scholarly journals Neoplasia de células dendríticas plasmocitoides blásticas

10.33821/572 ◽  
2021 ◽  
Vol 31 (3) ◽  
pp. 251-259
Author(s):  
Veronica Maribel Hurtado Hurtado ◽  
Andrea del Rocío Noboa Cercado ◽  
Lisette Elianna Moran Mosquera
Keyword(s):  
Diabetes Mellitus ◽  
Pet Ct

Introducción: La neoplasia de células dendríticas plasmocitoides blásticas (NCDPB) es una patología agresiva y representa menos del 1% de neoplasias hematológicas, se caracteriza por lesiones cutáneas nodulares violáceas sin evidencia de adenopatías en la mayoría de casos. Estudios observacionales demuestran que el Protocolo de quimioterapia Hyper-CVAD y la consolidación con trasplante de células progenitoras hematopoyéticas se han asociado con una mayor supervivencia general. Caso Clínico: mujer de 82 años con antecedentes de Diabetes Mellitus tipo con cinco meses de lesiones hiperpigmentadas, elevadas, induradas, violáceas no dolorosas en mejilla, brazos, tórax anterior y posterior y piernas. Evolución: En  citometría de flujo se determinó un fenotipo compatible con células patológicas (5.86%) con CD123++, HLADR+++, NG2++, CD56+++, CD4++, que sugiere una NCDPB. La biopsia de médula ósea presentó infiltración. PET CT posterior a terapia corticoide: no evidencia enfermedad tumoral macroscópica metabólicamente activa. Se inicia tratamiento con Dexametasona, con lo que las lesiones cutáneas disminuyeron en un 80%. Se inició Quimioterapia Protocolo CHOP like, ha recibido 6 ciclos hasta octubre del 2021, actualmente en remisión completa. Conclusión: En el presente caso el curso clínico de la NCDPB no fue agresivo hasta el momento del cierre del caso presentando disminución del 80% de las lesiones.

Abstract 14602: Vascular Calcification is Associated With Major Adverse Cardiovascular Events and Mortality in Men With Recurrent Prostate Cancer Undergoing PET/CT Imaging

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Preet Ayoub Shaikh ◽  
Avira Som ◽  
Daniel Lenihan ◽  
Kathleen W Zhang
Keyword(s):  
Prostate Cancer ◽  
Diabetes Mellitus ◽  
Vascular Calcification ◽  
Cardiovascular Events ◽  
Primary Outcome ◽  
Aortic Calcification ◽  
Recurrent Prostate Cancer ◽  
Cardiovascular Comorbidities ◽  
Increased Risk ◽  
Pet Ct

Background: Hormone therapy is a front-line therapy for men with prostate cancer and is associated with adverse cardiovascular events. The utility of vascular calcification for cardiovascular risk stratification in men with prostate cancer is unknown. Methods: 211 consecutive patients who underwent 18F-fluciclovine positron emission tomography (PET)/computed tomography (CT) at a single institution for recurrent prostate cancer were retrospectively identified. Clinical and demographic data were obtained from the medical record. Coronary and aortic calcification were qualitatively assessed on non-gated CT scans using standardized scoring systems. The primary outcome was a composite of subsequent major adverse cardiovascular event (MACE; myocardial infarction, stroke, coronary or peripheral revascularization, heart failure hospitalization) or all-cause mortality. Results: Median age was 69 (IQR 64, 75) years and cardiovascular comorbidities were common (70% hypertension, 65% hyperlipidemia, 47% current or former smoking, 20% diabetes mellitus). Over a median of 16.5 months, 8 patients (4%) met the primary outcome. Patients with MACE or death were older and had higher prevalence of traditional cardiovascular comorbidities (risk ratio [RR] 1.3 for hypertension, 1.4 for hyperlipidemia, 1.3 for diabetes mellitus; p>0.05 for all). Coronary and aortic calcification were more common in patients with MACE or death. Severe coronary calcification (RR=6.1, 95% CI 1.6-23.2, p=0.008) and severe thoracic aortic calcification (RR=9.9, 95% CI 2.0-47.6, p=0.004) were associated with significantly increased risk of MACE or death. Conclusions: Coronary and aortic calcification on PET/CT imaging are associated with significantly increased risk of MACE or death in men with recurrent prostate cancer. Vascular calcification may have utility for cardiovascular risk stratification in men receiving hormone therapy for prostate cancer.

