Here - American Geriatrics Society
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P OSTER<br />
A BSTRACTS<br />
and its sum of boxes. DLB patients without Capgras were able to tolerate<br />
and continue taking cholinesterase inhibitors (p=0.03) without<br />
other significant differences in medication management.<br />
Conclusions<br />
We found that DLB-C patients had more visual hallucinations,<br />
and that caregivers of DLB-C patients endorse greater caregiver burden.<br />
We were unable to discern specific patient characteristics or psychometric<br />
performance data to help us predict who may be at greater<br />
risk of developing Capgras syndrome. Future research is needed to<br />
evaluate management and treatment options for the clinically challenging<br />
behavioral sequelae of DLB and Capgras syndrome.<br />
A140<br />
Computational Modeling of Aging in Cardiac Myocytes.<br />
P. Dalal, E. Sobie. Pharmacology and Systems Therapeutics, Mt. Sinai<br />
School of Medicine, New York, NY.<br />
Supported By: This research is supported by the Medical Student<br />
Training in Aging Research (MSTAR) at Mount Sinai School of<br />
Medicine.<br />
BACKGROUND: The risk of susceptibility to more serious<br />
forms of cardiac arrhythmia rises significantly with normal aging.<br />
These forms of arrhythmia can manifest as palpitations, fibrillation,<br />
and even sudden death. One indicator of arrhythmia risk is action potential<br />
duration in cardiac myocytes. Specifically, the prolongation of<br />
action potential leads to a larger vulnerability period towards after<br />
depolarization. Such rogue depolarization can result in dangerous,<br />
self-sustaining circular currents. Animal studies in the past have<br />
shown that age associated molecular changes in cardiac myocytes include:<br />
a 40% reduction in SERCA pump protein, a 20% reduction in<br />
the transient outward current, a 59% increase in the peak L-Type calcium<br />
channel current, and a 142% increase in the inactivation time<br />
constant of the L-Type calcium channel. Additionally, the action potential<br />
is prolonged by 92% in older rats when compared with<br />
younger rats and the calcium transient decay is slower in aged rats<br />
while its amplitude remains the same.<br />
HYPOTHESIS: Implementing the molecular changes in rat myocytes<br />
into the computational models of Hund (2004), et al and Ten<br />
Tusscher (2004), et al will prolong the action potentials and slow the<br />
calcium transient decay of these models, creating a computational<br />
tool to study age associated arrhythmia risk.<br />
RESULTS: After implementing the four major molecular<br />
changes associated with cardiac aging, the action potential was prolonged<br />
by 4% in the Hund (2004) model and by 77% in the Ten Tusscher<br />
(2004) model. The calcium transient decay was slower in both<br />
models while the calcium transient amplitude was only unchanged in<br />
the Ten Tusscher (2004) model. In the Hund (2004) model, the amplitude<br />
was increased.<br />
CONCLUSIONS: It is possible to generate a computational<br />
model that replicates the age associated changes seen in cardiac myocytes.<br />
The Ten Tusscher (2004) model more accurately replicates<br />
these changes than the Hund (2004) model.<br />
A141<br />
Isolated CNS Post-transplant Lymphoproliferative Disorder in a<br />
Kidney Transplant Recipient.<br />
S. Dahiya, W. Ooi, A. Asik. Internal Medicine/Division of Hematology<br />
and Oncology, Baystate Medical Center, Springfield, MA.<br />
Introduction<br />
Post-transplantation lymphoproliferative disorder(PTLD)is a<br />
very well recognized complication of solid organ transplantation. Its<br />
incidence varies, depending on the graft recipient’s age,the type and<br />
intensity of immunosuppression, and the organ type transplanted.<br />
Extranodal involvement is common in PTLD, although the central<br />
nervous system (CNS) is an uncommon site of disease, especially in<br />
isolation. Literature review suggests less than handful of cases in geriatric<br />
population.<br />
Case<br />
65 year old female presented with complaints of intermittent expressive<br />
