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Chapter 9 · Hematology

Amyloidosis in the head and neck region usually mani-

fests as vocal cord thickening causing hoarseness of the voice, tongue intrinsic muscles deposition causing macroglossia, supra- and subglottic larynx, and periorbital deposition causing bleeding and ecchymoses (the raccoon sign). Amyloidosis of the paranasal sinuses can be seen as a sinusoidal mass with “ u y-bone appearance” of the adjacent bone.

Signs on Plain Radiographs

5 Pulmonary amyloidosis can be seen as a diffuse

interstitial nodular pattern or (rarely) as a single solitary mass (amyloidoma) (. Fig. 9.9.43 ).

5 When an amyloidoma involves a bone, it is usually

visualized as an osteolytic mass lesion.

5 Dialysis-related amyloid arthropathy is detected as

periarticular bony cysts or erosions.

Signs on US

5 Amyloidosis is one of the rare cases of enlarged

kidneys with high echogenicity.

5 Hepatic amyloidosis may appear as multiple foci of

increased liver parenchymal echogenicity.

Signs on CT and MRI

5 The affected kidney is normal or larger than

normal in early stages of amyloidosis. In later stages, renal fibrosis shrinkage with parenchymal calcification is often seen.

5 Hepatic amyloidosis can be seen on nonenhanced CT

as a di usely enlarged liver with hypoattenuation. Other radiological signs are nonspeci c.

5 Splenic manifestations of amyloidosis include

splenomegaly, calcification, and lack of enhancement after contrast injection. The lack of contrast enhancement is thought to be due to vascular amyloid angiopathy and diffuse parenchymal infiltration by amyloid proteins.

5 Small and large bowel involvement results in

diffuse or nodular wall thickening.

5 Cardiac amyloidosis can show many nonspecific

findings, such as biventricular hypertrophy that mimics hypertrophic cardiomyopathy (. Fig. 9.9.44 ), thickening of the papillary muscles and the valvular leaflets, and pleural or pericardial effusion. Biatrial enlargement and enhancement is a characteristic sign, but unfortunately not always seen. On MRI, a relatively characteristic pattern of myocardial amyloidosis seen on postgadolinium injection consists of strong subendocardial and subepicardial late enhancement (zebra enhancement pattern) (. Fig. 9.9.45 ).

. Fig. 9.9.43 Posteroanterior plain radiograph ( a ) and coronal HRCT ( b ) of a patient with multiple myeloma who developed pulmonary

amyloidosis shows di use bilateral nodular interstitial pattern lung disease

9.9 · Amyloidosis

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. Fig. 9.9.44 Short-axis white blood pool cardiac MRI in diastolic ( a ) and systolic ( b ) phases show hypertrophy of the right and left

ventricles in a patient with systemic amyloidosis

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. Fig. 9.9.45 Axial, four-chambers postcontrast cardiac MR

illustration of a patient with cardiac amyloidosis shows subendocardial and subepicardial enhancement that is described as a zebra enhancement pattern

5 Pulmonary amyloidosis on HRCT may resemble the

features of bronchiolitis obliterans, may diffuse interstitial nodular pattern (nodules <15mm in diameter) which may cause a “budding tree” appearance, or may (rarely) present as a solitary solid mass with calcification (amyloidoma) (. Fig. 9.9.43 ). Tracheal and bronchial wall

thickening are other characteristic signs of amyloidosis of the bronchial tree.

5 Paranasal sinuses amyloidoma is seen as a mass

with “ u y-bone appearance” of the adjacent bone. However, a biopsy is required to con rm diagnosis.

5 On MRI, synovial thickening that resembles

pigmented villonodular synovitis can be seen, which characteristically lacks the chronic hemorrhage and hemosiderin T1 and T2 hypointense signal intensities.

5 Amyloid proteins on MRI typically show low T1 and

T2 signal intensities and contrast enhancement. Therefore, signs of high signal intensity on T2W images in amyloidosis are usually due to the in ammatory reaction evoked by the amyloidosis, not by the amyloid proteins themselves.

