Positron Emission Tomogram Research Articles

Posterior Primary Progressive Prosopagnosia: Imaging and Neuropathology

AbstractBackgroundProsopagnosia is common with right temporal lesions, often in the fusiform gyrus when caused by vascular pathology. When caused by frontotemporal dementia, the lesion typically begins in the temporal tip. We are reporting advanced imaging, including tau and inflammation, as well as neuropathology in a patient with pathology centered at the posterior extent of the fusiform gyrus.MethodA 69‐year‐old man with apperceptive prosopagnosia and a negative amyloid positron emission tomogram (PET) underwent MRI and PET using 11C‐PBR28, an inflammation tracer, and 18F‐flortaucipir. V T values for 11C‐PBR28 were calculated with the Logan plot and a metabolite‐corrected arterial input function. For 18F‐flortaucipir, the SUV ratio over the cerebellar gray matter was calculated for t = 80‐100 min. A neuropathological examination was conducted using standard procedures as well as phospho‐tau histochemistry.ResultAtrophy and 18F‐flortaucipir uptake involved a similar region at the posterior extent of the right fusiform gyrus and, minimally, a symmetrical region of the left fusiform gyrus and an area in right premotor cortex. Involving the same regions, the 11C‐PBR28 signal was however more extensive than atrophy or 18F‐flortaucipir signal. At autopsy, the patient had corticobasal degeneration (CBD), with severe 4R tau involvement of temporo‐occipital, inferior parietal, and frontal cortices, as well as limbic regions and subcortical nuclei. The location of CBD pathology in this patient was highly atypical, as shown by comparing the neuropathological findings with the findings in two typical CBD patients.ConclusionAlthough prosopagnosia from ischemic and other lesions in the right posterior temporo‐occipital region is common, primary progressive prosopagnosia in the absence of amyloid has been described mostly with involvement of the right anterior temporal region. As exemplified by our patient, it can rarely happen with posterior temporal involvement and in this case the pathology was not TDP‐43 type C, as present in most patients with anterior temporal involvement, but corticobasal degeneration, a 4R tauopathy.

Posterior Primary Progressive Prosopagnosia: Imaging and Neuropathology

AbstractBackgroundProsopagnosia is common with right temporal lesions, often in the fusiform gyrus when caused by vascular pathology. When caused by frontotemporal dementia, the lesion typically begins in the temporal tip. We are reporting advanced imaging, including tau and inflammation, as well as neuropathology in a patient with pathology centered at the posterior extent of the fusiform gyrus.MethodA 69‐year‐old man with apperceptive prosopagnosia and a negative amyloid positron emission tomogram (PET) underwent MRI and PET using 11C‐PBR28, an inflammation tracer, and 18F‐flortaucipir. VT values for 11C‐PBR28 were calculated with the Logan plot and a metabolite‐corrected arterial input function. For 18F‐flortaucipir, the SUV ratio over the cerebellar gray matter was calculated for t = 80‐100 min. A neuropathological examination was conducted using standard procedures as well as phospho‐tau histochemistry.ResultAtrophy and 18F‐flortaucipir uptake involved a similar region at the posterior extent of the right fusiform gyrus and, minimally, a symmetrical region of the left fusiform gyrus and an area in right premotor cortex. Involving the same regions, the 11C‐PBR28 signal was however more extensive than atrophy or 18F‐flortaucipir signal. At autopsy, the patient had corticobasal degeneration (CBD), with severe 4R tau involvement of temporo‐occipital, inferior parietal, and frontal cortices, as well as limbic regions and subcortical nuclei. The location of CBD pathology in this patient was highly atypical, as shown by comparing the neuropathological findings with the findings in two typical CBD patients.ConclusionAlthough prosopagnosia from ischemic and other lesions in the right posterior temporo‐occipital region is common, primary progressive prosopagnosia in the absence of amyloid has been described mostly with involvement of the right anterior temporal region. As exemplified by our patient, it can rarely happen with posterior temporal involvement and in this case the pathology was not TDP‐43 type C, as present in most patients with anterior temporal involvement, but corticobasal degeneration, a 4R tauopathy.

