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 Table of Contents  
Year : 2019  |  Volume : 14  |  Issue : 3  |  Page : 229-235

Acute pancreatitis in rheumatology practice, with emphasis on systemic lupus erythematosus: A case series and newer concepts

1 Omkar Rheumatology Clinic, Director, Nashik, Maharashtra, India
2 Shree Bhausaheb Hire Government Medical College, Dhule, Maharashtra, India
3 Dr. Vasantrao Pawar Medical College, Nashik, Maharashtra, India
4 Center for Arthritis and Rheumatic Diseases, Director, Mumbai, Maharashtra, India

Date of Web Publication30-Oct-2019

Correspondence Address:
Dr. Praveen Pratap Jadhav
Omkar Rheumatology Clinic, Gaikwad Mala, Behind Regimental Plaza, Nasik Road, Nashik - 422 101, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/injr.injr_33_19

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Acute pancreatitis is seen in many rheumatological disorders, of which, systemic lupus erythematosus (SLE) is the most common. SLE is a multisystemic disease, affecting the gastrointestinal system in about half of the patients. Acute pancreatitis is a rare but life-threatening complication of SLE. Here, we report three intriguing cases of SLE wherein patients suffering from SLE presented with acute pancreatitis either as the initial symptom of the disease or as a flare. Another patient in this series is of dermatomyositis. Literature is reviewed, and newer concepts are discussed.

Keywords: Acute pancreatitis, antiphospholipid antibody syndrome, autoimmune hemolytic anemia, pancreatitis, systemic lupus erythematosus

How to cite this article:
Jadhav PP, Desai SR, Jadhav JP, Bichile LS. Acute pancreatitis in rheumatology practice, with emphasis on systemic lupus erythematosus: A case series and newer concepts. Indian J Rheumatol 2019;14:229-35

How to cite this URL:
Jadhav PP, Desai SR, Jadhav JP, Bichile LS. Acute pancreatitis in rheumatology practice, with emphasis on systemic lupus erythematosus: A case series and newer concepts. Indian J Rheumatol [serial online] 2019 [cited 2021 Jul 29];14:229-35. Available from:

  Introduction Top

Acute pancreatitis is a complication of many rheumatological diseases. From our combined patient database of around 6000 rheumatology patients, we found four patients who had acute pancreatitis, of which three were in patients with systemic lupus erythematosus (SLE), whereas one was in a patient with dermatomyositis. SLE is a chronic autoimmune inflammatory disorder of unknown etiology which affects various organs. The usual manifestations of SLE include skin rashes, arthritis, anemia, nephritis, and vasculitis. Pancreatitis is an uncommon presentation in SLE and its diagnosis should be considered in all patients of SLE presenting with abdominal pain.

  Case Reports Top

Case 1

A 30 year old female was admitted with complaints of ecchymosis, easy fatigability, and menorrhagia of 6 months. In addition, she had persistent arthralgia, photosensitivity, and hair loss. She had no history of alcohol consumption or smoking.

Physical examination revealed malar rash and pallor. There was no swelling and deformity of the joints. Systemic examination was unremarkable.

Hematological examination revealed microcytic hypochromic anemia with red blood cell (RBC) fragments and hemoglobin (hb) of g%. Total leukocyte count was 7800/mm[3]. Platelet levels were significantly reduced to 40,000/mm[3]. Renal functions were normal. A homogeneous, positive antinuclear antibody (ANA) was observed at 1:1000. Anti-double-stranded-DNA antibody (dsDNA) was positive. The C3 level at 84 mg/dL was normal. However, C4 was considerably low at 6 mg/dL. Coombs test was also positive. Reticulocyte count and lactate dehydrogenase (LDH) were not reported. Albumin level was within the normal range at 3.8 mg/dL. Globulin at 4 mg/dL was elevated. Serum bilirubin and alkaline phosphatase were normal. Lupus anticoagulant was not found. Prothrombin time and partial thromboplastin time were normal, and the patient had no thrombotic manifestation of the disease at this stage.

Her diagnosis at this stage was made as SLE with autoimmune hemolytic anemia (AIHA) associated with thrombocytopenia and antiphospholipid antibody (APS) positivity.

