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Cincinnati, United States

Glueck C.J.,Cholesterol and Metabolism Center | Freiberg R.A.,Cincinnati Medical Center | Wang P.,Cholesterol and Metabolism Center
Orthopedics | Year: 2014

In 6 patients with stage II knee osteonecrosis, all 6 with thrombophilia and 4 with concurrent hypofibrinolysis, the authors prospectively determined whether anticoagulation with enoxaparin could prevent collapse and progression to osteoarthritis, ameliorate pain, and restore function. The 6 patients were treated with enoxaparin (40 to 60 mg/d for 3 or more months) as mandated by a US Food and Drug Administration-approved protocol. In post-enoxaparin prospective follow-up, patients were reassessed clinically every 4 to 6 months, and radiographs were obtained every year. The 6 patients followed up at 15.1, 7.5, 3.9, 2.25, 2, and 1 year, respectively. None progressed to joint collapse or severe osteoarthritis. Four became and remained asymptomatic at 2-, 3.9-, 7.5-, and 15.1-year follow-up, respectively. A fifth patient did not progress to collapse or severe osteoarthritis but had residual pain at 2.25-year follow-up. The sixth patient had no symptomatic benefit on enoxaparin but improved on rivaroxaban at 1-year follow-up. Two patients had recurrences of knee pain 1 and 4 years after their initial treatment with enoxaparin. One resolved after a second course of enoxaparin, and the other, with a second recurrence 1 year after the second course, resolved after a third course. Pretreatment, all 6 patients required canes, crutches, or wheelchairs, but after enoxaparin, no patient required them, and walking was unrestricted. Thrombophilia-hypofibrinolysis contributes to the pathogenesis of knee osteonecrosis. Thrombophilic-hypofibrinolytic patients with stage II knee osteonecrosis treated with enoxaparin have had no collapse or progression to severe osteoarthritis, and most have had resolution of pain and restoration of full function. This represents a major improvement compared with the natural history of untreated spontaneous knee osteonecrosis. Source


Morrison J.A.,Childrens Hospital of Cincinnati | Glueck C.J.,Cholesterol and Metabolism Center | Wang P.,Cholesterol and Metabolism Center
Metabolism: Clinical and Experimental | Year: 2012

The objective was to assess whether pediatric risk factors predict cardiovascular disease (CVD), impaired fasting glucose (IFG) + type 2 diabetes mellitus (T2DM), and high blood pressure (HBP) in young adulthood. We performed a prospective follow-up of 909 public-parochial suburban schoolchildren first studied at ages 6 to 18 years and 26 years later at a mean age of 38 years. Pediatric triglycerides (TGs), blood pressure, low-density lipoprotein cholesterol, body mass index, and glucose above and high-density lipoprotein cholesterol below established pediatric cutoffs, along with race, cigarette smoking, family history of CVD, T2DM, and HBP, were assessed as determinants of young adult CVD, a composite variable including IFG + T2DM and HBP. By stepwise logistic regression, adult CVD (19 yes, 862 no) was associated with pediatric high TG (odds ratio [OR], 5.85; 95% confidence interval [CI], 2.3-14.7). High TG in pediatric probands with young adult CVD was familial and was associated with early CVD in their high-TG parents. Adult IFG + T2DM (114 yes, 535 no) was associated with parental T2DM (OR, 2.2; 95% CI, 1.38-3.6), high childhood glucose (OR, 4.43; 95% CI, 2-9.7), and childhood cigarette smoking (OR, 1.64; 95% CI, 1.03-2.61). Adult HBP (133 yes, 475 no) was associated with pediatric high body mass index (OR, 2.7; 95% CI, 1.7-4.3) and HBP (OR, 2.5; 95% CI, 1.5-4.3). Pediatric risk factors are significantly, independently related to young adult CVD, IFG + T2DM, and HBP. Identification of pediatric risk factors for CVD, IFG + T2DM, and HBP facilitates initiation of primary prevention programs to reduce development of adult CVD, IFG + T2DM, and HBP. © 2012 Elsevier Inc. All rights reserved. Source


Morrison J.A.,Cincinnati Childrens Hospital Medical Center | Glueck C.J.,Cholesterol and Metabolism Center | Wang P.,Cholesterol and Metabolism Center
Journal of Pediatrics | Year: 2012