Tumor-to-tumor metastasis of diffuse large B cell lymphoma to gastric adenocarcinoma via CXCL12 (SDF-1)/CXCR4 axis: a case report

BackgroundTumor-to-tumor metastasis is the rare phenomenon in which one tumor exhibits metastatic deposits from another. To the best of our knowledge, there has been no prior reported case of tumor-to-tumor metastasis of a diffuse large B cell lymphoma (DLBCL) to a primary gastric adenocarcinoma.Case presentationA 70-year-old man presented with chest discomfort. An echocardiogram showed the presence of a right ventricular tumor. A positron emission tomogram showed multiple foci of abnormal activity in right cervical lymph nodes, cardiac wall, and stomach. A right cervical lymph node biopsy specimen revealed histological features of DLBCL. An esophagogastroduodenoscopy showed a large circumferential ulceration on the gastric body. Subsequent biopsy revealed adenocarcinoma cells surrounded by infiltrating lymphoma cells. On immunohistochemical staining, lymphoma cells were positive for CXCR4 and adenocarcinoma cells were positive for CXCL12/SDF-1. The patient was treated with six cycles of R-CHOP chemotherapy regimen, resulting in a complete remission.ConclusionsThis patient’s case implies that the interaction between a chemokine and its receptor may be the underlying mechanism for the observed tumor-to-tumor metastasis. Specifically, our case would suggest an involvement of the CXCL12 (SDF-1)/CXCR4 axis in the observed metastasis of DLBCL to primary gastric adenocarcinoma.

Atrioventricular block after COVID-19: What is the mechanism, site of block, and treatment?

A 49-year-old healthy woman presented with exertional shortness of breath and palpitations of 3 months’ duration. Baseline electrocardiogram (ECG) was normal. Figure 1 shows selected tracings recorded during treadmill stress testing. Transthoracic echocardiogram showed no structural abnormalities. Cardiac positron emission tomogram showed normal myocardial perfusion and no abnormal fluorodeoxyglucose uptake. Antibody titers for Lyme disease were undetectable. Figure 2 shows selected tracings from an invasive electrophysiological (EP) study.

Epilepsy surgery in India

The history of epilepsy surgery dates back to the era before computerized tomography, magnetic resonance imaging (MRI), positronemission tomogram imaging, and electroencephalogram (EEG). Victor Horsley's resection of a cortical scar in 1886, based purely on localization is considered as the first epilepsy surgery recorded in history. In India, Prof. Jacob Chandy performed a pediatric hemispherotomy in 1952 at the Christian Medical College, Vellore. Prof. Malla Bhaskar Rao did a cortico-amygdalohippocampectomy in 1995 for hippocampal sclerosis at Sree Chitra Institute, Trivandrum. With over 1 million patients suitable for epilepsy surgery in India, the burden of disease is alarmingly high. The spectrum of epilepsy surgery resections in India has expanded tremendously over the past decade, but the centers performing them are few and far in between. Hence, the “surgical gap” (which includes eligible patients awaiting surgery) is ever increasing. With just around 1000 procedures performed every year, the surgical epilepsy programs in India need a massive overhaul in terms of skilled workforce and infrastructure. Sophisticated presurgical workup modalities, such as MEG, stereo-EEG, EEGfunctional MRI, etc., are have already been popularized in India. The results of epilepsy surgery in India are also at par with the world's state-of-art centers. As medical and surgical epileptology grows further over the years in India, the surgical treatment gap hopes to be effectively addressed.

Case of Complete Remission of Breast Cancer Metastasized to Lung Treated by Traditional Korean Therapy

This report is aimed to investigate the effect of Traditional Korean Therapy (TKT) in treating recurred breast cancer metastasized to lung. A 53-year-old woman who was diagnosed as left breast cancer and underwent surgery, adjuvant chemotherapy and radiotherapy in early 2009 was admitted for the treatment of recurred, metastatic lung cancer in late 2012. She was treated with TKT including acupuncture, moxibustion and pharmacopuncture. The effect was evaluated with positron emission tomogram and computed tomogram (PET-CT). The metastatic tumors in both lungs were disappeared after the treatment for about 2 months. These results suggest that TKT is a therapeutic method to treat metastatic lung cancer originated from breast cancer.

