Alphabetical list of conditions

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Alphabetical list of conditions


An AD (80% new mutation rate) skeletal dysplasia resulting from activating mutations in fibroblast growth factor receptor type 3 (FGFR3). This results in impaired enchondral bone growth.

Acquired immune deficiency syndrome

Widespread use of highly active antiretroviral therapy (HAART) has significantly changed the patterns of presentation of HIV-related disease in adults in developed nations. Opportunistic infections are less common, whereas non-AIDS-defining cancers and disorders related to immune reconstitution are being seen with greater frequency. In non-developed countries, without widespread access to HAART, the profile of AIDS-related diseases has changed little.

A Chest

Many patients present acutely with chest presentations. The likely causes of chest infection will vary with CD4+ count: below 500 cells/µl but above 200 cells/µl, bacterial, mycobacterial and candidal infections predominate. Below 200 cells/µl predisposes patients to pneumocystis pneumonia and with counts below 100 cell/µl, viral, protozoal and other fungal infections become common.

CXR and CT changes rarely provide definitive diagnosis.

Opportunistic infections

1. Pneumocystis jiroveci – most common opportunistic (fungal) infection. Associated with CD4+ count < 200 cells/µl. With effective chemoprophylaxis and antiretroviral treatment, incidence has fallen. Chest radiographs may be normal at presentation but typically progresses to show bilateral perihilar or diffuse ground-glass opacification and reticulation. Without treatment, there is rapid progression to air-space opacification. Diffuse ground-glass opacification, thickened interlobular septa and consolidation are the key findings on HRCT. Thin-walled cysts are present in ~30%. Less common imaging features include:

2. Mycobacterium tuberculosis – an important infection in HIV-positive patients, and diagnosis is difficult. Imaging features depend on severity of immune compromise: depressed but near-normal CD4+ levels are associated with similar radiological features to non-immunocompromised patients (upper lobe nodules ± cavitation). With more severe depression, more atypical patterns (non-upper lobe predilection; lower propensity for cavitation) and disseminated infection are likely.

B Abdomen


Dependent on level of immunocompromise: CD4 < 400 – TB, Candida; CD4 < 200 – Candida, Histoplasma, Cryptosporidium, Pneumocystis; CD4 < 100 – CMV, herpes simplex, MAI.

1. Primary HIV – oesophageal ulceration.

2. Candida – usually oropharynx and oesophagus. AIDS defining. Mucosal plaques, fold thickening, ‘shaggy’ oesophagus on barium swallow.

3. Herpes – small discrete ulcers on barium swallow.

4. CMV – most common gastrointestinal infection. Can occur anywhere but usually lower gastrointestinal tract. Oesophagus – large mid-oesophageal ulcer; CMV gastritis, enteritis and colitis – superficial progressing to deep ulceration (mimic Crohn’s), extensive bowel wall thickening on CT, US; segmental or diffuse, lymphadenopathy not prominent.

5. TB – ileocaecal jejunoileum most common sites (upper gastrointestinal tract less common). Segmental ulcers, wall thickening, strictures, and mass-like lesions of the caecum and terminal ileum. Regional low-attenuation necrotic lymphadenopathy. Hepatosplenomegaly (occasional focal lesions).

6. Chlamydia trachomatis – causes lymphogranuloma venereum. Generally in men who have sex with men as a HIV coinfection. Introduced anally and causes a proctocolitis. May have inguinal lymphadenopathy and collections.

7. Mycobacterium avium complex – usually small bowel. Mimics Whipple’s (irregular fold thickening and mild dilatation). Prominent lymphadenopathy. Hepatosplenomegaly (occasional focal lesions).

8. Cryptosporidium – diffuse fold thickening, flocculation of barium (mimics sprue). No lymphadenopathy.

9. Rochalimaea henselae (peliosis hepatis) – fever, sweats, right upper quadrant pain. Sonographically liver inhomogeneous, with hyperechoic and hypoechoic regions. Cavities may be visible on CT (if large).