The patient was prescribed with 1 mg/kg amount of prednisolone, daily escalating dose of azathioprine from 50 to 150 mg, tablet hydroxychloroquine 400 mg daily, 5 mg of folic acid, and calcium and Vitamin D supplements. The patient was followed up for 10 years and was continued with 5 mg/day of prednisolone, 12.5–25 mg of azathioprine, and 400 mg of hydroxychloroquine.

Ten years later, she presented to a gastroenterologist with fever, jaundice, vomiting, and pain in the right hypochondriac region. Hematological examination at this point revealed low Hb levels of 8 gm%, a total white cell count of 10,500/mm[3], erythrocyte sedimentation rate (ESR) of 90 mm/h, serum bilirubin level of 6.2 mg% – direct 1 mg% and indirect 5.2 mg%, alkaline phosphatase of 104 IU/L, blood urea nitrogen (BUN) of 10 mg/dL, serum creatinine of 0.8 mg/dL, presence of ANA, and low levels of complements C3 and C4. Abdominal sonography divulged the presence of a stone in the bile duct. This was removed with endoscopic retrograde cholangiopancreatography (ERCP). No sonological abnormality was found in the pancreas. The patient was discharged asymptomatic.

The following week, the patient was readmitted with symptoms of fever, abdominal pain, vomiting, and a blood pressure (BP) of 80/60 mmHg. Investigations were sent to rule out sepsis and acute pancreatitis. Blood analysis revealed elevated serum amylase and lipase levels of 5800 and 3200 U/L, respectively. The patient also had ascites and left-sided pleural effusion. Abdominal ultrasonography (USG) suggested inflammation of the pancreas. She was started on analgesics, injection octreotide, and other supportive treatment. Steroids were planned to be started after ruling out sepsis. In spite of intensive treatment, the patient succumbed in just 48 h.

Case 2

A 26-year-old woman, an ayurvedic doctor, was transferred from peripheral place for ventilatory support. She was diagnosed as SLE 3 years ago, but had been treating herself for arthralgias, photosensitivity, rashes, fever, and bleeding gums, with indigenous medicines. She had also taken three units of blood transfusions for 3 g% of Hb. She was anuric when she was transferred. She was naïve for treatment with steroids and other allopathic medicines.

On examination, her heart rate was 150/min and BP was 60 mmHg systolic. She was brought on ambu bag ventilation. Further examination revealed the presence of pallor, generalized edema, presence of fluid in the knee joint, and absence of lymphadenopathy. She was also found to have tense ascites. Deep tendon reflexes and plantars were absent. Bilateral air entry at the bases was absent. She was put on ventilatory support.

Hematological investigation revealed Hb levels of 5 g%. Leukocyte count was 10,500/mm[3]. ESR was 110 mm/h. C-reactive protein (CRP) levels were elevated at 2.8 mg/l. BUN level was 110 mg%, and serum creatinine was 5.8 mg%. Serum calcium levels were reduced at 7.6 mg/dL. Serum albumin and globulin levels were 2.5 and 3.5 g/dL, respectively. Total serum bilirubin level was observed to be 0.8 mg/dL, whereas direct and indirect serum bilirubin levels were 0.6 and 0.2 mg/dL, respectively. A homogeneous, positive ANA was observed at dilution 1:360. The presence of anti-dsDNA was observed at a dilution of 1/160. C3 levels at 35 mg/dL and C4 at 8 mg/dL were below the normal range. Coombs test was positive. A urine report dated 6 months prior to her admission revealed a nephritic picture with lots of RBCs, pus cells, proteins, and granular casts. USG of the kidney revealed the presence of medical renal disease. Based on these investigations, she was diagnosed with SLE, AIHA, and lupus nephritis. In view of respiratory distress and shock, a possible differential diagnosis of SLE carditis, sepsis, pancreatitis with shock, and acute respiratory distress syndrome (ARDS) was considered.

Further investigations at this stage revealed a serum amylase level of 12,000 U/L and serum lipase level of 9000 U/L. Ascitic fluid was drained later and was sent for culture and cytology and routine examinations. While the culture was sterile, it showed fifty cells of which 70% were polymorphs and 30% were lymphocytes. The adenosine deaminase levels in ascitic fluid were normal. Spot serum albumin level was low at 1.1 mg% at that time. An X-ray confirmed bilateral pleural effusion and ARDS.