5 Cerebral amyloidosis may present on

noncontrast-enhanced CT as intracranial hemorrhage due to CAA or (rarely) diffuse leptomeningeal thickening and enhancement.

5 Amyloidoma in any body region is usually seen as a

solid tissue mass that may cause bone osteolysis and contains calci cation. However, this appearance is nonspeci c, and biopsy is crucial to establish the diagnosis.

5 Dialysis-related amyloid arthropathy is detected on CT

as bony erosions and as formation of bony cysts. On MRI, the amyloid changes are detected as thickening and irregularity of the supraspinatus tendon, thickening of the iliofemoral portion of the hip joint capsule, and  uid collection within the bursae of the joints. Soft-tissue amyloid deposition can be seen in the spine, carpal tunnel, and knee synovium as typical low signal intensity on both T1W and T2W images.

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Chapter 9 · Hematology

Further Reading

Garcia-Muñoz R, et al. Splenic marginal zone lymphoma

with Evans’ syndrome, autoimmunity, and peripheral gamma/delta T cells. Ann Hematol. 2009;88:177–8. doi:10.1007/s00277-008-0555-z.

Máiz L, et al. Bronchiolitis obliterans organizing pneumonia

associated with Evans syndrome. Respiration. 2001;68:631–4.

Miyamae T, etal. An infant with γ-globulin-induced hypersensi-

tivity syndrome who developed Evans’ syndrome a er a second γ-globulin treatment. Mod Rheumatol. 2004;14:314–9.

Savasan S, etal.  e spectrum of Evans’ syndrome. Arch Dis

Child. 1997;77:245–8.

Shiozawa Z, etal. Superior sagittal sinus thrombosis associ-

ated with Evans’ syndrome of haemolytic anaemia. J Neurol. 1985;232:280–2.

Tsang KWT, etal. Rhodococcus equi lung abscess complicat-

ing Evans’ syndrome treated with corticosteroid. Respiration. 1998;65:327–30.

Ucci G, etal. A case of Evans’ syndrome in a patient with

ulcerative colitis. Dig Liver Dis. 2003;35:439–41.

9.11 Other Lymphatic Disorders

 is topic discusses some of the uncommon lymphatic disorders occasionally encountered in radiology and that can be mistaken initially for lymphoma or in ammatory conditions causing lymphadenopathy.

Castleman’s Disease (Angiofollicular Lymph Node Hyperplasia)

Castleman disease (CD) is a rare benign process of unknown cause, characterized by lymph nodes hyperplasia.

CD is liable to be misdiagnosed as other hypervascular tumors by radiology and pathology examinations. Lymph node hyperplasia may occur anywhere along the lymphatic chain within the body; however, it is commonly described in the mediastinum, abdomen, and pelvis.

 e main pathology in CD concerns lymph nodes hyperplasia and the related small blood vessels.  e lymph nodes are enlarged with high blood vessel proliferation and hypervascularity. CD is divided into two types: localized type and di use type.

 e localized type is characterized by proliferation of the lymph nodes in a certain region within the body. Di erential diagnoses of the localized type include tuberculosis lymphadenitis (ruled out by TB serology) and pheochromocytoma due to its hypervascularity (rules out by biochemistry investigations). CD diagnosis should be considered in di erential diagnosis of hypervascular tumor in the retroperitoneum.

 e di use type is characterized by lymph node proliferation through the body.  e main di erential diagnosis is lymphoma. Lymph node biopsy is the gold standard method to diagnose CD.

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Signs on CT

5 There are enlarged lymph nodes located within

the mediastinum or the retroperitoneum (. Figs. 9.11.47 and 9.11.48 ).

5 The lymph nodes in CD are characterized by

homogenous high-contrast enhancement in the early phase of dynamic enhancement that can exceed the enhancement of pheochromocytoma due to the hypervascularity of the lymph nodes. The high enhancement persists in the delayed phases.

5 Typically, there is absence of necrosis or cystic

changes within the enlarged lymph nodes, due to the abundant vascular supply. However, cystic changes may be found in 22 % of cases, especially when the lymph node is >5cm in diameter.

