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PubMed1989

Four strand recombination models.

A main point of this paper is to develop the idea that synapsis of DNA duplexes might take place by Watson-Crick base pairing between essentially intact duplex structure to form a four stranded intermediate. This intermediate is the same regular and compact four strand structure already discussed (e.g., McGavin, 1971a, J. molec. Biol., 55, 293-298; 1979, J. theor. Biol., 77, 83-99) and which has been used in several related recombination models (see, for example, McGavin, 1977, Heredity, 39, 15-25; 1984, J. theor. Biol., 107, 37-56; Wilson, 1979, Proc. natn. Acad. Sci. U.S.A., 76, 3641-3645; Nash et al., 1980, Cold Spring Harbor Symposium of Quantitative Biology, 45, 417-428; Nash, 1981, A. Rev. Genetics, 15, 143-167). These models can also be related to one recently suggested by Hopkins (1986, J. theor. Biol. 120, 215-222). An immediate stimulus to the development of the idea was the recent work of Griffith & Nash (1985, Proc. natn. Acad. Sci. U.S.A., 82, 3124-3128), on the site specific recombination system of the lambda bacteriophage. They observed trefoil knots with exclusively positive nodes among the products of the interaction of two relatively inverted attachment sites within circular molecules. The model discussed here may though be of interest in itself. The paper also compares several closely related models for recombination which involve formation of either identical or closely related four strand secondary structures.

DNA↗

PubMed2003

Drug-induced steatohepatitis.

Drugs rarely cause steatohepatitis, but amiodarone, perhexiline, and DH, have unequivocally been found to independently induce the histologic picture of alcoholic liver disease or NASH. All three agents have similar pathogenetic mechanisms of hepatotoxicity, targeting mitochondrial ATP production and fatty acid catabolism. Other drugs that occasionally cause steatohepatitis, most importantly steroid hormones, likely exacerbate the pathogenetic mechanisms leading to NASH. Similar to NASH, lipid peroxidation resulting from mitochondrial injury may account for all of the histologic findings in drug-induced steatohepatitis. Further research should determine the mechanisms by which drug-induced steatosis, a benign lesion, evolves to steatohepatitis and progressive fibrosis.

Amiodarone↗

PubMed1998

Nonalcoholic steatohepatitis.

NASH is an important form of chronic liver disease that is increasingly recognized. The diagnosis is secured by biopsy findings with similarities to alcoholic hepatitis in a patient with a confirmed history of abstinence. Obesity is a major risk factor, but the disease also occurs in the nonobese. In 20% to 40% of patients the disease can progress to various stages of fibrosis and ultimately cause cirrhosis and death from end-stage liver disease. For this reason, recognition of NASH is important, and establishing the diagnosis provides a further impetus for performing a liver biopsy as part of the evaluation of unexplained liver abnormalities. The mainstay of treatment is weight reduction in the obese. For those individuals who are not obese, continued observation is the only option currently available. Patients who develop decompensated cirrhosis should be considered for liver transplantation unless advanced age or other underlying medical illnesses are a problem. With the increasing knowledge about the pathophysiology of hepatic steatosis, it is hoped that better diagnostic tests for specific causes of NASH will be available and lead to efficacious therapy.

Biopsy↗

PubMed2002

Nonalcoholic steatohepatitis: risk factors for liver fibrosis.

The purpose of this study was to clarify the clinicopathological features of nonalcoholic steatohepatitis (NASH) and identify risk factors for severe hepatic fibrosis. MATERIALS AND METHODS: Eighty-one patients with biopsy-proven NASH were studied. In all patients, the diagnosis of NASH was established on the basis of following criteria: (1) the presence of steatosis, lobular inflammation, and ballooning degeneration on liver biopsy, (2) intake of less than 20 g of ethanol per week, and (3) appropriate exclusion of other liver diseases. RESULTS: The median age was 54 years (range: 21-82 years) and 41 patients were women (51%). Obesity was present in 58 patients (72%), while 25 patients (31%) had diabetes mellitus and 33 patients (41%) had hyperlipidemia. Histologically, 58 patients (72%) had trivial to moderate fibrosis, 6 patients (7%) had bridging fibrosis, and 17 patients (21%) had established cirrhosis. Multiple logistic regression analysis assessed clinical, laboratory and histological factors showed that the risk factors for fibrosis were a low platelet count (P=0.0016), a high AST/ALT ratio (P=0.0229), and the presence of Mallory bodies (P=0.0209). To exclude factors that were a consequence of liver cirrhosis, variables included in the multiple logistic analysis were age, gender, diabetes, obesity, and hyperlipidemia. This showed that older age (P=0.0037) and the absence of hyperlipidemia (P=0.0150) were risk factors for fibrosis. CONCLUSIONS: We found that a low platelet count, a high AST/ALT ratio, and the presence of Mallory bodies were significant predictors of severe liver fibrosis.