aphasia. Her medical history was remarkable for polycystic<br />
kidney disease leading to kidney failure and thus requiring transplant.<br />
Her transplant history includes, failed first transplant in 1995<br />
from a deceased donor and subsequent living-related donor transplant<br />
in 2005 from her son with unrelated blood type requiring heavy<br />
immunosuppresion. She was on mycophenolate, tacrolimus and prednisone<br />
for immunosuppressive regimen. Her neurological exam was<br />
significant for word finding difficulty and left eye ptosis. Rest of the<br />
physical exam was within normal limits. A spinal tap showed slight elevation<br />
of proteins to 149mg/dl and decreased glucose to 36mg/dl,<br />
raising a question of ongoing infectious process. An urgent MRI was<br />
obtained which showed multiple discrete enhancing lesions throughout<br />
the supratentorial and infratentorial white matter with leptomeningeal<br />
involvement. An extensive infectious workup looking<br />
for various causes of enhancing lesion in this severely immunosuppressed<br />
patient was negative. A brain biopsy was eventually performed,<br />
which showed monomorphic PTLD, categorized as EBV-associated<br />
diffuse large B-cell lymphoma. Given her kidney disease, she<br />
was started on a rather unconventional regimen with weekly rituximab<br />
for 8 weeks and 4 cycles of monthly intrathecal cytarabine. Her<br />
immunosuppresive regimen was changed to sirolimus only. She has<br />
been in remission since last 1 year, but unfortunately developed allograft<br />
rejection because of reduction in immunosuppressive regimen.<br />
Discussion<br />
Isolated CNS-PTLD following kidney transplant is exceedingly<br />
rare. However, it must be considered as a differential in transplant patients<br />
with CNS symptoms to avoid delay in diagnosis. Advanced age<br />
is considered as a poor prognostic factor, but this elderly patient did<br />
rather well with the unconventional regimen as outlined above.<br />
A142<br />
Deep Vein Thrombosis and Pulmonary Embolism (DVT/PE) with<br />
JAK2 positive Polycythemia Vera (PCV) and mild hematologic<br />
findings.<br />
R. Lands, S. Kelley. Department of Medicine, University of Tennessee,<br />
Knoxville, TN.<br />
An 81-year-old man came to the emergency room after becoming<br />
suddenly short of breath while taking a shower. Any exertion<br />
after that exacerbated his dyspnea but was relieved by lying down. He<br />
did not have chest pain, pleuritic or otherwise. He had no preceding<br />
illness, immobilization or prolonged travel. He was previously<br />
healthy with a history of hypertension and gout, but he was on no<br />
meds at the time of admission. Physical examination showed him to<br />
be in no distress at rest while wearing oxygen. Lungs were without<br />
rales or rhonci and his respiratory effort was normal. There was no<br />
edema of either lower extremity. High sensitivity D-Dimer was<br />
greater than 5000 ng/ml. EKG demonstrated right heart strain. Chest<br />
x-ray demonstrated elevation of the hemidiaphragm. Creatinine was<br />
1.9 mg/dl. Ventilation perfusion scan of the lungs was interpreted as<br />
high probability for left and right lower lobe pulmonary emboli.<br />
Doppler venous studies demonstrated bilateral deep vein thromboses<br />
of the lower extremities.<br />
Hgb was 17 g/dl and Hct 53%. WBC was 32,000 without basophilia<br />
or eosinophilia. Cells containing JAK-2 V617F mutation<br />
were present. BCR/ABL was absent. Erythropoietin was 1 mIU/ml.<br />
No further imaging was performed given his marginal renal function.<br />
Review of his old records demonstrated a very mild leukocytosis and<br />
upper normal hemoglobin levels for several years prior to this admission.<br />
One month after discharge, he followed up in the hematology<br />
clinic where his WBC was 15x103 and his hemoglobin 15.8mg/dL.<br />
Discussion: JAK2 is a gain of function mutation with tyrosine kinase<br />
activity that is present in 90% of patients with PCV. While it is<br />
primarily a diagnostic marker now, there is evidence that it might<br />
S64<br />
AGS 2012 ANNUAL MEETING