Internists, Rheumatologist
25 years of experience
Video profile
Accepting new patients
4815 Liberty Ave
Suite 222
Pittsburgh, PA 15224
Locations and availability (9)

Education ?

Medical School Score Rankings
University of Pittsburgh (1985)
  • Currently 4 of 4 apples
Top 25%

Awards & Distinctions ?

Castle Connolly America's Top Doctors® (2009, 2012 - 2014)
Castle Connolly's Top Doctors™ (2012 - 2013)
Patients' Choice Award (2008 - 2009, 2011 - 2012)
American Board of Internal Medicine
American College of Rheumatology
Antiphospholipid Antibody Syndrome Foundation of America

Affiliations ?

Dr. Manzi is affiliated with 14 hospitals.

Hospital Affilations



  • Forbes Regional Hospital
    2570 Haymaker Rd, Monroeville, PA 15146
    • Currently 4 of 4 crosses
    Top 25%
  • Alle-Kiski Medical Center
    1301 Carlisle St, Natrona Heights, PA 15065
    • Currently 4 of 4 crosses
    Top 25%
  • Allegheny General Hospital
    320 E North Ave, Pittsburgh, PA 15212
    • Currently 4 of 4 crosses
    Top 25%
  • Magee-Womens Hospital of UPMC Health System
    300 Halket St, Pittsburgh, PA 15213
    • Currently 3 of 4 crosses
    Top 50%
  • Western Pennsylvania Hospital
    4800 Friendship Ave, Pittsburgh, PA 15224
    • Currently 3 of 4 crosses
    Top 50%
  • West Penn - Forbes Regional Campus
  • UPMC Mercy
  • West Penn Allegheny Health System
  • UPMC Presbyterian
  • West Penn Hospital
  • VA Pittsburgh Healthcare System-University Dr. Div
  • Magee Womens Hospital
  • Allegheny U. Hospital - Allegheny General
  • UPMC Presbyterian/Shadyside
  • Publications & Research

    Dr. Manzi has contributed to 4 publications.
    Title Clinical Quality Measures for Electrodiagnosis in Suspected Cts: Comments.
    Date November 2010
    Journal Muscle & Nerve
    Title Differences in Subclinical Cardiovascular Disease Between African American and Caucasian Women with Systemic Lupus Erythematosus.
    Date March 2009
    Journal Translational Research : the Journal of Laboratory and Clinical Medicine

    Racial differences exist in disease rates and mortality in both cardiovascular disease (CVD) and systemic lupus erythematosus (SLE). The objective of this cross-sectional study was to compare the frequency and risk factors for subclinical CVD in African American (AA) and Caucasian women with SLE and no prior CVD events. Traditional CVD risk factors and SLE-related factors were assessed in 309 SLE women. Subclinical CVD was assessed by carotid ultrasound to measure intimamedial thickness (IMT) and plaque, and electron beam computed tomography (EBCT) was used to measure coronary artery calcium (CAC). AA women had less education and higher levels of body mass index, blood pressure, lipoprotein(a), C-reactive protein (CRP), fibrinogen, and erythrocyte sedimentation rate (ESR). However, AA women had lower albumin, more and longer duration of corticosteroid use, higher SLE disease activity and damage, and more dsDNA antibodies compared with Caucasian women after adjustment for age and study site. More AA women had carotid plaque (adjusted odds ratio [OR], 1.94; 95% confidence interval [CI], 1.03-3.65) and higher carotid IMT (0.620 vs 0.605 mm, P = 0.07) but similar CAC compared with Caucasians. A multivariate analysis revealed that the following risk factor variables were significantly different between the racial groups and associated with plaque: blood pressure, current corticosteroid use, SLE disease activity, and SLE damage. All factors contributed to the result, but no individual risk factor fully accounted for the association between race and plaque. In conclusion, the presence of carotid plaque was higher in AA compared with Caucasian women with SLE, in contrast to studies of non-SLE subjects, in which AA have similar or less plaque than Caucasians. A combination of SLE-related and traditional CVD risk factors explained the racial difference in plaque burden.

    Title Use of a Multiantigen Detection Algorithm for Diagnosis of Kaposi's Sarcoma-associated Herpesvirus Infection.
    Date November 2006
    Journal Journal of Clinical Microbiology

    The ability to readily and accurately diagnose Kaposi's sarcoma-associated herpesvirus (KSHV, or human herpesvirus 8) infection in individuals remains a demanding task. Among the available diagnostic methods, sensitivities and specificities range widely, and many are inadequate for large-scale screening studies. We examined a serological algorithm for detecting KSHV in human sera having high sensitivity and specificity. This method uses previously described open reading frame (ORF) K8.1 and ORF65 peptide-based enzyme-linked immunosorbent assays and a novel purified recombinant full-length LANA1 protein. We generated two multiantigen algorithms: one that maximized sensitivity and one that maximized specificity. These serological algorithms were then used to evaluate seroprevalence rates among populations of clinical and epidemiological importance. The serological algorithms yielded sensitivities of 96% and 93% and specificities of 94% and 98% for the more sensitive and specific algorithms, respectively. Among kidney donors, seroprevalence was low, 4.0% (2/50), and similar to that of blood donors (P = 0.46; odds ratio [OR], 1.4; confidence interval [CI], 0.14 to 7.9) using the highly specific algorithm. Using the sensitive algorithm, 8.0% (4/50) were infected compared to 6.4% (16/250) observed among blood donors (OR, 1.3; CI, 0.41 to 4.0; P = 0.43). Among subjects requiring bone marrow transplantation, seroprevalence rates were not elevated compared to those of blood donors (OR, 2.0; 95% CI, 0.10 to 122.9; P = 0.50). Because the need for high-quality KSHV detection methods are warranted and because questions remain about the optimal methods for assessing KSHV infection in individuals, we propose a systematic approach to standardize and optimize the assessment of KSHV infection rates using a combination of established and novel serological assays and methods.

    Title The Bbz/wor Rat: Clinical Characteristics of the Diabetic Syndrome.
    Date December 1993
    Journal Diabetologia

    The BBZ/Wor rat is a model of obesity and autoimmune diabetes mellitus developed by crossing the BB/Wor and Zucker rats. We studied circulating glucose and insulin levels, islet morphology and lymphocyte subsets in lean and obese BBZ/Wor rats before and after the onset of diabetes, and studied the clinical course of diabetes in animals after interruption of exogenous insulin therapy. Lean BBZ/Wor rats developed insulin-dependent diabetes and died in ketoacidosis within 1 week after cessation of insulin injections. Diabetes also developed in obese rats, but these animals were not insulin-dependent and survived for months without insulin therapy. The islets of the lean diabetic rats revealed complete destruction of pancreatic beta cells and plasma insulin levels were virtually undetectable. In contrast, the islets of the obese rats revealed insulitis and substantial beta-cell loss, however autoimmune beta-cell destruction was incomplete, and residual beta cells were presumably responsible for the presence of measurable levels of plasma insulin and the long-term survival of obese diabetics without insulin therapy. Obese rats were hyperinsulinaemic, developed diabetes significantly earlier, and with a greater incidence than lean rats, suggesting a possible relationship between enhanced beta-cell metabolic activity and immune destruction. Obese males became diabetic more frequently and at an earlier age than obese females and lean rats of both sexes, suggesting a role for gender in the pathogenesis of diabetes. We conclude that the BBZ/Wor rat is a unique animal model for investigating the interaction of obesity, beta-cell metabolism, autoimmune insulitis and genetic predisposition to diabetes.

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