scholarly journals The difference between steroid diabetes mellitus and type 2 diabetes mellitus: a whole-body 18F-FDG PET/CT study

2020 ◽  
Vol 57 (11) ◽  
pp. 1383-1393
Author(s):  
Qingqing Zhao ◽  
Jinxin Zhou ◽  
Yu Pan ◽  
Huijun Ju ◽  
Liying Zhu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Type 2 Diabetes Mellitus ◽  
Glucose Metabolism ◽  
Glycogen Storage ◽  
Β Cells ◽  
Pet Ct ◽  
Fdg Pet Ct

Abstract Aims Steroid diabetes mellitus (SDM) is a metabolic syndrome caused by an increase in glucocorticoids, and its pathogenesis is unclear. 18F-FDG PET/CT can reflect the glucose metabolism of tissues and organs under living conditions. Here, PET/CT imaging of SDM and type 2 diabetes mellitus (T2DM) rats was used to visualize changes in glucose metabolism in the main glucose metabolizing organs and investigate the pathogenesis of SDM. Methods SDM and T2DM rat models were established. During this time, PET/CT imaging was used to measure the %ID/g value of skeletal muscle and liver to evaluate glucose uptake. The pancreatic, skeletal muscle and liver were analyzed by immunohistochemistry. Results SDM rats showed increased fasting blood glucose and insulin levels, hyperplasia of islet α and β cells, increased FDG uptake in skeletal muscle accompanied by an up-regulation of PI3Kp85α, IRS-1, and GLUT4, no significant changes in liver uptake, and that glycogen storage in the liver and skeletal muscle increased. T2DM rats showed atrophy of pancreatic islet β cells and decreased insulin levels, significantly reduced FDG uptake and glycogen storage in skeletal muscle and liver. Conclusions The pathogenesis of SDM is different from that of T2DM. The increased glucose metabolism of skeletal muscle may be related to the increased compensatory secretion of insulin. Glucocorticoids promote the proliferation of islet α cells and cause an increase in gluconeogenesis in the liver, which may cause increased blood glucose.

Metabolic Syndrome and Diabetes Mellitus in Mexico: the Role of PET/CT in Endothelial Dysfunction and Cardiovascular Disease Detection

2017 ◽  
Vol 10 (3) ◽  
Author(s):  
Erick Alexánderson Rosas ◽  
Jonathan Badin Castro ◽  
Diego Adrián Vences Anaya ◽  
Juan José del Moral Díez ◽  
Jessy Steve Masso Bueso ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Endothelial Dysfunction ◽  
Disease Detection ◽  
Pet Ct

The difference between steroid diabetes mellitus and type 2 diabetes mellitus: A whole-body 18F-FDG PET/CT study

2020 ◽  
Author(s):  
Qingqing Zhao ◽  
Jinxin Zhou ◽  
Yu Pan ◽  
Huijun Ju ◽  
Liying Zhu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Type 2 Diabetes Mellitus ◽  
Glucose Metabolism ◽  
Fdg Pet ◽  
Glycogen Storage ◽  
Pet Ct ◽  
Fdg Pet Ct

