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Dr. Meetu  Agrawal  Md image

Dr. Meetu Agrawal Md

1450 Mercantile Ln Suite 111
Largo MD 20774
301 257-7610
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: D77379
NPI: 1679821458
Taxonomy Codes:
207R00000X

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Publications

Extensive osteolytic skull base amyloidoma simulating malignancy: A rare pseudotumor producing a diagnostic dilemma. - Journal of cancer research and therapeutics
Although amyloidomas are quite well-known, intracranial, and especially skull base lesions have been rarely reported. Extensive lesions in the skull base frequently simulate malignancy clinicoradiologically. Diagnosis of these lesions is important as they offer a favorable prognosis. We describe a large infiltrating osteolytic skull base tumor-like lesion in a 45-year-old male without evidence of associated plasma cell dyscrasia. Squash smears and histopathology revealed a plasma cell-rich lesion with abundant amyloid, confirming amyloidoma. To conclude, amyloidoma of the skull base is a rare tumor-like lesion, with timely diagnosis and management offering a good prognosis.
Sclerosing Angiomatoid Nodular Transformation of the Spleen: A New Entity or a New Name? - Turk patoloji dergisi
Sclerosing angiomatoid nodular transformation of the splenic red pulp has been described quite recently; many of the lesions previously diagnosed as splenic exuberant granulation tissue, multinodular hemangioma, and inflammatory pseudotumor could actually belong to this category. The lesion has been well reported intermittently in the past, but new cases with still newer associations keep appearing from time to time. There are no known risk factors and no inciting triggers have been proven. We report two such cases- one of which has extensive extramedullary haematopoiesis; a feature that has never been reported earlier. Clinico-morphological and radiological features along with pathogenesis are discussed in detail.
Aspergillus colonization in hydatid cyst: Addition of a case. - Lung India : official organ of Indian Chest Society
Aspergillus is a common saprophytic fungus that causes invasive or non-invasive disease in humans. It commonly colonizes pre-existing lung cavities. It has been earlier reported to coexist in previously operated or ruptured hydatid cysts. However there have been only few case reports of its occurrence in previously unoperated cysts in immunocompetent hosts. The present case adds to this category.
A forgotten disease reminds itself with a rare complication. - Indian journal of dermatology
Diagnosed cases of sexually transmitted diseases (STD) represent tip of the iceberg and Donovanosis in one of them. Donovanosis, in most cases is obvious clinically, but rely for its confirmation on the demonstration of donovan bodies in histological sections and cytological preparation. In an extremely rare setting, this disease may get complicated by the development of squamous cell carcinoma. We report this occurrence in an 18-year-old girl to review the currently forgotten status of donovanosis amongst the STDs and the poor outcome of the disease if left untreated.
Teratomas in central nervous system: a clinico-morphological study with review of literature. - Neurology India
Cranio-spinal axis teratomas are rare. This subset is interesting because symptoms can be varied, depending on the location. Histopathology is diagnostic; most of the lesions are benign. Rarely, malignancy develops in any of the somatic components.To study the demographic, clinico-morphological and follow-up data of central nervous system (CNS) teratomas.Cases diagnosed as mature or immature teratomas in the CNS over a 20-year period were included in the study. Clinico-radiological, demographic and follow-up data of these cases were analyzed.A total of 14 tumors were diagnosed as teratomas. Of these, 11 were mature cystic teratomas; and 1 case each, of teratoma with malignant transformation, terato-carcinoma and mixed germ cell tumor (immature teratoma with germinoma). Six of the 14 cases were intracranial and 8 were spinal. Presenting features varied according to the location. Radiologically, contrast enhancement with predominantly solid component was suggestive of malignancy or an aggressive tumor. Morphologically, a variety of tissue derivatives were seen in the cases. Excision was curative or provided symptomatic relief in most cases; terato-carcinoma and mixed germ cell tumor patients needed adjuvant radiotherapy.CNS teratomas are rare. Morphology and location decide outcome.
Experimental therapeutics for patients with myeloproliferative neoplasias. - Cancer
Philadelphia chromosome (Ph)-negative myeloproliferative neoplasms (MPNs) are characterized by stem cell-derived, unrestrained clonal myeloproliferation. The World Health Organization classification system, proposed in 2008, identifies 7 distinct categories of Ph-negative MPNs including essential thrombocythemia (ET); polycythemia vera (PV); primary myelofibrosis (PMF); mastocytosis; chronic eosinophilic leukemia; chronic neutrophilic leukemia; and MPN, unclassifiable. For many years, the treatment of ET, PV, and PMF, the most frequently diagnosed Ph-negative MPNs, has been largely supportive. In recent years, that paradigm has been challenged because of the discovery of a recurrent point mutation in the Janus kinase 2 (JAK2) gene (JAK2(V617F)). This mutation can be detected in the vast majority of patients with PV and approximately half of patients with ET or PMF and serves as both a diagnostic marker as well as representing a putative molecular target for drug development. Several putative targeted agents with significant in vitro JAK2 inhibitory activity and various degrees of JAK2 specificity are currently undergoing clinical evaluation. Furthermore, other investigational non-tyrosine kinase inhibitor approaches such as immunomodulatory agents and pegylated interferon- have also shown promising results in MPNs.© 2010 American Cancer Society.
Chronic myeloid leukemia in the tyrosine kinase inhibitor era: what is the "best" therapy? - Current oncology reports
The introduction of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), has revolutionized the treatment of chronic myeloid leukemia (CML). By directly targeting the Bcr-Abl kinase, imatinib leads to durable cytogenetic remissions and in turn improved survival. However, many patients with CML develop resistance, fail to respond, or become intolerant to imatinib due to side effects. This has spurred interest in developing second-generation TKIs to overcome the mechanisms of resistance that lead to treatment failure, specifically Bcr-Abl1 kinase domain mutations. Two second-generation TKIs, nilotinib and dasatinib, are approved for the treatment of CML after imatinib failure or intolerance. Unfortunately, many patients fail subsequent treatment with these agents, as they can develop highly resistant mutations such as T315I. Various other strategies are now in use to optimize the treatment of CML, including dose optimization of imatinib, combination therapy, upfront use of second-generation TKIs, and use of maintenance therapy with interferon-alpha and vaccines. This review highlights progress made in the treatment of CML in the past year.
Tyrosine kinase inhibitors: the first decade. - Current hematologic malignancy reports
The treatment of chronic myeloid leukemia (CML) drastically changed with the introduction of imatinib mesylate, a Bcr-Abl1 tyrosine kinase inhibitor (TKI), in 1998. By directly targeting this leukemogenic protein kinase, imatinib affords patients with CML sustained chromosomal remissions, which translate into prolonged survival. However, there has been concern over the emergence of resistance to imatinib, and some patients fail to respond or are intolerant of imatinib therapy because of untoward toxicity. This has spurred interest in developing novel TKIs to overcome the mechanisms of resistance that lead to treatment failure-most importantly, Bcr-Abl1 kinase domain mutations. Two of these second-generation TKIs, nilotinib and dasatinib, are approved worldwide for the treatment of CML after imatinib failure or intolerance. Although these agents are active, they fail in many patients because of the development of highly resistant mutations such as the T315I, against which several novel agents are currently being tested in clinical trials. This review provides an account of the progress made in the field of TKI therapy for CML over the past decade.

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1450 Mercantile Ln Suite 111 Largo, MD 20774
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