. Results At 24 h aftertreatment there were some HTK expressed cells found in group C and peal(at 72 h after treatment.While compare with group B and group C,there existed significant difference(112±6.1,68±4.2,59±3.9,P<0.05).At 72 h after treatment,the NSS of group C was significantly lower than that ofgruop B and A(6.70±0.16,8.13±0.16,7.93±0.20,P<0.05);7 days after the treatment,the difference was more significant(5.14±0.18,7.82±0.14,7.91±0.10,P<0.01).Apoptotic cells were mostly seen around the infarct area.The ratsinpAdCMV-HTK group showed significantly reduced number of cells positive for TUNEL staining as compared to those in the saline and blank control groups at 3 days(10.1±0.9,16.7±1.1,and 20.4±0.8,respectively)and 7 days after the treatment(15.2±1.2,33.6±1.3,and 28.8±1.7,respectively)(P<0.05).The mRNA levels ofbc1-2.bax and caspasc-3 were elevated in all the groups at 24 h,peaked at 72 h,and decreased gradually till 7 days alter the treatment.Compared with those in the other two groups，bcl-2 mRNA level in the pAdCMV-HTK group increased slightly P>0.05) while bax and caspase-3 mRNA levels decreased markedly(P<0.05) 72 h and 7 days after the treatment.Conclusion Kallikrein can inhibit neuronal apoptosis around the cerebral infarct and improve the neurological fimction of rats following cerebral infarction probably by reducing the expressions of such apoptotic factors as bax and caspase-3.
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Objective To investigate the effects ofkallikrein gene transfer on microvascularproliferation around the cerebral infarct and on the recovery of regional cerebral blood flow (rCBF)following ischemia/reperfusion injury in rats. Methods The rats with cerebral ischemia/reperfusioninjury induced by middle cerebral artery occlusion (MCAO) were randomly assigned into blank controlgroup, saline group, and pAdCMV-HTK treatment group and received corresponding injections into thetissues around the infarct area. Each group was divided into 3 subgroups (n=10) for observation at 12, 24and 72 h after the treatment. The neurological deficits of the rats before and after the treatment wereevaluated using neurological severity scores (NSS), and the expressions of exogenous human tissuekallikrein (HTK) and vascular endothelial growth factor (VEGF) in the brain tissues were detectedimmunohistochemically. TIC staining was performed to measure the changes in the infarct size.14C-iodoantipyrine tracing technique was used to define the rCBF in the rats. Results Compared tothe blank control group, the cerebral infarct size was significantly reduced in pAdCMV-HTK group 24 hafter the treatment, and was further reduced at 72 h (P<0.05). At 24 h after the treatment, the NSS inpAdCMV-HTK group was significantly lower than that in the blank euntrol and saline groups (P<0.05),and was further reduced at 72 h (P<0.01). After MCAO, the VEGF-positive cells were found mostly inthe cortex and the white matter around the infarct area. The expression of VEGF in pAdCMV-HTK groupwas markedly higher than that in the other two groups at 12, 24, and 72 h after the treatment (P<0.05). Inall the 3 groups, the rCBF around the infarct was slightly decreased as compared to that in thecontralateral hemisphere, pAdCMV-HTK slightly increased the rCBF 12 h after the injection (P>0.05),and significant increase in the rCBF occurred 24 h and 72 h after the injection (P<0.05). ConclusionKallikrein gene transfer following cerebral ischemia/reperfusion injury promotes vascular proliferationaround the infarct and increases the rCBF to reduce the infarct volume and attenuate neurological deficitsin rats.