Abstract Background Steroid diabetes mellitus (SDM) is a metabolic syndrome caused by an increase in glucocorticoids, and its pathogenesis is unclear. 18F-FDG PET/CT can reflect the glucose metabolism of tissues and organs under living conditions, and plays an important role in diabetes research. Here, PET/CT imaging of SDM and type 2 diabetes mellitus (T2DM) rats was used to observe the changes of glucose metabolism in major glucose metabolism organs and immunohistochemical analysis to explore the possible pathogenesis of SDM. Results The SDM rat model was successfully established, which showed increased FBG and insulin levels; 18F-FDG PET/CT imaging showed increased FDG uptake in skeletal muscle, but no significant increase in liver uptake (15d);Immunohistochemistry showed that islet α-cell and β-cell proliferation, GLUT-4 and IRS-1, PI3Kp85α expression in skeletal muscle increased, and glycogen storage in liver and skeletal muscle increased.T2DM rats showed atrophy of pancreatic islet β cells and decreased insulin levels; Significantly reduced FDG uptake and glycogen storage in skeletal muscle and liver; IRS-1 expression in skeletal muscle decreased, and GLUT-4 and PI3Kp85α did not change significantly. Conclusion The pathogenesis of SDM is different from that of T2DM. The increased glucose metabolism of skeletal muscle may be related to the increased compensatory secretion of insulin; glucocorticoids promote the proliferation of islet α cells and cause the increase of gluconeogenesis in the liver may be the cause of its increased blood glucose.

scholarly journals Reacción leucemoide que simula una neoplasia mieloproliferativa crónica en mieloma múltiple indolente : reporte de caso y revisión de la literatura.

2019 ◽  
Vol 6 (2) ◽  
pp. 40-40
Author(s):  
Humberto Martínez ◽  
Jaime Valdés
Keyword(s):  
Diabetes Mellitus ◽  
Jak2 V617f ◽  
Pet Ct

Introducción: la reacción leucemoide (RL) en el contexto de neoplasias de células plasmáticas se ha descrito en reportes de casos. No hemos encontrado asociación en la literatura de RL con mieloma indolente. Métodos: se describe un caso de RL que simula una neoplasia mieloproliferativa crónica en mieloma múltiple indolente. Resultados: mujer de 68 años con antecedente de diabetes mellitus tipo 2 y rosácea, con astenia, adinamia y malestar general. Dentro de los laboratorios inicialmente solicitados, se reporta una leucocitosis de 74.690 x mm3 con 67.190 x mm3 neutrófilos, sin anemia y recuento plaquetario normal. Se comienza tratamiento extrainstitucional con hidroxiurea y, posteriormente, con nilotinib. Se confirma la ausencia de cromosoma Filadelfia y mutación JAK2 V617F, por lo cual se suspende nilotinib y se documenta infiltración del 30% por neoplasia de células plasmáticas en médula ósea, y una paraproteinemia IgA lambda de 3,2 g/dl, sin componente CRAB por ausencia de anemia, alteración renal e hipercalcemia con PET/CT negativo para lesiones líticas o plasmocitomas, cadenas livianas relación menor de 100. Se considera mieloma múltiple indolente de alto riesgo por IgA y se inicia tratamiento con lenalidomida y dexametasona. La paciente se encuentra en aceptables condiciones generales, tolerando satisfactoriamente la quimioterapia. Conclusión: este es el primer caso conocido por nosotros de mieloma múltiple indolente asociado con reacción leucemoide en la literatura mundial.

scholarly journals Imaging of Hidradenitis Suppurativa and Its Complications

2014 ◽  
Vol 2014 ◽  
pp. 1-5
Author(s):  
Feng Poh ◽  
Siew Kune Wong
Keyword(s):  
Diabetes Mellitus ◽  
Hidradenitis Suppurativa ◽  
Tissue Specimen ◽  
Imaging Findings ◽  
Natural Progression ◽  
Pet Ct ◽  
Perianal Fistulae ◽  
History Of ◽  
Well Differentiated ◽  
Sacral Osteomyelitis

We present a 56-year-old man with known diabetes mellitus and a 10-year history of hidradenitis suppurativa (HS) and highlight, through MR imaging findings, the relentless natural progression of the disease, characterized by recurrent exacerbations of abscesses and fistulae and complications of perianal fistulae and sacral osteomyelitis. We also demonstrate the appearance of this condition on PET-CT with F-18 FDG, which was performed for staging after postexcision tissue specimen revealed well-differentiated squamous cell carcinoma. The association of arthritis and possible dactylitis was also manifested in our patient. Discussion of HS in the radiology literature is limited and, to our knowledge, there has been no case report describing these imaging findings in the same patient.

