Browse Health
Urologist
9 years of experience
Video profile
Accepting new patients

Education ?

Medical School Score
Drexel University (2001)
  • Currently 2 of 4 apples

Awards & Distinctions ?

Associations
American Board of Urology
American Urological Association

Affiliations ?

Dr. Griffin Merriam is affiliated with 13 hospitals.

Hospital Affilations

Score

Rankings

  • Bryn Mawr Rehabilitation Hospital
    414 Paoli Pike, Malvern, PA 19355
    • Currently 4 of 4 crosses
    Top 25%
  • Chester County Hospital
    701 E Marshall St, West Chester, PA 19380
    • Currently 4 of 4 crosses
    Top 25%
  • Main Line Hospital - Bryn Mawr
    Urology
    130 S Bryn Mawr Ave, Bryn Mawr, PA 19010
    • Currently 4 of 4 crosses
    Top 25%
  • Riddle Memorial Hospital
    1068 W Baltimore Pike, Media, PA 19063
    • Currently 3 of 4 crosses
    Top 50%
  • Brandywine Hospital
    201 Reeceville Rd, Coatesville, PA 19320
    • Currently 3 of 4 crosses
    Top 50%
  • Main Line Hospital Paoli
    255 W Lancaster Ave, Paoli, PA 19301
    • Currently 2 of 4 crosses
  • Main Line Hospital Lankenau
    Urology
    100 E Lancaster Ave, Wynnewood, PA 19096
    • Currently 1 of 4 crosses
  • M L Health-Paoli Memorial Hospital
  • -Lankenau Hospital - On staff since 2007
  • Lankenau Medical Center
  • Bryn Mawr Hospital - On staff since
  • Lankenau Medical Center - On staff since
  • Paoli Hospital - On staff since
  • Publications & Research

    Dr. Griffin Merriam has contributed to 7 publications.
    Title Rhabdomyolysis After Laparoscopic Nephrectomy.
    Date February 2008
    Journal Jsls : Journal of the Society of Laparoendoscopic Surgeons / Society of Laparoendoscopic Surgeons
    Excerpt

    BACKGROUND AND OBJECTIVES: Laparoscopic renal surgery has become a widely applied technique in recent years. The development of postoperative rhabdomyolysis is a known but rare complication of laparoscopic renal surgery. Herein, 4 cases of rhabdomyolysis and a review of the literature are presented with respect to pathogenesis, treatment, and prevention of this dire complication. METHODS: A retrospective review of over 600 laparoscopic renal operations over the past 8 years was performed. All cases of postoperative rhabdomyolysis were identified. A Medline search was performed to find articles related to the development of postoperative rhabdomyolysis. Cases of rhabdomyolysis developing after laparoscopic renal surgery and common risk factors between cases were identified. RESULTS: The incidence of postoperative rhabdomyolysis in our series is 0.67%. It is similar to the rate reported in other series. Male sex, high body mass index, prolonged operative times, and the lateral decubitus position are all risk factors in its development. CONCLUSION: The prevention and optimal management of postoperative rhabdomyolysis following laparoscopic renal surgery has yet to be defined. The risk factors we identified should be carefully addressed and minimized. A better understanding of the pathogenesis of rhabdomyolysis will also be a key component in its prevention.

    Title New Imaging Techniques in Prostate Cancer.
    Date November 2006
    Journal Current Urology Reports
    Excerpt

    Correct staging of prostate cancer at initial diagnosis, as well as accurate staging and tumor localization with biochemical recurrence, remains generally inaccurate with current imaging techniques. Newer modalities are being investigated to accurately identify patients with prostate cancer at different stages of disease. Identification of locally recurrent disease or distant metastasis at the time of biochemical failure after local therapy will help guide treatment options and avoid potentially toxic salvage therapies in patients who will not benefit. A review of prostate cancer imaging literature over the past 12 months was performed to identify emerging imaging modalities that may be beneficial in the management of prostate cancer. Enhanced transrectal ultrasonography modalities, including ultrasound contrast agents, color and power Doppler, and elastrography, have demonstrated incremental benefit when combined with standard gray-scale ultrasonography to accurately target and diagnose prostate cancer. Endorectal MRI, with contrast enhancement and spectroscopic imaging, shows promise in the initial staging of prostate cancer prior to local therapy. The use of positron-emission tomography scan for prostate cancer remains to be defined, but may help delineate the site of recurrence with biochemical failure after local therapy. Several new imaging modalities show promise for the evaluation of the patient with prostate cancer. Enhanced ultrasonography techniques may prove to be more accurate in diagnosing prostate cancer over standard gray-scale ultrasonography. Accumulating evidence supports the use of endorectal MRI and spectroscopy to help treatment planning with either surgical or radiotherapeutic approaches. Although intriguing, the available data for positron-emission tomography in prostate cancer remains too shallow to advocate routine use.

    Title Relationship Between P53 Mutations and Inducible Nitric Oxide Synthase Expression in Human Colorectal Cancer.
    Date January 1999
    Journal Journal of the National Cancer Institute
    Title P53 and Vascular Endothelial Growth Factor Regulate Tumor Growth of Nos2-expressing Human Carcinoma Cells.
    Date December 1998
    Journal Nature Medicine
    Excerpt

    The finding of frequent nitric oxide synthase expression in human cancers indicates that nitric oxide has a pathophysiological role in carcinogenesis. To determine the role of nitric oxide in tumor progression, we generated human carcinoma cell lines that produced nitric oxide constitutively. Cancer cells expressing inducible nitric oxide synthase that had wild-type p53 had reduced tumor growth in athymic nude mice, whereas those with mutated p53 had accelerated tumor growth associated with increased vascular endothelial growth factor expression and neovascularization. Our data indicate that tumor-associated nitric oxide production may promote cancer progression by providing a selective growth advantage to tumor cells with mutant p53, and that inhibitors of inducible nitric oxide synthase may have therapeutic activity in these tumors.

