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Dr. Viktoria  Kaplan  Md image

Dr. Viktoria Kaplan Md

1721 E 19Th Ave #468
Denver CO 80218
303 630-0501
Medical School: University Of Wisconsin Medical School - 2001
Accepts Medicare: No
Participates In eRX: Yes
Participates In PQRS: Yes
Participates In EHR: No
License #: 43421
NPI: 1669422457
Taxonomy Codes:
174400000X

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Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. Viktoria Kaplan is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:99204 Description:Office/outpatient visit new Average Price:$250.00 Average Price Allowed
By Medicare:
$155.57
HCPCS Code:99214 Description:Office/outpatient visit est Average Price:$128.60 Average Price Allowed
By Medicare:
$100.33

HCPCS Code Definitions

99204
Office or other outpatient visit for the evaluation and management of a new patient, which requires these 3 key components: A comprehensive history; A comprehensive 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, 45 minutes are spent face-to-face with the patient and/or family.
99214
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.

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1073538047
Neurology
167
1184656407
Diagnostic Radiology
66
1497752448
Diagnostic Radiology
44
1912947995
Diagnostic Radiology
43
*These referrals represent the top 10 that Dr. Kaplan has made to other doctors

Publications

Activity of lung neutrophils and matrix metalloproteinases in cyclophosphamide-treated mice with experimental sepsis. - International journal of experimental pathology
Sepsis in patients receiving chemotherapy may result in acute respiratory distress syndrome, despite decreased number of blood neutrophils [polymorphonuclear neutrophils (PMNs)]. In the present study, we investigated the correlation of cyclophosphamide (CY)-induced neutropenia with the destructive potential of lung PMN in respect to formation of septic acute lung injury (ALI). Mice were treated with 250 mg/kg of CY or saline (control) and subjected to cecal ligation and puncture (CLP) or sham operation. ALI was verified by histological examination. Lung PMNs and matrix metalloproteinases (MMPs) were assessed by flow cytometry and gelatin zymography. CLP in CY-treated mice induced a typical lung injury. Despite profound neutropenia, CY treatment did not attenuate CLP-induced ALI. This might relate to only a partial suppression of PMN: CY has significantly reduced PMN influx into the lungs (P = 0.008) and suppressed their oxidative metabolism, but had no suppressive effect on degranulation (P = 0.227) and even induced MMP-9 activity (P = 0.0003). In CY-untreated animals, peak of CLP-induced ALI coincided with massive PMN influx (P = 0.013), their maximal degranulation (P = 0.014) and activation of lung MMP-9 (P = 0.002). These findings may indicate an important role of the residual lung PMN and activation of MMP-9 in septic lung injury during CY chemotherapy.
Response of lung NK1.1-positive natural killer cells to experimental sepsis in mice. - Shock (Augusta, Ga.)
Natural killer cells (NKC) participate in the initiation of the immune response and coordination between innate and adaptive immune mechanisms. Their role in systemic inflammation induced by trauma or infection (sepsis) is still controversial. In the present study, lung NKC and their response to experimental sepsis were investigated. Mice were subjected to cecal ligation and puncture (CLP) to induce sepsis and acute lung injury (ALI). Animals were sacrificed 1, 4, and 7 days postoperatively, and lung histopathology, pulmonary vascular permeability, and inflammatory cells accumulation were assessed. On day 4, parameters of ALI were most prominent, and lung NK1.1+CD3- cells were isolated and studied by flow cytometry. Although CLP did not change the absolute number of lung NKC (2.47 +/- 0.52 x 10(5)/lung compared with 2.97 +/- 0.27 x 10(5)/lung in the sham group), the peak of the CLP-induced ALI was associated with severe dysfunction of lung NKC. Cell cytotoxicity decreased to 25.1 +/- 2.4% (P = 0.002), and percentage of perforin-positive NKC to 2.7 +/- 0.5% (P = 0.03). Cytokine profile of lung NK1.1+CD3- cells was prominently changed. The percentage of IFN-gamma-positive cells decreased to 19.7 +/- 5.7% (P = 0.047), but TNF-alpha-positive cells grew to 26.7 +/- 3.3% (P = 0.02). In summary, severe CLP-induced dysfunction of lung NK1.1+CD-3 cells was demonstrated. This may influence the outcome of the animals during sepsis and acute lung damage.
Response of lung gammadelta T cells to experimental sepsis in mice. - Immunology
Gammadelta T cells link innate and adaptive immune systems and may regulate host defence. Their role in systemic inflammation induced by trauma or infection (sepsis) is still obscured. The present study was aimed to investigate functions of lung gammadelta T cells and their response to experimental sepsis. Mice were subjected to caecal ligation and puncture (CLP) to induce sepsis and acute lung injury (ALI), or to the sham operation. Animals were killed 1, 4, and 7 days postoperatively; lungs were examined by histology, and isolated cells were studied by flow cytometry. Absolute number of gammadelta T cells progressively increased in lungs during sepsis, and reached a seven-fold increase at day 7 after CLP (3.84 +/- 0.41 x 10(5)/lung; P = 0.0002 versus sham). A cellular dysfunction was revealed one day after CLP, as manifested by low cytolytic activity (22.3 +/- 7.1%; P < 0.05 versus sham), low interferon-gamma (IFN-gamma; 8.5 +/- 2.5%; P < 0.05 versus control) and interleukin-10 (IL-10) expression, and high tumour necrosis factor-alpha expression (19.5 +/- 1.7%; P < 0.05 versus control). The restoration of cytotoxicity, and increase in IFN-gamma and IL-10 expression was observed at day 7 of CLP-induced sepsis. In summary, our results demonstrate significant progressive accumulation of gammadelta T cells in lungs during CLP-induced ALI. The temporary functional suppression of lung gammadelta T cells found early after CLP may influence the outcome of sepsis, possibly being associated with uncontrolled inflammatory lung damage.

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1721 E 19Th Ave #468 Denver, CO 80218
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