Objective: To evaluate children's cardiovascular disease (CVD) risk factors as predictors of parents' subsequent CVD, type 2 diabetes mellitus (T2DM), and high blood pressure (HBP). Study design: We conducted a 26-year prospective follow-up of 852 5- to 19-year-old black and white schoolchildren (mean age, 12 years; Lipid Research Clinics, 1973-8), and parents (mean age, 40 years) from 519 families in Princeton Schools, Cincinnati, Ohio. Schoolchildren were reassessed in the Princeton Follow-up study 1999-2003 at mean age 39 years; CVD, T2DM, and HBP history of their 1038 parents were reassessed by mean age 66 years. We assessed relationships of childhood risk factors with parental CVD, T2DM, and HBP. Child-probands identified with triglyceride (TG) levels, blood pressure, low-density lipoprotein cholesterol levels, body mass index (BMI), and glucose level greater than and high-density lipoprotein cholesterol levels less than established cutoff points. Results: Pediatric HBP (P =.006) and low high-density lipoprotein cholesterol (P =.018) were predictive of parental CVD at age ≤50 years. Pediatric HBP (P =.02) and high TG (P =.03) were predictive of parental CVD at age ≤60 years. Pediatric high TG (P =.009) and high low-density lipoprotein cholesterol (P =.04) were predictive of parental CVD by age 66 years. Pediatric high BMI (P =.0006) were predictive of parental T2DM. Pediatric high BMI (P =.003) and black race (P =.004) were predictive of parental HBP. Conclusions: Pediatric risk factors identify families with parents at increased risk for CVD, T2DM, and HBP, emphasizing the usefulness of the child as proband. Copyright © 2012 Mosby Inc. All rights reserved. Source


Pandit R.S.,Cholesterol and Metabolism Center | Glueck C.J.,Cholesterol and Metabolism Center
Blood Coagulation and Fibrinolysis | Year: 2014

Our specific aim is to describe the development of thrombotic osteonecrosis of the jaws after testosterone-anastrozole therapy in a 55-year-old white man subsequently found to have previously undiagnosed factor V Leiden heterozygosity. Before the diagnosis of V Leiden heterozygosity, he was given testosterone gel, 50mg/day, and on testosterone, serum testosterone (963ng/dl) and estradiol were high (50pg/ml). Anastrozole was started, and testosterone was continued. Six months later, osteonecrosis of the jaws was diagnosed. Exogenous testosterone is aromatized to estradiol and estradiol-induced thrombophilia, when superimposed on underlying familial thrombophilia, as in this case, may lead to thrombosis and osteonecrosis. We recommend that before giving testosterone, at a minimum, screening for the factor V Leiden and G20210A mutations, and factor VIII and XI activity be carried out, to avoid unanticipated thrombosis. © 2014 Wolters Kluwer Health Lippincott Williams & Wilkins. Source


Glueck C.J.,Cholesterol and Metabolism Center | Morrison J.A.,Heart Institute | Wang P.,Cholesterol and Metabolism Center | Woo J.G.,Heart Institute | Woo J.G.,Cincinnati Childrens Hospital Medical Center Cincinnati
Metabolism: Clinical and Experimental | Year: 2013

Objective We determined whether simple, clinical information on late and early menarche could help identify adult women with metabolic syndrome (MetS) and oligomenorrhea. Materials/Methods We carried out a 26-year prospective follow-up of 272 suburban schoolgirls from ages 5-22 to 30-46. Results Early menarche (≤ 10 years, 5.2% of girls) and late menarche (≥ 16 years, 6.7% of girls) were both associated with oligomenorrhea (≥ 42 days) in adulthood, 29% and 11%, vs. 5% for normal menarche (11-15 years), p =.004. Early menarche was characterized by high childhood BMI (LS mean ± SE: 21.2 ± 1.0 kg/m2) and by high childhood and adult MetS (15%, 36%). Girls with late menarche had the lowest childhood BMI (18.1 ± 1.0), no childhood MetS, and the highest adult MetS (47%). Increasing age at menarche was associated with uniformly decreasing childhood BMI and MetS, but with a U-shaped pattern of BMI (p =.05), MetS (p =.008), and oligomenorrhea (p =.02) in adulthood. Change to MetS from median ages 13 to 38 was associated with early-late menarche (OR = 3.11, 95% CI 1.37-7.07, p =.007). MetS in adulthood was associated with childhood MetS (OR = 8.03, 95% CI 2.57-25.08, p =.0003) and with early-late menarche (OR = 3.43, 95% CI 1.44-8.15, p =.005). Conclusions Menarche age had a curvilinear ('U' shaped) relationship with MetS and oligomenorrhea in adulthood. Late menarche and early menarche are risk factors for adult oligomenorrhea, MetS, and cardiometabolic abnormalities. Girls with early (≤ age 10) and with late menarche (≥ 16) represent a group at high risk for adult cardiometabolic abnormalities and oligomenorrhea that is easily identifiable by physicians. © 2013 Elsevier Inc. Source

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