Association between an Alzheimer’s Disease-Related Index and APOE ε4 Gene Dose

BackgroundWe introduced a hypometabolic convergence index (HCI) to characterize in a single measurement the extent to which a person’s fluorodeoxyglucose positron emission tomogram (FDG PET) corresponds to that in Alzheimer’s disease (AD). Apolipoprotein E ε4 (APOE ε4) gene dose is associated with three levels of risk for late-onset AD. We explored the association between gene dose and HCI in cognitively normal ε4 homozygotes, heterozygotes, and non-carriers.MethodsAn algorithm was used to characterize and compare AD-related HCIs in cognitively normal individuals, including 36 ε4 homozygotes, 46 heterozygotes, and 78 non-carriers.ResultsThese three groups differed significantly in their HCIs (ANOVA, p = 0.004), and there was a significant association between HCIs and gene dose (linear trend, p = 0.001).ConclusionsThe HCI is associated with three levels of genetic risk for late-onset AD. This supports the possibility of using a single FDG PET measurement to help in the preclinical detection and tracking of AD.

Paraneoplastic disseminated lentigines heralding aggressive Langerhans cell sarcoma

Dear Editor, A 21-year-old man presented with a rapidly growing (9 cm), non-tender right flank mass with superficial excoriation and inflammation (Fig. 1a). The lesion was accompanied by rapid onset of disseminated brown papules, involving the torso, back, and limbs (Fig. 1b). Facial and axillary skins were spared, and there was no particular direction of spread. The skin patches did not coalesce or show pruritus or inflammation. There was also weight loss of 15 lb in 3 months. A positron emission tomogram scan (PET) showed FDG uptake in the right waist (SUV 5.8) and right groin (SUV 2.1) (Fig. 1c). Wide margin resection of the mass and lymph node excision was performed with clear margins. Histology of both specimens showed sheets and loose clusters of pleomorphic malignant cells infiltrating the dermis and subcutis with frequent mitosis (Fig. 1d). In view of the anaplastic morphology and unusual presentation, extensive immunophenotyping was performed. The cells were positive for CD1a, S100, and Langerin stains. They were negative for melanocytic markers (HMB45, melan-A, MITF) EMA, cytokeratin (CK, Cam 5.2, 34betaE12), actin, desmin, CD31, CD34, c-kit, B and T markers (CD20, CD79a, CD3), CD68, CD30, CD56, CD21, MPO, and ALK1. Electron microscopy for Birbeck granules was not performed. The picture was compatible with Langerhans cell sarcoma (LCS). A separate skin biopsy of a pigmented lesion on the torso showed elongated rete ridges with increased basal melanin pigmentation within keratinocytes and the tips, with no increased Langerhans cells and no evidence of malignancy or dysplasia. The lesion was compatible with common lentigo. The patient was treated with consolidation radiotherapy to the primary sites, but there was no regression of the skin lentiges. Fig. 1 a Clinical photo showing the flank mass with impending ulceration. b Widespread lentiginous lesion all over the trunk heralding the rapid growth of the malignant lesion. c PET with maximum intensity projection showing two sites of active lesions in the ... In the World Health Organization classification, LCS is the malignant end of the spectrum of benign Langerhans cell histiocytosis (LCH) [1]. The typical LCH cell is replaced by pleomorphic tumor cells in the LCS, only identifiable by phenotype or ultrastructure. Initial unifocal subcutaneous involvement is not unusual. However progressive disease, especially with multifocal dissemination, is highly fatal, despite multi-agent chemotherapy. It remains to be seen whether systemic progression may occur in our patient. Our patient demonstrated two hitherto unreported phenomena, namely paraneoplastic manifestation of LCS and acquired rampant disseminated lentigines as a new paraneoplastic dermatosis. The clinical history and histological findings do not suggest an underlying disseminated cutaneous LCH. Common paraneoplastic dermatoses (e.g., acanthocis nigricans) are well characterized and are putatively caused by neoplastic humoral secretions. Acquired melanocytic nevi are mostly related to solar exposure and are therefore localized. Recently, some cases of acral lentigines are debated to be paraneoplastic [2]. Disseminated lentigines are usually only found in familial lentiginosis syndromes (e.g., LEOPARD syndrome, Peutz–Jeghers, Carney complex, PTEN hamartoma syndrome). The neoplastic associations of these syndromes come from their primary systemic gene mutations [3]. The rapidly acquired disseminated growth of lentigines in our case is highly unusual and is somewhat induced by the abnormal aggressive transformation of the LCS cells. Skin pigmentation is usually under exquisite humoral control [4], and cutaneous Langerhans cells interact closely with melanocytes and keratinocytes [5]. It is impossible, however, to retrospectively work out the exact mechanism how the localized growth induced a systemic pigment response, since interval archival specimens are unavailable and the list of possible mediators are extensive. In any case, extirpation of the primary lesion appeared to halt further skin lesions.