The patient was put on vasomotor and respiratory support. She was also given 1 g intravenous methyl prednisolone, a shot of 500 mg of cyclophosphamide, and other supportive treatment. Plasmapharesis was planned, but deferred due to hypotension. However, she succumbed in few days.

Case 3

A 52-year-old male, smoker and nonalcoholic, was referred for inability to climb stairs for the past 3 months. He also had a history of intermittent fever rising up to 99° F–100°F, inability to raise his neck from the pillow, pain in the thighs, rashes over the upper eyelids, and generalized arthralgia for the past 3 months. He did not have dysphagia.

On examination, he had a heliotrope rash over the eyelids, Gottron's papules over the knuckles, mechanic's hand, tenderness over the thighs, and mild generalized tenderness all over the body. The cardiovascular system was normal except that the BP was 150/90 mmHg. No gallop rhythm was auscultated. Respiratory and abdominal examinations were normal. The muscles showed mild tenderness, and deep tendon reflexes were present. A diagnosis of dermatomyositis was suspected on the basis of the history.

Hematological investigations revealed the following: Hb of 14 gm%; total leukocyte count of 9500/mm[3] with 68% polymorphs, 28% lymphocytes, and 4% monocytes; ESR of 96 mm/h; and CRP level of 30 mg/L. A +2 positive ANA test with nucleolar pattern and a negative anti-dsDNA test were observed. Anti-cyclic citrullinated protein and rheumatoid factor tested negative. Serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase (SGPT) levels were found to be 360 and 660 units, respectively. LDH levels were 12,000 U/L. Creatine phosphokinase levels were raised to 7200 U/L. BUN level of 40 mg% and serum creatinine level of 1.3 mg% were noted. USG, X-ray chest, and two-dimensional echocardiography were normal. Electromyography study was consistent with the diagnosis of inflammatory myositis.

He was started on tablet prednisolone 1 mg/kg with gradual tapering of dose over 3 months. Tablet methotrexate 25 mg weekly was prescribed and was later reduced to 15 mg weekly. High-dose methotrexate caused adverse effects in the form of nausea and occasional vomiting. Folic acid and calcium and Vitamin D supplements were prescribed along with bisphosphonates. Physiotherapy of the neck, pelvic, and shoulder girdle was advised, to which the patient was compliant. The patient improved well and resumed his duties in 3 months.

After about 6 months, with regular treatment of methotrexate and prednisolone, he presented with bouts of abdominal pain and vomiting. A USG report revealed gall stones, distended gallbladder, and pancreatic swelling. Pancreatitis was confirmed with high amylase and lipase levels. He was treated for the same and settled over 2 weeks. A follow-up computed tomography (CT) scan of the abdomen revealed a pseudocyst of pancreas and stone in the biliary duct.

However, the patient refused surgery and continued to take tablet prednisolone 7.5 mg daily and 15 mg methotrexate weekly.

Case 4

A 23-year-old female was admitted with the chief complaint of severe upper abdominal pain. She had a history of fever associated with anorexia, bodyache, and headache over the past 2 months. She also complained of joint pain for the past 4–5 months. Fever was low grade, almost continuous and without chills. The joints involved were mostly of hands, including the small joints, not associated with swelling and an hour of early-morning stiffness. She also had recurrent oral ulcers.

On examination, her pulse rate was 100/min and BP was 100/70 mmHg. The cardiovascular, nervous, and respiratory systems presented normally. The abdomen showed marked tenderness in the epigastric region.

As severe epigastric pain was her presenting symptom, she was investigated for the same. Laboratory investigations revealed an Hb of 8.1 g/dL. The total leukocyte count was 10,700 cells/mm[3], and platelet counts were within normal levels. ESR was 20 mm in 1 h. Serum creatinine was 1.2 mg/dL, and SGPT was 13.6 IU/L. Serum amylase levels and serum lipase were high at 505 and 323 units/L, respectively. Serum protein and albumin levels slightly decreased at 4.7 and 3 g/dL, respectively. Ultrasound of the abdomen and pelvis revealed moderate ascites. The pancreas was bulky suggestive of pancreatitis. Pseudo thickening of the gallbladder wall and mild splenomegaly were also seen.