10. PCP – liver/spleen/kidneys – hypoechoic/hypoattenuating masses or multiple tiny echogenic/hyperattenuating foci (calcified).

Common symptoms/signs

1. Dysphagia – common. Usually due to candidiasis, but occasionally caused by viral oesophagitis or Kaposi’s sarcoma.

2. Hepatosplenomegaly – non-specific. Seen in many infections (CMV, TB, MAI) and lymphoma.

3. Diarrhoea – common. Usually CMV colitis if mild, or Cryptosporidium (protozoa) if severe. Giardia, Clostridium difficile and Mycobacterium may also occur.

4. Retroperitoneal/mesenteric lymphadenopathy

5. AIDS cholangiopathy – right upper quadrant pain, nausea, vomiting and fever. Due to infection by CMV or Cryptosporidium. Gallbladder wall thickening, pericholecystic fluid, intrahepatic and extrahepatic bile duct strictures, diverticula, intraluminal filling defects and strictures of the juxta-ampullary pancreatic duct.

6. HIV nephropathy – proteinuria and rapidly progressive renal failure. Usually, globally enlarged kidneys.

7. Pyelonephritis and renal abscesses.

D Musculoskeletal

Further Reading

Boiselle, P. M., Crans, S. A., Jr., Kaplan, M. A. The changing face of Pneumocystis carinii pneumonia in AIDS patients. AJR Am J Roentgenol. 1999; 172:1301–1309.

Burns, J., Shaknovich, R., Lau, J., et al. Oncogenic viruses in AIDS: mechanisms of disease and intrathoracic manifestations. AJR Am J Roentgenol. 2007; 189:1082–1087.

Ferrand, R. A., Desai, S. R., Hopkins, C., et al. Chronic lung disease in adolescents with delayed diagnosis of vertically-acquired HIV infection. Clin Infect Dis. 2012; 55:145–152.

Guihot, A., Couderc, L. J., Rivaud, E., et al. Thoracic radiographic and CT findings of multicentric Castleman disease in HIV-infected patients. J Thorac Imaging. 2007; 22:207–211.

Kuhlman, J. E. Imaging pulmonary disease in AIDS: state of the art. Eur Radiol. 1999; 9:395–408.

Logan, P. M., Finnegan, M. M. Pictorial review: pulmonary complications in AIDS: CT appearances. Clin Radiol. 1998; 53:567–573.

Major, N. M., Tehranzadeh, J. Musculoskeletal manifestations of AIDS. Radiol Clin North Am. 1997; 35:1167–1190.

Provenzale, J. M., Jinkins, J. R. Brain and spine imaging findings in AIDS patients. Radiol Clin North Am. 1997; 35:1127–1166.

Redvanly, R. D., Silverstein, J. E. Intra-abdominal manifestations of AIDS. Radiol Clin North Am. 1997; 35:1083–1126.

Reeders, J. W., Goodman, P. C., 2001. Radiology of AIDS. Springer, Heidelberg.

Reeders, J. W., Yee, J., Gore, R. M., et al. Gastrointestinal infection in the immunocompromised (AIDS) patient. Eur Radiol. 2004; 14(Suppl 3):E84–E102.

Restrepo, C., Lemos, D., Gordillo, H. Imaging findings in musculoskeletal complications of AIDS. Radiographics. 2004; 24:1029–1049.

Restrepo, C. S., Ocazionez, D. Kaposi’s sarcoma: imaging overview. Semin Ultrasound CT MR. 2011; 32(5):456–469.

Richards, P. J., Armstrong, P., Parkin, J. M., et al. Chest imaging in AIDS. Clin Radiol. 1998; 53:554–566.

Spencer, S. P., Power, N., Reznek, R. H. Multidetector computed tomography of the acute abdomen in the immunocompromised host: a pictorial review. Curr Probl Diagn Radiol. 2009; 38(4):145–155.

