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Biomedical subjects

Y S Kang

Publications and source records attributed to Y S Kang.

At least 19 recordsLinked to original sources
PubMed2006

Spironolactone ameliorates renal injury and connective tissue growth factor expression in type II diabetic rats.

Administration of spironolactone provides a beneficial effect in various animal models of renal injury. In this study, we investigated whether spironolactone prevents the progression of diabetic nephropathy through reduction of connective tissue growth factor (CTGF) synthesis in type II diabetic rats. In addition, we evaluated the effect of aldosterone and spironolactone on CTGF and collagen production in cultured cells. Renal functional and morphologic changes were examined in Otsuka Long-Evans Tokushima Fatty rats with or without spironolactone treatment (20 mg/kg/day) for 8 months, as well as in non-diabetic age-matched Long-Evans Tokushima Otsuka rats. Spironolactone treatment did not induce any significant differences in body weight, kidney/body weight ratio, serum creatinine concentration, blood glucose levels, or systolic blood pressure. However, urinary protein and albumin excretion were significantly decreased in the spironolactone treatment group, which was associated with amelioration of glomerulosclerosis. In addition, renal CTGF, collagen synthesis demonstrated marked decreases in the spironolactone treatment group. In cultured MC and PTC, aldosterone induced significant increases in CTGF gene expression and protein synthesis associated with increased collagen synthesis, which was abolished by prior treatment with spironolactone. However, aldosterone treatment did not induce transforming growth factor (TGF)-beta1 overproduction, and inhibition of TGF-beta1 by neutralization of TGF-beta1 protein did not significantly prevent aldosterone-induced CTGF production. These results suggest that the antifibrotic effects of spironolactone may be mediated by CTGF through a TGF-beta1-independent pathway in this animal model of diabetic nephropathy.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2005

Urinary concentration of transforming growth factor-beta-inducible gene-h3(beta ig-h3) in patients with Type 2 diabetes mellitus.

AIMS: The expression of TGF beta-inducible gene h3(beta ig-h3) has been used to assess the biological activity of TGF beta in the kidney. In this study, we investigated whether the urinary concentration of beta ig-h3 is associated with diabetic nephropathy in patients with Type 2 diabetes mellitus. We also evaluated the relationship between the urinary concentration of beta ig-3 and proteinuria and microalbuminuria (AER) in a normal healthy population and in Type 2 diabetes patients. METHODS: Four hundred and seventy-nine Type 2 diabetic patients without non-diabetic kidney diseases and 528 healthy control subjects were enrolled. The study subjects were divided into five groups: a non-diabetic healthy control group with normal ACR (n = 443), a non-diabetic healthy control group with microalbuminuria (n = 85), a normoalbuminuric diabetic group (n = 198), a microalbuminuric diabetic group (n = 155) and an overt proteinuria group (n = 126). Urinary levels of beta ig-h3 were measured by enzyme-linked immunosorbent assay. RESULTS: (i) Urinary excretion of beta ig-h3 was significantly higher in the diabetic groups than in the controls, even in the normoalbuminuric stage (25.02 +/- 8.84 vs. 18.67 +/- 6.56, P = 0.03). In diabetic patients, urinary beta ig-h3 levels increased significantly as diabetic nephropathy advanced (25.02 +/- 8.84 vs. 34.06 +/- 24.55 vs. 169.63 +/- 57.33, P < 0.001). (ii) Proteinuria was found to be significantly correlated with urinary beta ig-h3 (healthy control; r = 0.137, P = 0.019, diabetic patients; r = 0.604, P < 0.001). ACR was also found to be significantly related with urinary beta ig-h3 in diabetic patients (r = 0.383, P = 0.006). (iii) In diabetic patients, urinary beta ig-h3 was significantly related with systolic and diastolic blood pressure (systolic blood pressure: r = 0.436, P = 0.024; diastolic blood pressure, r = 0.365, P = 0.042), total cholesterol and HbA(1c) (cholesterol: r = 0.169, P = 0.03, HbA(1c); r = 0.387, P = 0.044). Logistic regression analyses showed that urinary beta ig-h3 was associated with a significant increase in the risk of microalbuminuria and proteinuria in diabetic patients. CONCLUSIONS: Longitudinal monitoring of urinary beta ig-h3 may improve the likelihood of detecting diabetic nephropathy at an earlier stage and beta ig-h3 could be a sensitive marker of diabetic kidney disease progression.

