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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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Case study: 24-year-old male presenting with polyarthralgias.

Anusha Vakiti ; Saad Javed ; Kevin C. King .

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Last Update: February 20, 2023 .

• Case Presentation

A 24-year-old white male with no known medical history presented to the hospital with chief complaints of 2 weeks of progressively worsening pain and swelling of his right wrist and left ankle joints. He did not report any fevers, chills, night sweats, weight loss or rash. He was employed as a fireman. He denied alcohol use disorder, smoking cigarettes, or any recreational drugs. Family history was significant for hypertension in father and ovarian cancer in the mother. His vital signs were within normal limits on presentation. On physical examination, the patient had significant swelling of multiple joints including the right wrist, right elbow, and left ankle. The joints were erythematous and tender to touch. Due to severe pain, he had limited range in the involved joints.

• Initial Evaluation

Initial laboratory workup for the swollen joints included a complete blood count which revealed an elevated white blood cell count (WBC) of 14000/microliter with neutrophil predominance, ESR of 118 mm per hour, and CRP of 8 mg/dL. A comprehensive metabolic panel was within normal limits. Infectious workup, which included blood and urine cultures, was negative. Immunological workup revealed elevated ANA titer (1:320), positive lupus anticoagulant, and high dsDNA antibodies. Ultrasound of the right elbow and left ankle joints revealed effusion in the joints and the surrounding soft tissue swelling. MRI of the right wrist revealed heterogeneous signal and enhancement of multiple carpal bones involving the second through fifth metacarpals, subcutaneous and deep soft tissue of the wrist and proximal hand. Based on the clinical and laboratory evidence, the patient was diagnosed with systemic lupus erythematosus (SLE) by the rheumatologist and was started on steroids, Plaquenil, and methotrexate. The patient’s clinical condition initially improved with the regimen, but his symptoms relapsed when weaning the steroids. He was discharged on a slow tapering dose of prednisone.

• Differential Diagnosis

The differential diagnosis for a young male (before fourth decade) with polyarthralgia is more inclined towards rheumatologic conditions like SLE, sarcoid arthritis, scleroderma, or gout. If associated with signs and symptoms of infection, gonococcal joint infection is high on the differential. Rheumatoid arthritis and polymyalgia rheumatica usually affect the older population (after the fourth decade). Based on the distribution of the joints, duration of symptoms, and association with other organ systems the classification of polyarthralgia is very broad and makes for a very challenging diagnosis. The most common differentials for a patient presenting with polyarthralgia are Rheumatoid arthritis, Lupus, Lyme, Septic arthritis, Gonorrheal joint arthritis, or Gout.

• Confirmatory Evaluation

During a follow-up appointment a few weeks later, he complained of multiple subcutaneous nodules. On physical exam, multiple, tender, non-erythematous subcutaneous nodules were noted along with a palpable, non-tender mass on the left side of the abdomen. CT abdomen showed a large heterogeneous mass measuring 20.1 by 10.7 by 18.1 cm, in the left quadrant of the abdomen along with a poorly defined low attenuation mass measuring 2.9 by 3 cm in the right hepatic lobe. CT guided biopsy of the left-sided abdominal mass was non-diagnostic. He underwent exploratory laparotomy, with excision of the left-sided abdominal mass along with splenectomy and distal pancreatectomy. There were multiple abnormal areas in the liver concerning for metastases. Pathology of the resected mass revealed sheets of malignant acinar cells with no intervening ductal structures or islets. Tumor cells were positive for trypsin and cytokeratin and were negative for CD117 and synaptophysin, consistent with pancreatic acinar cell carcinoma. Serum CA 19-9 levels were high. Lipase levels were elevated at 40,000U/dL. At this point, based on the biopsy and staging, the patient was diagnosed with stage IV pancreatic acinar cell carcinoma, but the cause of his polyarthralgia was still uncertain. Adjuvant chemotherapy was initiated with leucovorin, 5-fluorouracil (5-FU) and oxaliplatin for the carcinoma. During his treatment, his joint swelling and pain progressed and involved new joints of right ankle and left knee. Imaging studies of the joints showed joint effusion and soft tissue swelling. Arthrocentesis of the right ankle joint was performed, and the synovial fluid studies were consistent with infection and cultures were positive for methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas. He was treated with antibiotics including vancomycin and piperacillin–tazobactam without any improvement. Due to progressive worsening of the right ankle joint, he required irrigation and debridement with arthrotomy. Repeat cultures were negative, but his symptoms continued to worsen, and he had persistent drainage of milky colored fluid from the surgical site and eventually required a below-knee amputation. Surgical pathology of the right knee joint revealed acute on chronic inflammation with the presence of granulation and fibrin tissue, without any evidence of malignancy. For further evaluation, arthrocentesis of left knee, left ankle, and right wrist was done and yielded milky colored fluid. His lipase levels continued to remain above 20,000 U/dL despite being treated with chemotherapy.