C11-acetate PET for docetaxel prednisone (DP) response assessment in castrate-resistant prostate cancer (CRPC).

e15143 Background: C11- acetate (acetate) positron-emission tomogram (PET) has shown promise in detection of metastasis in prostate cancer in recent studies. Our study tested the feasibility of acetate-PET to predict early response to DP in CRPC. Methods: Men with metastatic CRPC for whom DP was indicated were enrolled in a prospective study of acetate-PET imaging and bone scans. Patients (pts) were imaged with both modalities at study entry and after 3 cycles of DP. DP was continued beyond cycle 3 until PCWG2-defined progression or toxicity. Treating physicians were blinded to acetate-PET results. No pts were on statins. The study was IRB-approved. Results: 6 pts with documented bone metastases were imaged (5 both pre and post-therapy.) Pre-therapy acetate-PET identified osseous metastases in all 6 pts. Remarkably, in one pt with previous radiation therapy, pre-therapy acetate-PET was negative for disease in the radiated area whereas bone scan showed persistent activity. The median number of DP cycles was 7 (5-16). 4 pts had ≥ 50% PSA decline. The median time to progression (TTP) was 5 months (mo). Of the 4 pts with PSA response, 2 had response on acetate-PET with TTP 5 mo and 10 mo respectively. One pt had > 50% PSA response but progression after 3 cycles based on PET, and met PCWG2 criteria for progression at 3.5 mo. The 4th pt with PSA response had stable findings on post-therapy PET and had 13 mo TTP. The pt who had no PSA response had stable post-therapy PET and had 2 mo TTP. Bone scan was stable in 3 pts, showed progression in 1pt and showed response in 1 pt. Conclusions: Response or progression on acetate-PET can be seen after a few chemotherapy cycles for CRPC. This study supports the exploratory inclusion of acetate-PET in future therapeutic clinical trials, with the potential to enhance the early prediction of treatment outcome. Acetate-PET might also allow more precise identification of viable target lesions than bone scan.

Concomitant plasmacytoma and B cell lymphoma with discordant light chain expression but clonal identity

