Relationship between Degenerative Disc Disease and Lipid Profiles in Older Adults

BACKGROUND: Lumbar degenerative disc disease (LDDD) is associated with obesity; however, there are only a few studies on the relationship between LDDD and the specific risk of obesity, such as dyslipidemia. We aimed to identify the independent association between LDDD and serum lipid profiles in older adults.METHODS: A retrospective case-control study was performed with the patients with LDDD, such as spinal stenosis and lumbosacral disc prolapse, and control patients. Sixty-eight patients with LDDD aged 65–85 years were recruited in the LDDD group. Thirty-seven age- and sex-matched controls without LDDD were also enrolled. Logistic regression analysis was performed after adjusting for age, sex and body mass index to assess the association between LDDD and serum lipid profiles.RESULTS: Total cholesterol and triglyceride levels were significantly higher in the LDDD group. The subjects with abnormal triglyceride level (>150 mg/dL) showed a significant odds ratio (7.274, 95% confidence interval [1.552–34.095], P-value=0.012) for LDDD.CONCLUSION: The study findings suggest that higher total cholesterol level may be associated with the patients with LDDD. Therefore, the association between serum triglyceride level and risk of LDDD must be studied further.

Association with inflammatory cells and apolipoproteins to the progression of atherosclerosis / 대한외과학회지

PURPOSE: Inflammatory cells are known to be associated with the progression of atherosclerosis and plaque rupture. However, the relation to inflammatory cells and apolipoproteins on the progression of atherosclerosis is unknown. This study was aimed at examining the different expressions of inflammatory cells and evaluate the effect of apolipoprotein (APO) C1 and APO E during the progression of atherosclerosis. METHODS: Ten atherosclerotic tissues were compared with five non-atherosclerotic tissues. The presence of vascular smooth muscle cells (VSMCs), macrophages, T-cells, APO C1, and APO E were identified by Western blotting and immunohistochemical analysis with antibodies. The senescence was analyzed by senescence-associated beta-galactosidase. RESULTS: The protein expression and senescence of macrophages, APO C1 and APO E were significantly higher in the main atherosclerotic lesion than the non-atherosclerotic lesion. A high concentration of inflammatory cells and the paucity of VSMCs were present in the shoulder area. In addition, macrophage and T-cells are expressed in the early stage of atherosclerotic development and more expanded in advanced atherosclerotic plaques. APO C1 was expressed mainly within the necrotic core, and APO E existed mostly around the necrotic core and the fibrous cap in advanced atherosclerotic plaques. CONCLUSION: Our study indicated that the expression and the senescence of macrophage and T-cells may be closelyrelated to induction and deposition of APO C1 and APO E. This contributes to the development and progression of atherosclerotic plaque by expanding the necrotic core.

Expression of apoC1 and FTL Genes in Human with Carotid Atherosclerosis

PURPOSE: The pathogenesis of carotid atherosclerosis (CA) is known to involve several pathologic processes, such as lipid disturbances, thrombosis, oxidative stress and apoptosis. However, the genetic factors contributing to the development of CA, are, poorly understood. Thus, this study was performed to clarify the genes that are related with CA by comparing the expression patterns of mRNA in the arteries of a control group and in the arteries of a CA patients group. MATHODS: The total RNAs in the arteries of both groups were obtained from the abdominal aorta of 5 brain death donors and also the carotid arteries of 10 CA patents, and the DNAs were then reversely transcribed into complementary DNA (cDNA). The annealing control primer (ACP) method was applied to identify the differentially expressed messenger RNAs (mRNAs). RESULTS: The prominently expressed genes in the CA group compared with the control group were those of apolipoprotein C1 (apoC1) and ferritin light chain (FTL). There was a difference in the gene and protein expressions in the development of vascular disease between the coronary and carotid arteries, i.e., the transcriptional pathway for the FTL expression in CA patient arteries, and the posttranscriptional pathway in the coronary artery disease. The ApoC1 gene was another prominently expressed gene in the current study, and it has been reported to promote apoptosis in the cultured smooth muscle cells of human aorta. CONCLUSION: The increased expression of the apoC1 and FTL genes in the carotid artery might increase the possibility of CA via the apoptosis and oxidation of the increased LDL and VLDL.

