Waldenström macroglobulinemia: Imaging Checklist

Waldenström macroglobulinemia (WM) is a lymphoplasmacytic lymphoma that is associated with an immunoglobulin M (IgM) monoclonal protein (M-protein). To establish the diagnosis of WM, it is necessary to demonstrate IgM monoclonal protein in the serum, along with histologic evidence of lymphoplasmacytic cells in the bone marrow. There is a similar spectrum of disease to that seen multiple myeloma (MGUS, smoldering myeloma, and frank myltiple myeloma) in WM: IgM monoclonal gammopathy of undetermined significance, smoldering macroglobulinemia, and WM.

WM is more common in men and in whites. The most common presenting symptom is fatigue related to a normochromic or normocytic anemia. Patients can also have peripheral neuropathy. Hyperviscosity syndrome, which includes epistaxis, gingival bleeding, and retinal hemorrhage is related to high plasma IgM concentrations and is becoming less common due to earlier diagnosis. It is rarely seen in patients with IgM concentration of <4,000 mg/dL.

The checklist for reviewing images in these patients includes clinical features, complications of the disease, and potential mimickers. These include:

• Lymph nodes: The majority of patients have adenopathy on FDG-PET and CT.
• Bone marrow: Almost half of patients show diffuse increased uptake on PET, and about 90% will show marrow signal changes on MRI (diffuse in more than half). This can be due to marrow infiltration or hyperplasia due to anemia.
• Spleen size: Between 10-20% of patients will have splenomegaly on imaging
• Liver size: Hepatomegaly can be seen in patients, but the prevalence on imaging has not been reported.
• Viscera: Between 10-20% of patients will have visceral or extra-nodal sites of involvement on imaging.
• Venous patency: To assess for thrombosis due to hyperviscosity from high IgM protein
• Vessel walls: To assess for immune complex vasculitis due to IgM protein
• Presence of hemorrhage: Due to low levels of von Willebrand factor
• Central nervous system: To assess for presence of Bing-Neel syndrome, which is perivascular infiltration of small lymphocytes, lymphoplasmacytoid cells, and plasma cells in the brain parenchyma and/or spine.
• Amyloidosis: Imaging features of amyloidosis should be sought, since it can also present with an IgM monoclonal protein and neuropathy (particularly if the light-chain isotype is lambda).

WM can be difficult to differentiate from marginal zone lymphoma. MYD88 mutation L265P is more commonly seen in WM (67% of cases), and less commonly in splenic marginal zone lymphoma (4%) and mucosa-associated lymphatic tissue lymphoma (7%).

Because the M-protein of patients with WM is almost always IgM, a broad differential should be considered for lucent bone lesions (the M-protein of multiple myeloma is usually IgG, followed by IgA and IgD, with IgM myeloma making up about 1% of cases). The same can be said for sclerotic bone lesions with or without peripheral neuropathy (the M-protein of POEMS is usually IgG and IgA, with IgM POEMS being very rare). However, this information is not always available when interpreting initial staging studies for patients with newly diagnosed plasma cell dyscrasia.

References

• Banwait R, O'Regan K, Campigotto F, Harris B, Yarar D, Bagshaw M, Leleu X, Leduc R, Ramaiya N, Weller E, Ghobrial IM. The role of 18F-FDG PET/CT imaging in Waldenstrom macroglobulinemia. Am J Hematol. 2011 Jul;86(7):567-72.
• Gertz MA. Waldenström macroglobulinemia: 2013 update on diagnosis, risk stratification, and management. Am J Hematol. 2013 Aug;88(8):703-11.
• Moulopoulos LA, Dimopoulos MA, Varma DG, Manning JT, Johnston DA, Leeds NE, Libshitz HI. Waldenström macroglobulinemia: MR imaging of the spine and CT of the abdomen and pelvis. Radiology. 1993 Sep;188(3):669-73.

Sarcoid-Like Reaction in Oncology

Sarcoid is thought to develop in predisposed individuals by a cross-reaction to tumor, bacterial, viral, or inorganic antigens or immunogenes. Patients respond by forming noncaseating granulomas, which are most commonly intrathoracic. Sarcoid-like reaction (SLR) refers to the development of noncaseating granulomas in patients who do not fulfill the criteria for systemic sarcoidosis.