Dear Editor, A 63-year-old patient presented with abdominal pain. A computerized tomogram scan showed a gallbladder mass (Fig. 1a). A positron emission tomogram revealed additional FDG-avid lesions in the sternum, ribs, bilateral humeri, vertebral column, and pelvic bone (Fig. 1b). Magnetic resonance imaging confirmed vertebral lytic lesions (Fig. 1c). A serum protein electrophoresis showed a monoclonal band (IgA λ 16.2g/l), and he was referred for suspected plasma cell myeloma (PCM). A bone marrow biopsy, however, showed 19 % infiltration by monoclonal B cells, expressing CD20, but negative for CD3−, CD5, CD10, CD138, IgA, IgG, and IgM (Fig. 1d). These cells showed κ−light chain restriction (Fig. 1e, f). Staining with CD138 highlighted less than 1 % plasma cells, while the lymphoma cells do not express CD138. In view of the discrepancy, cholecystectomy was performed showing a plasmacytoma (Fig. 1g). The plasma cells were CD138 positive, CD20 negative, and also positive for cytoplasmic lambda chain and IgA, but negative for IgG, IgM, and κ−light chain restriction. (Fig. 1h, i). They also expressed CD56 and cyclin D1. The double pathology was treated with R-CEOP ×6 (rituximab, cyclophosphamide, epirubicin, vincristine, and prednisolone) together with maintenance with thalidomide and bortezomib (weekly × 16 doses) and radiotherapy to both humerus. A complete remission by radiological and serum immunofixation assessment was shown at 1 year. He refused an autologous stem cell transplantation (SCT). The clonal relationship between the two lesions was investigated by polymerase chain reaction using IgH VJ primers followed by cloning and sequencing, using DNA from the homogeneous plasmacytoma and microdissected lymphoma cells from the trephine biopsy [1]. This showed a direct relationship between the two B cell clones in terms of band size and sequence homology (Fig. 1j and k). Fig. 1 a Computerized tomogram scan showing a gallbladder lesion (arrow). b Positron emission tomogram scan showing FDG avid uptake (arrows) in the porta hepatis as well as in the sternum, ribs, and femur. c Magnetic resonance imaging showing osteolytic lesions ... This case is interesting in terms of pathogenesis and treatment. In terms of pathogenesis, cases of concomitant B cell lymphoproliferation and plasma cell dyscrasia are rare and usually of independent clones [2]. The immunophenotyping and light chain expression do not suggest a common evolution from a lymphoplasmacytoid lymphoma. Our case is characterized by clonal homology but discordant light chain expression, immunophenotype, and morphology. Plasma cell myeloma with discordant light chain secretion is well documented [3]. Posttreatment switch in monoclonal protein may also occur after SCT [4]. More dramatically, changes in immunophenotype, morphology, and light chain expression in B cell malignancies after rituximab treatment are also recognized [1, 5, 6]. However, in our case, the clones occurred concomitantly and upfront in distinct cell lineages. This may theoretically result from plasma cell differentiation of the malignant B lymphocytes or a divergent evolution from a primordial B cell clone. Pools of malignant clonotypic B cells are known to exist in PCM patients [7]. In terms of treatment, a combination of lymphoma and PCM treatment seems to be effective in controlling both lesions with minimal overlap of toxicity. It is uncertain whether this patient may have survival benefit from an autologous SCT.

C11-acetate PET for docetaxel prednisone (DP) response assessment in castrate-resistant prostate cancer (CRPC).

83 Background: C11-acetate (acetate) positron-emission tomogram (PET) has shown promise in detection of metastasis in prostate cancer in recent studies. Our study tested the feasibility of acetate-PET to predict early response to DP in CRPC. Methods: Men with metastatic CRPC for whom DP was indicated were enrolled in a prospective study of acetate-PET imaging and bone scans. Patients (pts) were imaged with both modalities at study entry and after 3 cycles of DP. DP was continued beyond cycle 3 until PCWG2-defined progression or toxicity. Treating physicians were blinded to acetate-PET results. No pts were on statins. The study was IRB-approved. Results: 6 pts with documented bone metastases were imaged (5 both pre and post-therapy.) Pre-therapy acetate-PET identified osseous metastases in all 6 pts. Remarkably, in one pt with previous radiation therapy, pre-therapy acetate-PET was negative for disease in the radiated area whereas bone scan showed persistent activity. The median number of DP cycles was 7 (5-16). 4 pts had ≥ 50% PSA decline. The median time to progression (TTP) was 5 months (mo). Of the 4 pts with PSA response, 2 had response on acetate-PET with TTP 5 mo and 10 mo respectively. One pt had > 50% PSA response but progression after 3 cycles based on PET, and met PCWG2 criteria for progression at 3.5 mo. The 4th pt with PSA response had stable findings on post-therapy PET and had >10 mo TTP. The pt who had no PSA response had stable post-therapy PET and had 2 mo TTP. Bone scan was stable in 4 pts and showed progression in 1 pt. Conclusions: Response or progression on acetate-PET can be seen after a few chemotherapy cycles for CRPC. This study supports the exploratory inclusion of acetate-PET in future therapeutic clinical trials, with the potential to enhance the early prediction of treatment outcome. Acetate-PET might also allow more precise identification of viable target lesions than bone scan.