She was diagnosed as acute pancreatitis and admitted in the intensive care unit. She was started on injection octreotide 25 mg twice a day, analgesics, antibiotics (piperacillin + tazobactum), and supportive treatment.

Although she was diagnosed and treated as acute pancreatitis, in view of her long-term fever and polyarthritis, she was further investigated for rheumatologic causes. Anti-cyclic citrullinated protein was negative, and ANA was positive at a dilution of 1:320, with a homogenous pattern. ANA blot revealed positivity for antibodies against SSA, SSB, dsDNA, and histones.

Hence, she was diagnosed as SLE, satisfying four of eight (arthritis, mucosal ulcers, positive ANA, and positive dsDNA) criteria based on the 1997 Revised American College of Rheumatology criteria.

To the treatment, pulsed doses of methylprednisolone 500 mg a day for 3 days were added, which were later converted to oral prednisolone. Oral hydroxychloroquine 200 mg twice a day and azathioprine 50 mg were also added. Supportive treatment was also started.

With this treatment, the patient improved symptomatically in 3–4 days. Her amylase dropped to 179 U/L, Hb improved to 9 g/dL, and white cell count became 11,100 cells/mm[3]. Her abdominal pain subsided totally and so did her fever, arthralgia, and bodyache.

She was discharged asymptomatically in 8 days with a diagnosis of SLE with acute pancreatitis.

She was followed up at regular intervals for the next 3 years and was well maintained on tapering dose of steroids, azathioprine, and hydroxychloroquine. Her last follow-up was on 2 years after the initial presentation and was asymptomatic till then.

She has not followed up since then. Telephonic follow-up has confirmed that she is asymptomatic till now and on irregular treatment.

  Discussion Top

The above four cases represent a varied presentation of acute pancreatitis in rheumatologic diseases. Although rheumatoid arthritis is the most common diagnosis encountered in rheumatology practice, we did not find any patients with this diagnosis complicated by acute pancreatitis in our database.

To sum up, the likely causes of acute pancreatitis in these cases were as follows:

  • In case 1, the patient had AIHA, which could have contributed to the development of acute pancreatitis. Long-term azathioprine intake may have played a role in her predisposition. However, the pancreatic instrumentation in the form of ERCP was the precipitating factor and the most likely cause. A combination of all the above factors may have led to acute pancreatitis
  • In case 2, high SLE activity was contributing to acute pancreatitis. ARDS, due to undiagnosed cause, led to shock, which in turn could have propagated the pancreatitis. It can also be argued that initial pancreatitis, either due to active SLE or unknown cause, could have been complicated by shock and ARDS. Her AIHA may also have contributed to pancreatitis
  • In case 3, gallstones seem to be the cause of pancreatitis, with a quite underlying disease and good outcome. Here, the cause of pancreatitis seems to be unrelated dermatomyositis
  • In case 4, acute pancreatitis was the presenting feature of SLE, thus suggesting an active disease itself as a cause of pancreatitis.

Acute pancreatitis is a rare complication of SLE. It is seen in 0.2%–8.2% of all lupus patients. Most of the times, it presents as a lupus flare.[1],[2] Sometimes, it can be a presenting major symptom of SLE.[3],[4],[5],[6],[7],[8] The term “major symptom” needs to be specified here, as prior minor constitutional symptoms can be missed. In one report, of the 99 cases of SLE with pancreatitis, 10 had pancreatitis as their first symptom.[3] In our series, one of the four cases had pancreatitis as the first major symptom of lupus. This patient had a Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score of at least 7 (4 for arthritis, 2 for mucosal ulcers, and 1 for fever, complements were not estimated), suggesting a mild-to-moderate SLE activity. Early diagnosis and prompt treatment leads to rapid control of symptoms and disease activity. Pancreatitis as an initial symptom, at least in some patients, suggests SLE itself as the primary etiologic reason for the development of pancreatitis. This case suggests that, in young females presenting with pancreatitis, SLE should be borne in mind as an etiology. Conversely, in a patient with known SLE presenting with acute abdominal pain, a diagnosis of pancreatitis should always be considered.