Albuminuria↗
PubMed2005

Characteristics of population with normal serum creatinine impaired renal function and: the validation of a MDRD formula in a healthy general population.

BACKGROUND AND AIMS: Glomerular filtration rate (GFR) provides the most accurate estimation of renal function. This study investigated the clinical characteristics of patients with impaired renal function having a normal serum creatinine level. We also validated whether the new Modification of Diet in Renal Disease (MDRD) formula can be applied in a healthy general population. MATERIAL AND METHODS: A total 393 participants who had serum creatinine concentration below 132.6 micromol/L without underlying diseases were randomly selected on an address basis in Ansan City. According to the level of GFR, they were divided into 3 groups and we analyzed their clinical characteristics. In 75 subjects, who were randomly selected 25 cases in each group based on GFR estimated by Cockcroft-Gault (C-G) formula, true GFR was measured using the 99mTc-DTPA renal clearance method. RESULTS: A total 393 (male: 106, female: 287) participants were as follows: GFR < 60 ml/min/1.73 m2; 4% (n = 25); 60 < or = GFR < 90 ml/min/1.73 m2; 26.2% (n = 103); GFR > or = 90 ml/min/1.73 m2; 67.4% (n = 265). In the group of decreased GFR, the mean age was older (67.4+/-10.7 vs. 48.7+/-12.8 vs. 39.4+/-8.2 years, p < 0.001), the gender was male (90.33+/-28.77 vs. 110.55+/-31.64, p < 0.001), and amount of proteinuria more increased (0.61 (0.56) vs. 0.33 (0.34) vs. 0.38 (0.33) gm/day, p = 0.007). The accuracy and precision of each formula were assessed by the difference in GFR measured by the 99mTc-DTPA renal clearance method--estimated GFR by each formula (deltaGFR), and the coefficient of determination (r2) of different predictive equations. The results were as follows: deltaGFR = -14.78+/-46.03, r2 = 0.79 (24-hour urinary creatinine clearance), deltaGFR=-16.79+/-57.32, r2 = 0.66 (100/serum creatinine), deltaGFR = 9.54+/-39.18, r2 = 0.87 (C-G formula), deltaGFR = -12.30+/-54.31, r2 = 0.66 (AASK formula), deltaGFR = 8.70+/-37.62, r2 = 0.79 (MDRD formula). Multiple linear regression analysis and logistic regression analysis showed that age, serum creatinine, total cholesterol and 24-hour urinary protein excretion were independently related to GFR and associated with a significant increase in the risk of decrement of GFR. CONCLUSIONS: From these results, a more accurate assessment of renal function should be required in a population characterized by older age, male gender and more proteinuria. The MDRD study formula and Cockcroft-Gault formula have greater accuracy and precision with true GFR, and this equation can be applied in subjects with healthy general population.

Adult↗
PubMed2004

Plasma and urinary vascular endothelial growth factor and diabetic nephropathy in Type 2 diabetes mellitus.