Long-term survival of 42 patients with resected N2 non-small-cell lung cancer: the impact of 2-18F-fluoro-2-deoxy-d-glucose positron emission tomogram mediastinal staging

Prognostic information known preoperatively allows stratification of patients to surgery; induction therapy and surgery; or definitive chemoradiotherapy and may prevent a futile thoracotomy. Attention has focussed on the standard uptake value (SUV) of the primary tumour but less has been described regarding the 18F-fluoro-2-deoxy-D-glucose (18F-FDG) avidity of mediastinal nodes. We aimed, in a group of surgically resected cN0-1 but pN2 tumours, to compare the survival of patients with and without 18F-FDG avid mediastinal nodes. Retrospective review of a surgical database identified cN0-1 non-small-cell lung cancer (NSCLC) patients with pN2 disease after resection. Survival of non-FDG avid N2 versus FDG avid N2 groups was compared after stratification according to variables found on univariate analysis to affect survival. From January 1993 to December 2006, 42 patients were identified; 27 (64%) had non-FDG avid N2 disease. Five-year and median survival were better in the non-FDG avid N2 disease group, 25% versus 0% and 30 (16-44) versus 13 (10-16) months, respectively (p=0.02). After 1998, the difference in survival was 41% versus 0% and 35 (14-56) versus 12 (16-18) months, respectively (p=0.02). After resection, patients with non-FDG avid N2 disease have better survival than patients with FDG avid N2 disease. Exploratory thoracotomy alone (after frozen section analysis) cannot be advocated in patients with non-FDG avid N2 disease as survival after resection appears at least equivalent to alternate therapeutic approaches in this group. This assertion may be tempered if right pneumonectomy is required or R0 resection is unachievable. Mediastinal nodal avidity may improve stratification in future studies of long-term survival in NSCLC.

Papillary Thyroid Carcinoma Tall Cell Variant

The most common of the aggressive variant of papillary thyroid carcinoma (PTC) is the tall cell variant (TCV). Because there are serious prognostic and management implications to a diagnosis of TCV, we review the entity to inform clinicians about the many facets of TCV. The TCV of PTC is characterized by cells having the nuclear features of PTC and whose height is at least twice or thrice their width. There is disagreement regarding the proportion of tall cells and the cell height required to diagnose TCV. In view of its blurred definition and rarity, studies have shown that TCV is still underdiagnosed. We propose that PTC be diagnosed as TCV if it is composed of > or =50% tall cells. The latter should have a height that is at least twice their width, an eosinophilic cytoplasm, and the nuclear features of PTC. Whatever its definition, there is a consensus that TCV has a higher recurrence and death rate than classical PTC. Most authorities believe that TCV's worse prognosis is related to its older age at presentation, larger tumor size, and high frequency of extrathyroid extension (ETE). However, in a recent article, TCV without ETE was shown to have a more aggressive behavior than classical PTC without ETE independent of age, gender, and tumor size. The aggressive behavior of TCV could be related to the high expression of Muc1 and matrix metalloproteinase and to the higher prevalence of B-RAF mutations when compared to classical PTC. The importance of TCV is accentuated by the fact that it is overrepresented in those fluorodeoxyglucose positron-emission tomogram (FDG-PET)-positive thyroid carcinomas that are refractory to radioactive iodine (RAI) therapy constituting 20% of these incurable tumors. TCV is a biologically and clinically aggressive form of PTC that is still underdiagnosed. TCV is overrepresented in patients with RAI refractory disease. It has a high prevalence of B-RAF mutations making the latter an attractive target in RAI refractory cases. Imaging modalities that can detect RAI refractory disease such as FDG-PET scanning are needed in many patients and a requirement in those with extensive ETE. More studies are needed to identify those TCV that become RAI refractory and develop effective target therapies against these incurable carcinomas.