5 Punctuate or coarse calcification may be seen in

30 % of cases (lymphomas do not calcify unless treated).

5 A thin rim-like enhancement sign may be noticed

in the arterial phase, with several enhancing feeding vessels that surround the nodes.

5 To differentiate CD from pheochromocytoma in the

retroperitoneum, MRI should be done. Pheochromocytoma show higher signal intensity on T2W images compared to CD.Contrast-enhanced images may be similar due to the high vascular blood supply of the lymph nodes in CD.

5 CD shows higher contrast enhancement than any

other retroperitoneal sarcoma.

. Fig. 9.11.47 Axial abdominal portal phase,

contrast-enhanced CT shows diffuse lymphadenopathy in the retroperitonium around the aorta and the inferior vena cava ( arrowheads ) in a patient with Castleman’s disease

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Chapter 9 · Hematology

Kimura’s Disease

Kimura’s disease (KD) is a chronic in ammatory disease characterized by tumor-like so -tissue swelling and lymphoid tissue hyperplasia (. Fig. 9.11.49 ).

KD is characterized histopathologically by lymphoid hyperplasia with so -tissue in ltration by eosinophils, which is a constant  nding in this disease.  e cause of this disease is unknown, but it is thought to be caused by chronic allergic reaction due to the eosinophilia and high serum immunoglobulin E in patients with KD.

KD has predominance in young males and is usually seen in Asian populations, especially in Japan and China (80 %). Patients o en present with asymptomatic, unilateral so tissue swelling involving lymph nodes or salivary glands (e.g., the parotid glands). Regional lymphadenopathy is found in 66 % of cases.  e head and neck region is a ected in 70 % of cases. Atopic disorders can be seen in patients with KD.Rare manifestations include masses formation in the

. Fig. 9.11.48 Coronal abdominal portal phase,

contrast-enhanced CT of the same patient shows the enlarged lymph nodes separating the inferior vena cava from the aorta ( arrowhead )

external auditory meatus, tongue, orbits, epiglottis, larynx, groin (15 %), and extremities (12 %). Nephrotic syndrome is found in 12 % of cases.

De nite diagnosis requires mass biopsy with laboratory evidence of eosinophilia that is not related to parasitic infection.

Kikuchi–Fujimoto Disease (Histiocytic Necrotizing Lymphadenitis)

Kikuchi–Fujimoto disease (KFD) is a rare, self-limiting condition, characterized by the development of fever, weight loss, malaise, and lymphadenitis (commonly cervical).

KFD is o en mistaken for tuberculous lymphadenitis, lymphoma, systemic lupus lymphadenitis, and infectious lymphadenitis.  e misdiagnosis rate is up to 40 % of cases.

 e disease is self-limiting and benign, with a course lasting 6–8 weeks.  e recurrence rate is 3 % of cases. Laboratory  ndings are not speci c and usually show high C-reactive protein and erythrocyte sedimentation rate, mild lymphocytosis, leukopenia, and atypical lymphocytes. De nite diagnosis is done by  ne-needle lymph node biopsy.

 e disease is of unknown origin, a ects mainly females (mean age of 30 years), and may be associated with Epstein– Barr virus activation and systemic lupus erythematosus.

Signs on CT

Neck and mediastinal CT often show lymphadenopathy similar to the picture seen in lymphoma and tuberculous adenitis. History, laboratory investigations, and the biopsy report are the main elements for establishing the diagnosis.

. Fig. 9.11.49 An illustration demonstrating left parotid

enlargement in a patient with Kimura disease

9.12 · Mastocytosis

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Signs on CT

5 When the salivary glands are affected, an

irregularly shaped subcutaneous mass with heterogeneous contrast enhancement is commonly found. The adjacent bone is often not disturbed.

5 Enlargement of the lachrymal gland in a unilateral

or bilateral fashion, mimicking Sjögren’s syndrome, may be seen.

5 Abdominal lymphadenopathy may be enlarged,

mimicking lymphoma or localized CD.

Signs on MRI

MR features are nonspeci c, and diagnosis is essentially by laboratory investigation and biopsy. MR examination helps to exclude other di erential diagnoses.