Primärer Hyperaldosteronismus – warum diagnostizieren wir immer noch so wenige Patienten?

2020 ◽  
Vol 145 (11) ◽  
pp. 716-721
Author(s):  
Laura Handgriff ◽  
Martin Reincke
Keyword(s):  
Diabetes Mellitus ◽  
Primary Aldosteronism ◽  
Outcome Study ◽  
Adrenal Hyperplasia ◽  
Primärer Hyperaldosteronismus ◽  
Oder Eine ◽  
Pet Ct ◽  
Jüngere Patienten ◽  
Bilateral Adrenal Hyperplasia ◽  
Captopril Test

Was ist neu? Definition, Klassifizierung und Prävalenz Der primäre Hyperaldosteronismus (PA) ist die häufigste chirurgisch therapierbare Form der sekundären Hypertonie. Hauptursachen des PA sind ein 1-seitiges Aldosteron-produzierendes Nebennierenadenom oder eine bilaterale idiopathische Nebennierenrindenhyperplasie (Bilateral Adrenal Hyperplasia, BAH). In den letzten Jahren ist das Phänomen der autonomen Kortisol-Co-Sekretion (ACS) im Rahmen des Conn-Syndroms in den Fokus gerückt. Während der Mineralokortikoidexzess für die Hypertonie verantwortlich ist, scheint die ACS vor allem zu metabolischen Komorbiditäten wie erhöhtem BMI, gestörter Glukosetoleranz und Diabetes mellitus Typ 2 zu führen. Das sogenannte „Connshing“-Syndrom (zusammengezogen von Conn- und Cushing-Syndrom) wird als neuer metabolischer Subtyp angesehen. Diagnose Folgende Hypertoniegruppen sollen unter anderem gescreent werden (etwa 50 % aller Hypertoniker): Patienten mit therapierefraktärer Hypertonie, mit arterieller Hypertonie und Hypokaliämien, mit arterieller Hypertonie und obstruktivem Schlafapnoe-Syndrom (OSAS), mit arterieller Hypertonie und adrenalem Nebennierenzufallstumor, mit Hypertonie und Blutdruck > 150/90 mmHg sowie jüngere Patienten mit Hypertonie. Das Screening erfolgt mittels des Aldosteron-Renin-Quotienten. Der nächste Schritt ist häufig die Bestätigung der Diagnose PA mittels Kochsalzbelastungs- und/oder Captopril-Test. Neu ist, dass bei sehr ausgeprägtem biochemischem Phänotyp, z. B. bei Patienten mit spontaner Hypokaliämie sowie maximal supprimierten Renin- und Aldosteron-Werten > 550 pmol/l, ohne weiteren Bestätigungstest direkt eine Subtypdifferenzierung erfolgen kann. Die Subtypdifferenzierung erfolgt mittels CT-Bildgebung der Nebennieren und (als Goldstandard) Nebennierenvenenkatheterisierung. Bei technisch nicht erfolgreichen Katheterisierungen werden nuklearmedizinische Verfahren (z. B. CXCR4-PET/CT) in Einzelfällen eingesetzt. Therapie Bei gesichertem unilateralem PA ist eine Adrenalektomie indiziert. Entsprechend der Primary-Aldosteronism-Surgical-Outcome-Study-Kriterien profitieren Frauen, jüngere Patienten (< 50 Jahre), Patienten mit geringerer Laufzeit der Hypertonie (< 5 Jahre) und Patienten mit geringerer Anzahl (< 2) von Antihypertensiva am meisten von einer Adrenalektomie. Im Fall einer BAH sollte eine Therapie mittels Spironolacton (initial 25–50 mg/d) eingeleitet werden, mit entsprechender Steigerungsoption zum Anheben des Renin als Ziel.

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