Dr. Sergio  Fazio  Md,Phd image

Dr. Sergio Fazio Md,Phd

3303 Sw Bond Ave
Portland OR 97239
503 189-9008
Medical School: Other - 1983
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: Yes
License #: MF165476
NPI: 1366526477
Taxonomy Codes:
207RC0000X 207RE0101X

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy


Dr. Sergio Fazio is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:99214 Description:Office/outpatient visit est Average Price:$237.00 Average Price Allowed
By Medicare:
HCPCS Code:99213 Description:Office/outpatient visit est Average Price:$160.00 Average Price Allowed
By Medicare:
HCPCS Code:36415 Description:Routine venipuncture Average Price:$24.00 Average Price Allowed
By Medicare:
HCPCS Code:85610 Description:Prothrombin time Average Price:$17.00 Average Price Allowed
By Medicare:

HCPCS Code Definitions

Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: A detailed history; A detailed examination; Medical decision making of moderate complexity. Counseling and/or coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of moderate to high severity. Typically, 25 minutes are spent face-to-face with the patient and/or family.
Office or other outpatient visit for the evaluation and management of an established patient, which requires at least 2 of these 3 key components: An expanded problem focused history; An expanded problem focused examination; Medical decision making of low complexity. Counseling and coordination of care with other physicians, other qualified health care professionals, or agencies are provided consistent with the nature of the problem(s) and the patient's and/or family's needs. Usually, the presenting problem(s) are of low to moderate severity. Typically, 15 minutes are spent face-to-face with the patient and/or family.

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found


Doctor Name
Cardiovascular Disease (Cardiology)
Cardiovascular Disease (Cardiology)
*These referrals represent the top 10 that Dr. Fazio has made to other doctors