AIMS: Vascular endothelial growth factor (VEGF) has been implicated in the pathogenesis of diabetes mellitus. We determined whether alterations of plasma and urinary VEGF levels are related to diabetic nephropathy in Type 2 diabetic patients. METHODS: One hundred and seven patients and 47 healthy controls were studied. Study subjects were divided into four groups using urinary albumin-to-creatinine ratio (ACR): a non-diabetic healthy control group (n = 47), a normoalbuminuric diabetic group (n = 37), a microalbuminuric diabetic group (n = 37) and an overt proteinuric diabetic group (n = 33). VEGF levels were measured by enzyme-linked immunosorbent assay. RESULTS: (i) Urinary VEGF concentrations were significantly higher in the diabetic groups, even at the normoalbuminuric stage (log VEGF/Cr, normoalbuminuria; 4.33 +/- 1.06 vs. control; 3.53 +/- 0.79, P = 0.009). Urinary VEGF excretions increased as diabetic nephropathy advanced. (ii) Plasma and urinary VEGF levels were higher in hypertensive diabetic patients than in the normotensive individuals with diabetes. (iii) In those with diabetes, plasma VEGF levels were found to be positively correlated with plasma urea (r = 0.398, P = 0.039) and urinary ACR (r = 0.251, P = 0.044), and urinary VEGF to be positively correlated with urinary ACR (r = 0.645, P < 0.001), and creatinine (r = 0.336, P = 0.009), and to be negatively correlated with serum albumin (r = -0.557, P < 0.001). Urinary VEGF and serum creatinine were independently correlated with urinary ACR. CONCLUSIONS: Urinary excretion of VEGF increased during the earlier stage of diabetic nephropathy and was significantly correlated with urinary albumin excretion. This suggests that urinary VEGF might be used as a sensitive marker of diabetic nephropathy and for predicting disease progression.

Albuminuria↗
PubMed2001

Role of reactive oxygen species in apoptosis induced by N-ethylmaleimide in HepG2 human hepatoblastoma cells.

We have previously reported that N-ethylmaleimide induces apoptosis through activation of K(+), Cl(-)-cotransport in HepG2 human hepatoblastoma cells. In this study, we investigated the role for reactive oxygen species as a mediator of the apoptosis induced by N-ethylmaleimide. N-ethylmaleimide induced a significant elevation of intracellular level of reactive oxygen species. Treatment with antioxidants (N-acetyl cysteine, N,N'-diphenyl-p-phenylenediamine) which markedly suppressed generation of reactive oxygen species, significantly inhibited the N-ethylmaleimide-induced activation of K(+), Cl(-)-cotransport and apoptosis. Inhibitors of NADPH oxidase (diphenylene iodonium, apocynin, D-(+)-neopterine) also significantly blunted the generation of reactive oxygen species, activation of K(+), Cl(-)-cotransport and apoptosis induced by N-ethylmaleimide. These results suggest that reactive oxygen species generated through activation of NADPH oxidase may play a role in the N-ethylmaleimide-induced stimulation of K(+), Cl(-)-cotransport and apoptosis in HepG2 cells.

Apoptosis↗
PubMed2001

Apoptosis signal-regulating kinase 1 controls the proapoptotic function of death-associated protein (Daxx) in the cytoplasm.

Although Daxx (death-associated protein) was first reported to mediate the apoptotic signal from Fas to JNK in the cytoplasm, other data suggested that Daxx is mainly located in the nucleus as a transcriptional regulator. Here, we demonstrated that cellular localization of Daxx could be determined by the relative concentration of a proapoptotic kinase, apoptosis signal-regulating kinase 1 (ASK1) by using immunofluorescence and transcriptional reporter assay. ASK1 sequestered Daxx in the cytoplasm and inhibited the repressive activity of Daxx in transcription. In addition, Daxx was bound to the activated Fas only in the presence of ASK1, accelerating the Fas-mediated apoptosis. These results suggest that Daxx requires ASK1 for its cytoplasmic localization and Fas-mediated signaling. Taken together, we could conclude that ASK1 controls the dual function of Daxx as a transcriptional repressor in the nucleus and as a proapoptotic signal mediator in the cytoplasm.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Involvement of K(+)-Cl(-)-cotransport in the apoptosis induced by N-ethylmaleimide in HepG2 human hepatoblastoma cells.

