Download as pdf or txt
Download as pdf or txt
You are on page 1of 10

ARTICLE IN PRESS

Benign Cutaneous and Subcutaneous Lesions


on FDG-PET/CT
Ur Metser, MD, FRCPC,*,† and Noam Tau, MD*,†

18
F-FDG, the most commonly used PET radiopharmaceutical in clinical practice, can also accu-
mulate in inflammatory and infectious conditions. This may account for false-positive PET findings
when staging or restaging a patient with malignancy. As clinical use of FDG-PET-CT is increas-
ing, nuclear medicine physicians are encountering a myriad of cutaneous and subcutaneous lesions,
many of which are incidental and benign. The most common cause for the FDG avidity of these
lesions is inflammation. Although a specific diagnosis may not always be possible, background
clinical history and morphologic features of the lesion on CT may help narrow the differential di-
agnosis. This article aims to familiarize nuclear medicine physicians and radiologists with various
benign cutaneous and subcutaneous conditions encountered in routine clinical practice.
Semin Nucl Med ■■:■■–■■ © 2017 Elsevier Inc. All rights reserved.

Pathophysiology of 18F-FDG Inflammation is triggered by innate immune receptors that


identify pathogens and abnormal or damaged cells, and may
Uptake in Inflammation be induced by infection, injury, or exposure to toxins. In-

T he most common etiologies for increased FDG uptake


in the skin or subcutaneous tissues are inflammatory or
infectious (Table 1). FDG is a glucose analog with a meta-
flammation is a complex cascade of cytokine-mediated
immunologic events that result in increased glucose metabo-
lism and FDG uptake.4 The earliest stages of inflammation
bolic pathway similar to that of glucose, including uptake by involve vasodilation, increased vascular permeability, and in-
cell surface transporter proteins (mainly GLUT-1) and phos- creased blood flow, which then result in increased flux of FDG
phorylation by hexokinase.1 In 1923, Otto Heinrich Warburg into cells. This facilitates the recruitment of leukocytes, plasma
suggested that most malignant cells produce energy by a high proteins, and fluids. Activated inflammatory cells show in-
rate of glycolysis followed by lactic acid fermentation in the creased expression of glucose transporters, and the affinity
cytosol. This nonoxidative metabolism of glucose generates of these transporter proteins to glucose is increased via
more energy than the low rate of glycolysis followed by oxi- cytokines.5 Hexokinase is also upregulated during this process,
dation of pyruvate in mitochondria of most normal cells. This increasing the retention of FDG within these cells. Both pro-
energy production process was termed the “Warburg effect.”2 cesses together cause FDG accumulation in recruited
In 1992, Kubota et al reported that FDG uptake in tumors inflammatory cells. FDG uptake appears to correlate well with
is due to uptake not only in tumor cells but also in tumor- the density of inflammatory cells in both acute and chronic
associated inflammatory cells.3 In fact, accumulation of FDG inflammations.6 The neutrophil is a key effector cell of the
is often higher in the inflammatory cells than in tumor cells, immune system and is an important component of host
enabling use of FDG-PET in imaging of inflammation and defense. Neutrophil responds to external insults such as bac-
infection. terial infection via chemotaxis, phagocytosis, degranulation,
and generation of toxic reactive oxygen intermediates. Acti-
*Joint Department of Medical Imaging, University Health Network, Mount
vated neutrophils, either responding to an infection or as part
Sinai Hospital and Women’s College Hospital, University of Toronto, of inflammatory response, have increased glucose uptake and
Toronto, Ontario, Canada. metabolism.
†Department of Medical Imaging, University of Toronto, Toronto, Ontario, In the past decade and a half, there has been an increase
Canada. in clinical use of FDG-PET, most commonly for staging or
Address reprint requests to Ur Metser, MD, FRCPC, Joint Department of
Medical Imaging, Princess Margaret Hospital, University Health Network,
restaging of various malignancies, or for therapy response as-
610 University Ave, Suite 3-960, Toronto, ON, Canada M5G 2M9. E-mail: sessment. PET may also be utilized for non–malignancy-
ur.metser@uhn.ca related reasons, such as identifying a source of infection in

http://dx.doi.org/10.1053/j.semnuclmed.2017.02.007 1
0001-2998/© 2017 Elsevier Inc. All rights reserved.
ARTICLE IN PRESS
2 U. Metser and N. Tau