In oncological patients, SLR most commonly occurs in the lymph nodes draining a malignant tumor, but can also be observed in the organ of tumor origin and distant tissues. It develops after antineoplastic treatment with biologic modifiers (e.g., interferon and interleukin-2), single or combination chemotherapy agents, or even after surgery without chemotherapy.

The patient above has a history of melanoma of the left lower extremity with recurrent ipsi- and contra-lateral inguinal nodal involvement that has been treated with surgery (most recently 8 months ago) and chemotherapy in the remote past (cisplatin, vinblastine, and dacarbazine). The PET from 3 months ago (left panel) was clear. The new PET (right panel) shows new supraclavicular (red arrow), intra-thoracic (yellow arrows), and upper abdominal (blue arrow) adenopathy. The lymph nodes are highly FDG-avid and most prominent in the chest, where we see the symmetric hilar and mediastinal adenopathy typical of sarcoid and would be atypical for nodal involvement from lower extremity melanoma. It is important to keep SLR in mind in order to avoid over-calling disease progression. This can be more problematic in cases of intrathoracic neoplasms that would be expected to recur in the chest and involve hilar and mediastinal lymph nodes. Symmetrical hilar involvement can be a helpful hint in these cases.

References

• Inoue K, Goto R, Shimomura H, Fukuda H. FDG-PET/CT of sarcoidosis and sarcoid reactions following antineoplastic treatment. Springerplus. 2013 Dec;2(1):113.
• Tchernev G, Tana C, Schiavone C, Cardoso JC, Ananiev J, Wollina U. Sarcoidosis vs. Sarcoid-like reactions: The Two Sides of the same Coin? Wien Med Wochenschr. 2014 Jul;164(13-14):247-259.

Hypertrophic Osteoarthropathy

Hypertrophic osteoarthropathy (HO), formerly and incorrectly referred to as hypertrophic pulmonary osteoarthropathy, has primary and secondary forms. The primary form (pachydermoperiostosis) is often familial and is more commonly seen in males.

The secondary form can be seen in a variety of pulmonary and hepatic conditions, including:

• Lung cancer
• Mesothelioma
• Carcinomas of liver and gut
• Inflammatory bowel disease
• Liver cirrhosis
• Congenital cyanotic heart disease
• Pulmonary fibrosis
• Empyema
• Graves disease
• Thalassemia

Patients can present with clubbing of fingers, periostosis of distal long bones, thickening of skin over face and ankles, gynecomastia, and arthritis and synovitis. The synovitis is accompanied by a viscous, non-inflammatory effusion.

Various etiologies have been proposed, but the most recent thought is that it is due to arteriovenous shunting (e.g., in the liver, lung, or various tumors). The idea is that unfragmented megakaryocytes get delivered to distal sites in systemic circulation instead of being filtered in the lungs. This leads to production of growth factors (PDGF and VEGF), which lead to angiogenesis, endothelial hyperplasia. In certain lung tumors, there is de novo production of these growth factors by tumor, which makes it to the peripheral circulation.

A neurogenic role has also been proposed. This is supported by the fact that pain and deformity resolve with peripheral vagotomy in both primary and secondary forms, even with the primary tumor intact.

Differential diagnosis for Multifocal Periostitis in Adults and children were covered earlier.

References

Armstrong DJ, et al. Hypertrophic pulmonary osteoarthropathy (HPOA) (Pierre Marie-Bamberger syndrome): two cases presenting as acute inflammatory arthritis. Description and review of the literature. Rheumatol Int. 2007 Feb;27(4):399-402.

The Hurricane Sign

SPECT studies are often used with myocardial perfusion studies for evaluation of ischemia. Long acquisition times for SPECT images increase susceptibility to artifacts, especially those caused by patient motion. The hurricane sign refers to an artifact caused by lateral patient motion during image acquisition. On the short axis views a circular object with spirals extending from the 12:00 and 6:00 positions causing discontinuity in the ventricular walls is seen. This pattern does not correspond with normal coronary artery anatomy.