Acquired immune deficiency syndrome (AIDS) in children

The majority of cases (~80%) are due to transmission from an infected mother, with a 25% risk of acquiring infection. Acquisition from transfusions (in the neonatal period or because of diseases such as thalassaemia and haemophilia) is rare in the West but still occurs in developing countries. 50% of those infected congenitally will present in the first year of life.

AIDS in children differs from AIDS in adults in the following ways:


1. PCP – may be localized initially but typically there is rapid progression to generalized lung shadowing, which is a mixed alveolar and interstitial infiltrate. 50% of infections occur at age 3–6 months. Two-thirds of infections are the first and only infective episode.

2. CMV pneumonia.

3. LIP/PLH – in 50% of patients. Insidious onset of clinical symptoms. CXR shows a diffuse, symmetrical reticulonodular or nodular pattern (2–3 mm in diameter) which is most easily seen at the bases and periphery of the lungs ± hilar or mediastinal lymphadenopathy. The nodules consist of collections of lymphocytes and plasma cells without any organisms. Children with LIP are more likely to have generalized lymphadenopathy, salivary gland enlargement (particularly parotid) and finger clubbing than those with CXR changes due to opportunistic infection, and the prognosis for LIP is better. Long-standing LIP may be complicated by lower lobe bronchiectasis or cystic lung disease (resembling that seen in histiocytosis).

4. Mediastinal or hilar adenopathy may be secondary to PLH, M. tuberculosis, MAI, CMV, lymphoma or fungal infection.

5. Cardiomyopathy, dysrhythmias and unexpected cardiac arrest.


1. Hepatosplenomegaly – due to chronic active hepatitis, hepatitis A or B, CMV, EBV and M. tuberculosis, generalized sepsis, tumour (fibrosarcoma of the liver) or congestive cardiac failure.

2. Oesophagitis – Candida, CMV or herpes simplex.

3. Chronic diarrhoea – in 40–60% of children. Infectious agents are only infrequently found but include Candida, CMV and Cryptosporidium. Radiological findings are non-specific and include a malabsorption-type pattern with thickening of bowel wall and mucosal folds and dilatation. Fine ulceration may be seen.

4. Pneumatosis coli.

5. Mesenteric, para-aortic and retroperitoneal lymphadenopathy – due to MAI, lymphocytic proliferation (lymph-node syndrome), non-Hodgkin’s lymphoma or Kaposi’s sarcoma (rare in childhood).

6. HIV nephropathy – children may present with proteinuria, fluid and electrolyte imbalances and/or acute or chronic renal failure. US shows enlarged echogenic kidneys and CT shows enlarged pyramids. Simple cysts may be present.

7. UTI – in up to 50% of AIDS patients. May be due to common organisms or unusual agents, e.g. CMV, Cryptococcus, Candida, Aspergillus, Mycobacterium and Pneumocystis.


1. HIV encephalopathy is divided into two types:

Imaging may show:

2. Intracranial calcifications – in up to 33% of HIV-infected children. Usually bilateral and symmetrical and most commonly seen in the globus pallidus and putamen; less commonly in the subcortical frontal white matter and cerebellum. Usually not seen before 10 months of age; early calcifications are more likely because of congenital infections.

3. Malignancy – most commonly high-grade B-cell lymphoma associated with EBV infection.

4. Cerebrovascular accidents.

5. Infections:

6. Chronic otitis media and sinusitis.

Further Reading

Haller, J. O. AIDS-related malignancies in pediatrics. Radiol Clin North Am. 1997; 35(6):1517–1538.

Haller, J. O., Cohen, H. L. Pediatric HIV infection: an imaging update. Pediatr Radiol. 1994; 24:224–230.

Martinoli, C., Pretolesi, F., Del Bono, V., et al. Benign lymphoepithelial parotid lesions in HIV-positive patients: spectrum of findings at gray-scale and Doppler sonography. AJR Am J Roentgenol. 1995; 165(4):975–979.