Table 1 Infectious and Inflammatory Cutaneous and Subcutaneous Disorders That May Be FDG-avid
Systemic conditions involving skin Sarcoidosis
and subcutaneous tissues Gout
Medium- and small-vessel vasculitides
Cutaneous disorders Autoimmune Psoriasis
Pemphigus (various types)
Inflammatory Insect bite
Acne vulgaris
Hidradenitis suppurativa
Granulomatous vasculitis
Febrile neutrophilic dermatosis (Sweet syndrome)—paraneoplastic
Acquired perforating dermatosis
Steatocystoma multiplex (rare)
Necrobiotic xanthogranuloma (rare)
Infectious Erysipelas
Abscess
Herpes zoster
Furuncle/carbuncle
Rhinophyma
Mycobacteria—tuberculosis, MAC, and other nontuberculous mycobacteria
Toxoplasma
Lesions primarily involving Fat necrosis—breast, post surgery
subcutaneous tissues Lipodystrophy or lipoatrophy in HIV patients
Panniculitis—including erythema nodosum
Eosinophilic fasciitis, nodular fasciitis
Epidermoid cysts—uncomplicated or ruptured
Pilonidal sinus
Hematoma
Iatrogenic cutaneous and Wound healing
subcutaneous lesions Scars and keloids
Injections site granulomas
Drug reactions, including extravasation (ie, erlotinib, BCG, anakinra, silicone)
Foreign body reaction—mesh, gossypiboma, calcium hydroxylapatite dermal
filler, breast implant, and other implants
Infected foreign body
MAC, Mycobacterium avium complex.

patients with fever of unknown origin or febrile neutropenia.7 to therapy, or to evaluate for cardiac involvement.8,9 This sys-
Whatever the indication, benign skin or subcutaneous lesions temic autoimmune, inflammatory disease shows cutaneous
may be incidentally encountered. A familiarity with the various involvement more commonly than usually clinically appre-
etiologies and their imaging appearance may be helpful in ciated, with skin being the second most common site of disease
deriving a concise differential diagnosis. after the lungs. Reports show that 30%-35% of systemic sar-
coidosis patients have various skin findings, and in 10% of
patients, skin is the first or only site of disease.10 Acute forms
of sarcoidosis usually present with a discreet nodular appear-
Systemic Conditions Involving ance (macules, papules, or other types), whereas plaque-
Cutaneous and Subcutaneous like disease usually accompanies the chronic form of disease.11
As expected, the PET appearance follows the clinical presen-
Tissues tation, with cutaneous FDG-avid lesions apparent in locations
Systemic inflammatory disorders may involve cutaneous and of involved skin, whether as discreet nodules or plaque-like12
subcutaneous tissues at different disease stages. The skin and (Fig. 1).
subcutaneous tissues can manifest as the sole site of disease, Subcutaneous involvement is less common, with 2%-6%
as may be seen in cutaneous sarcoidosis, or may appear as a of patients developing subcutaneous lesions during the course
further site of disease during the course of illness. of disease. In the chronic form, these subcutaneous, hard, in-
Sarcoidosis is the hallmark of a systemic disorder that may durated nodules are often asymptomatic but may present as
involve the cutaneous and subcutaneous tissues and mani- mildly tender.13 These nodules may also be the first or only
fest as FDG-avid lesions on PET. PET may be used in systemic sign of disease.14,15 Subcutaneous sarcoid nodules are more
sarcoidosis to determine disease activity, to assess response common in Caucasian women in the fifth and sixth decades.
ARTICLE IN PRESS
Benign lesions on FDG-PET/CT 3

Figure 1 Cutaneous sarcoidosis involvement of the right breast. On PET, there is a metabolically active cutaneous lesion in the right inframammary fold,
with corresponding focal skin thickening on CT. Note the multiple foci of abnormal FDG uptake in the spleen in keeping with splenic involvement.