REFERENCES
Burrell S and MacDonald A. Artifacts and pitfalls in myocardial perfusion imaging. J Nucl Med Technol 2006;34:193-211.
Sorrell V, Figueroa B, Hansen CL. The "hurricane sign": evidence of patient motion artifact on cardiac single photon emission computed tomographic imaging. J Nucl Cardiol 1996;3:86-8.

Bone Scan vs. FDG-PET in Pediatric Sarcomas

Walter et. al compared ¹⁸F-FDG PET/CT and ^99mTc-MDP in 29 patients with bone and soft tissue sarcomas. They found that ^99mTc-MDP did not add any diagnostic value over ¹⁸F-FDG PET/CT. The superiority of ¹⁸F-FDG PET/CT is most pronounced in patients with Ewing sarcoma family of tumors, in whom tumor tends to infiltrate the bone marrow rather than the mineralized bone, and bone destruction is dominated by osteoclastic activity, rather than osteoblastic activity.

	18F-FDG PET/CT	99mTc-MDP
Sensitivity	100%	70%
Specificity	100%	95%
Accuracy	100%	82%

The image above is from a patient with Ewing sarcoma of the distal left femur. The primary lesion (black arrow) and bony metastases are clearly seen on the MIP image from the ¹⁸F-FDG PET study, while the bone scan only shows the uptake in the area of periosteal reaction (pink arrow) and a right anterior rib lesion that likewise was associated with cortical breakthrough and a periosteal reaction. MRI shows the primary lesion (black arrow), as well as metastases in the left and right femurs (blue arrows).

References

• Völker T, Denecke T, Steffen I, Misch D, Schönberger S, Plotkin M, Ruf J, Furth C, Stöver B, Hautzel H, Henze G, Amthauer H. Positron emission tomography for staging of pediatric sarcoma patients: results of a prospective multicenter trial. J Clin Oncol. 2007 Dec 1;25(34):5435-41.
• Walter F, Czernin J, Hall T, Allen-Auerbach M, Walter MA, Dunkelmann S, Federman N. Is there a need for dedicated bone imaging in addition to 18F-FDG PET/CT imaging in pediatric sarcoma patients? J Pediatr Hematol Oncol. 2012 Mar;34(2):131-6.

Drugs and Cardiac FDG Uptake

Certain drugs and patient factors can affect cardiac uptake of FDG.

Drug	Effect	Comment
Insulin	↑	Similar to the effect of eating close to FDG administration. Will also cause diffuse increase in muscle uptake and a decrease in liver uptake.
Bezafibrate	↑	Fibrate drug used for hyperlipidemia.
Benzodiazepines	↑
Levothryoxine	↓
Metformin	↓	Shown above. Increases colonic FDG uptake and can result in a competitive decrease in cardiac FDG uptake.

In addition to the above, certain patient factors can increase cardiac FDG uptake: Male gender, younger patients (< 30 years), fasting duration of <5 hours, and patients with heart failure tend to have higher cardiac FDG uptake.

References

• Israel O, Weiler-Sagie M, Rispler S, Bar-Shalom R, Frenkel A, Keidar Z, Bar-Shalev A, Strauss HW. PET/CT quantitation of the effect of patient-related factors on cardiac 18F-FDG uptake. J Nucl Med. 2007 Feb;48(2):234-9.
• Maurer AH, Burshteyn M, Adler LP, Steiner RM. How to differentiate benign versus malignant cardiac and paracardiac 18F FDG uptake at oncologic PET/CT. Radiographics. 2011 Sep-Oct;31(5):1287-305.

F18-FDG PET in Neuroendocrine Tumors

Somatostatin receptor scintigraphy (e.g., octreoscan) is more sensitive than both ¹²³I-MIBG scintigraphy and ¹⁸F-FDG PET for neuroendocrine tumors. However, ¹⁸F-FDG PET is more sensitive for detection of aggressive tumors, with a sensitivity of around 90%, compared to ~70% and ~45% for somatostatin receptor and ¹²³I-MIBG scintigraphy for tumors with proliferation index above 15%.

In these aggressive tumors, somatostatin receptor and ¹²³I-MIBG scintigraphy can underestimate the extent of disease dissemination and lead to suboptimal treatment for these patients (aggressive disease is treated with systemic chemotherapy, while less aggressive disease is treated with somatostatin analogs or α-interferon).