However, in most patients, acute pancreatitis occurs as a generalized flare. Its cause could be varied. The causes may or may not be related to SLE. Makol et al. have suggested that hypertriglyceridemia, psychosis, recent viral infection, and drug toxicity as risk factors for developing pancreatitis.[2] Others have suggested various underlying mechanisms such as complement activation and autoimmune reactions, viral infection, hypotension, microthrombi formation, vasculitis, and intimal thickening that may lead to pancreatitis.[9],[10]

Because almost all patients with SLE are on long-standing drugs, these have been implicated in the development of pancreatitis. Steroids have been long suspected, but not conclusively proven to cause pancreatitis. Studies suggest that steroids have a mild inhibitory effect on pancreatic secretion, which may lead to increase in its viscosity. This may lead to stasis of pancreatic secretions and predisposition to pancreatitis.[11] However, in real-world study, it was found that, in patients of rheumatoid arthritis on oral glucocorticoids, there was a reduction in the risk of acute pancreatitis.[12] In contrast, azathioprine is more firmly linked with pancreatitis.[13],[14] In our series, only case 1 had a history of taking azathioprine for more than 10 years. However, in this patient, the link between azathioprine and pancreatitis appears weak, and the role of pancreatic intervention appears stronger. Azathioprine-induced pancreatitis has been reported 22 days after the initiation of azathioprine,[14] and not so late. In addition, it is known that azathioprine-induced pancreatitis is transient and reversible on withdrawal of the drug.[15] Hence, it is unlikely that azathioprine is a major etiology of pancreatitis.

Pancreatic instrumentation in the form of ERCP is a known risk factor for pancreatitis.[16] In patients undergoing ERCP, female gender, younger age (<55 years), and other associated causes of pancreatitis confer higher risk for instrumentation-induced acute pancreatitis. In Case 1, the patient deteriorated after ERCP. The temporal relation of the procedure and event suggested ERCP as the cause of her deterioration. Although this patient had a reason to undergo ERCP in view of the gallstone, she may have had a subclinical pancreatitis also. She had three major risk factors to develop post-ERCP pancreatitis – young age, female gender, and gallstones. This case may endorse the view that it may be risky for SLE patients with risk factors to undergo instrumentation. If it absolutely essential, then great caution needs to be exercised during and post procedure.

Another striking feature in our series is that two patients, case 1 and case 2, had a strong possibility of an additional AIHA. In recent times, there have been increasing reports of association between AIHA and pancreatitis in SLE.[17],[18] The exact cause is not known. In fact, any condition that causes massive hemolysis can give rise to acute pancreatitis. In a retrospective study by Druml et al., it was found that the prevalence of pancreatitis was 20% in forty patients who had massive hemolysis (defined as 12% drop of hematocrit in 12 h).[19] The authors concluded that the back pain often found in acute hemolysis may be due to pancreatitis pancreatitis, rather than coming from the kidneys. Hemolysis as a cause of pancreatitis has also been confirmed in experimental models. Histological changes in the pancreas following massive hemolysis have been observed in these models.[20] Thus, in SLE, at least a few cases of acute pancreatitis can be attributed to hemolysis secondary to AIHA. From our series, it can be suggested that the association between pancreatitis and AIHA can lead to increased mortality.

APS syndrome is another associate of SLE that seems to be closely linked with the development of acute pancreatitis. The association of APS with acute pancreatitis is being increasingly recognized.[21],[22],[23] In APS, vascular occlusion is due to thromboembolism, whereas in SLE, the primary abnormality is vasculitis. Combination of both pathologies may synergistically work toward the development of pancreatitis. Interestingly, in a single postmortem case of pancreatitis due to APS associated with SLE, the pathological abnormality was vascular occlusion due to thromboembolism.[24]

Shock, especially septic shock, could be a contributory cause to pancreatitis in cases 1 and 2. Pancreatic injury is common in septic shock. The probable mechanisms include tissue hypoperfusion, oxidative damage, and cellular apoptosis. Severe septic shock causes hypoperfusion and ischemia of vital organs. However, whether there is hypoperfusion of the pancreas is not well studied. Increase in pancreatic enzymes in shock without overt manifestations of pancreatitis does not seem to alter the course of shock and is not associated with higher mortality.[25] Hence, it is more likely that shock is the effect rather than the cause of pancreatitis.