Macrophage SR-BI Mediates Efferocytosis via Src/PI3K/Rac1 Signaling and Reduces Atherosclerotic Lesion Necrosis. - Journal of lipid research
Macrophage apoptosis and efferocytosis are key determinants of atherosclerotic plaque inflammation and necrosis. Bone marrow transplantation studies in ApoE and LDLR deficient mice revealed that hematopoietic SR-BI deficiency results in severely defective efferocytosis in mouse atherosclerotic lesions, resulting in 17-fold higher ratio of free to macrophage-associated dead cells in lesions containing SR-BI-/- cells, 5-fold more necrosis, 65.2% less lesional collagen content, nearly 7-fold higher dead cell accumulation, and 2-fold larger lesion area. Hematopoietic SR-BI-/- deletion elicited a maladaptive inflammatory response (higher IL-1Beta, IL-6 and TNF-alpha, lower IL-10 and TGF-Beta. Efferocytosis of apoptotic thymocytes was reduced by 64% in SR-BI-/- versus WT macrophages, both in vitro and in vivo. In response to apoptotic cells, macrophage SR-BI bound with phosphatidylserine and induced Src phosphorylation and cell membrane recruitment, which led to downstream activation of PI3K and Rac1 for engulfment and clearance of apoptotic cells, as inhibition of Src decreased PI3K, Rac1-GTP, and efferocytosis in WT cells. Pharmacological inhibition of Rac1 reduced macrophage efferocytosis in a SR-BI dependent fashion, and activation of Rac1 corrected the defective efferocytosis in SR-BI-/- macrophages. Thus, deficiency of macrophage SR-BI promotes defective efferocytosis signaling via the Src/PI3K/Rac1 pathway, resulting in increased plaque size, necrosis, and inflammation.Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
Residual Cardiovascular Risk in Chronic Kidney Disease: Role of High-density Lipoprotein. - Archives of medical research
Although reducing low-density lipoprotein-cholesterol (LDL-C) levels with lipid-lowering agents (statins) decreases cardiovascular disease (CVD) risk, a substantial residual risk (up to 70% of baseline) remains after treatment in most patient populations. High-density lipoprotein (HDL) is a potential contributor to residual risk, and low HDL-cholesterol (HDL-C) is an established risk factor for CVD. However, in contrast to conventional lipid-lowering therapies, recent studies show that pharmacologic increases in HDL-C levels do not bring about clinical benefits. These observations have given rise to the concept of dysfunctional HDL where increases in serum HDL-C may not be beneficial because HDL loss of function is not corrected by or even intensified by the therapy. Chronic kidney disease (CKD) increases CVD risk, and patients whose CKD progresses to end-stage renal disease (ESRD) requiring dialysis are at the highest CVD risk of any patient type studied. The ESRD population is also unique in its lack of significant benefit from standard lipid-lowering interventions. Recent studies indicate that HDL-C levels do not predict CVD in the CKD population. Moreover, CKD profoundly alters metabolism and composition of HDL particles and impairs their protective effects on functions such as cellular cholesterol efflux, endothelial protection, and control of inflammation and oxidation. Thus, CKD-induced perturbations in HDL may contribute to the excess CVD in CKD patients. Understanding the mechanisms of vascular protection in renal disease can present new therapeutic targets for intervention in this population.Copyright © 2015 IMSS. Published by Elsevier Inc. All rights reserved.
Plasma lipid levels and colorectal adenoma risk. - Cancer causes & control : CCC
Abnormalities in lipid levels have been associated with colorectal neoplasm risk; however, few studies have adjusted for use of cholesterol-lowering medications. The objective of this study was to determine the association of plasma lipid levels with adenoma risk while accounting for statin medication use.We included 254 subjects with advanced adenoma, 246 with single small adenoma, 179 with multiple small adenoma cases, and 403 control participants in the Tennessee Colorectal Polyp Study who also had plasma lipid measurements performed. Data on the use of statin medications were available for 83.4% of these participants. The association between plasma lipids and adenoma risk was evaluated using logistic regression models.Participants in the highest quartile of HDL cholesterol (range 52-106 mg/dl) had an adjusted odds ratio of 0.49 (95% CI 0.23, 1.07), 0.35 (95% CI 0.13, 0.91), and 0.22 (95% CI 0.09, 0.54) for single small, multiple small, and advanced adenomas compared to the lowest quartile (range 12-34 mg/dl), respectively. Participants with the highest quartile of triglyceride levels (range 178-721 mg/dl) had an adjusted odds ratio of 2.40 (95% CI 1.26, 4.55), 1.67 (95% CI 0.66, 4.23), and 2.79 (95% CI 1.25, 6.23) for single small, multiple small, and advanced adenoma, respectively, compared to the lowest quartile (range 40-84 mg/dl). When restricted to individuals with known statin medication use, adjusting for statin use did not appreciably affect these results.We found a direct association between triglyceride plasma levels and an inverse association between plasma HDL cholesterol levels and adenoma risk. Both effects were not appreciably changed when accounting for the regular use of statin medication.
Isolevuglandin-type lipid aldehydes induce the inflammatory response of macrophages by modifying phosphatidylethanolamines and activating the receptor for advanced glycation endproducts. - Antioxidants & redox signaling