In the example above, FDG-PET shows uptake in several areas not seen on octreoscan. One example is an enlarged retroperitoneal lymph node that is not hot on octreoscan, but light s up on FDG-PET (black arrows).

References

Binderup T, Knigge U, Loft A, Mortensen J, Pfeifer A, Federspiel B, Hansen CP, Højgaard L, Kjaer A. Functional imaging of neuroendocrine tumors: a head-to-head comparison of somatostatin receptor scintigraphy, 123I-MIBG scintigraphy, and 18F-FDG PET. J Nucl Med. 2010 May;51(5):704-12.

Focal Nodular Hyperplasia on F-18 FDG-PET

Focal nodular hyperplasia (FNH) characteristically has FDG avidity similar to (more common) or lower than the surrounding liver. In rare circumstances, FNH can present as a hypermetabolic lesion, creating some confusion.

The case above shows the typical appearance of focal nodular hyperplasia on CT. FDG-PET shows that the uptake of the lesion (arrow) is similar to the adjacent liver.

Differential considerations on FDG-PET include adenoma, hemangioma, and hepatocellular carcinoma.

References

• Aznar DL, Ojeda R, Garcia EU, Aparici F, Sánchez PA, Flores D, Martínez C, Sopena R. Focal nodular hyperplasia (FNH): a potential cause of false-positive positron emission tomography. Clin Nucl Med. 2005 Sep;30(9):636-7.
• Kurtaran A, Becherer A, Pfeffel F, Müller C, Traub T, Schmaljohann J, Kaserer K, Raderer M, Schima W, Dudczak R, Kletter K, Virgolini I. 18F-fluorodeoxyglucose (FDG)-PET features of focal nodular hyperplasia (FNH) of the liver. Liver. 2000 Dec;20(6):487-90.

FDG and Lactating Women

Lactating women have increased uptake in the breast(s) used for breastfeeding. For example, a breast that is consistently refused by baby or breasts in non-breastfeeding women, do not have significantly increased uptake.

No significant radiotracer is excreted in the breast milk, and the radiation dose received by the baby is more from close contact with the breast than from ingestion of radioactive milk.

References

Hicks RJ, Binns D, Stabin MG. Pattern of uptake and excretion of (18)F-FDG in the lactating breast. J Nucl Med. 2001 Aug;42(8):1238-42.

Infradiaphragmatic Brown Fat Uptake

Brown fat uptake in FDG-PET is usually fairly characteristic in the neck, shoulder and costovertebral regions: bilateral, symmetric, intense uptake that is usually multifocal although linear uptake is also possible.

Infradiaphragmatic brown fat uptake poses a challenge when asymmetrical or focal, and may be mistaken for adrenal malignancy or misregistration due to respiration. Correlation with PET images shows the uptake to be located in infradiaphragmatic fat.

References

• Bar-Shalom R, Gaitini D, Keidar Z, Israel O. Non-malignant FDG uptake in infradiaphragmatic adipose tissue: a new site of physiological tracer biodistribution characterised by PET/CT. Eur J Nucl Med Mol Imaging. 2004 Aug;31(8):1105-13.
• Reddy MP, Ramaswamy MR. FDG uptake in brown adipose tissue mimicking an adrenal metastasis: source of false-positive interpretation. Clin Nucl Med. 2005 Apr;30(4):257-8.

FDG Embolism

Thrombus formation during intravenous administration of FDG can result in small pulmonary emboli that present as a focus (or foci) of intense FDG activity in the lung without a corresponding CT abnormality. These generally resolve after a few days and can even be seen to migrate peripherally in scans obtained on the same day.

The mechanism is thought to be related to FDG uptake by platelets at the site of injection and by neutrophils at the site of embolism. Vascular injury during FDG injection can lead to thrombus formation and platelet activation. Activated platelets have increased energy requirements and glucose uptake (5–6 times normal), which can lead to concentration of FDG in the thrombus. Activated neutrophils that respond to vascular injury after pulmonary embolism also have increased glucose uptake and can cause focal FDG uptake at the site of embolism.