Miller, C. R. Pediatric aspects of AIDS. Radiol Clin North Am. 1997; 35:1191–1222.

Safriel, Y. I., Haller, J. O., Lefton, D. R., et al. Imaging of the brain in the HIV-positive child. Pediatr Radiol. 2000; 30:725–732.

Stoane, J. M., Haller, J. O., Orentlicher, R. J. The gastrointestinal manifestations of pediatric AIDS. Radiol Clin North Am. 1996; 34(4):779–790.

Zinn, H. L., Haller, J. O. Renal manifestations of AIDS in children. Pediatr Radiol. 1999; 29:558–561.


The effect of excessive growth hormone on the mature skeleton.


The absence of homogentisic acid oxidase leads to the accumulation of homogentisic acid and its excretion in sweat and urine. The majority of cases are AR.

Ankylosing spondylitis

A seronegative spondyloarthropathy manifesting as an inflammatory arthritis affecting the sacroiliac joints and entire spine, leading ultimately to fusion. Onset 20–40 years; M : F ratio = 3 : 1.

Axial skeleton

1. Involved initially in 70–80%. Initial changes in the sacroiliac joints followed by the thoracolumbar and lumbosacral regions. The entire spine may be involved eventually.

2. The radiological changes in the sacroiliac joints (see 3.12) are present at the time of the earliest spinal changes. MRI most sensitive technique for early disease and all changes except syndesmophytes.

3. Spondylitis – anterior and posterior erosion of vertebral end-plates (Romanus). Enthesitis of annulus fibrosis. Then sclerosis causing ‘shiny corner’ (osteitis).

4. Discovertebral – inflammatory involvement of intervertebral disc (Andersson).

5. Syndesmophytes – bony outgrowths from vertebral margins.

6. Squaring of vertebrae – due to bone proliferation.

7. Arthritis – facet, costovertebral and costotransverse joints (synovitis, erosion, ankylosis).

8. Enthesitis – interspinous ligaments with osteitis.

9. Ankylosis – fusion of spine from 5–7 plus bony extension through 4. Leads to ‘bamboo spine’.

10. Fracture – insufficiency in ankylosed spine (especially cervicothoracic and thoracolumbar junctions).

11. Osteoporosis – with long-standing disease.

12. Kyphosis.

13. Arachnoiditis – rare and late. Arachnoid diverticulae, laminar erosions, dural calcification.

Asbestos inhalation

Lung and/or pleural disease caused by the inhalation of asbestos fibres (a group of fibrous silicates; different morphological forms – crocidolite, amosite, tremolite and chrysotile; widely utilized in industry). Long latency (> 20–30 years) between exposure and lung/pleural disease. Disease is more common with crocidolite (blue asbestos) than chrysotile (white asbestos). Pleural disease alone 50%; pleura and lung parenchyma 40%; lung parenchyma alone 10%.


1. Pleural plaques – commonest manifestation of asbestos exposure developing 20–30 years after exposure. Typically seen on parietal pleural on undersurface of ribs, diaphragmatic pleura and adjacent to spine; virtually pathognomonic. Sharply angulated, ‘holly-leaf’ opacities on chest radiography and sharply demarcated. Discrete ‘punched-out’ appearance at CT.

2. Benign pleural effusion – most common ‘early’ (< 10 years) manifestation; occurs in < 10%. Exudative fluid. May be unilateral or bilateral and may be followed by residual benign diffuse pleural thickening in around 50% or regions of rounded atelectasis (‘folded lung’).

3. Diffuse pleural thickening – less specific for asbestos exposure than plaques.

4. Rounded atelectasis – (folded lung, Blesovsky syndrome). Rounded mass, adjacent pleural thickening and parenchymal bands/distortion (‘comet tail’ appearance). Can be seen with other exudative effusions.

5. Malignant pleural mesothelioma – long latency (30–40 years). Lobulated pleural thickening involving mediastinal pleura ± large pleural effusion but minimal mediastinal shift. (NB. Can occur in peritoneum.)