A 12-year-old female came to clinic with a 3 month history of ankle pain. It initially started in the right ankle after she had turned her ankle during dancing. This got somewhat better but then her left ankle and foot also became more painful. She had continued her activities which included multiple dance activities, gymnastics, Tae Kwon Do and two weeks previously she had started cross-country running. The pain had increased in the couple of days after she started cross-country. The running occurred mainly on sidewalks and roads. She said she had no pain in the morning but it slowly increased over the day and was worse when she started her activities in the afternoon or evening. Sometime she would limp during practices. The pain decreased with rest after the activities and with warm baths. She denied any pain at night, swelling or warmth of the joint, night sweats, weight loss, rashes, fevers or chills. She denied any other joints being affected. The past medical history was non-contributory. The family history had no specific orthopaedic, rheumatologic or immune problems. The pertinent physical exam revealed a healthy female with growth parameters in the 10-50%. She was tall and thin. The ankles, feet and toes did not show any erythema or edema. No specific pain could be elicited. The joints were freely mobile. The rest of her extremities, back, and TMJ joints were negative. She had no skin changes.
The radiologic evaluation showed no bony changes in the feet or ankles. The diagnosis of general overuse resulting in ankle pain was made. The patient was instructed to significantly decrease or stop her activities and let her body rest more until the pain subsided. She then could increase her activities as tolerated. She had a health maintenance examination already scheduled in 3 weeks so followup would be done then. After the visit the medical student was reviewing the differential diagnosis of joint pain with the attending and included gout as one of the entities. “I’ve only seen hyperuricemia with patients with tumor lysis syndrome or with a metabolic problem. I’ve never seen gout. It’s really an adult disease and certainly on the differential diagnosis for adults, but we really don’t see it in children,” the attending noted.
Purines are heterocyclic aromatic organic compounds. Common ones are adenine, guanine, xanthine, hypoxanthine, uric acid and caffeine. The most common sources of purines are meat (especially liver, kidney, and brain), certain fish (herring, mackerel, anchovies, sardines), and in lower amounts in beans, and certain plants and yeast. Purines are synthesized, used by the body, then they are degraded by a variety of enzymes. They then can be salvaged to resynthesize purines or are eliminated primarily by the kidney.
When intake or synthesis outweighs elimination then hyperuricemia can result. Hyperuricemia can occur in patients with obesity and metabolic syndrome, psoriasis, medications (thiazide diuretics), genetic diseases such as Lesch Nyhan disease, and kidney disease including transplantation. Myeloproliferative disease including leukemia, lymphoma and tumor lysis syndrome also have increased risk of hyperuricemia.
Hyperuricemia can lead to the deposition of monosodium urate crystals in the joint and periarticular tissue. Crystal deposition stimulates interleukin-1 release from monocytes that causes an inflammatory response. Painful joints and gout are the result. Overtime gouty trophi may occur that can cause bony erosions. As it can take 20 years or more for this process of hyperuricemia and crystal deposition to occur, gout generally does not occur often in the typical pediatric patient. Therefore gout is not usually considered in the differential diagnosis of joint or limb pain in the pediatric population as it is in the adult population.
The causes of leg pain can be reviewed here.
The causes of limp can be reviewed here.
In the adult population, gout had a prevalence rate of 1.4 – 4% in the western countries of the United States, United Kingdom, Germany and Australia.
Juvenile gouty arthritis is uncommon in the pediatric population. A review found only 66 cases of primary gout over a period from 1769-1971.
Secondary gout occurs more often but is uncommon too occurring in the diseases listed above. In adult renal transplant patients hyperuricemia (80%) and gout (10%) are frequent complications. In the pediatric renal transplant populations, one study found 50% of patients had hyperuricemia, but rarely had gout. The gout occurred > 5 years after transplant.
Questions for Further Discussion
1. What is the differential diagnosis of joint swelling?
2. What signs and symptoms are consistent with idiopathic juvenile arthritis?
3. What is pseudogout?
- Symptom/Presentation: Foot Pain
- Age: School Ager
To Learn More
To view pediatric review articles on this topic from the past year check PubMed.
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Available from the Internet at http://en.wikipedia.org/wiki/Purine (rev. 1/2/15, cited 1/12/15).
Wikipedia. Purine metabolism.
Available from the Internet at http://en.wikipedia.org/wiki/Purine_metabolisme (rev.11/3/14 cited 1/12/15).
Treadwell BL. Juvenile gout. Ann Rheum Dis. 1971 May;30(3):279-84.
Yarom A, Rennebohm RM, Strife F, Levinson JE. Juvenile gouty arthritis. Two cases associated with mild renal insufficiency. Am J Dis Child. 1984 Oct;138(10):955-7.
Sparta G, Kemper MJ, Neuhaus TJ.
Hyperuricemia and gout following pediatric renal transplantation. Pediatr Nephrol. 2006 Dec;21(12):1884-8.
Truck J, Laube GF, von Vigier RO, Goetschel P. Gout in pediatric renal transplant recipients. Pediatr Nephrol. 2010 Dec;25(12):2535-8.
Kim HK, Zbojniewicz AM, Merrow AC, Cheon JE, Kim IO, Emery KH. MR findings of synovial disease in children and young adults: Part 2. Pediatr Radiol. 2011 Apr;41(4):512-24
Robinson PC, Taylor WJ, Merriman TR. Systematic review of the prevalence of gout and hyperuricaemia in Australia. Intern Med J. 2012 Sep;42(9):997-1007.
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital