Mary P Toye

Publications (2)0.88 Total impact

• Article: Metabolic abnormalities in human immunodeficiency virus-infected children: two-year follow-up.

  Jens C Krause, Mary P Toye, Donna J Fisher, Barbara W Stechenberg, Edward O Reiter, Holley F Allen
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  ABSTRACT: HIV-associated lipodystrophy (LD) manifests with fat maldistribution, dyslipidemia, and insulin resistance in some HIV-infected children on antiretroviral therapy. To assess whether lipid abnormalities in patients with HIV are stable over time. The perinatally HIV-infected cohort at a medium-sized urban US teaching hospital. This prospective, observational study consisted of five visits (at entry and 3, 6, 24, and 30 months after entry) during which fasting venous blood samples were drawn for HIV-1 RNA, CD4 lymphocytes, lipid profile, free fatty acids (FFA), glucose, insulin, and adiponectin. IGF-I/IGFBP-3 levels were measured at the first and fifth visits. Of 36 study participants, seven were lipodystrophic, and 30 patients completed all five study visits. LDL-cholesterol, total cholesterol (TC), triglycerides (TG), and FFA levels were significantly higher in patients taking protease inhibitors (PIs). Patients with LD had higher TC and TG levels (both p < 0.05), and higher FFA (p = 0.0532). Adiponectin levels did not differ between PI/non-PI and LD/non-LD groups. HDL-cholesterol seemed to decrease, and FFA to increase over time. All IGF-I and all but one IGFBP-3 level were within normal range for age and Tanner stage. Dyslipidemia remained relatively constant over our study period. Adiponectin was not useful as a marker of LD in our population.
  Journal of pediatric endocrinology & metabolism: JPEM 04/2009; 22(4):345-51. · 0.88 Impact Factor
• Article: HIV--associated lipodystrophy in children.

  Jens C Krause, Mary P Toye, Barbara W Stechenberg, Edward O Reiter, Holley F Allen
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  ABSTRACT: Lipodystrophy (LD) with varying degrees of lipohypertrophy, lipoatrophy, hyperlipidemia, and insulin resistance is one of the complications of highly active antiretroviral therapy (HAART) and occurs in one to 33 % of HAART-treated, HIV infected children. We summarize the data on the role of leptin, adiponectin, the growth hormone axis, glucocorticoids, sterol response element binding protein 1c (SREBP-1c), the tumor necrosis factor alpha axis (TNF-alpha), interleukin-6 (IL-6), interleukin- 18 (IL-18), interferon-alpha (IFN-alpha), tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1) in the pathophysiology of LD. Adiponectin levels are generally decreased in LD, whereas leptin levels are increased. Systemic cortisol levels are not elevated in LD, even though glucocorticoids seem to play an important role in LD and the phenotype can be reminiscent of Cushing syndrome. GH resistance in LD needs to be better characterized. While some cytokines show promise as markers for LD, it is difficult to tell whether their derangement is a cause of or the effect of LD.
  Pediatric endocrinology reviews: PER 10/2005; 3(1):45-51.