Journal Article↗

PubMed2004

Comparison of three colorimetric reagents in the determination of methanol with alcohol oxidase. Application to the assay of pectin methylesterase.

Three colorimetric reagents for the determination of formaldehyde, the Nash reagent (ammonia plus acetylacetone), Purpald (4-amino-3-hydrazino-5-mercapto-1,2,4-triazole), and N-methylbenzothiazolinone-2-hydrazone (MBTH), were compared for the determination of methanol when used in conjunction with alcohol oxidase. The combination of alcohol oxidase plus the commonly used Nash reagent was specific for methanol versus ethanol, but had the lowest sensitivity of the three reagents tested. Substituting Purpald for the Nash reagent increased the sensitivity 3-fold while still maintaining a high (59-fold) selectivity for methanol versus ethanol. Using MBTH increased the sensitivity still further, but with a loss of the selectivity toward methanol. Since MBTH reacted with aldehydes under neutral conditions, it could be included along with the alcohol oxidase to act as an aldehyde trap. This prevented further oxidation reactions by alcohol oxidase and allowed for extended incubations. A procedure for assaying low levels of pectin methylesterase activity that relies on this trapping ability is described. In addition, alcohol oxidase plus Purpald is shown to be a simple and sensitive way to measure the methanol released from plant material following the thermal activation of endogenous pectin methylesterase.

Alcohol Oxidoreductases↗

PubMed2004

[Alcoholic and non-alcoholic steatohepatitis].

Chronic aethylism has always been a major social as well as health problem. It may lead, at least in some patients, to steatohepatitis (ASH) which is known to progress to cirrhosis more rapidly. Because of the fact that the prevalence of obesity in association with the metabolic syndrome (insulin resistance) is strikingly increasing in the Western world, we will more and more often be faced with a second form of steatohepatitis, the so called non-alcoholic steatohepatitis (NASH). Clinical differentiation between these two entities may often be difficult. The use of the CAGE-questions as well as interviewing family members can help to indentify hidden alcohol abuse. Clinically, the presence of both diseases can only be speculated. To get the diagnosis, liver biopsy must be performed to show the typical histologic feature of fatty liver with hepatocyte necrosis as well as infiltration of polymorphcellular leukocytes. Histology cannot differentiate between ASH and NASH. Therefore, similar pathogenetic mechanisms are supposed. However, therapeutic approaches are different. Treatment of choice in ASH is alcohol abstinence, that of NASH the reduction of insulin resistance, primarily by weight loss.

Alcoholism↗

PubMed2004

Hepatic steatosis in obese Chinese children.