The persistent drainage of milky colored fluid from all the involved joints led to diagnosing the cause of polyarthralgia in this patient. Based on the diagnosis of metastatic acinar cell pancreatic carcinoma, evidence of elevated lipase levels, subcutaneous nodules, and the arthrocentesis yielding milky colored fluid, the patient’s polyarthralgia were believed to be due to hyperlipasemia, a rare paraneoplastic manifestation of pancreatic acinar cell carcinoma. The painful subcutaneous lesions are caused by an inflammatory process known as panniculitis which has been studied to be associated with polyarthralgia in a patient with pancreatic acinar cell carcinoma. Pancreatic polyarthritis and panniculitis are hypothesized to be caused by the peripheral lipolytic activity of lipase circulating systemically due to the pancreatic disease. [1] [2]

Initial adjuvant chemotherapy was with leucovorin, 5-fluorouracil (5-FU) and oxaliplatin but given the lack of response, his chemotherapy was switched to capecitabine and subsequently to gemcitabine and Abraxane. In spite of chemotherapy, the patient did not have any response, and his clinical condition worsened. After goals of care discussion with the patient and his family, he was transitioned to hospice care given his poor prognosis and chemotherapy was discontinued.

Paraneoplastic syndromes are a rare group of heterogeneous disorders that are triggered by an altered immune system response to a neoplasm. The symptoms may involve any organ system ranging from cutaneous manifestations to involvement of the neuromuscular or musculoskeletal systems. As seen in this patient, the paraneoplastic syndrome can be the initial presentation of the malignancy and can lead to delayed diagnosis and treatment. It is of great significance to understand the various paraneoplastic syndromes associated with a neoplasm. Few examples of common paraneoplastic syndromes are hypercalcemia of malignancy associated with breast cancer, SIADH associated with small cell carcinoma of the lung. Hyperlipasemia syndrome is a rare paraneoplastic syndrome associated with acinar cell carcinomas. Few cases have been reported of pancreatic panniculitis and polyarthralgia caused by hyperlipasemia. [3] [4]

Acinar cell carcinomas fall into the category of malignant epithelial neoplasms with an incidence of about 1% to 2% of the pancreatic neoplasms. The usual presentation of these tumors is solid, but they can also present either as cystic lesions or mixed with both solid and cystic components. They can present at any age but are often seen in older patients (sixth decade) and predominant in males than in females. Most patients present with vague symptoms such as abdominal pain, weight loss, fatigue or nausea. They are characterized by the production of zymogen granules containing pancreatic exocrine enzymes, in the tumor cells. A consequence of this is a rare paraneoplastic syndrome called hyperlipasemia or lipase hypersecretion syndrome. Serum lipase levels in such cases are usually above 10,000 U/dl and can result in multiple subcutaneous fat nodules and necrosis, termed as pancreatic panniculitis and polyarthralgia due to effusions and sclerotic lesions in the bones. This syndrome can be the initial manifestation of the neoplasm and is associated with poor prognosis. Histologically, these neoplasms are characterized by malignant cells with acinar cell differentiation, which stain positive for immunohistochemical stains such as trypsin, chymotrypsin, elastase, or lipase. Zymogen granules can be noted on the ultrastructure examination. KRAS, SMAD4, the mutations commonly associated with ductal adenocarcinomas are not seen in acinar cell carcinomas. Compared to patients with ductal adenocarcinoma, the overall prognosis for patients with acinar cell carcinoma is better. However, the presence of paraneoplastic syndrome association can worsen the prognosis and affect the quality of life as seen in this case. [5]