On PET, these appear as discreet FDG-avid nodules in the may be seen secondary to systemic factors, such as infec-
subcutaneous fat. tion, inflammation, vaccination, or drug exposure. In up to
The most common form of acute subcutaneous involvement 21%-25% of patients, there may be an underlying malig-
is erythema nodosum, which may be seen in approximately 10%- nancy, mostly hematologic, and the dermatosis may be its
35% of patients with subcutaneous sarcoidosis. Erythema nodosum presenting symptom.18,19 The syndrome manifests acutely with
usually presents with painful erythematous rounded nodules, most fever and rapidly appearing tender erythematous nodules,
often located on the anterior surface of lower extremities, and may mostly on the face, neck, and upper limbs, which may co-
also be accompanied by systemic symptoms such as malaise, fever, alesce to form plaques. On pathology, these nodules have dense
and arthralgia. On pathology, erythema nodosum shows septal pan- neutrophil infiltrates, which may account for their FDG avidity.
niculitis without granulomas. Although not specific to sarcoidosis, As with Sweet syndrome but much less common, pem-
when a young patient presents with erythema nodosum, sarcoid- phigus can be the cutaneous expression of a paraneoplastic
osis should be suspected.16 Löfgren syndrome, a subtype of syndrome, and is then termed paraneoplastic pemphigus.20
sarcoidosis, manifests as an acute triad of erythema nodosum, hilar This specific pemphigus subset also has a strong relation-
lymphadenopathy, and arthritis and is considered self-limiting, with ship with hematologic malignancies. Unlike the predictable
a better prognosis than systemic sarcoidosis.17 appearance of skin lesions in Sweet syndrome, paraneoplastic
pemphigus has a variable appearance, including pemphigus
vulgaris, bullous pemphigoid, or mimicking various other
nodular or plaque-like skin conditions. Therefore, a skin biopsy
Autoimmune and Inflammatory is often necessary for a definitive diagnosis.
Cutaneous Conditions
There is a myriad of FDG-avid inflammatory skin condi-
tions. However, as PET is not routinely used to diagnose or
manage them, most FDG-avid cutaneous lesions are encoun- Skin Infections
tered incidentally. Location of lesions and demographic and Skin infections have variable clinical and imaging appear-
clinical data such as patient’s age may help in making the di- ances. Localized infections such as furuncles and abscesses
agnosis. For example, FDG-avid lesions in skin folds may usually have a focal appearance both clinically and radio-
suggest hidradenitis suppurativa (Fig. 2). Nonetheless, a defi- logically, and are easily differentiated from more widespread
nite diagnosis would require clinical examination. infections such as cellulitis (Fig. 3A, B).
A clinically important entity that should be kept in mind Acne vulgaris is a common skin disorder in teenagers and
is the cutaneous manifestations of paraneoplastic syn- presents a frequent indication for dermatology consulta-
dromes. Sweet syndrome (acute febrile neutrophilic dermatosis) tions. Nonetheless, there is still an open debate on the role

Figure 2 Hidradenitis suppurativa of the left groin. PET performed for restaging of squamous cell carcinoma of tongue showed incidental FDG
uptake in left groin, corresponding to irregular thickening on CT. This corresponded to tiny non–tender erythematous skin nodules shown
to represent hidradenitis suppurativa.
ARTICLE IN PRESS
4 U. Metser and N. Tau

Figure 3 Focal and diffuse infections. (A) Cutaneous nodule with high metabolic activity in the left groin in keeping with a furuncle. (B) In
contrast, diffuse involvement pattern on PET, with subcutaneous fat stranding on CT, corresponding to right flank cellulitis.