OBJECTIVES THE AIMS OF OUR STUDY WERE: (1) to determine the prevalence of asymptomatic hepatic steatosis and presumed nonalcoholic steatohepatitis, in our local population of obese Chinese children referred for medical assessment; and (2) to assess the correlation between severity of ultrasonographic hepatic steatosis and degree of obesity, insulin resistance and serum biochemical abnormalities. DESIGN: Cross-sectional study. METHODS: In total, 84 obese children, 25 girls and 59 boys with median age and body mass index (BMI) of 12.0 years (interquartile range (IR): 9.5-14.0) and 30.3 kg/m(2) (IR: 27.1-33.4), respectively, referred for medical assessment were studied. All subjects underwent physical examination, anthropometric and dual energy X-ray absorptiometry (DEXA) scan measurements and real-time ultrasonographic (US) examination of the liver. Fasting blood samples were collected for the measurement of liver function, hepatitis status, levels of serum glucose and insulin and lipid profile. Degree of fatty infiltration of the liver was graded according to ultrasonic appearance of liver echotexture, liver-diaphragm differentiation in echo amplitude, hepatic echo penetration and clarity of hepatic blood vessels. RESULTS: All recruited subjects had no history of alcohol abuse and tests for Hepatitis B or C virus were negative. Thorough examination showed all of them to be in general good health without signs of chronic liver disease. Hepatic steatosis identified by defined ultrasonic appearances was diagnosed in 65 subjects (77%); 17 girls and 48 boys. The severity of fatty liver was positively related to anthropometric measurements including BMI, waist and hip circumference, subscapular skinfold thickness; insulin resistance markers [QUICKI and homeostasis model assessment (HOMA)], and hypertriglyceridaemia. Multvariate ordinal regression analysis showed that BMI and raised alanine aminotransferase (ALT) were positively associated with fatty liver. Combination of hepatic steatosis with raised ALT (presumptive NASH) was found in 19 subjects (24%). This group of patients had significantly higher waist hip ratio and conicity index compared to those with isolated hepatic steatosis. Boys with presumed NASH were also found to have significantly higher insulin resistance. CONCLUSION: Nonalcoholic fatty liver disease (NAFLD) was common among our cohort of obese children referred for medical assessment. The prevalence of simple steatosis and presumed NASH was 77 and 24%, respectively. The severity of US steatosis was positively correlated with BMI, raised ALT, insulin resistance and hypertryglyceridaemia. Ultrasonography being noninvasive and readily available could be used for the monitoring of the progression of hepatic steatosis. Further longitudinal studies are required to determine the natural disease progression and the role of insulin resistance and other factors in the pathophysiology of NAFLD.

Adolescent↗

PubMed1999

Does steatohepatitis impair liver regeneration? A study in a dietary model of non-alcoholic steatohepatitis in rats.

BACKGROUND: Impaired liver regeneration is a feature of alcoholic hepatitis, but the relative importance of alcohol, nutritional imbalance and inflammatory mediators in causing this effect is unclear. Non-alcoholic steatohepatitis (NASH) is a form of liver disease with similar morphology to alcoholic hepatitis, but the effect of this disorder on liver regeneration is unclear. We, therefore, examined the status of liver regeneration in a rat nutritional model of hepatic steatosis with inflammation, which is morphologically identical to NASH in humans. METHODS: Male Wistar rats received a methionine-choline-deficient diet (MCDD) for 4 weeks before experiments and both isocaloric pair-fed and ad libitum-fed rats were used as controls. Following partial hepatectomy (68%), the extent of hepatic regeneration was determined 24 h later using [3H]-thymidine incorporation and restitution of liver mass. RESULTS: There was no significant difference of [3H]-thymidine incorporation in MCDD-fed, pair-fed and ad libitum-fed rats (80+/-27, 78+/-11 and 80+/-6.3 d.p.m./microg DNA, respectively). Similarly, restituted liver masses in three groups of rats were not significantly different (17+/-3.8, 18+/-1.8 and 17+/-3.1% initial liver weight, respectively). CONCLUSIONS: The similarities in hepatic histology and cytochrome P450 2E1 induction between this nutritional model of hepatic steatohepatitis and alcoholic steatohepatitis imply that these two disorders share pathogenetic mechanisms. However, liver regeneration is not altered by NASH in rats, indicating that the nutritional and inflammatory changes that appear similar to those of alcoholic liver disease do not cause impairment of liver regeneration.

Animal Feed↗

PubMed2000

Hepatic stellate cell activation in nonalcoholic steatohepatitis and fatty liver.