Hyperlipasemia syndrome is associated with poor prognosis of the acinar cell carcinoma, and the management modalities vary. Surgical resection is often the curative option for cases with local early-stage acinar cell carcinomas. However, often these acinar cell carcinomas are diagnosed in advanced or metastatic stages, and such cases often require adjuvant chemotherapy. Given the presence of APC gene/beta-catenin pathway genetic alterations, as seen in colorectal carcinomas, acinar cell carcinomas are often treated with 5-FU/leucovorin. Other chemotherapeutic agents that can be used include irinotecan,  doxorubicin, erlotinib, gemcitabine, cisplatin, docetaxel, capecitabine, oxaliplatin, sunitinib, and sirolimus. Lowery et al. published a study in 2011 that highlighted the use of combination therapy, to use gemcitabine or 5-FU-based combination chemotherapy along with platinum analogs such as irinotecan in patients with advanced studies validated to have improved chemosensitivity. [6] [7] [8]

• Pearls of Wisdom
• Pancreatic acinar cell cancer is a rare malignancy of the pancreas and often seen in the elderly population.
• Usually dominated by symptoms of abdominal pain, and less frequently jaundice.
• The hypersecretion subtype may present with fever, arthralgia, rash, hypereosinophilia, and panniculitis. 
• Imaging will usually reveal large lesions with sharp boundaries.
• Tissue is required to confirm diagnosis.
• Surgery is the treatment of localized lesions.
• For metastasis lesions, various chemotherapy protocols have been developed, which can result in long-term survival. 
• Current day suggests that oxaliplatin-based chemotherapy is most effective.
• Compared to pancreatic adenocarcinomas, these malignancies carry a better prognosis.

It is important to be aware of the various paraneoplastic manifestations of malignancies, as the paraneoplastic presentation might be the initial sign of malignancy and could be misleading.

• Review Questions
• Access free multiple choice questions on this topic.
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CT abdomen image obtained from owner

Disclosure: Anusha Vakiti declares no relevant financial relationships with ineligible companies.

Disclosure: Saad Javed declares no relevant financial relationships with ineligible companies.

Disclosure: Kevin King declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Vakiti A, Javed S, King KC. Case Study: 24-Year-Old Male Presenting With Polyarthralgias. [Updated 2023 Feb 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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• Case Report
• Open access
• Published: 15 October 2008

Chronic tophaceous gout presenting as acute arthritis during an acute illness: a case report

• Abhijeet Dhoble 1 ,
• Vijay Balakrishnan 1 &
• Robert Smith 1  

Cases Journal volume  1 , Article number:  238 ( 2008 ) Cite this article

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Metrics details

Gout is a metabolic disease that can manifest as acute or chronic arthritis, and deposition of urate crystals in connective tissue and kidneys. It can either manifest as acute arthritis or chronic tophaceous gout.

Case presentation

We present a 39-year-old male patient who developed acute arthritis during his hospital course. Later on, after a careful physical examination, patient was found to have chronic tophaceous gout. The acute episode was successfully treated with colchicines and indomethacin.

Gout usually flares up during an acute illness, and should be considered while evaluating acute mono articular arthritis. Rarely, it can also present with tophi as an initial manifestation.

