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Dr. Michael  Pearlman  Md image

Dr. Michael Pearlman Md

256 Salem End Rd
Framingham MA 01702
617 202-2230
Medical School: Tufts University School Of Medicine - 1970
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: Yes
Participates In EHR: No
License #: 33601
NPI: 1699861948
Taxonomy Codes:
2084P0800X

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Awards & Recognitions

About Us

Practice Philosophy

Conditions

Dr. Michael Pearlman is associated with these group practices

Procedure Pricing

HCPCS Code Description Average Price Average Price
Allowed By Medicare
HCPCS Code:90801 Description:Psy dx interview Average Price:$185.00 Average Price Allowed
By Medicare:
$159.39
HCPCS Code:90862 Description:Medication management Average Price:$79.99 Average Price Allowed
By Medicare:
$61.79

Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found

Referrals

NPI
Doctor Name
Specialty
Count
1053385732
Diagnostic Radiology
104
1972540474
Diagnostic Radiology
85
*These referrals represent the top 10 that Dr. Pearlman has made to other doctors

Publications

Brain tumors in children--current therapies and newer directions. - Indian journal of pediatrics
Brain tumors are the second most common malignancy and the major cause of cancer related mortality in children. Though significant advances in neuroimaging, neurosurgery, radiation therapy and chemotherapy have evolved over the years, overall survival rate remains less than 75%. Malignant gliomas, high risk medulloblastoma with recurrence and infant brain tumors continue to be a major cause of therapeutic frustration. Even today diffuse pontine gliomas are universally fatal. Though tumors like low grade glioma have an overall excellent survival, recurrences and progression in eloquent areas pose therapeutic challenges. As research continues to unravel the biology including key molecules and signaling pathways responsible for the oncogenesis of different childhood brain tumors, novel targeted therapies are profiled. Identification of major targets like the Epidermal Growth factor Receptor (EGFR), Platelet Derived Growth Factor Receptor (PDGFR), Vascular Endothelial Growth factor (VEGF) and key signaling pathways like the MAPK and PI3K/Akt/mTOR has enabled us over the recent years to better understand tumor behavior and design tailored therapy. These efforts have improved overall survival of children with brain tumors. This review article discusses the current status of common brain tumors in children and the newer therapeutic approaches.
Evaluating disparities in door-to-EKG time for patients with noncardiac chest pain. - Journal of emergency nursing: JEN : official publication of the Emergency Department Nurses Association
Our objective was to examine gender, racial, and age differences in door-to-EKG time in patients diagnosed with non-cardiac chest pain.This was a prospective cohort study of adult patients with an explicitly stated chief complaint of chest pain at an urban, academic ED. Primary study outcome variable was time to initial EKG. Predictor variables included gender, race, and age.The final sample consisted of 214 patients. The overall median time to EKG in this cohort of patients was 29 minutes. No difference in time to EKG was found between gender or racial category. Time to EKG was significantly greater for patients in age categories 18-39 and 40-59 when compared with subjects greater than 60 years old.In this prospective cohort study of non-STEMI/ACS patients with a chief complaint of chest pain, there were no gender or racial disparities in door-to-EKG time.
Dexrazoxane's protection of jejunal crypt cells in the jejunum of C3Hf/Kam mice from doxorubicin-induced toxicity. - Cancer chemotherapy and pharmacology
Dexrazoxane (DEX) is used clinically to reduce doxorubicin-induced cardiotoxicity. Because DEX inhibits anthracycline-induced toxicity, we set out to investigate DEX's ability to reduce the incidence and severity of gastrointestinal toxicity associated with anthracycline administration in C3Hf/Kam mice. Doxorubicin and idarubicin, two commonly used anthracyclines, were each examined in combination with DEX. A jejunal crypt survival assay demonstrated that DEX increased crypt survival from 40% (doxorubicin 22.5 mg/kg) to 63% at a DEX/doxorubucin dose ratio of 10:1 ( P<0.05). When doxorubicin was increased to a dose of 27.5 mg/kg, crypt survival increased from 18% to 40% at a DEX:Dox ratio of 5:1 ( P<0.05). At ratios of 10:1 and 20:1, DEX had no protective effect on idarubicin-induced crypt cell toxicity. Our findings support the use of DEX to prevent or ameliorate mucositis in patients receiving anthracycline-based therapy and the use of DEX with high-dose doxorubicin to treat refractory disease.
Dexrazoxane in combination with anthracyclines lead to a synergistic cytotoxic response in acute myelogenous leukemia cell lines. - Leukemia research
In an attempt to improve current therapeutic strategies for acute myelogenous leukemia (AML), we studied the effects of a commercially available drug, dexrazoxane (DEX), which protects against anthracycline-induced cardiotoxicity. The rationale was that DEX would permit higher doses of cardiotoxic drugs to be given. The drug itself may have therapeutic potential as well. Finally, there are concerns that the drug may, as a protective agent, diminish the effectiveness of various chemotherapeutics. To help resolve the question about potential drug antagonism, we undertook a series of in vitro analyses of DEX and various combinations with anthracyclines and other agents. Colony-forming assays were used to evaluate stem-cell renewal of myeloid cells in vitro, and median-effect analysis was used to evaluate antagonism, synergism, and additivity. The anthracyclines doxorubicin, daunorubicin, and idarubicin were individually combined with DEX to study in vitro effects in leukemic myeloid cell lines. In the hope, we could extend the findings to non-anthracyclines, etoposide and cytosine arabinoside were also evaluated in combination with DEX using the same in vitro model and method. We found that the effects of DEX in combination with any of the anthracyclines were schedule dependent. The antitumor effect was greater for each combination than for any anthracycline alone except when DEX was administered 24h before doxorubicin or daunorubicin. These data were corroborated through median-effect analysis. Etoposide in combination with DEX was synergistic for all combinations and schedules, and the combination of cytosine arabinoside and DEX was effective depending on the schedule used. DEX appears to be a promising drug in the treatment of AML and warrants further clinical study involving novel drug combinations.

Map & Directions

256 Salem End Rd Framingham, MA 01702
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