infection has in the course of disease, and especially Propi- Lesions Primarily Involving
onibacterium acnes bacterium. One view supports a purely
inflammatory response to overexcretion of sebum from se-
Subcutaneous Tissues
baceous glands, whereas other views claim the disease is purely Subcutaneous tissues include adipose cells, blood vessels, nerves,
infectious. Treatment trends have shifted accordingly between hair follicles, and collagen fibers. FDG-avid lesions may arise from
antibiotic and anti-inflammatory drugs, with current treat- these structures or may extend from a cutaneous process. It should
ment regimens being aimed at both.21 Regardless of the precise be kept in mind that although uncommon, subcutaneous metas-
etiology, both processes may be FDG-avid. tases exist and should always be considered in the appropriate
Although acne is a benign condition with mostly cos- clinical context, especially in melanoma patients.28,29
metic implications, there are systemic infections that may also Fat necrosis is a benign inflammatory condition of fat, usually
involve the skin, and often prove detrimental to patients’ well- appearing secondary to local tissue insult, including trauma,
being as they are difficult to treat. Although more commonly surgery, biopsy, and radiation injury. Fat necrosis is common
present in immunocompromised patients, either due to HIV in the breast, where it has been well documented, but can
infection of secondary to immunosuppressive drugs, these sys- appear in any subcutaneous tissue. Fat necrosis is usually FDG-
temic infections can also affect patients following trauma and avid. A diagnosis can often be made based on PET and
surgery, and even immunocompetent patients. Toxoplasmo- morphological findings on CT, in the appropriate clinical context
sis, tuberculosis, and other nontuberculous mycobacteria may (Fig. 4). However, it is important to keep in mind that other
all involve the skin in the course of the disease.22-24 The clini- conditions such as lipodystrophy, panniculitis, and even T-cell
cal and radiological appearances of all these conditions overlap lymphoma may have a similar appearance.30,31
and may include multiple discreet nodules, ulcers, and skin Panniculitis is a general term for a group of pathologic pro-
abscesses. Biopsies and cultures should be directed to the most cesses consisting of adipocyte necrosis with surrounding
metabolically active lesion, whether cutaneous or other. inflammatory cells. The latter may be secondary to the ne-
Although herpes zoster is common in elderly patients, there has crosis or the precipitating factor. As panniculitis may be a
been an increased incidence in young immunocompromised pa- marker of a systemic disorder such as lupus or scleroderma,
tients in recent decades. Herpes zoster is a reactivation of varicella- biopsy of the involved fat is necessary for specific diagnosis.32
zoster virus dormant in the dorsal nerve root and cranial sensory Panniculitis-like T-cell lymphoma is an important differen-
ganglia of patients previously infected with chickenpox. The re- tial diagnosis, and as it is not a benign process, it requires
activation process causes the virus to multiply and spread within prompt diagnosis and treatment.33,34
the ganglion, through sensory nerves and later to the skin, causing Patients receiving antiretroviral therapy for HIV may undergo
an intense inflammatory process and neuronal necrosis. This process changes in their body fat distribution, termed HIV
then results in the characteristic dermatomal rash characteristic lipodystrophy.35,36 The most stigmatizing of these changes is
of the disease.25,26 On PET, this appearance can be best appreci- loss of subcutaneous fat (lipoatrophy), especially in the face.
ated using maximum intensity projection reconstruction or coronal This is more common in patients receiving nucleoside analog
views, where the cutaneous FDG avid lesions appear along a single, reverse-transcriptase inhibitors, but other culprit antiretroviral
or rarely multiple dermatome.27 drugs have also been implicated. Regardless of the exact cause,
ARTICLE IN PRESS
Benign lesions on FDG-PET/CT 5

Figure 4 Fat necrosis. PET performed for assessing sarcoidosis 3 months post abdominoplasty showing abnormal metabolic activity in diffuse
fat stranding of subcutaneous abdominal fat in keeping with fat necrosis.

the common end pathway is adipose cell apoptosis with in- FDG-avid (Fig. 6). However, the most common cause of
flammatory changes surrounding it, causing loss of fat tissue. FDG uptake along a surgical wound is inflammation during
This process is FDG-avid and should be always considered wound healing (Fig. 7). Persistent FDG update may be due
when imaging treated HIV patients37,38 (Fig. 5A, B). to keloid formation.39 Foreign body response such stitch
granuloma, mesh response, and others is also FDG-avid
Iatrogenic Cutaneous and (Fig. 8A, B). In fact, the inflammatory response to foreign
bodies can last for years after surgery.40,41 Another common
Subcutaneous Lesions finding on PET is injection site granuloma. Variable acute
Postoperative wound infection and infected subcutaneously or chronic inflammatory responses with high-level FDG
placed devices such as ports or pacemakers are usually uptake were reported in patients receiving immunotherapy

Figure 5 Cheek augmentation due to HIV lipoatrophy. (A) Moderate FDG uptake in
the left premaxillary area corresponding to high signal intensity on fat saturated in-
version recovery MRI (B). Both PET and MRI findings can be secondary to HIV
lipoatrophy and cheek augmentation performed 10 years earlier in this patient.
ARTICLE IN PRESS
6 U. Metser and N. Tau

Figure 6 Infected right chest wall port site, confirmed clinically.