Gout is a metabolic disease, which is characterized by acute or chronic arthritis, and deposition of monosodium urate crystals in joint, bones, soft tissues, and kidneys [ 1 – 4 ]. In 18 th century, Garrod proposed a causative relationship between elevated uric acid and urate crystal formation, which is underlying pathology for gout [ 4 ]. Gout can either manifest as acute arthritis or chronic arthropathy, which is also called tophaceous gout [ 1 , 2 , 5 ].

A 39-year-old African American male patient was admitted with one-day history of acute left lower quadrant pain, and was diagnosed with acute uncomplicated diverticulitis, confirmed by computed tomography (CT) of the abdomen. His medical and surgical history was unremarkable, and he denied any medication use. He denied smoking or illicit drug use, but admitted occasional alcohol use on every other weekend. He did not follow any particular diet. He had an average built with BMI of 29.6. He was started on intravenous antibiotics and pain medication, which led to significant clinical improvement within two days.

On the third day of hospitalization, he developed acute, severe pain and swelling of the left elbow. Within next few hours, pain worsened and he was unable to move the elbow joint, which was tender, erythematous, and swollen on examination (figure 1 ). Never investigated in the past, we also noted a firm 4 × 6 cm mass on each elbow, and another one surrounding the proximal inter-phalangeal joint of right middle finger (figure 2 ). There was no overlying edema or cellulitis. There were no other swellings or tophi noted especially on toes or ears. When asked particularly, he denied similar episodes in the past. He also denied any episode of swelling of great toe in the past.

Tophus at the back of right elbow.

Tophi/tophus around the proximal inter-phalangeal joint of right middle finger.

Plain radiography of left elbow showed joint effusion, and soft tissue swelling. Radiography of other joints including hands and feet was not performed. Laboratory values on the third day are given in table 1 . Liver function test was also performed, and the results were unremarkable. Diagnostic arthocentesis was performed on both the elbows, and revealed negatively birefringent needle-shaped crystals using polarized microscopy in both samples. Detailed analysis of synovial fluid is given in table 2 . The swelling on the right elbow was aspirated to determine the etiology because patient had that swelling for a long time.

The patient responded partially to colchicine, but later had great relief with indomethacin. Colchicine was used at the dose of 0.6 mg every two hourly. He received total of six doses, but it was stopped because he developed severe nausea and vomiting. He admitted that his pain was reduced to 4/10 in intensity from 9/10 before treatment, but swelling was persistent. We initiated indomethacin at 50 mg every eight hourly, and his pain and swelling was relieved to great extent in 48 hours.

Gout is a metabolic disease that can manifest as acute or chronic arthritis, and deposition of urate crystals in connective tissue and kidneys. All patients have hyperuricemia at some point of their disease. But, either normal or low serum uric acid levels can occur at the time of acute attack; and asymptomatic hyperuricemic individuals may never experience a clinical event resulting from urate crystal deposition [ 1 – 4 ]. Low to normal uric acid concentration can be due to excessive excretion of uric acid, crystal formation, or systemic inflammatory state [ 6 , 7 ]; however, exact mechanism is still not completely understood. A diagnosis of gout is most accurate when supported by visualization of uric acid crystals in a sample of joint or bursal fluid, or demonstrated histologically in excised tissue. Synovial fluid analysis of our patient was consistent with inflammatory arthritis. Mild leucocytosis in this patient was due to systemic inflammatory response.

Visible or palpable tophi, as this patient exhibited, are usually noted only among those patients who are hyperuricemic and have had repeated attacks of acute gout, often over many years. However, presentation of tophaceous deposits in the absence of gouty arthritis is also reported [ 5 , 8 ]. Pain and inflammation are manifested when uric acid crystals activate the humoral and cellular inflammatory processes [ 9 ].

During an acute illness, if systemic inflammatory state prevails, such as in an acute infection, cytokines and chemokines triggers inflammation and cause arthritis in the presence of urate crystals [ 10 , 11 ]. Phagocytosis of these crystals by macrophages in the synovial lining cells precedes influx of neutrophils in the joint [ 9 – 11 ]. This process releases various mediators of inflammation locally [ 12 , 13 ].