The role of K(+)-Cl(-)-cotransport in apoptosis in human cancer cells was investigated. N-Ethylmaleimide, a K(+)-Cl(-)-cotransport activator, induced apoptosis in a dose-dependent manner in HepG2 human hepatoblastoma cells. N-Ethylmaleimide induced Cl(-)-dependent K(+) efflux, indicating that K(+)-Cl(-)-cotransport is functionally present in HepG2 cells. Calyculin-A and genistein, inhibitors of K(+)-Cl(-)-cotransport, significantly prevented both K(+)-Cl(-)-cotransport activation and apoptosis induced by N-ethylmaleimide. These results demonstrate, for the first time, a novel role for K(+)-Cl(-)-cotransport in apoptosis in human hepatoma cells. These results further suggest that K(+)-Cl(-)-cotransport may be a valuable target for therapeutic interventions for human hepatoma.

Apoptosis↗
PubMed2001

Facilitated olefin transport by reversible olefin coordination to silver ions in a dry cellulose acetate membrane.

The highly selective dry complex membrane AgBF4-cellulose acetate (CA) was prepared and tested for the separation of ethylene/ethane and propylene/propane mixtures. The maximum selectivity for olefin over paraffin was found to be 280 for the ethylene/ethane mixture and 200 for the propylene/propane mixture. Solid-state interactions of AgBF4 with cellulose acetate (CA) and/or olefins have been investigated by using FT-IR, UV, and X-ray photoelectron spectroscopy (XPS). FT-IR and XPS studies clearly show that the silver ions are coordinated by carbonyl oxygen atoms among three different types of oxygen atoms present in CA-two in the acetate group and one in the ether linkage. Upon incorporation of AgBF4 into CA, the carbonyl stretching frequency of the free cellulose acetate at 1750 cm(-1) shifts to a lower frequency by about 41 cm(-1). The binding energy corresponding to a carbonyl oxygen atom in the O 1s XPS spectrum shifts to a more positive binding energy by the incorporation of AgBF4. Reversible olefin coordination to silver ions has been observed by FT-IR and UV studies. Treatment of the AgBF4-CA membrane placed in a gas cell with propylene produces a propylene-coordinated membrane in which coordinated propylene is easily replaced by other olefins such as 1,3-butadiene.

Journal Article↗
PubMed2001

Role of pertussis toxin-sensitive G-proteins in intracellular Ca2+ release and apoptosis induced by inhibiting cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels in HepG2 human hepatoblastoma cells.

Previously, we have reported that inhibition of cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels by glibenclamide induced intracellular Ca2+ release from IP(3)-sensitive stores and apoptosis in HepG2 human hepatoblastoma cells (Kim JA, Kang YS, Lee SH, Lee EH, Yoo BH, Lee YS. 1999. Biochem Biophys Res Commun 261:682-688). In this study we investigated the upstream signals involved in the mechanism of these actions of glibenclamide. Treatment with glibenclamide initiated production of inositol 1,4,5-trisphosphate (IP(3)) in a dose- and time-dependent manner. The glibenclamide-induced formation of IP(3) was significantly inhibited by CFTR activators (levamisole and bromotetramisole). The intracellular Ca2+ release and apoptosis induced by glibenclamide were significantly suppressed by treatment with phospholipase C (PLC) inhibitors (U-73122 and manoalide) or by pretreatment with pertussis toxin (PTx). In addition, PTx-catalyzed ADP-ribosylation of GTP-binding proteins (G-proteins) was markedly enhanced by treatment with glibenclamide in a time-dependent manner. Taken together, these results suggest that PTx-sensitive G-proteins coupled to PLCbeta may mediate the intracellular Ca2+ release and apoptosis induced by inhibiting CFTR Cl- channels in HepG2 cells. These results further suggest that the PTx-sensitive G-proteins may be a valuable target for the therapeutic intervention of human hepatomas.