Figure 7 Abnormal FDG uptake in left abdominal surgical wound 5 weeks post surgery. This may be inflammatory, although clinical corre-
lation is needed to exclude wound infection.

in the form of subcutaneous bacillus Calmette–Guérin metabolically active tissue capable of generating heat and is com-
injections, but have also been described in other types of monly encountered on PET, mostly in young, thin women, more
injected drugs42,43 (Fig. 9). often in cold conditions. Therefore, it is not surprising that
hibernomas are highly metabolically active as well48,49 (Fig. 10).
The FDG avidity of hibernomas helps to differentiate them from
Benign Tumors their yellow fat counterparts—lipomas. Hibernomas commonly
Benign cutaneous and subcutaneous tumors are uncom- arise in areas where brown adipose tissue would normally be ex-
mon in general and even rarer on FDG-PET due to their low pected and usually do not recur after resection. Although
metabolic cellular activity. However, there are a few excep- hibernomas have a typical imaging appearance of a well-
tions that should be noted (Table 2). demarcated, heterogeneous low-attenuation lesion on CT with high
Dermatofibroma (superficial benign fibrous histiocytoma) is the FDG uptake, biopsy may be obtained to exclude a more sinister
most common mesenchymal tumor of the skin, with an uncer- process such as liposarcoma.50,51
tain etiology. Dermatofibroma is composed of fibroblasts and Neurofibromatosis type 1 (NF1) is a common genetic disease
histiocytes and appears mostly on limbs of young to middle- affecting 1 in 2500 live births and is caused by mutation of
aged adults, especially women.44,45 Almost all subtypes of this tumor the tumor-suppressor gene “neurofibromin”, resulting in a pre-
are benign and do not require treatment. Most are limited to the disposition to developing tumors, both benign and malignant,
skin, although cases of deep penetrating or purely subcutaneous termed neurofibromas.52 Cutaneous neurofibromas have no
dermatofibromas have been described.46,47 On PET, dermatofi- malignant potential. The subcutaneous form may be nodular
bromas appear as small cutaneous (and less commonly or diffuse, with the latter termed plexiform neurofibroma.
subcutaneous) focal soft tissue nodules with high FDG uptake. These deeper and more complex benign tumors may undergo
Dermatofibromas can easily be confused with furuncles on imaging, transformation to malignant peripheral nerve sheath tumors.
and clinical correlate is needed. Up to 10% of NF1 patients will develop malignant periph-
In contrast to the cutaneous nature of dermatofibroma, eral nerve sheath tumor during their lifetime, and these tumors
hibernomas are subcutaneous brown fat tumors. Brown fat is a are one of the leading causes of death in this patient
population.53-55 Studies show that both benign and malig-
nant tumors in NF1 patients are FDG-avid (Fig. 11A, B), with
Table 2 Benign FDG-avid Tumors various FDG uptake thresholds suggested for detecting ma-
Dermatofibroma—superficial benign fibrous histiocytoma lignant transformation.56-58
Hibernoma Pilomatricoma, also known as pilomatrixoma or calcify-
Neurofibroma and schwannoma in neurofibromatosis ing epithelioma of Malherbe, is a benign tumor of hair follicles,
Cholesterol granuloma commonly appearing in the head and neck regions of pedi-
Pilomatricoma atric patients.59,60 Although this tumor has a typical appearance
Purely cutaneous Rosai-Dorfman disease on ultrasound, CT, and MRI (Fig. 12), a definite diagnosis
ARTICLE IN PRESS
Benign lesions on FDG-PET/CT 7

Figure 8 Postsurgical foreign body granuloma. (A) Patient’s 10 years’ postexploratory laparotomy showing high metabolic activity in a soft
tissue nodule located deep in the surgical scar, in keeping with a stitch granuloma. (B) Sagittal image in another patient post orchiectomy
shows FDG-avid nodule at resected tip of the spermatic cord in keeping with postorchiectomy suture granuloma.

Figure 9 Patient with malignant melanoma treated with subcutaneous injections of BCG to the abdominal wall. Note the intense abnormal
metabolic activity in the subcutaneous tissues in the right lower abdomen, corresponding to injection site.

Figure 10 Hibernoma. Metabolically active mass in posterior left thigh in keeping with histologically proven hibernoma.
ARTICLE IN PRESS
8 U. Metser and N. Tau

Figure 11 Neurofibroma. Patient with neurofibromatosis type 1. (A) Left parasternal chest wall skin thickening on CT, with low-level meta-
bolic activity on PET, corresponding to a high T2-weighted signal on MRI in a known neurofibroma (B).