Factors associated with the development of fibrosis in nonalcoholic steatohepatitis (NASH) are largely unknown, although an association with increased hepatic iron has been suggested. Hepatic stellate cells are the principal collagen-producing cells in many liver diseases and when activated express alpha-smooth muscle actin (alpha-SMA). Hepatic stellate cell activation and association with fibrosis, necroinflammatory activity, steatosis, and stainable iron in 60 cases of NASH and 16 cases of steatosis were evaluated. All 76 patients were obese or had other risk factors for NASH. All biopsy specimens were stained for alpha-smooth muscle actin to evaluate the pattern of hepatic stellate cell activation and were evaluated for inflammatory activity (0 to 3), fibrosis (0 to 4), and stainable iron stores (0 to 4). The zonal location of activated stellate cells was recorded, and the degree of activation was graded as high-grade or low-grade based on the percentage of lobular alpha-SMA+ cells. Activated stellate cells were identified in the hepatic lobule in 74 of 76 biopsy specimens and graded as low-grade in 26 and high-grade in 48. Zone 3 was involved in 72 of 74 positive cases, and in 33 cases, the activated stellate cells were preferentially located in zone 3. The degree of stellate cell activation correlated with fibrosis but not with inflammatory activity, severity of steatosis, or stainable iron. In most cases, the degree of stellate cell activation paralleled the degree of hepatic fibrosis, but in 25 cases, the degree of hepatic stellate cell activation was greater than expected, raising the question of whether such patients are at risk for disease progression.

Actins↗

PubMed2002

Cryptogenic cirrhosis: clinicopathologic findings at and after liver transplantation.

The incidence of cryptogenic cirrhosis (CC) has decreased since the discovery of hepatitis C virus (HCV), still the etiology in 5% of cases with cirrhosis remains unresolved. Our aims were to define the clinicopathologic features of CC at liver transplantation (LT), evaluate the post-LT course with outcome and define the possible pathogenetic mechanisms. 27/534 LT recipients (5%) over a period of 16.5 years were entered in the LT database as cases of CC. A detailed analysis of pre- and post-LT clinical and all liver pathology specimens was performed. Based on clinicopathologic findings, a more definite diagnosis was possible in 23 of 27 (85%): Nonalcoholic steatohepatitis (NASH) in 9 (33%), autoimmune liver disease (AILD) in 6 (22%), alcoholic liver disease in 4, secondary biliary cirrhosis in 2 and 1 each of hepatitis C and portal venopathy. 4/27 cases remained unresolved. In the NASH group, native livers had focal steatosis, Mallory's hyalin, glycogenated hepatocytic nuclei, high-grade inflammation, and 3+ bile duct proliferation. Large cell dysplasia was more common in this group compared to other patients. Two patients had recurrence of NASH after LT. In AILD group native livers had little or no bile duct proliferation. Two patients had recurrence in AILD group. Of 27 patients 19 are alive (70%) with a follow-up of 407-3647 days. Based on the study results, the following conclusions were reached: (1) CC results from varying etiologies, which can be defined by a careful clinicopathologic analysis in a majority (85%) of cases; (2) Nonalcoholic steatohepatitis (33%) and AILD (22%) are the common underlying causes of CC; and (3) Post-LT outcome for CC is disease dependent with, recurrent disease seen in both nonalcoholic steatohepatitis (22%) and autoimmune liver disease (33%).

Adolescent↗

PubMed2004

The pathogenesis of nonalcoholic steatohepatitis and other fatty liver diseases: a four-step model including the role of lipid release and hepatic venular obstruction in the progression to cirrhosis.

Fatty liver disease involves the accumulation of triglycerides in hepatocytes, necrosis of hepatocytes, inflammation, and often fibrosis with progression to cirrhosis. The two-hit model summarizes the important early metabolic events leading to hepatocellular necrosis in nonalcoholic steatohepatitis (NASH). In this article, we provide evidence of lipid release from hepatocytes in posttransplant fat necrosis and in NASH and quantify vascular obliteration in a series of biopsies with NASH. Obliteration of small hepatic veins (<30 microm) in small numbers is compensated by collateral flow. Obliteration of larger hepatic veins (>30 microm) is associated with fibrotic collapse lesions that are not easily resorbed. Based on these observations, we propose a new four-step model that includes the later events that lead to cirrhosis after necrosis has occurred. This model is applicable to nonalcoholic fatty liver disease (NAFLD), alcoholic disease, postjejunoileal bypass disease, and posttransplant fat necrosis. The first step is steatosis facilitated by insulin, and the second is necrosis induced by intracellular lipid toxicity or lipid peroxidation, or both, modified by alcohol, drugs, and ischemia. The third step is release of bulk lipid from hepatocytes into the interstitium leading to direct and inflammatory injury to hepatic veins. The fourth step is venous obstruction with secondary collapse and ultimately fibrous septation and cirrhosis.