Understanding anesthesia through functional imaging

This review will highlight the recent functional magnetic resonance imaging, positron emission tomogram scan and connectivity studies in anesthesia and analgesia. In regional cerebral blood flow (rCBF) studies with isoflurane and sevoflurane, there is a consistent pattern of rise in rCBF in the anterior cingulate cortex and insula while the thalamus, lingual cortex and cerebellum show a decrease in rCBF, in a dose range of 0.2-1 minimum alveolar concentration. Even 0.25 minimum alveolar concentration causes a predominant decrease of rCBF in the cortical regions and increase of rCBF in the subcortical regions. This minimum alveolar concentration level primarily affects the association cortices. Thalamus and thalamo-cortical pathways seem to be linked to the hypnotic effects of anesthesia and deep sedation. Connectivity studies also confirm this. The electroencephalogram equivalent of this appears to be a transition from 'alpha' wave activity to 'delta' wave activity. Anterior cingulate cortex, S1 and S2 are the regions consistently activated in acute pain. Remifentanil infusion in acute pain decreases the activation in pain perception regions while activating the pain modulation regions. In chronic pain states, prefrontal cortex and insula are activated whereas there is a decrease in activity in the thalamus. Slowly, a pattern of neuronal activity reflecting hypnosis, analgesia, amnesia and reflex suppression seems to be emerging giving us a better insight into the central nervous system effects of anesthesia.

Histological Aggressiveness of Fluorodeoxyglucose Positron-Emission Tomogram (FDG-PET)-Detected Incidental Thyroid Carcinomas

We previously reported a high incidence of primary thyroid cancer in fluorodeoxyglucose positron-emission tomogram (FDG-PET)-detected incidental thyroid abnormalities. The aim of our study was to determine if these FDG-PET-detected thyroid malignancies represent a more-aggressive variant of primary thyroid carcinoma. All patients that underwent operative intervention for FDG-PET-detected incidental thyroid abnormalities were identified (June 2003 to April 2006). Patients with a diagnosis of primary thyroid carcinoma on final histopathology were included in the study. The patient demographics and histopathological findings were analyzed to identify adverse prognostic features. In 11,500 patients, 17,250 FDG-PET scans were performed; 377 of these patients (3.2% of patients and 2.1% of FDG-PET scans) had findings positive for thyroid abnormality. Of the 32 patients that underwent operative intervention, 22 patients with a final diagnosis of primary thyroid malignancy were included in the study. A greater number of patients [12 patients, (54%)] were noted to harbor poor prognostic variants of primary thyroid carcinoma on final histopathology [tall-cell variant: 11 patients (50%) and poorly differentiated thyroid carcinoma: 1 patient (4%)]. Extra-thyroidal extension (ETE) was noted in the majority of patients [14 patients (63%)]. In patients with tall cell variant on final histopathology, the rate of ETE was even higher [10 patients (90%)]. Thyroid malignancies incidentally detected on FDG-PET scan harbor a high rate of unfavorable prognostic features and may represent a more-aggressive variant of primary thyroid carcinoma. These patients need to be subjected to further investigation with a view to possible operative intervention.

Intrathecal rituximab treatment for pediatric post‐transplant lymphoproliferative disorder of the central nervous system

Post-transplant lymphoproliferative disorder (PTLD) in the central nervous system (CNS) has a poor prognosis. New therapeutic approaches should be explored. We report our experience with intrathecal administration of rituximab in a 10-year-old kidney allograft recipient with PTLD in the CNS. After standard treatment had failed, we tried to treat the patient by administering rituximab directly into the cerebral ventricle through an Omaya reservoir, in addition to conventional intrathecal and systemic chemotherapy. This strategy resulted in a disappearance of clinical symptoms and a negative positron emission tomogram. Intrathecal administration of rituximab may be a feasible approach in children with PTLD in the CNS. However, its specific role in our patient remains uncertain.