Figure 12 FDG-avid cutaneous lesion in the left neck of a 14-year-old adolescent boy who was previously treated for Hodgkin lymphoma. CT
shows fine calcifications in the lesion. Ultrasound shows a 2-cm large well-defined ovoid lesion with a hypoechogenic rim and central echogenic
foci, consistent with pilomatricoma. Despite its characteristic CT and ultrasonographic appearance, excisional biopsy was performed due to
the patient’s history. Histopathology confirmed pilomatricoma.(Case courtesy of Dr. H.J.A. Adams and Dr. T.C. Kwee.)
ARTICLE IN PRESS
Benign lesions on FDG-PET/CT 9

can only be reached on postexcisional pathology.61,62 The level 25. Cohen JI: Clinical practice: Herpes zoster. N Engl J Med 369:255-263,
of FDG uptake in these tumors is highly variable, and there- 2013
26. Cohen JI, Straus SE, Arvin AM: Varicella-zoster virus replication,
fore PET is usually not helpful in reaching a specific diagnosis. pathogenesis and management, in Knipe D.M., Howley P.M. (eds):
Tumor recurrence after complete excision is rare. Fields Virology (ed 5). Philadelphia, PA, Lippincott Williams & Wilkins,
In summary, focal FDG uptake in the skin or subcutane- 2007
ous tissues is a common incidental finding on PET. FDG 27. Egan C, Silverman E: Increased FDG uptake along dermatome
uptake is not specific for malignancy and may be due to in- on PET in a patient with herpes zoster. Clin Nucl Med 38:744-745,
2013
flammation, infection, or a benign tumor. Although a specific 28. Nguyen NC, Chaar BT, Osman MM: Prevalence and patterns of soft tissue
diagnosis may not always be possible, background clinical metastasis: Detection with true whole-body F-18 FDG PET/CT. BMC
history and morphologic features of the lesion on CT may Med Imaging 7:8, 2007
help in narrowing the differential diagnosis. 29. Beaman FD, Kransdorf MJ, Andrews TR, et al: Superficial soft-tissue
masses: Analysis, diagnosis, and differential considerations. Radiographics
27:509-523, 2007
References 30. Seo YY, Yoo I, Hyun OJ, et al: FDG uptake in fat necrosis following
1. Waki A, Fujibayashi Y, Yonekura Y, et al: Reassessment of FDG uptake transverse rectus abdominis myocutaneous (TRAM) flap reconstructed
in tumor cells: High FDG uptake as a reflection of oxygen-independent breasts: 3 cases. Clin Nucl Med 35:283-285, 2010
glycolysis dominant energy production. Nucl Med Biol 24:665-670, 1997 31. Lee SA, Chung HW, Cho KJ, et al: Encapsulated fat necrosis mimicking
2. Warburg O: Metabolism of tumours. Biochem Z 142:317-333, 1923 subcutaneous liposarcoma: Radiologic findings on MR, PET-CT, and US
3. Kubota R, Yamada S, Kubota K, et al: Intratumoral distribution of imaging. Skeletal Radiol 42:1465-1470, 2013
fluorine-18-fluorodeoxyglucose in vivo: High accumulation in 32. Segura S, Requena L: Anatomy and histology of normal subcutaneous
macrophages and granulation tissues studied by microautoradiography. fat, necrosis of adipocytes, and classification of the panniculitides.
J Nucl Med 33:1972-1980, 1992 Dermatol Clin 26:419-424, 2008
4. Ashley NT, Weil ZM, Nelson RJ: Inflammation: Mechanisms, costs, and 33. Huang CT, Yang WC, Lin SF: Positron-emission tomography
natural variation. Annu Rev Ecol Evol Syst 43:385-406, 2012 findings indicating the involvement of the whole body skin in
5. Paik JY, Lee KH, Choe YS, et al: Augmented 18F-FDG uptake in activated subcutaneous panniculitis-like T cell lymphoma. Ann Hematol 90:853-
monocytes occurs during the priming process and involves tyrosine 854, 2011
kinases and protein kinase C. J Nucl Med 45:124-128, 2004 34. Ravizzini G, Meirelles GS, Horwitz SM, et al: F-18 FDG uptake in
6. Condliffe AM, Kitchen E, Chilvers ER: Neutrophil priming: subcutaneous panniculitis-like T-cell lymphoma. Clin Nucl Med
Pathophysiological consequences and underlying mechanisms. Clin Sci 33:903-905, 2008
94:461-471, 1998 35. de Waal R, Cohen K, Maartens G: Systematic review of antiretroviral-
7. Vos FJ, Bleeker-Rovers CP, Oyen WJ: The use of FDG-PET/CT in patients associated lipodystrophy: Lipoatrophy, but not central fat gain, is an