References

• Farsad M, Ambrosini V, Nanni C, Castellucci P, Boschi S, Rubello D, Fabbri M, Franchi R, Fanti S. Focal lung uptake of 18F-fluorodeoxyglucose (18F-FDG) without computed tomography findings. Nucl Med Commun. 2005 Sep;26(9):827-30.
• Ha JM, Jeong SY, Seo YS, Kwon SY, Chong A, Oh JR, Song HC, Bom HS, Min JJ. Incidental focal F-18 FDG accumulation in lung parenchyma without abnormal CT findings. Ann Nucl Med. 2009 Aug;23(6):599-603.
• Kavanagh PV, Stevenson AW, Chen MY, Clark PB. Nonneoplastic diseases in the chest showing increased activity on FDG PET. AJR Am J Roentgenol. 2004 Oct;183(4):1133-41.

Bone Infarction on FDG-PET

Bone infarction/avascular necrosis can have increased FDG activity, likely from peri-infarct inflammation. This hasn't been very well studied in the literature and can sometimes result in a false-positive interpretation in the evaluation of metastatic disease. The image above shows mild FDG activity in the left femoral head, corresponding to avascular necrosis seen on the coronal T1-weighted image.

References

Grigolon MV, Delbeke D. F-18 FDG uptake in a bone infarct: a case report. Clin Nucl Med. 2001 Jul;26(7):613-4.

Diffusely Increased FDG Activity in the Thyroid

The thyroid may occasionally have diffusely increased uptake on FDG-PET scans obtained for malignancy elsewhere. Between 1%-3% of patients undergoing a PET scan will have such uptake. This finding can be seen as a normal variant or associated with chronic lymphocytic (Hashimoto) thyroiditis, with or without the presence of hypothyroidism and can be seen even in patients receiving thyroid hormone replacement therapy.

Focal uptake in the thyroid should raise concern for carcinoma or metastasis.

References

• Chen YK, Chen YL, Cheng RH, Yeh CL, Lee CC, Hsu CH. The significance of FDG uptake in bilateral thyroid glands. Nucl Med Commun. 2007 Feb;28(2):117-22.
• Karantanis D, Bogsrud TV, Wiseman GA, Mullan BP, Subramaniam RM, Nathan MA, Peller PJ, Bahn RS, Lowe VJ. Clinical significance of diffusely increased 18F-FDG uptake in the thyroid gland. J Nucl Med. 2007 Jun;48(6):896-901.
• Shreve PD, Anzai Y, Wahl RL. Pitfalls in oncologic diagnosis with FDG PET imaging: physiologic and benign variants. Radiographics. 1999 Jan-Feb;19(1):61-77; quiz 150-1.

Perirectal Artifact on FDG PET/CT

Differences in position of rectal gas between acquisition of CT and PET images can lead to a perirectal artifact on attenuation-corrected PET images.

The artifact is caused by localized attenuation over-correction at the margin of the rectum due to movement of gas: There is soft tissue attenuation in the rectum at CT acquisition, and gas during PET acquisition. The proximity of the high-signal urinary bladder results in a high-intensity region extending posterior to the bladder and around the rectum immediately adjacent to a region of rectal gas. The artifact is not observed when rectal gas is absent.

This artifact is reportedly seen in 15% of PET/CTs and has a maximum standardized uptake value of ~5.

References

Lodge MA, Chaudhry MA, Udall DN, Wahl RL. Characterization of a perirectal artifact in 18F-FDG PET/CT. J Nucl Med. 2010 Oct;51(10):1501-6.

Leiomyosarcoma vs. Leiomyoma on FDG-PET

While uterine leiomyosarcomas usually have moderate to intense FDG uptake and uterine leiomyomas usually have low to moderate FDG uptake, there is overlap in findings on FDG-PET. This, unfortunately, means that FDG PET cannot reliably differentiate leiomyosarcoma from leiomyoma.

The image above shows a uterine leiomyoma (arrow) with intense FDG activity (maximum SUV of around 10). It has remained stable in size and activity on 4 years of follow-up PET/CT.

References

• Kitajima K, Murakami K, Kaji Y, Sugimura K. Spectrum of FDG PET/CT findings of uterine tumors. AJR Am J Roentgenol. 2010 Sep;195(3):737-43.