Adenosine Diphosphate Ribose↗
PubMed2001

Identification of a mutation in the human raloxifene response element of the transforming growth factor-beta 3 gene.

The human transforming growth factor-beta 3 (TGF-beta 3) is an important cytokine to maintain bone mass by inhibiting osteoclast differentiation. Recently raloxifene response element (RRE), a new enhancer with a polypurine sequence for estrogen receptor (ER)-mediated gene activation, was identified on the TGF-beta 3 gene. Functional analysis of the RRE-mediated pathway has shown that this would be an important pathway for bone preserving effect. We found a novel mutation in the RRE sequence by single-strand conformational polymorphism analysis in one of 200 Korean women. Cloning and sequencing revealed a heterozygote in which one allele had an insertion of 20 nucleotides (AGAGAGGGAGAGGGAGA GGG) between nucleotide +71 and +72 and a point mutation at nucleotide +75 (G-A transition), and the other allele had normal sequence. The insertion was a nearly perfect tandem duplication of the wild type DNA sequence. The bone mineral density of the affected woman was not much lower than that of age-matched controls. Transient transfection of the mutant allele showed no significantly different activity compared with that of the wild type allele. These observations suggest that the heterozygote variation of the RRE sequence seems not to be operative in determination of bone mass.

Estrogen Antagonists↗
PubMed2001

Deflazacort increases osteoclast formation in mouse bone marrow culture and the ratio of RANKL/OPG mRNA expression in marrow stromal cells.

Information on precise effects of deflazacort on bone cell function, especially osteoclasts, is quite limited. Therefore, the present study was undertaken to test effects of deflazacort on osteoclast-like cell formation in mouse bone marrow cultures and on the regulation of osteoprotegerin (OPG) and its ligand (RANKL) mRNA expressions by RT-PCR in the ST2 marrow stromal cells. TRAP-positive mononuclear cells increased after the treatment of deflazacort at 10(-9) to 10(-7) M alone for 6 days in a dose-dependent manner. Number of TRAP-positive multi-nucleated cells (MNCs) increased significantly with combined treatment of deflazacort at 10(-7) M and 1,25-(OH)2D3 at 10(-9) M compared to that of cultures treated with 1,25-(OH)2D3 alone (p<0.05). Exposure to deflazacort at 10(-7) M in the presence of 1,25-(OH)2D3 at 10(-9) M in the last 3-day culture had greater stimulatory effect on osteoclast-like cell formation than that of the first 3-day culture did. Deflazacort at 10(-10) -10(-6) M downregulated OPG and upregulated RANKL in mRNA levels in a dose-dependent manner. These observations suggest that deflazacort stimulate osteoclast precursor in the absence of 1,25-(OH)2D3 and enhance differentiation of osteoclasts in the presence of 1,25-(OH)2D3. These effects are, in part, thought to be mediated by the regulation of the expression of OPG and RANKL mRNA in marrow stromal cells.

Animals↗
PubMed2001

Polychlorinated naphthalenes, biphenyls, dibenzo-p-dioxins, and dibenzofurans as well as polycyclic aromatic hydrocarbons and alkylphenols in sediment from the Detroit and Rouge Rivers, Michigan, USA.