with febrile neutropenia. Semin Nucl Med 43:340-348, 2013 antiretroviral adverse drug reaction. PLoS ONE 8:e63623, 2013
8. Youssef G, Leung E, Mylonas I, et al: The use of 18F-FDG PET in the 36. Carr A: HIV lipodystrophy: Risk factors, pathogenesis, diagnosis and
diagnosis of cardiac sarcoidosis: A systematic review and metaanalysis management. AIDS 17:S141-S148, 2003 (suppl 1)
including the Ontario experience. J Nucl Med 53:241-248, 2012 37. Bleeker-Rovers CP, van der Ven AJ, Zomer B, et al: F-18-
9. Valeyre D, Prasse A, Nunes H, et al: Sarcoidosis. Lancet 383:1155-1167, fluorodeoxyglucose positron emission tomography for visualization of
2014 lipodystrophy in HIV-infected patients. AIDS 18:2430-2432, 2004
10. Wanat KA, Rosenbach M: Cutaneous sarcoidosis. Clin Chest Med 38. Torriani M, Zanni MV, Fitch K, et al: Increased FDG uptake in association
36:685-702, 2015 with reduced extremity fat in HIV patients. Antivir Ther 18:243-248,
11. Sanchez M, Haimovic A, Prystowsky S: Sarcoidosis. Dermatol Clin 2013
33:389-416, 2015 39. Ozawa T, Okamura T, Harada T, et al: Accumulation of glucose in keloids
12. Li Y, Berenji GR: Cutaneous sarcoidosis evaluated by FDG PET. Clin with FDG-PET. Ann Nucl Med 20:41-44, 2006
Nucl Med 36:584-586, 2011 40. Koljevic-Markovic A, Orcurto MV, Doenz F, et al: Persistent FDG uptake
13. Kalb RF, Epstein W, Grossman ME: Sarcoidosis with subcutaneous around an inguinal mesh prosthesis 25 years after implantation. Clin
nodules. Am J Med 85:731-736, 1988 Nucl Med 32:242-243, 2007
14. Higgins EM, Salisbury JR, Du Vivier AW: Subcutaneous sarcoidosis. Clin 41. Aide N, Deux JF, Peretti I, et al: Persistent foreign body reaction around
Exp Dermatol 18:65-66, 1993 inguinal mesh prostheses: A potential pitfall of FDG PET. AJR Am J
15. Marcoval J, Moreno A, Mañá J, et al: Subcutaneous sarcoidosis. Dermatol Roentgenol 184:1172-1177, 2005
Clin 26:553-556, 2008 42. Prosch H, Mirzaei S, Oschatz E, et al: Case report: Gluteal injection site
16. Chowaniec M, Starba A, Wiland P: Erythema nodosum—review of the granulomas: False positive finding on FDG-PET in patients with
literature. Reumatologia 54:79-82, 2016 non-small cell lung cancer. Br J Radiol 78:758-761, 2005
17. Mañá J, Gómez-Vaquero C, Montero A, et al: Löfgren’s syndrome 43. Sogge SM, Fotos JS, Tulchinsky M: Bacillus Calmette-Guerin injections
revisited: A study of 186 patients. Am J Med 107:240-245, 1999 for melanoma immunotherapy: Potential for a false-positive PET/CT.
18. Paydas S: Sweet’s syndrome: A revisit for hematologists and oncologists. Clin Nucl Med 40:368-369, 2015
Crit Rev Oncol Hematol 86:85-95, 2013 44. Mentzel T: Cutaneous mesenchymal tumours: An update. Pathology
19. Cohen PR, Kurzrock R: Sweet’s syndrome and cancer. Clin Dermatol 46:149-159, 2014
11:149-157, 1993 45. Luzar B, Calonje E: Cutaneous fibrohistiocytic tumours—an update.
20. Yong AA, Tey HL: Paraneoplastic pemphigus. Australas J Dermatol Histopathology 56:148-165, 2010
54:241-250, 2013 46. Fletcher CD: Benign fibrous histiocytoma of subcutaneous and deep soft
21. Tilles G: Acne pathogenesis: History of concepts. Dermatology 229:1-46, tissue: A clinicopathologic analysis of 21 cases. Am J Surg Pathol
2014 14:801-809, 1990
22. Mawhorter SD, Effron D, Blinkhorn R, et al: Cutaneous manifestations 47. Laughlin CL, Carrington PR: Deep penetrating dermatofibroma. Dermatol
of toxoplasmosis. Clin Infect Dis 14:1084-1088, 1992 Surg 24:592-594, 1998
23. Kumar B, Muralidhar S: Cutaneous tuberculosis: A twenty-year 48. Richard D, Picard F: Brown fat biology and thermogenesis. Front Biosci
prospective study. Int J Tuberc Lung Dis 3:494-500, 1999 (Landmark Ed) 16:1233-1260, 2011
24. Gonzalez-Santiago TM, Drage LA: Nontuberculous mycobacteria: Skin 49. Dempersmier J, Sul HS: Shades of brown: A model for thermogenic fat.
and soft tissue infections. Dermatol Clin 33:563-577, 2015 Front Endocrinol (Lausanne) 6:71, 2015
ARTICLE IN PRESS
10 U. Metser and N. Tau