18F-Fluorodeoxyglucose Uptake in Thyroid From Positron Emission Tomogram (PET) for Evaluation in Cancer Patients: High Prevalence of Malignancy in Thyroid PET Incidentaloma

18F-Fluorodeoxyglucose Uptake in Thyroid From Positron Emission Tomogram (PET) for Evaluation in Cancer Patients: High Prevalence of Malignancy in Thyroid PET Incidentaloma

18F-Fluorodeoxyglucose Uptake in Thyroid from Positron Emission Tomogram (PET) for Evaluation in Cancer Patients: High Prevalence of Malignancy in Thyroid PET Incidentaloma

To investigate the prevalence of incidental thyroid F-fluorodeoxyglucose (FDG) uptake in positron emission tomogram (PET) scan for evaluation in cancer patients and the role of standard uptake value (SUV) measurement in differentiation of thyroid malignancy from benign disease. Retrospective single-center study. Four thousand one hundred thirty-six subjects had been given FDG-PET scan for evaluation of known malignancies not associated with thyroid. The maximum SUVs of the thyroid lesions were recorded and reviewed. Fine needle aspiration was performed in patients with definite nodule by palpation or ultrasonography. Ninety-four (2.2%) were identified to have focal (n = 45, 1.1%) or diffuse (n = 45, 1.1%) thyroid FDG uptake. The incidence of focal or diffuse thyroid FDG uptake was higher in women (2.7% or 1.9%) than in men (0.4% or 0.7%). Cytologic diagnosis was available in 32 of 45 focal thyroid FDG uptakes. In 16 (50%) patients, the tumor was found to be malignant; 14 were papillary thyroid carcinoma (surgically confirmed in 7 cases), 2 were metastatic tumor from breast and esophagus. Sixteen were cytologically diagnosed as follicular cell lesions: follicular neoplasm (n = 2), nodular hyperplasia (n = 7), indeterminate follicular lesion (n = 7). There was no significant difference in maximum SUV between benign and malignant nodules. From 45 patients with diffuse thyroid FDG uptake, presumptive diagnosis of chronic thyroiditis was possible in 34 patients by clinical and laboratory findings. Our data suggest that a cytologic diagnosis of focal thyroid FDG-PET incidentaloma regardless of SUV is mandatory considering the very high prevalence of thyroid malignancy.

High-dose chemotherapy with autologous blood stem cell transplantation for aggressive subcutaneous panniculitis-like T-cell lymphoma

High-dose chemotherapy with autologous blood stem cell transplantation for aggressive subcutaneous panniculitis-like T-cell lymphoma

Metastatic liver cancer: A rare case

Hemangiopericytoma is a rare tumor especially when it rises in the peritoneal cavity. We present a case of a 60-year-old woman with an isolated recurrent hemangiopericytoma of the liver. The patient presented with a palpable right upper quadrant abdominal mass, which occurred 7 years after undergoing resection of a malignant hemangiopericytoma arising from the greater omentum. She had not followed up 6 mo after surgery. Various imaging studies showed a single large, well-capsulated liver tumor with central necrosis, accompanied by hypervascularity typical of a vascular tumor. Preoperative laboratory HBsAg and anti-HCV workup were both negative. Under the impression of recurrent malignant hemangiopericytoma, right trisegmentectomy was performed to completely resect the tumor. Pathological examination confirmed the diagnosis of recurrent hemangiopericytoma. Even though the incidence of the hemangiopericytoma is relatively low, malignant hemangiopericytoma has a tendency to recur frequently after a long-term disease-free interval. Also, the recurrent hemangiopericytoma is not easily detected early during follow-up until it becomes symptomatic because there are no specific tumor markers, and because of the diversity with regard to site of recurrence. The authors suggest that Positron Emission Tomogram (PET) may be a useful tool for the detection of recurrent hemangiopericytoma. We describe herein some characteristics and behaviors of malignant hemangiopericytoma, particularly after surgical resection.