Further Reading

Chen HC, etal. Systemic lupus erythematosus with simul-

taneous onset of Kikuchi-Fujimoto’s disease complicated with antiphospholipid antibody syndrome: a case report and review of the literature. Rheumatol Int. 2005; 25:303–6.

Chidambara Murthy S, et al. Kikuchi’s disease associated

with systemic lupus erythematosus. Indian J Dermatol Venereol Leprol. 2005;71:338–41.

Ching ASC, etal. Extranodal manifestations of Kimura’s dis-

ease: ultrasound features. Eur Radiol. 2002;12:600–4.

Hiwatashi A, etal. Kimura’s disease with bilateral auricular

masses. Am J Neuroradiol. 1999;20:1976–8.

Hrycek A, et al. Kikuchi-Fujimoto disease: a case report.

Rheumatol Int. 2005;26:179–81.

Irsutti M, etal. Castleman disease: CT and MR imaging

features of a retroperitoneal location in association with paraneoplastic pemphigus. Eur Radiol. 1999;9: 1219–21.

Jeong YY, etal. Imaging of Kimura’s disease involving teh

abdomen. AJR Am J Roentgenol. 2006;187:W131–2.

Kaicker S, etal. PET-CT scan in patient with Kikuchi disease.

Pediatr Radiol. 2008;38:596–7.

Kodama T, etal. Kimura’s disease of the lacrimal gland. Acta

Opthalmol Scand. 1998;76:374–7.

Liu PI, etal. Kimura’s disease in upper arm: a case report and

imaging  ndings. Chin J Radiol. 2007;32:153–6.

Ortak T, etal. Kimura disease: a brief clinical report. Eur J

Plast Surg. 2008;31:253–7.

Zheng X, etal. Localized Castleman disease in retroperito-

neum: newly discovered features by multi- detector helical CT.Abdom Imaging. 2008;33:489–92.

Zhou LP, etal. Imaging  ndings in Castleman disease of the

abdomen and pelvis. Abdom Imaging. 2008;33:482–8.

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9.12 Mastocytosis

Mastocytosis is a group of diseases characterized by abnormal proliferation of mast cells both in the bone marrow and the peripheral tissues such as the skin, gastrointestinal tract, liver, and spleen. Mastocytosis not only a ects predominantly children (75 %) but also adults with more severe manifestations (25 %). Mastocytosis is classi ed into four clinical categories based on their clinical manifestations, prognosis, and pathological  ndings: 1 . Indolent mastocytosis : this type generally has a good prog-

nosis. It is subdivided into patients with isolated skin mastocytosis ( type IA , urticaria pigmentosa ) and systemic mastocytosis with visceral and bone involvement ( type IB ) .

2 . Mastocytosis with hematologic disease : this type is

characterized by mastocytosis associated with myeloproliferative/myelodysplastic disorders.  e prognosis is determined based on the severity of the hematologic disease.

3 . Aggressive mastocytosis : this type is characterized by

rapidly deteriorating clinical course with increase mastocytes burden.  e patient develops eosinophilia with generalized lymphadenopathy; prognosis is poor.

4 . Mast cell leukemia : this type is extremely rare and carries

the worst prognosis.

Patients with urticaria pigmentosa present classically with small, yellow-tan to reddish brown macules. Nodules or plaque-like lesions may be seen.  ese skin lesions are seen in the upper and lower limbs sparing the palms, soles, face, and scalp.  e thorax and the abdomen may be a ected.  e skin lesions are also found in 90 % of patients with systemic mastocytosis and 50 % in mastocytosis with hematological disorders.

Darier ’ s sign is a term used to describe erythematous skin lesion that rises a er rubbing or scratching lesions of cutaneous mastocytosis.  e erythema appears 2–5min a er rubbing the skin and lasts from 30min to several hours. Mast cells contain histamine, heparin, and prostaglandin. When the skin is rubbed, there is degranulation of mast cells with the release of mast cell contents within the dermis. Darier’s sign is caused by the e ect of histamine. Darier’s sign can be also seen in leukemia cutis, lymphoma, and Langerhans cell histiocytosis. Mastocytomas are rare skin lesions that typi- cally occur before 6 months of age as solitary or multiple skin nodules.