50. Lin D, Jacobs M, Percy T, et al: High 2-deoxy-2[F-18]fluoro-D-glucose 57. Combemale P, Valeyrie-Allanore L, Giammarile F, et al: Utility of
uptake on positron emission tomography in hibernoma originally thought 18F-FDG PET with a semi-quantitative index in the detection of
to be myxoid liposarcoma. Mol Imaging Biol 7:201-202, 2005 sarcomatous transformation in patients with neurofibromatosis type 1.
51. Kim JD, Lee HW: Hibernoma: Intense uptake on F18-FDG PET/CT. PLoS ONE 9:e85954, 2014
Nucl Med Mol Imaging 46:218-222, 2012 58. Chirindel A, Chaudhry M, Blakeley JO, et al: 18F-FDG PET/CT
52. Ferner RE, Gutmann DH: International consensus statement on malignant qualitative and quantitative evaluation in neurofibromatosis type 1
peripheral nerve sheath tumors in neurofibromatosis. Cancer Res patients for detection of malignant transformation: Comparison of early
62:1573-1577, 2002 to delayed imaging with and without liver activity normalization. J Nucl
53. Ducatman BS, Scheithauer BW, Piepgras DG, et al: Malignant peripheral Med 56:379-385, 2015
nerve sheath tumors. A clinicopathologic study of 120 cases. Cancer 59. Lan MY, Lan MC, Ho CY, et al: Pilomatricoma of the head and neck:
57:2006-2021, 1986 A retrospective review of 179 cases. Arch Otolaryngol Head Neck Surg
54. Walker L, Thompson D, Easton D, et al: A prospective study of 129:1327-1330, 2003
neurofibromatosis type 1 cancer incidence in the UK. Br J Cancer 60. Kwon D, Grekov K, Krishnan M, et al: Characteristics of pilomatrixoma
95:233-238, 2006 in children: A review of 137 patients. Int J Pediatr Otorhinolaryngol
55. Rasmussen SA, Yang Q, Friedman JM: Mortality in neurofibromatosis 78:1337-1341, 2014
1: An analysis using U.S. death certificates. Am J Hum Genet 68:1110- 61. Lim HW, Im SA, Lim GY, et al: Pilomatricomas in children: Imaging
1118, 2001 characteristics with pathologic correlation. Pediatr Radiol 37:549-555,
56. Ferner RE, Golding JF, Smith M, et al: [18F]2-fluoro-2-deoxy-D-glucose 2007
positron emission tomography (FDG PET) as a diagnostic tool for 62. Bulman JC, Ulualp SO, Rajaram V, et al: Pilomatricoma of childhood:
neurofibromatosis 1 (NF1) associated malignant peripheral nerve sheath A common pathologic diagnosis yet a rare radiologic one. AJR Am J
tumours (MPNSTs): A long-term clinical study. Ann Oncol 19:390-394, Roentgenol 206:182-188, 2016
2008

You might also like