Iodine-131: Half-Life

In the United States, patients treated with ¹³¹I ablation for hyperthyroidism or thyroid carcinoma are sent home with instructions on hygiene and limitations on social interactions. The instructions vary a bit among different centers, but are based on a balance between insurance reimbursement for inpatient isolation, patient comfort, and public safety.

The duration of isolation is usually decided empirically based on the administered dose, ranging from 2-7 days. This is based on the effective half-life of ¹³¹I, which is eliminated mainly through urine, but also in stool.

The physical half-life of ¹³¹I is fixed by nature at approximately 8 days. The effective half-life, however, depends on a number of patient factors. In healthy subjects, the effective half-life for the clearance of ¹³¹I is between 5-7 days. The effective half-life is similar in patients being treated for thyrotoxicosis. In patients with thyroid carcinoma who have been treated with total thyroidectomy, ¹³¹I clears faster because of the absence of significant thyroid tissue. The effective half-life in these patients is between 10 hours - 15 hours.

References

• Greenlee C, Burmeister LA, Butler RS, Edinboro CH, Morrison SM, Milas M; American Thyroid Association Radiation Safety Precautions Survey Task Force. Current safety practices relating to I-131 administration for diseases of the thyroid: a survey of physicians and allied practitioners. Thyroid. 2011 Feb;21(2):151-60.
• Ravichandran R, Binukumar J, Saadi AA. Estimation of effective half life of clearance of radioactive Iodine (I) in patients treated for hyperthyroidism and carcinoma thyroid. Indian J Nucl Med. 2010 Apr;25(2):49-52.

Central Venous Obstruction in the Chest

Collateral vessels can be recruited to bypass central venous obstruction in the chest via three routes. More central obstructions (superior vena cava) tend to recruit more inferior collaterals, while the more peripheral obstructions (subclavian or brachiocephalic veins) tend to recruit more superior collaterals.

The three routes are:

• Superior route: Seen with subclavian or brachiocephalic vein obstruction. Blood flows via through the ipsilateral external jugular vein into horizontal veins that communicate across the midline via the transverse arch of the anterior jugular venous system. Once on the contralateral side, blood flows into the external jugular vein into the subclavian vein, and finally into the superior vena cava.
• Posterior route: Seen in cases of obstruction at the level of the supraazygos superior vena cava. This leaves the azygos vein as a conduit for blood to get into the superior vena cava. Blood from the head and neck flows through paravertebral collaterals into intercostal and paravertebral veins and then the superior intercostal vein, which drains into the azygos vein.
• Anterolateral: Seen in cases of central superior vena cava obstruction (shown above). Blood flows through anterior intercostal, internal mammary (pink arrow), and long thoracic veins, which, flow to the inferior vena cava (green arrow) via pericardiophrenic (yellow arrow), musculophrenic (blue arrow), lumbar, and hepatic veins. The internal mammary vein can also connect to the left portal vein via the paraumbilical vein and result in increased activity or enhancement in segment IV of liver (white arrow) and is the basis of the focal hepatic hot spot sign on ^99mTc sulfur colloid "liver and spleen" scans. IN the image above, we also see aortopulmonary window collaterals (red arrow) that drain into the infraazygos superior vena cava(S), in this patient with combined infraazygos superior vena cava and azygos vein obstruction.

References

• Dickson AM. The focal hepatic hot spot sign. Radiology. 2005 Nov;237(2):647-8.
• Gosselin MV, Rubin GD. Altered intravascular contrast material flow dynamics: clues for refining thoracic CT diagnosis. AJR Am J Roentgenol. 1997 Dec;169(6):1597-603.
• Lee KR, Preston DF, Martin NL, Robinson RG. Angiographic documentation of systemic-portal venous shunting as a cause of a liver scan ""hot spot'' in superior vena caval obstruction. AJR Am J Roentgenol. 1976 Oct;127(4):637-9.
• Godwin JD, Chen JT. Thoracic venous anatomy. AJR Am J Roentgenol. 1986 Oct;147(4):674-84.

FDG-PET Appearance of Rectus Femoris Origin Injuries

Strain or avulsion injury of the proximal tendon of the rectus femoris muscle can lead to increased FDG activity at the level of the anterior inferior iliac spine and superior acetabular ridge. Recognition of this entity can help avoid confusion for neoplasm on PET and offer a non-neoplastic etiology for pain in this region.