    Title Up-regulation of Inducible Nitric Oxide Synthase Expression in Cancer-prone P53 Knockout Mice.
    Date August 1998
    Journal Proceedings of the National Academy of Sciences of the United States of America
    Excerpt

    High concentrations of nitric oxide (NO) cause DNA damage and apoptosis in many cell types. Thus, regulation of NO synthase (NOS) activity is essential for minimizing effects of cytotoxic and genotoxic nitrogen oxide species. We have shown previously that NO-induced p53 protein accumulation down-regulates basal and cytokine-modulated inducible NOS (NOS2) expression in human cells in vitro. To further characterize the feedback loop between NOS2 and p53, we have investigated NO production, i.e., urinary nitrate plus nitrite excretion, and NOS2 expression in homozygous p53 knockout (KO) mice. We report here that untreated p53 KO mice excreted 70% more nitrite plus nitrate than mice with wild-type (wt) p53. NOS2 protein expression was constitutively detected in the spleen of untreated p53 KO mice, whereas it was undetectable in the spleen of wt p53 controls. Upon treatment with heat-inactivated Corynebacterium parvum, urinary nitrite plus nitrate excretion of p53 KO mice exceeded that of wt controls by approximately 200%. C. parvum treatment also induced p53 accumulation in the liver. Splenectomy reduced the NO output of C. parvum-treated p53 KO mice but not of wt p53 controls. Although NO production and NOS2 protein expression were increased similarly in KO and wt p53 mice 10 days after injection of C. parvum, NOS2 expression returned to baseline levels only in wt p53 controls while remaining up-regulated in p53 KO mice. These genetic and functional data indicate that p53 is an important transrepressor of NOS2 expression in vivo and attenuates excessive NO production in a regulatory negative feedback loop.

    Title Vascular Endothelial Growth Factor and Nitric Oxide Synthase Expression in Human Lung Cancer and the Relation to P53.
    Date August 1998
    Journal British Journal of Cancer
    Excerpt

    Vascular endothelial growth factor (VEGF) expression and mutations of cancer-related genes increase with cancer progression. This correlation suggests the hypothesis that oncogenes and tumour suppressors regulate VEGF, and a significant correlation between p53 alteration and increased VEGF expression in human lung cancer was reported recently. To further examine this hypothesis, we analysed VEGF protein expression and mutations in p53 and K-ras in 27 non-small-cell lung cancers (NSCLC): 16 squamous cell, six adenocarcinomas, one large cell, two carcinoids and two undifferentiated tumours. VEGF was expressed in 50% of the squamous cell carcinomas (SCC) and carcinoids but none of the others. p53 mutations occurred in 14 tumours (52%), and K-ras mutations were found in two adenocarcinomas and one SCC; there was no correlation between the mutations and VEGF expression. As nitric oxide also regulates angiogenesis, we examined NOS expression in NSCLC. The Ca2+-dependent NOS activity, which indicates NOS1 and NOS3 expression, was significantly reduced in lung carcinomas compared with adjacent non-tumour tissue (P < 0.004). Although the Ca2+-independent NOS activity, which indicates NOS2 expression, was low or undetectable in non-tumour tissues and most carcinomas, significant activity occurred in three SCC. In summary, our data do not show a direct regulation of VEGF by p53 in NSCLC. Finally, we did not find the up-regulation of NOS isoforms during NSCLC progression that has been suggested for gynaecological and breast cancers.

    Title Frequent Nitric Oxide Synthase-2 Expression in Human Colon Adenomas: Implication for Tumor Angiogenesis and Colon Cancer Progression.
    Date February 1998
    Journal Cancer Research
    Excerpt

    An increased expression of nitric oxide synthase (NOS) has been observed in human colon carcinoma cell lines as well as in human gynecological, breast, and central nervous system tumors. This observation suggests a pathobiological role of tumor-associated NO production. Hence, we investigated NOS expression in human colon cancer in respect to tumor staging, NOS-expressing cell type(s), nitrotyrosine formation, inflammation, and vascular endothelial growth factor expression. Ca2+-dependent NOS activity was found in normal colon and in tumors but was significantly decreased in adenomas (P < 0.001) and carcinomas (Dukes' stages A-D: P < 0.002). Ca2+-independent NOS activity, indicating inducible NOS (NOS2), is markedly expressed in approximately 60% of human colon adenomas (P < 0.001 versus normal tissues) and in 20-25% of colon carcinomas (P < 0.01 versus normal tissues). Only low levels were found in the surrounding normal tissue. NOS2 activity decreased with increasing tumor stage (Dukes' A-D) and was lowest in colon metastases to liver and lung. NOS2 was detected in tissue mononuclear cells (TMCs), endothelium, and tumor epithelium. There was a statistically significant correlation between NOS2 enzymatic activity and the level of NOS2 protein detected by immunohistochemistry (P < 0.01). Western blot analysis of tumor extracts with Ca2+-independent NOS activity showed up to three distinct NOS2 protein bands at Mr 125,000-Mr 138,000. The same protein bands were heavily tyrosine-phosphorylated in some tumor tissues. TMCs, but not the tumor epithelium, were immunopositive using a polyclonal anti-nitrotyrosine antibody. However, only a subset of the NOS2-expressing TMCs stained positively for 3-nitrotyrosine, which is a marker for peroxynitrite formation. Furthermore, vascular endothelial growth factor expression was detected in adenomas expressing NOS2. These data are consistent with the hypothesis that excessive NO production by NOS2 may contribute to the pathogenesis of colon cancer progression at the transition of colon adenoma to carcinoma in situ.

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