Sediment from the upper Detroit and lower Rouge Rivers in southeastern Michigan, USA, were analyzed to examine the distribution of polychlorinated naphthalenes (PCNs), biphenyls (PCBs), dibenzo-p-dioxins (PCDDs), and dibenzofurans (PCDFs) as well as polycyclic aromatic hydrocarbons (PAHs) and alkylphenolic compounds such as butylphenol, octylphenol, and nonylphenol (NP). Sediments from a non-point source location in Lake Michigan were also analyzed for target compounds. Concentrations of target compounds in the upper Detroit and lower Rouge Rivers varied considerably among locations, and notable spatial variation existed. Concentrations of PCNs and PCDDs/PCDFs in sediments from the upper Detroit and lower Rouge Rivers ranged from 0.08 to 187 ng/g and 69 to 1420 pg/g dry weight, respectively. Total PCBs, PAHs, and NP concentrations ranged from 8 to 25,000, 17 to 44,000, and < 10 to 60,000 ng/g dry weight, respectively. Concentrations of all target compounds except PCNs were significantly correlated with total organic carbon content of sediments. Similarly, concentrations of PCBs, PCDDs, and PCDFs were significantly correlated with each other. The distribution of organic contaminants in the upper reaches of the Detroit River and lower Rouge River suggested the presence of localized, but multiple, sources of contamination for each compound class. Conners Creek combined sewer overflow has been identified as one of the potential sources for the upper Detroit River, where the highest concentrations PCBs and PCDDs/PCDFs were found. Polycyclic aromatic hydrocarbon and NP concentrations were consistently high in sediment from the lower Rouge River. Analysis of data from selected locations suggested that PCNs contributed a greater proportion of the dioxin-like activity than PCBs and PCDDs/PCDFs contributed.

Benzofurans↗
PubMed2001

Characterization of dioxin-like activity of sediments from a Czech river basin.

Synthetic organic chemicals are present in environmental compartments as complex mixtures and therefore their potential effects are difficult to predict. In this study, in vitro bioassays using wild-type fish and rat hepatoma cell lines and their corresponding recombinant cell systems were used to evaluate 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-like activity in extracts of sediments collected from rivers of the Czech Republic. All the sediment extracts elicited statistically significant responses in all the cell lines tested. For most sediment extracts, a complete dose-response relationship was obtained. The maximal efficacy of the samples was between 57 and 143% of the maximal induction elicited by TCDD. Greater responsiveness, sensitivity, and reproducibility were observed for recombinant than wild-type cells. Cell line-specific differences in the sensitivity to compounds present in the complex sediment extracts were observed. The TCDD equivalents (TCDD-EQs) determined from the different cell bioassays were correlated. Greater concentrations of TCDD-EQs were obtained with fish cell lines. The TCDD-EQs calculated from the results of chemical analysis of toxic equivalents (TEQs) were in good agreement with those determined by bioassays; the arly hydrocaron receptor (AhR)-effects of the identified chemicals appear to be generally additive. This indicates that most of the TCDD-like activity was accounted for by the compounds identified and quantified by instrumental analysis. Fractionation along with mass-balance calculations allowed identification of the active fractions and classes of compounds. Polycyclic aromatic hydrocarbons (PAHs) were found to be responsible for most of the AhR-mediated activity in sediments.

Animals↗
PubMed2000

Nucleolar localization of human methionyl-tRNA synthetase and its role in ribosomal RNA synthesis.

Human aminoacyl-tRNA synthetases (ARSs) are normally located in cytoplasm and are involved in protein synthesis. In the present work, we found that human methionyl-tRNA synthetase (MRS) was translocated to nucleolus in proliferative cells, but disappeared in quiescent cells. The nucleolar localization of MRS was triggered by various growth factors such as insulin, PDGF, and EGF. The presence of MRS in nucleoli depended on the integrity of RNA and the activity of RNA polymerase I in the nucleolus. The ribosomal RNA synthesis was specifically decreased by the treatment of anti-MRS antibody as determined by nuclear run-on assay and immunostaining with anti-Br antibody after incorporating Br-UTP into nascent RNA. Thus, human MRS plays a role in the biogenesis of rRNA in nucleoli, while it is catalytically involved in protein synthesis in cytoplasm.

Antibodies↗
PubMed2000

Caveolin internalization by heat shock or hyperosmotic shock.