Biopsy↗

PubMed2004

Effects of weight loss surgeries on liver disease.

Obesity is the single most significant risk factor for the development of nonalcoholic fatty liver disease (NAFLD) in children and adults. NALFD is estimated to occur in 30 to 100% of obese adults, and in approximately 53% of obese children. The majority of obese patients have ultrasonographic evidence of fatty liver; 30% have histologically documented nonalcoholic steatohepatitis (NASH). Up to 25% of patients with NASH may progress to cirrhosis. In the United States, an estimated 65% of adults are overweight and 31% are obese. Between 2001 and 2002, the number of people with severe obesity, who are more than 100 pounds overweight, rose to nearly 11 million. Since 1970, levels of childhood and teen overweight have climbed to approximately 16% in those aged 6 to 19 years. Recent findings indicate that key features of NAFLD and NASH improve or resolve dramatically with weight loss. This article discusses weight loss surgeries and their effects on liver disease.

Adipose Tissue↗

PubMed2006

Crohn's disease-induced non-alcoholic fatty liver disease (NAFLD) sensitizes for severe acute hepatitis B infection and liver failure.

Non-alcoholic fatty liver disease (NAFLD) commonly is associated with chronic inflammatory bowel disease (CIBD) and usually is considered to be stable and benign. However, NAFLD -- and in particular its subset, non-alcoholic steatohepatitis (NASH) -- may lead to progressive liver disease. Moreover, NAFLD sensitizes the liver to injury and increases the risk of developing acute-on-chronic liver failure following a "third hit". We here present one patient with NASH, as probably induced by long-standing Crohn's disease in the absence of ethanol consumption or abuse. The patient acquired an acute HBV infection and died from complications. As based on the clinical and histological findings, Crohn's disease appears to be a risk factor for developing NAFLD and thus to contribute to the progression into NASH. In conclusion, we suggest that Crohn's disease-related NAFLD may increase the vulnerability of the liver, which indicates that patients with a known history of CIBD merit special attention.

Crohn Disease↗

PubMed1989

Advocacy, prejudice, and role modeling in the deaf community.

Prejudiced attitudes toward deaf people are a well-established phenomenon (Higgins & Nash, 1982; Moores, 1982; Quigley & Kretschmer, 1982). In recent years, however, a new phenomenon has appeared, and some members of the deaf population now openly express prejudice against the hearing (Boros & Stuckless, 1982; Nash & Nash, 1981). The phenomenon may be an interesting example of Allport's (1954) classical analysis: The victims of the prejudice may tend to reciprocate and/or internalize the prejudice to which they have been exposed. The purpose of our analysis is to examine this phenomenon in more detail, particularly from the perspective of social learning theory as described by Bandura and Walters (1963), Walters (1966), and Bandura (1977).

Deafness↗

PubMed2006

Endotheliitis in chronic viral hepatitis: a comparison with acute cellular rejection and non-alcoholic steatohepatitis.