Patients with systemic mastocytosis present o en with abdominal pain, diarrhea, nausea, peptic ulcers, and gastrointestinal bleeding. Symptoms can be precipitated by narcotics, nonsteroidal anti-in ammatory drugs, penicillin, cold or hot temperature, exercise and emotions, and alcohol. Other features include malabsorption, hepatosplenomegaly (50 %), and lymphadenopathy (60 %). Laboratory investigations classically show anemia (50 %) and eosinophilia (25 %). Bleeding tendency may occur due to high levels of heparin released by mast cells or vitamin K de ciency due to malabsorption.

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Chapter 9 · Hematology

Diagnosis is established by measurement of serum concentration of both mature and α-tryptase, which re ects mast cell numbers (normal level up to 11ng/mL). Systemic mastocytosis is strongly suspected if serum tryptase level is >20 ng/ mL. is test is best done during acute events caused by mastocytosis.  e other method to detect mastocytosis is to measure 24-h urinary histamine concentration.  e latter method is used when serum tryptase level measurement is unavailable.

Signs on Chest Radiographs

Pulmonary mastocytosis is rarely detected in systemic mastocytosis as bilateral di use interstitial nodular pattern.

Signs on Skeletal Radiographs

1. Classically, mastocytosis is seen as multiple nodular mixed osteolytic/osteosclerotic lesions that di usely a ects the skeleton (. Figs. 9.12.50 and 9.12.51 ). The osteolytic lesions are caused by granulomatous formation. In contrast, sclerotic lesions are caused by the e ect of histamine which is known to stimulate the formation of  brous tissue. Fibrous tissue will be later converted into osteoid, which will be converted into bony sclerotic lesions.

2. Osteoporosis may be seen due to the high heparin e ect or the bone resorption e ect of prostaglandin produced by mast cells.

. Fig. 9.12.50 Anteroposterior and lateral plain radiographs of the lumbar spine of a patient with

systemic mastocytosis show the classical, military, osteolytic/osteosclerotic pattern (both a & b )

9.13 · Myelo brosis andMyeloid Metaplasia

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. Fig. 9.12.51 Anteroposterior pelvic radiograph of the

same patient in . Fig. 9.12.50 show the classical, military, osteolytic/osteosclerotic pattern of mastocytosis

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reaction causing collagen  brosis, osteosclerosis, and angiogenesis of the bone marrow. MMM is accompanied by widespread extramedullary hematopoiesis. MMM is typically seen in patients >65 years of age. Death usually occurs 2–3 years a er the  rst onset of the disease. Clinical presentation is divided to myeloproliferation, cytopenia, and constitutional symptoms.

Myeloproliferative symptoms include splenomegaly, hepatomegaly, lymphadenopathy bone pain, portal hypertension (10 %), risk of leukemia, and extramedullary hematopoiesis. Cytopenic symptoms include fatigue, thrombosis, and bleeding. Constitutional symptoms include fatigue, weight loss, night sweat, and hyperuricemia that can lead to gout (5–20 %), arthralgia, and fever. Rare CNS manifestations due to meningeal hematopoiesis include headache, seizures, altered consciousness, and hemiplegia.

Diagnosis is con rmed by laboratory investigations which will show anemia, thrombocytopenia, and characteristic teardrop red blood cells.  e white blood count is initially high and then drops (leukopenia). Bone marrow aspiration histological results are nondiagnostic.

Signs on Barium Follow-Through

1. There is di use bowel wall thickening with nodular mucosa due to in ltration of the intestinal lamina propria by mast cells. Di erential diagnoses include Whipple’s disease, amyloidosis, and lymphangiectasia.

2. Multiple, large bull’s eye lesions may be detected. Di erential diagnoses of intestinal bull’s eye lesions include lymphoma, metastases, Kaposi sarcoma, and aberrant pancreas.

Signs on MRI

There is mosaic bone marrow pattern with high T2 signal intensity surrounded by hypointense rim, best to be seen in the vertebral column.