We investigated the cellular localization of caveolin, a landmark protein of caveolae, by indirect immunofluorescence after heat shock or hyperosmotic shock. Caveolin was internalized to the perinucleus by heat shock (43 degrees C) and relocalized in the plasma membrane after recovery of NIH3T3 cells at 37 degrees C for 4 h. The caveolin internalization was also observed after cells were exposed to hyperosmotic shock. Caveolin disappeared from detergent-insoluble complexes in the heat-shocked cells, but alkaline phosphatase was still there, suggesting that their responses to heat shock are quite different even though both of them were enriched in detergent-insoluble complexes of normal cells. Caveolin was internalized by the actin depolymerizer cytochalasin D, but not by the tubulin depolymerizer nocodazole. In addition, cellular exposure to hydrogen peroxide caused caveolin internalization along with disintegrated microfilaments and intact microtubules. Since cellular exposure to heat shock showed disintegrated microfilaments but intact microtubules, caveolin internalization might be due to depolymerized microfilaments. When cells were exposed to heat shock and allowed to recover for 4 h, actin depolymerization and caveolin internalization were not induced by a second heat shock, suggesting that some heat shock protein(s) might prevent actin depolymerization and caveolin internalization.

3T3 Cells↗
PubMed2000

Taurine transport mechanism through the blood-brain barrier in spontaneously hypertensive rats.

Taurine levels in the brain decrease when an animal is subjected to pathological conditions, such as ischemia-anoxia and seizure, but they tend to increase in hypertension. The present study investigated the blood-brain barrier (BBB) transport of [3H]-labelled taurine in spontaneously hypertensive rats (SHR) using internal artery carotid perfusion (ICAP) at a rate of 4 ml/min for 10, 15 and 30 seconds. The volume of distribution in brain (VD) and the permeability surface area product (PS) of [3H]-taurine through the BBB in SHR were calculated. The PS value for taurine at 15 s was higher than at the longer perfusion times. This could result from taurine efflux back into blood occurring after 15 s. As in the case of normotensive rats, taurine was shown to enter the brain via the sodium and chloride ion dependent carrier system.

Animals↗
PubMed2000

Transanally injected triamcinolone acetonide in levator syndrome.

PURPOSE: Several treatments are used for the treatment of levator syndrome, such as rectal massage, biofeedback, and galvanic stimulation. But their effects are inconsistent, and multiple treatment sessions are usually required. Triamcinolone acetonide and lidocaine mixture was injected locally into the tenderest point in levator syndrome under the hypothesis that levator syndrome is caused by tendinitis of pelvic floor musculature. METHODS: A mixture of 40 mg of triamcinolone acetonide and 1 ml of 2 percent lidocaine was injected into the tenderest point transanally in 104 patients (33 males; mean age, 51 years) with levator syndrome from December 1996 to May 1998 at Daehang Clinic. Additional injections were repeated at two-week intervals to a maximum of three injections in cases of poor response. Follow-up was performed prospectively concerning patient's perception of pain level using a visual analog scale. Depending on the response, the patients were classified into four groups: pain-free, good, fair, and no response. More than 50 percent pain reduction was classified as "good," and less than 49 percent reduction as "fair." RESULTS: The injection regions, where the tenderest points were identified on digital rectal compression, were left anterior anal canal in 71.2 percent of patients, right anterior in 3.8 percent of patients, and posterior in 25 percent of patients. The results of treatment were as follows: at three months after injection, response was classified as pain-free in 36.8 percent of patients, good in 35 percent of patients, fair in 19.5 percent of patients, and no response in 8.7 percent of patients; at six months the response was pain-free in 30.1 percent of patients, good in 46.5 percent of patients, fair in 18.2 percent of patients, and no response in 5.2 percent of patients. Most patients, except 8.7 percent at three months and 5.2 percent at six months, experienced treatment benefits. There were no complications during the follow-up periods. CONCLUSION: Transanal injection of triamcinolone acetonide and lidocaine mixture into the tenderest point is such a simple, safe, and very effective modality that it can be recommended as a primary therapy for levator syndrome.

Adolescent↗