References

Sopov V, Bernstine H, Stern D, Yefremov N, Sosna J, Groshar D. Spectrum of focal benign musculoskeletal 18F-FDG uptake at PET/CT of the shoulder and pelvis. AJR Am J Roentgenol. 2009 Apr;192(4):1029-35.

Aortitis: Differential Diagnosis

Aortitis, the inflammation of the aortic wall, can be due to infectious or noninfectious conditions. Patients present with nonspecific signs, symptoms, and laboratory findings that can include pain, fever, vascular insufficiency, and elevated levels of acute phase reactants.

Differential considerations include:

Noninfectious

• Large-vessel vasculitides (shown above):
  • Giant cell arteritis: Affects large and medium-sized vessels. Often involves the superficial cranial arteries.
  • Takayasu arteritis: Abdominal aorta most commonly affected. Descending thoracic aorta and aortic arch can also be involved. Look for stenosis or luminal narrowing of aorta and branch vessels. Aneurysmal dilatation less common, but can be seen after destruction of media. Arterial wall calcification (can be seen in chronic cases) is typically linear and spares the ascending aorta.
  • Rheumatoid arthritis: Aortitis is rare. Heart, aortic valve, and great vessels can be affected.
  • Systemic lupus erythematosus: Aortitis uncommon.
  • Ankylosing spondylitis: Aortic root and valve disease seen in 80% of cases. Aortic wall thickening is seen in 60% of affected patients.
  • Reiter syndrome:
• Medium- and small-vessel vasculitides:
  • Wegener arteritis:
  • Polyarteritis nodosa:
  • Behçet disease: Wall-enhancing saccular pseudoaneurysms can be seen in the aorta and branch vessels in 20% of patients.
  • Relapsing polychondritis: May manifest as aortic root dilatation and aortitis.
  • Cogan syndrome: Ocular, inner ear, and vascular inflammation. Patients are usually white young adults. Aortitis and valvulitis seen in ~10% of patients.
• Isolated aortitis: Isolated idiopathic (thoracic) aortitis, Chronic periaortitis (Idiopathic retroperitoneal fibrosis, inflammatory abdominal aortic aneurysm, perianeurysmal aortitis, idiopathic isolated abdominal periaortitis).
• Radiation-induced: Usually years after exposure to high-dose radiation. Can manifest as thrombosis, pseudoaneurysm, rupture, stenosis, and accelerated wall calcification.

Infectious

• Bacterial: Salmonella, Staphylococcus, Streptococcus pneumoniae
• Syphilis: The typical calcification of the ascending aorta is uncommon.
• Mycobacterial: Mycobacterium tuberculosis
• Viral: HIV.

References

• Gornik HL, Creager MA. Aortitis. Circulation. 2008 Jun 10;117(23):3039-51.
• Restrepo CS, Ocazionez D, Suri R, Vargas D. Aortitis: imaging spectrum of the infectious and inflammatory conditions of the aorta. Radiographics. 2011 Mar-Apr;31(2):435-51.

Metformin and 18F-FDG PET

Metformin has been shown to significantly increase ¹⁸F-FDG uptake in the colon and, to a lesser extent, the small bowel.

Cells of the intestinal wall are exposed to much higher concentrations of metformin for much longer times compared to other cell types. In addition, animal studies have shown that metformin increases glucose transfer into intestinal mucosal cells and can increase glucose utilization by up to 60%.

This results in intense, diffuse, and continuous uptake along the bowel on ¹⁸F-FDG PET imaging. The uptake is seen in both the wall and within the lumen (likely due to excretion of ¹⁸F-FDG into the stool).

The pattern is fairly characteristic and confusion with malignant focal bowel uptake is rare. The problem is that this diffuse uptake can mask an existing bowel malignancy and lead to a false-negative result.

References

Gontier E, Fourme E, Wartski M, Blondet C, Bonardel G, Le Stanc E, Mantzarides M, Foehrenbach H, Pecking AP, Alberini JL. High and typical 18F-FDG bowel uptake in patients treated with metformin. Eur J Nucl Med Mol Imaging. 2008 Jan;35(1):95-9.