Selected References

Avila NA, etal. Pulmonary and ovarian manifestations of sys-

temic mastocytosis. AJR. 1996;166:969–70.

Avila NA, etal. Mastocytosis: magnetic resonance imaging pat-

terns of marrow disease. Skeletal Radiol. 1998;27:119–26.

Haney K, etal. MRI characteristics of systemic mastocytosis

of the lumbosacral spine. Skeletal Radiol. 1996;25:171–3.

Jabbour SA, etal. Rare syndromes. Clin Dermatol. 2006;24:

299–316.

Quinn SF, etal. Bull’s-eye lesion: a new gastrointestinal presen-

tation of mastocytosis. Gastrointest Radiol. 1984;9:13–5.

9.13 Myelo brosis andMyeloid Metaplasia

Myelo brosis with myeloid metaplasia (MMM) is a rare disease characterized by abnormal stem cell proliferation within the bone marrow that is accompanied by intense bone marrow

Signs on Radiographs

1. There is di use bone sclerosis that can be patchy mimicking Paget’s disease or  uorosis with sandwich vertebrae. Unlike Paget’s disease, serum alkaline phosphatase levels are normal in myelo brosis.

2. Periostitis can be seen along the diaphyses of long bones mimicking osteosarcoma.

Signs on CT

1. Lymphadenopathy, massive splenomegaly, and hepatomegaly are usually present.

2. Bilateral paraspinal masses may be seen in the mid-thoracic segment due to extramedullary hematopoiesis.

3. Bilateral symmetrical nephromegaly without signs of hydronephrosis can be seen due to hematopoiesis. This sign is usually seen in in ltrative processes a ecting the kidneys like nephroblastomatosis, Beckwith–Wiedemann syndrome, acute glomerulonephritis, type I glycogen storage disease, and nephritic syndrome.

Signs on MRI

1. The bone marrow contains multiple patchy low T1–T2 signal intensity areas representing  brosis (. Fig. 9.13.52 ); however, low T1–T2 signal intensity lesions within the bone marrow can be seen in MRI in in ltrative processes like leukemia.

2. Extramedullary hematopoiesis masses can be seen in the paraspinal muscles in the mid-thoracic segments

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Chapter 9 · Hematology

extending into the spinal canal compressing the spinal cord or extending into the neural foramina compressing the spinal nerves. Characteristically, the masses show low signal in T1W images, high signal intensity on T2W images, and di use homogenous contrast enhancement after contrast injection (. Fig. 9.13.53 ).

3. CNS meningeal hematopoiesis is a rare complication of MMM that presents as intracranial masses located within the meninges or the falx cerebri and enhances homogenously after contrast injection similar to meningiomas. The history and clinical presentation is important to di erentiate between the two. Extramedullary hematopoiesis masses are sensitive to radiotherapy.

. Fig. 9.13.52 Sagittal T1W & STIR-W MR images of a patient with myelo brosis showing reduced signal intensity of the bone marrow

in the lumbar vertebrae ( arrowheads in a ) with increased T2 signal intensity of the posterior vertebral elements due to active extramedullary hematopoiesis ( arrow in b )

9.13 · Myelo brosis andMyeloid Metaplasia

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. Fig. 9.13.53 Axial T2W image of the same patient in

. Fig. 9.13.52 shows paraspinal muscle masses with high T2

signal intensity due to extramedullary hematopoiesis ( arrows )

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Selected References

Fernback SK, etal. Extramedullary hematopoiesis in the kid-

neys in infants siblings with myelo brosis. Pediatr Radiol. 1992;22:211–2.

Guermazi A, etal. Imaging of spinal cord compression due to

thoracic extramedullary haematopoiesis in myelo brosis. Neuroradiology. 1997;39:733–6.

Guermazi A, etal. Imaging  ndings in patients with myelo -

brosis. Eur Radiol. 1999;9:1366–75.

Mesa RA, etal. Myelo brosis and myeloid metaplasia: disease

review and non-transplant treatment options. Best Pract Res Clin Haematol. 2006;19(3):495–517.

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