Endotheliitis is an important histologic feature of acute cellular rejection (ACR) in the liver allograft. This change is not specific, however, and has been suggested to be associated with various liver diseases. End-stage liver disease owing to chronic hepatitis C is the leading indication for transplantation in North America, and its recurrence in allograft recipients is common. Because the presence of endotheliitis remains a diagnostic and therapeutic dilemma in transplant pathology, we investigated the prevalence and severity of endotheliitis in chronic liver diseases including hepatitis C. Endotheliitis was evaluated in 128 nontransplant liver biopsies of chronic liver diseases before therapy, including hepatitis C (HCV, n=62), hepatitis B (HBV, n=17), and nonalcoholic steatohepatitis (NASH, n=49). Eighty posttransplant biopsies with ACR were also reviewed. Subendothelial and supraendothelial endotheliitis were separately scored in the portal and central regions using a semiquantitative scoring system from 0 to 4. Pathologists were blinded to the clinical histories, and each biopsy was independently scored by 2 pathologists. Histologic activity index was also scored subsequently for cases of chronic HCV and HBV, using the modified Knodell (Ishak) score. Mean endotheliitis scores>1 were seen in 60%, 35%, and 6% of HCV, HBV, and NASH patients, respectively. The scores for portal subendotheliitis and supraendotheliitis were significantly higher in the viral hepatitis group than in the NASH group (P<0.01). There was no significant difference in the scores of endotheliitis comparing HCV to HBV. ACR group showed significantly higher scores in both portal and central subendotheliitis than any other group (P<0.00005). In the HBV and HCV groups with mean scores of portal subendotheliitis>1 (n=44), mean Ishak scores for portal inflammation and periportal injury were 2.43 and 2.34, respectively; whereas in those with less severe portal subendotheliitis (<or=1, n=35), Ishak scores were 1.66 and 1.37, respectively (P=0.00001 for portal inflammation and P=0.00001 for periportal injury, respectively). Our results suggest that minimal to mild subendotheliitis is common in portal veins in chronic hepatitis C and B, but is significantly less intense than that seen in ACR. The degree of endotheliitis correlates with inflammatory activity. These observations may help minimize the risk of overdiagnosing ACR when the patient has recurrent viral hepatitis, and may help clinicians avoid exposing patients to unnecessary immunosuppressive regimens when patients do not have cellular rejection.

Adult↗

PubMed2002

The clinicopathologic spectrum and management of nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFD) comprises a spectrum of conditions characterized by the presence of predominantly macrovesicular fatty change in the liver and the absence of alcohol consumption in amounts considered detrimental to the liver. The histologic spectrum of NAFLD includes fatty liver alone or steatohepatitis (NASH). Nonalcoholic steatohepatitis is associated with increasing fibrosis is some cases and may progress to cirrhosis. Nonalcoholic fatty liver disease is often associated with insulin resistance. It is likely that there are one or more additional pathophysiologic defects in those with NASH, rendering them more susceptible to injury from oxidative stress. The clinical and histologic features of NASH are described, and an approach to the diagnosis and treatment of NAFLD is provided.

Adolescent↗

PubMed2006

Altered hepatic expression of SREBP-1 and PPARgamma is associated with liver injury in insulin-resistant lipodystrophic HIV-infected patients.

BACKGROUND: HIV-infected patients with HAART-related lipodystrophy are frequently insulin resistant and at risk of non-alcoholic fatty liver disease (NAFLD) with steatohepatitis (NASH). The transcription factors, peroxisome proliferator activated receptors (PPARalpha, PPARgamma1/PPARgamma2) and sterol regulatory element binding proteins (SREBP-1) regulate liver lipid metabolism. Here, we examined whether their expression was modified and related to liver injury in HIV-infected patients. METHODS: Fourteen HAART-treated HIV patients (nine with and five without insulin resistance) who had liver biopsy because of unexplained elevated transaminases were compared with nine non-HIV age-and body mass index-matched patients with NAFLD and 10 controls without steatosis. Hepatic expression of PPARs and SREBP-1 was assessed by real time reverse transcriptase-polymerase chain reaction. RESULTS: Liver histology showed NASH in six of nine insulin-resistant lipodystrophic and two of five non-insulin-resistant HIV patients. Compared with NAFLD or control subjects, expression of SREBP-1 was significantly higher only in HIV-insulin-resistant patients (P = 0.04 and P = 0.02) whereas, compared to controls, HIV-insulin-resistant, HIV-non-insulin-resistant and NAFLD patients had lower expressions of PPARgamma1 (P = 0.03, P = 0.05 and P = 0.01) and PPARgamma2 (P = 0.04, P = 0.05 and P = 0.01). Among HIV patients, the percentage of steatosis was positively correlated with SREBP-1 expression (r = 0.62, P = 0.04) whereas the score of fibrosis was inversely correlated with PPARgamma1 and PPARgamma2 expression (r = -0.57, P = 0.03 and r = -0.6, P = 0.02, respectively). CONCLUSION: Insulin-resistant lipodystrophic HIV-infected patients may develop NASH. Steatosis is associated with overexpression of SREBP-1 and fibrosis with decreased expression of PPARgamma1 and PPARgamma2. These results suggest that altered expression of SREBP-1 and PPARgamma could contribute to the pathogenesis of steatosis and fibronecrotic changes in insulin-resistant lipodystrophic patients.