Finally, even in patients with SLE, nonlupus causes should be considered as a cause of pancreatitis. Gallstones are the most common cause of acute pancreatitis. Alcohol abuse, hypertriglyceridemia, and infections are the other common causes to be borne in mind.

The method of diagnosing pancreatitis in SLE does not differ as compared to non-SLE patients. Increased amylase and lipase forms the basis of diagnosis. Ultrasound and CT scan confirm the diagnosis. Estimation of complements C3 and C4 is important to determine the disease activity and severity of SLE.

Treatment of acute pancreatitis in SLE can be quite challenging. With the strong evidence of association between SLE and APS and/or AIHA, patients should be investigated for these conditions as early as possible. Any delay in diagnosing hemolysis or thrombotic tendency would possibly lead to poor outcome for the patient. It may be worthwhile here to introduce the concept of screening for these disorders as soon as pancreatitis is diagnosed in SLE. Initiating specific treatment early in the course of disease may help in preventing deadly outcome of this fatal disease. Corticosteroids are indicated in autoimmune hemolytic anemia. Apart from steroids, increasing evidence supports the use of rituximab in AIHA, particularly warm antibody AIHA.[26] In a study by Birgens et al., a satisfactory response was observed in 75% of the patients treated with rituximab and prednisolone, whereas it was observed only in 36% of those given prednisolone alone (P = 0.003). After 36 months, about 70% of the patients who had received rituximab and prednisolone were still in remission, compared with only 45% of those in the prednisolone group.[27] In patients with APS also, apart from anticoagulation, rituximab has been suggested to have an significant role.[28],[29] An European registry suggested an essential role of rituximab in catastrophic APS.[30] Thus, it can be suggested that, in SLE with acute pancreatitis associated with either AIHA or APS, lower threshold should be indicated for the use of rituximab. Going further, a case can be argued for the use of rituximab in SLE with associated AIHA or APS, even without pancreatitis. Prevention of hemolysis (in AIHA) will prevent the bilirubin from rising, which in turn will prevent the formation of gallstones. pancreatitis, as gall stones formation will lead to a reduced risk of pancreatitis as gallstones are known to be the strongest risk factors for the development of pancreatitis.

Apart from the treatment of these unusual associations, the rest of the treatment for acute pancreatitis will be on same lines as in nonlupus state.

Mortality of pancreatitis in lupus is very high. In a cohort of 4053 patients with SLE, 27 had SLE-related acute pancreatitis with a mortality of 37.04%. Mortality was higher in patients with higher SLE activity. In this longitudinal study, patients with pancreatitis presented with higher SLEDAI score (21.7 vs. 16.17, P = 0.03), more organ system involvement (5.7 vs. 3.96, P = 0.001), and higher mortality (37.04% vs. 0, P = 0.01).[4] When compared to non-SLE pancreatitis, 45% excess mortality was reported by Wang et al.[31] Treatment with corticosteroids or azathioprine was not associated with increased mortality. On the contrary, mortality was low in patients who were treated with these agents after the onset of pancreatitis (20% mortality, compared with 61% among those who were not treated with steroids for their pancreatitis, P = 0.005).[32]

Among other rheumatologic diseases, rheumatoid arthritis is another diagnosis which predisposes the patient to acute pancreatitis.[33] However, we did not find such a patient in our databases. Acute pancreatitis may also be associated with other rare rheumatologic disorders, but the discussion is beyond the scope of this article.

  Conclusion Top

Acute pancreatitis is a rare but dreaded complication of SLE. It can have varied presentations. It may be an initial presentation of SLE or can present as its flare. It must be suspected in any patient of SLE presenting with acute abdominal pain. Conversely, in any young female presenting with acute pancreatitis, SLE must be considered. Because development of acute pancreatitis is a function of disease activity of SLE, it is imperative that a tight control of its activity will go a long way in preventing this dangerous complication. Finally, in SLE with acute pancreatitis, APS and AIHA should be considered as predisposing factors, be investigated, and treated appropriately. Rituximab seems to be a promising drug for this association. A thought can also be given for prevention of acute pancreatitis, especially if SLE is associated with AIHA or APS. This can be achieved by strict control of the disease activity, and may be, by using rituximab.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

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