Hyperuricemia is often present in patients with tophaceous gout, and they can benefit from uric acid lowering therapy early during the course [ 14 , 15 ]. In our patient, serum uric acid and 24-hour urine uric acid level was within normal limits when measured in the hospital before his discharge from the hospital. It was decided to follow him up in the clinic in two weeks, and measure these values again during 'interval gout' before deciding to start him on any particular medication to prevent further attacks of acute arthritis.

Our patient presented with tophi as an initial presentation of gout, which is very rare, but has been reported [ 5 , 8 ]. Investigational studies due to acute elbow joint pain deciphered the underlying mystery of chronic swelling. Systemic inflammatory response secondary to diverticulitis exposed the joints to the effects of urate.

First-line treatments for an acute flare are either oral colchicine and/or non-steroidal anti-inflammatory agents. Systemic or intra-articular corticosteroids can also be used, and are equally effective, but with more side effects [ 16 , 17 ]. Interleukin-1 inhibitors are still under investigation, and are not approved for an acute attack of gout [ 18 ].

Gout usually flares up during an acute illness, and should always be considered while evaluating acute mono articular arthritis in hospitalized patients. Gout can present with tophi as an initial manifestation of the disease process.

Written informed consent was obtained from the patient for publication of this case report and accompanying images in Journal of Medical Case Reports. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

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Department of Internal Medicine, Michigan State University, East Lansing, Michigan, USA

Abhijeet Dhoble, Vijay Balakrishnan & Robert Smith

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Dhoble, A., Balakrishnan, V. & Smith, R. Chronic tophaceous gout presenting as acute arthritis during an acute illness: a case report. Cases Journal 1 , 238 (2008). https://doi.org/10.1186/1757-1626-1-238

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DOI : https://doi.org/10.1186/1757-1626-1-238

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• Diverticulitis
• Serum Uric Acid
• Uric Acid Level

Cases Journal

ISSN: 1757-1626

Rheumatoid arthritis: Differentiating between forms of crippling arthritis

Emma, a 32-year-old with existing foot and hand pain, visits her healthcare provider after hand pain, neck stiffness, and worsening fatigue over the last three months.

Emma’s healthcare provider conducts a full clinical history and physical examination and decides to test for rheumatoid arthritis.  

Emma is experiencing joint pain and fatigue. See how serological testing can help confirm a diagnosis of rheumatoid arthritis.

Patient History

Family history.

• Mother has unknown form of crippling arthritis.

Emma's Personal History

• Localized pain in knuckles of hand and pads of feet.
• Ibuprofen helps some, and acetaminophen does not.
• Imaging: Marginal erosions were detected on radiographs.
• Physical examination: Normal with the exception of the hands, which were tender when palpated over the second and third proximal interphalangeal joints.

Emma’s  Test Results

These results together with this patient's case history and symptoms, help confirm the diagnosis.  

Differential Diagnosis

REFINED DIAGNOSIS

• Inflammatory arthritis, rheumatoid.

HEALTHCARE PROVIDER MANAGEMENT PLAN

• Steroids and methotrexate initially.
• Biologics or triple therapy if inadequate response.
• Follow up every eight to 12 weeks in the beginning to assess therapies and monitor lab work.
• Healthcare provider visits may extend to every three to six months if well controlled.

The people, places, and events depicted in these case studies and photographs do not represent actual patients, nor are they affiliated in any way with Thermo Fisher Scientific.

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This Common Condition Can Damage Joints Long Before It’s Detected

Nearly 33 million Americans have osteoarthritis. Experts explain how it affects the body, and why it’s so hard to diagnose.

By Knvul Sheikh

It may start as a twinge in your knee or hip when you get out of bed. Over time, that twinge may turn into persistent pain, swelling or reduced range of motion — signs of a condition called osteoarthritis.