Adult↗

PubMed2005

Vertebral rotation and thoracic torsion in adolescent idiopathic scoliosis: what is the best radiographic correlate?

BACKGROUND: As a result of the increased appreciation of the three-dimensional nature of scoliosis and modern spinal instrumentation's improved corrective capabilities, there has been renewed interest in the correction and measurement of vertebral rotation. Computed tomography (CT), the gold standard for accuracy, is limited in its clinical utility owing to cost, radiation exposure, and the effects of postural changes on scoliosis curves and vertebral rotation. Consequently, the Perdriolle and Nash-Moe techniques remain the standard measurements for providing a reasonable estimate of pre- and postoperative vertebral rotation because of their simplicity. However, these techniques have considerable interobserver variability, and pedicle screw instrumentation obscures the landmarks necessary for utilizing these techniques for postoperative vertebral rotation assessment. The purpose of the present study was to assess the utility of alternate radiographic measures to assess vertebral rotation and thoracic torsion when compared with conventional measures on pre- and postoperative radiographs and CT evaluation. METHODS: We reviewed the preoperative, immediate postoperative, and final follow-up radiographs, as well as the pre- and postoperative CT scans, of 19 patients (average age 15 years, 6 months) with Lenke 1 curves (average 55 degrees , range 47-66 degrees ), all treated with anterior spinal fusion. Coronal and sagittal Cobb angles as well as vertebral rotation (Perdriolle and Nash-Moe) at the superior uninstrumented, superior instrumented, apical, inferior instrumented, and inferior uninstrumented vertebrae were measured on all films, and vertebral rotation was assessed on the CT scans by a previously described method. Additionally, several measures of thoracic torsion (as a proxy for vertebral rotation and overall deformity improvement) were assessed. These included the rib-vertebral angle difference (RVAD), apical rib hump prominence (RH), apical vertebral body-rib ratio (AVB-R), and apical rib spread difference (ARSD). RESULTS: The postoperative main thoracic curve averaged 26 degrees (range 16-39 degrees , 52% correction) and 29 degrees (range 22-40 degrees , 47% correction) at final follow-up. For apical derotation, the postoperative CT improved from -11.5 degrees to -6.6 degrees and correlated significantly with the Cobb main thoracic curves (42% correction, r = 0.48, P = 0.003). There was weakly positive, but statistically significant, correlation between the pre- and postoperative CT scans and the corresponding Perdriolle and Nash-Moe measures of segmental rotation (r = 0.32-0.40, all P < 0.0001). The RVAD demonstrated poor correlation with the main thoracic curve values and correction, Perdriolle rotation and correction, and CT rotation and correction (r = -0.22-0.37, all P > 0.20). The apical RH demonstrated good correlation with the main thoracic curve (r = 0.65, P < 0.0001), apical Perdriolle rotation (r = 0.57, P < 0.0001), and CT apical rotation (r = 0.53, P = 0.002). We also found moderate correlation between the AVB-R and the main thoracic Cobb, apical Perdriolle, and CT (r = 0.57, 0.59, and 0.49, respectively; all P < 0.005). Similar relationships were found with the ARSD (r = 0.51, 0.47, and 0.43, respectively; all P < 0.02). CONCLUSIONS: The RH, AVB-R, and the ARSD-measures of thoracic torsion-demonstrated moderate to good overall correlation with the main thoracic curve Cobb angles, apical Perdriolle rotation, and apical CT rotation. These should be useful as clinical measures for assessing three-dimensional deformity correction on plane radiographs, especially for the intraoperative evaluation of vertebral derotation and thoracic symmetry restoration.

Adolescent↗