Increased lipid peroxidation occurs in many conditions associated with inflammation. Because lipid peroxidation produces lipid aldehydes that can induce inflammatory responses through unknown mechanisms, elucidating these mechanisms may lead to development of better treatments for inflammatory diseases. We recently demonstrated that exposure of cultured cells to lipid aldehydes such as isolevuglandins (IsoLG) results in the modification of phosphatidylethanolamine (PE). We therefore sought to determine (i) whether PE modification by isolevuglandins (IsoLG-PE) occurred in vivo, (ii) whether IsoLG-PE stimulated the inflammatory responses of macrophages, and (iii) the identity of receptors mediating the inflammatory effects of IsoLG-PE.IsoLG-PE levels were elevated in plasma of patients with familial hypercholesterolemia and in the livers of mice fed a high-fat diet to induce obesity and hepatosteatosis. IsoLG-PE potently stimulated nuclear factor kappa B (NFκB) activation and expression of inflammatory cytokines in macrophages. The effects of IsoLG-PE were blocked by the soluble form of the receptor for advanced glycation endproducts (sRAGE) and by RAGE antagonists. Furthermore, macrophages derived from the bone marrow of Ager null mice failed to express inflammatory cytokines in response to IsoLG-PE to the same extent as macrophages from wild-type mice.These studies are the first to identify IsoLG-PE as a mediator of macrophage activation and a specific receptor, RAGE, which mediates its biological effects.PE modification by IsoLG forms RAGE ligands that activate macrophages, so that the increased IsoLG-PE generated by high circulating cholesterol levels or high-fat diet may play a role in the inflammation associated with these conditions. Antioxid. Redox Signal. 22, 1633-1645.
Targeting PCSK9 for therapeutic gains. - Current atherosclerosis reports
Even though it is only a little over a decade from the discovery of proprotein convertase subtilisin/kexin type 9 (PCSK9) as a plasma protein that associates with both hypercholesterolemia and low cholesterol syndromes, a rich literature has developed describing its unique physiology and the impact of antagonism of this molecule on cholesterol metabolism for therapeutic purposes. Indeed, the PCSK9 story is unfolding rapidly, with many answers and more questions. This review summarizes the most recent data from phase II/III clinical trials of PCSK9 inhibition with the three leading antibodies, highlights the clinical significance of the ongoing studies, and suggests future areas of investigation based on recent basic science discoveries on the physiology of PCSK9.
PCSK9 inhibition to reduce cardiovascular disease risk: recent findings from the biology of PCSK9. - Current opinion in endocrinology, diabetes, and obesity
Review novel insights into the biology of proprotein convertase subtilisin/kexin 9 (PCSK9) that may explain the extreme efficiency of PCSK9 inhibition and the unexpected metabolic effects resulting from PCSK9 monoclonal antibody therapy, and may identify additional patients as target of therapy.For over 20 years, the practical knowledge of cholesterol metabolism has centered around cellular mechanisms, and around the idea that statin therapy is the essential step to control metabolic abnormalities for cardiovascular risk management. This view has been embraced by the recent AHA/ACC guidelines, but is being challenged by recent studies including nonstatin medications and by the development of a new class of cholesterol-lowering agents that seems destined to early US Food and Drug Administration approval. The discovery of PCSK9 - a circulating protein that regulates hepatic low-density lipoprotein (LDL) receptor and serum LDL cholesterol levels - has led to a race for its therapeutic inhibition. Recent findings on PCSK9 regulation and pleiotropic effects will help identify additional patient groups likely to benefit from the inhibitory therapy and unravel the full potential of PCSK9 inhibition therapy.Injectable human monoclonal antibodies to block the interaction between PCSK9 and LDL receptor are demonstrating extraordinary efficacy (LDL reductions of up to 70%) and almost the absence of any side-effects. A more moderate effect is seen on other lipoprotein parameters, with the exception of lipoprotein(a) levels. We describe mechanisms that can explain the effect on lipoprotein(a), predict a potential effect on postprandial triglyderides, and suggest a new category of patients for anti-PCSK9 therapy.
The role of PCSK9 in intestinal lipoprotein metabolism: synergism of statin and ezetimibe. - Atherosclerosis. Supplements
Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a major role in the regulation of lipoprotein metabolism, mostly through control of low-density lipoprotein receptor degradation. Depletion of cellular cholesterol causes a compensatory increase in plasma PCSK9 levels, which can diminish the cholesterol-lowering power of statins and may lead to the overproduction of intestinal lipoproteins, mainly thorough the up regulation of microsomal triglyceride transfer protein and the Niemann-Pick C1-like 1 protein, the target of ezetimibe. Thus, ezetimibe therapy may counter this unwanted effect of statins, providing an additional theoretical rationale for combining the effect of ezetimibe on intestinal cholesterol absorption and that of statins on cholesterol synthesis.© 2015 Elsevier Ireland Ltd. All rights reserved.
Macrophage apoAI protects against dyslipidemia-induced dermatitis and atherosclerosis without affecting HDL. - Journal of lipid research
Tissue cholesterol accumulation, macrophage infiltration, and inflammation are features of atherosclerosis and some forms of dermatitis. HDL and its main protein, apoAI, are acceptors of excess cholesterol from macrophages; this process inhibits tissue inflammation. Recent epidemiologic and clinical trial evidence questions the role of HDL and its manipulation in cardiovascular disease. We investigated the effect of ectopic macrophage apoAI expression on atherosclerosis and dermatitis induced by the combination of hypercholesterolemia and absence of HDL in mice. Hematopoietic progenitor cells were transduced to express human apoAI and transplanted into lethally irradiated LDL receptor(-/-)/apoAI(-/-) mice, which were then placed on a high-fat diet for 16 weeks. Macrophage apoAI expression reduced aortic CD4(+) T-cell levels (-39.8%), lesion size (-25%), and necrotic core area (-31.6%), without affecting serum HDL or aortic macrophage levels. Macrophage apoAI reduced skin cholesterol by 39.8%, restored skin morphology, and reduced skin CD4(+) T-cell levels. Macrophage apoAI also reduced CD4(+) T-cell levels (-32.9%) in skin-draining lymph nodes but had no effect on other T cells, B cells, dendritic cells, or macrophages compared with control transplanted mice. Thus, macrophage apoAI expression protects against atherosclerosis and dermatitis by reducing cholesterol accumulation and regulating CD4(+) T-cell levels, without affecting serum HDL or tissue macrophage levels.Copyright © 2015 by the American Society for Biochemistry and Molecular Biology, Inc.
Smoking, sex, risk factors and abdominal aortic aneurysms: a prospective study of 18 782 persons aged above 65 years in the Southern Community Cohort Study. - Journal of epidemiology and community health
Abdominal aortic aneurysm (AAA) is a leading cause of death in the USA. We evaluated the incidence and predictors of AAA in a prospectively followed cohort.We calculated age-adjusted AAA incidence rates (IR) among 18 782 participants aged ≥65 years in the Southern Community Cohort Study who received Medicare coverage from 1999-2012, and assessed predictors of AAA using multivariable Cox proportional hazards models, overall and stratified by sex, adjusting for demographic, lifestyle, socioeconomic, medical and other factors. HRs and 95% CIs were calculated for AAA in relation to factors ascertained at enrolment.Over a median follow-up of 4.94 years, 281 cases were identified. Annual IR was 153/100,000, 401, 354 and 174 among blacks, whites, men and women, respectively. AAA risk was lower among women (HR 0.48, 95% CI 0.36 to 0.65) and blacks (HR 0.51, 95% CI 0.37 to 0.69). Smoking was the strongest risk factor (former: HR 1.91, 95% CI 1.27 to 2.87; current: HR 5.55, 95% CI 3.67 to 8.40), and pronounced in women (former: HR 3.4, 95% CI 1.83 to 6.31; current: HR 9.17, 95% CI 4.95 to 17). A history of hypertension (HR 1.44, 95% CI 1.04 to 2.01) and myocardial infarction or coronary artery bypass surgery (HR 1.9, 95% CI 1.37 to 2.63) was negatively associated, whereas a body mass index ≥25 kg/m(2) (HR 0.72; 95% CI 0.53 to 0.98) was protective. College education (HR 0.6, 95% CI 0.37 to 0.97) and black race (HR 0.44, 95% CI 0.28 to 0.67) were protective among men.Smoking is a major risk factor for incident AAA, with a strong and similar association between men and women. Further studies are needed to evaluate benefits of ultrasound screening for AAA among women smokers.Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
On the function and homeostasis of PCSK9: reciprocal interaction with LDLR and additional lipid effects. - Atherosclerosis
Proprotein convertase subtilisin kexin type 9 (PCSK9) is a circulatory ligand that terminates the lifecycle of the low-density lipoprotein (LDL) receptor (LDLR) thus affecting plasma LDL-cholesterol (LDL-C) levels. Recent evidence shows that in addition to the straightforward mechanism of action, there are more complex interactions between PCSK9, LDLR and plasma lipoprotein levels, including: (a) the presence of both parallel and reciprocal regulation of surface LDLR and plasma PCSK9; (b) a correlation between PCSK9 and LDL-C levels dependent not only on the fact that PCSK9 removes hepatic LDLR, but also due to the fact that up to 40% of plasma PCSK9 is physically associated with LDL; and (c) an association between plasma PCSK9 production and the assembly and secretion of triglyceride-rich lipoproteins. The effect of PCSK9 on LDLR is being successfully utilized toward the development of anti-PCSK9 therapies to reduce plasma LDL-C levels. Current biochemical research has uncovered additional mechanisms of action and interacting partners for PCSK9, and this opens the way for a more thorough understanding of the regulation, metabolism, and effects of this interesting protein.Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Map & Directions

3303 Sw Bond Ave Portland, OR 97239
View Directions In Google Maps

Nearby Doctors

3181 Sw Sam Jackson Park Rd
Portland, OR 97239
888 338-8305
3710 Sw Us Veterans Hospital Rd P3-Anes
Portland, OR 97239
503 208-8262
3181 Sw Sam Jackson Park Road Department Of Emergency Medicine
Portland, OR 97239
503 947-7500
3181 Sw Sam Jackson Park Rd Uhn67
Portland, OR 97239
503 946-6949
3181 Sw Sam Jackson Park Rd Uhn-80
Portland, OR 97239
503 948-8205
5200 Sw Macadam Ave
Portland, OR 97239
503 317-7854
5200 Sw Macadam Ave
Portland, OR 97239
503 317-7854
3375 Sw Terwilliger Blvd
Portland, OR 97239
503 947-7891
3181 Sw Sam Jackson Park Rd Mail Code 120
Portland, OR 97239
503 948-8211
3181 Sw Sam Jackson Park Rd
Portland, OR 97239
503 943-3442