But as with many other chronic conditions, doctors are unable to diagnose osteoarthritis until it has already progressed significantly and has interfered with everyday activities. Scientists are racing to find ways to diagnose osteoarthritis earlier and stave off or slow some of the damage from the disease, which affects over 32.5 million adults in the United States and more than 500 million people worldwide.

Research has started to show that osteoarthritis is not caused solely by everyday wear and tear on joints, like the deterioration of rubber treads on a tire over time. In some patients, persistent, low-grade inflammation might accelerate the progression of the disease or even cause it. And scientists now believe the damage can start long before symptoms appear. In a new study published last week, researchers from Duke University identified molecules circulating in the blood of women that might serve as markers of the disease up to eight years before an X-ray picked up changes in their bones.

“This tells us that there is an osteoarthritis continuum,” said Dr. Virginia Byers Kraus, lead author of the study and a professor of medicine at Duke. “You’re already on an escalator that’s leading you up the path to symptoms and X-ray changes way before we thought.”

What happens in the body in osteoarthritis?

The disease affects cartilage, a protective tissue that serves as padding between the bones in your joints, allowing them to glide over each other when you walk, climb stairs or bend to pick up groceries. It is constantly breaking down with exercise and everyday activities. “But our body typically knows how to repair itself,” said Dr. Elaine Husni, director of the Cleveland Clinic’s Arthritis and Musculoskeletal Center. The fluid surrounding joints contains enzymes that help cut up and remove worn cartilage, while special cells fix minor damage and rebuild cartilage.

But this cycle of breakdown and repair goes awry in people with osteoarthritis, Dr. Husni said. In some patients, those enzymes may be too aggressive in removing cartilage, or the healing process may be much slower than the cartilage breakdown. In others, the body senses damage or stress in the joints, which leads to inflammation. This inflammation tells cartilage-snipping enzymes that they need to come remove worn-down tissue. But if the body can’t dial the inflammation back down after repairs are completed, it can lead to more cartilage breakdown, Dr. Husni said.

Carrying extra body weight is one of the biggest risk factors for developing osteoarthritis. Injuries from sports or repetitive motion also increase the risk of osteoarthritis, as do conditions that involve increased inflammation throughout the body, such as diabetes.

Eventually, the cartilage loses its ability to cushion the bones. This leads to pain, a crackling sensation when moving your joints, reduced range of motion and swelling. The symptoms of osteoarthritis are most common in weight-bearing joints like the knee, hip and lower spine, though they may also occur in the small joints in fingers or feet, Dr. Husni said.

How is osteoarthritis diagnosed?

When a patient shows up with joint pain, a provider might start by feeling for swelling, testing a joint’s range of motion and ordering tests to rule out other problems or types of arthritis.

The current gold standard for diagnosing osteoarthritis is an X-ray, which can show changes in joint structure associated with the disease. The more worn the joint, the narrower the gap appears between bones.

However, by the time these changes show up on an X-ray, the damage to the joint is already done, Dr. Husni said. X-ray images also don’t always correspond to the severity of symptoms or pain that patients experience. “You could have two patients with the same amount of joint space narrowing — something like two or three millimeters on an X-ray — but one patient could have a ton of pain and the other may not,” Dr. Husni said.

While Dr. Kraus’s team and other researchers are studying biomarkers that might make osteoarthritis easier to diagnose, it may take years to prove a blood test is reliable enough to use in clinical settings. Researchers are also looking at whether these and other molecular markers can be used alongside drugs in trials, to measure whether experimental treatments for osteoarthritis are working or not, she said.

For now, patients have to rely on supportive treatments to manage pain, such as heating pads, physical therapy and over-the-counter medicines, Dr. Kraus said.

And people can use the knowledge that osteoarthritis is a slowly progressing disease to take steps to reduce the risk of disease or slow the inevitable wear and tear of joints, Dr. Kraus said: Keeping off excess weight, staying active and following a balanced diet rich in anti-inflammatory foods can help support your joint health and overall well-being.

Knvul Sheikh is a Times reporter covering chronic and infectious diseases and other aspects of personal health. More about Knvul Sheikh