No Association of TGF-beta Gene Polymorphism with the Progression of Autosomal Dominant Polycystic Kidney Disease(ADPKD) in Korean Patients / 대한신장학회잡지

BACKGROUND: Two genetic loci, PKD1 and PKD2, have been identified as being responsible for ADPKD, and PKD1 is known to be associated with poor prognosis. However, the presence of intrafamilial clinical diversity suggests the presence of disease-modifying loci. Because the mechanism of renal failure in ADPKD includes cystic growth and tubulointerstitial atrophy and fibrosis, we studied the associations between two cytokine gene polymorphisms in the TGF-beta gene, which are known to be related with chronic tubulointerstitial inflammation, and ADPKD progression in Korean patients. METHODS: 47 normal controls and 114 individuals with ADPKD were genotyped by PCR-RFLP, and the TGF-beta gene leader sequence of T869C(Leu10Pro) variant was compared with MspA1I and G915C (Arg25Pro) with BglI. Statistic significances were determined using the Chi-square test. RESULTS: The distribution of alleles for the TGF-beta Leu10Pro polymorphism in ADPKD was : T 52%, C 48%, which was similar to the Korean(56 : 44, p= 0.670) and Western controls(65 : 35), and in addition, no differences were found between the CRF and the non-CRF groups(p=0.571) or the early hypertension and the normotension groups(p=0.252). The distribution of alleles for the TGF-beta Arg25Pro polymorphism was all GG type, which was different from Western controls(90 : 10, p=0.000). CONCLUSION: Our results suggest that the polymorphism at Arg25Pro of TGF-beta in Korean population has different allele distribution from Western, and the polymorphism at Leu10Pro of TGF-beta has no association with the renal progression of Korean ADPKD patients.

Clinical Characteristics of End-stage Renal Disease in Korean Autosomal Dominant Polycystic Kidney Disease / 대한신장학회잡지

End stage renal disease(ESRD) is a well-known major complication of autosomal polycystic kidney disease(ADPKD). Several risk factors of renal progression in ADPKD were identified, such as PKD1 gene, male gender and earlier age of onset. In Korea, ADPKD is a cause of ESRD in 2% of hemodialysis patients. Until now, only a few detailed studies have been performed in regarding to evaluate the risk factor for ESRD especially in the Asian population. 148 ADPKD patients were registered to PKD clinic in our hospital(Mar. 1996-Dec. 1999). Among them, 34 patients(male : female = 14 : 20) who had started renal replacement therapy were studied to elucidate clinical characteristics including the nature of progression of renal failure. These data were compared with 14 patients(male : female = 3 : 11) who did not develop renal failure(serum creatinine 1g/24h), urolithiasis, upper urinary tract infection, hypertension and liver cysts were 69, 54, 16, 29, 85 % and 85%, respectively. 84% of these patients had family members with ADPKD and 10% of them had ESRD family members. PKD1 vs. PKD2 was 7 : 1 in 8 patients with ESRD and 1 : 1 in 2 patients of control group. Gross hematuria and proteinuria were more prevalent in ESRD patients than the control group(p=0.001 and p=0.0008, respectively). In 18 patients with ESRD, rates of renal progression were traced using a reciprocal of serum creatinine(1/Cr) curve. Once azotemia(serum creatinine value > OR =1.5 mg/dL) developed, the median rate of decline of 1/Cr was -0.073dL/mg/year(range : -0.046--0.114dL/mg/year), which was constant irrespective of either the age of onset or sex. In summary, in 34 patients, the renal function seemed to be maintained to a certain age. But, once azotemia developed, the renal function was rapidly declining with similar rate, ended up ESRD in 8.2 years. Presence of gross hematuria and proteinuria were associated with poor prognosis.

Genotype Analysis in Korean Families with Autosomal Dominant Polycystic Kidney Disease(ADPKD) / 대한신장학회잡지

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disease in adults, and its major morbidities are renal failure and cerebrovascular accident. The prevalence of this disease in the chronic haemodialysis patient population is known to be approximately 2% in Korea. So far, three genetic loci have been identified as being responsible for ADPKD, and approximately 85% of the cases in Western countries are related to the PKD1 gene. However, little information is available concerning the pattern of linkage analysis or the mutations present in Asian populations. For this study, 35 families with hereditary renal cysts were recruited from our ADPKD clinic from 1993 to the present, and their molecular genetic characteristics were studied. Subjects were chosen according to the criteria of Ravine et al. Linkage analysis was done with microsatellite markers(PKD1:SM7, UT581, AC2.5, KG8, D16S418, PKD2 : D4S423, D4S1534, D4S1542, D4S1544, D4S2460). Genomic DNA PCR and PAGE gel run were done, and the allele patterns were compared with sonographic findings. The results of this study showed that the ratio of PKD1 to PKD2 was 23 : 3, and PKD2 families showed the tendency of milder renal prognosis than PKD1 families. In conclusion, we confirmed the usefulness of linkage analysis for ADPKD in Korean population, and our data shows a similar percentage of PKD1(88%) and PKD2(12%) in Korean patients as in the Western population.