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Journal of Digestive Diseases 2014; 15; 327–330
doi: 10.1111/1751-2980.12146
Case report
Pancreatic panniculitis in acute pancreatitis Zhen Zhen GUO, Zhi Yin HUANG, Li Bin HUANG & Cheng Wei TANG Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China
INTRODUCTION Subcutaneous manifestations of acute pancreatitis (AP), including ecchymosis and pancreatic panniculitis, are seldomly seen in clinical settings.1 Compared with ecchymosis such as Cullen’s sign and Grey Turner’s sign, pancreatic panniculitis (subcutaneous fat necrosis) is much rarer. Clinicians, especially those with less experiences, may be unable to identify pancreatic panniculitis because few photographs of the subcutaneous manifestations are available under this condition. Pancreatic panniculitis is usually confirmed by subcutaneous biopsy.2 If the typical subcutaneous manifestations are consistently related to subcutaneous fat necrosis, it would be possible for patients to avoid an invasive biopsy. In this study, we presented a case of pancreatic panniculitis with subcutaneous manifestations at the early and late stage of severe acute pancreatitis (SAP). Previous case reports on pancreatic panniculitis were also reviewed. CASE REPORT A 27-year-old woman was diagnosed with gallstoneinduced AP, presenting as acute persistent upper abdominal pain for 10 h, with plasma amylase level of > 762 U/L (reference range 60–180 U/L), and diffuse swelling of the pancreas and gallbladder stones detected by abdominal ultrasonography. After 4 days of conventional medical treatment in a local Correspondence to: Cheng Wei TANG, Department of Gastroenterology, West China Hospital, Sichuan University, No. 37 Guo Xue Xiang, Wuhou District, Chengdu, Sichuan Province 610041, China. Email: [email protected] Conflict of interest: None. © 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
hospital her symptoms did not ameliorate, and her body temperature was elevated to 39°C and dyspnea occurred, thus she was admitted to our hospital. Physical examination on admission did not inspect any ecchymosis or rash. The results of laboratory tests were as follows: white blood cell count 11.23 × 109/L with 93.8% neutrophils, serum albumin 30.7 g/L (reference range 40–55 g/L), calcium 1.44 mmol/L (reference range 2.1–2.7 mmol/L), amylase 343 U/L (reference range 25–125 U/L), lipase 402 U/L (reference range 13–60 U/L), partial pressure of oxygen 67 mmHg, C-reactive protein (CRP) 49.4 mg/L (reference range < 5 mg/L), interleukin (IL)-6 1370 pg/mL (reference range < 7 pg/mL) and IL-10 18.1 pg/mL (reference range < 9.1 pg/mL). Serum bilirubin and triglyceride levels were normal. She accepted noninvasive mechanical ventilation, oral rehydration, empirical antibiotics (moxifloxacin and tinidazole), octreotide for anti-inflammation (intravenous infusion at 50 μg/h for 3 days → 25 μg/h for 4 days → hypodermic injection at 300 μg/day for 3 days) and other supportive therapies. Her dyspnea and abdominal pain were greatly relieved after 4 days of treatment but the fever persisted (37.7– 39.2°C). Bacterial cultures of blood and ascites were negative. On the 10th day after the onset of AP, extensive erythematous plaques on the buttocks appeared but in the absence of swelling, heat or tenderness (Fig. 1a). Subsequently, contrast-enhanced computed tomography revealed necrotizing pancreatitis, peripancreatic fluid collection, massive ascites and pelvic fluid (Fig. 1b,c). After another 10 days of medical treatment, her erythematous plaques on the buttocks began to fade (Fig. 1d) and body temperature returned to normal level. She was discharged after 23 days of hospital stay as the erythematous plaques continued to fade and ultrasonography showed an almost complete disappearance of ascites and pelvic fluids.
327
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ZZ Guo et al.
Journal of Digestive Diseases 2014; 15; 327–330
a
b
c
d
Figure 1. (a) Fresh erythematous plaques on the buttocks of the patient on the 10th day after the onset of AP. Abdominal computed tomography (CT) showing (b) necrotizing pancreatitis, peripancreatic fluid collection, massive ascites and (c) pelvic fluid (contrast-enhanced CT). (d) Fading erythematous plaques.
Her erythematous plaques completely subsided one month after discharge. DISCUSSION Acute pancreatitis is a common disease with an incidence of 4.9–73.4 cases per 100 000 population.3–5 However, we found that only 12 cases of AP with panniculitis have been reported since 1967 (Table 1).1,6–14 Therefore, pancreatic panniculitis may be considered a rare condition in AP. The patient’s subcutaneous manifestations of pancreatic panniculitis were obviously different from those of cellulitis, which generally presents with swelling, tenderness and heat. Of the 13 AP patients with pancreatic panniculitis including ours, 7 (53.8%) were males and the other 6 (46.2%) were females, with a mean age of 33.8 ± 16.6 years (range 6–57 years). At least nine of those patients presented with fever or ascites. Pancreatic panniculitis usually appears 10 to 15 days after the onset of AP and may be divided into three types: (i) with extensive erythematous plaques located usually at the buttocks and trunk (38.5%, 5/13); (ii) with scattered multiple nodular fat necrosis that often appears on the lower extremities (46.1%, 6/13); and (iii) a mixture of types (i) and (ii)
(15.4%, 2/13) (Table 1). Subcutaneous signs usually subside 15 to 30 days after their appearance when the patients recover from AP. SAP occurred in at least 80% of patients with extensive erythematous plaques but in only one-third of those with nodular fat necrosis, indicating that pancreatic panniculitis with extensive erythematous plaques may be associated with the development of SAP. The clinical outcomes of SAP patients with pancreatic panniculitis may benefit from advances of supportive therapy since all SAP patients died before the year 2000, while merely one of three patients have died in the 10 years since. In previous case reports of pancreatic panniculitis, most of extensive erythematous plaques on the buttocks consistently showed subcutaneous acute inflammation with diffuse fat necrosis by histological examination. Therefore, invasive biopsy can be avoided when a clinician is able to identify the typical subcutaneous manifestations of pancreatic panniculitis. As a complication of SAP, pancreatic panniculitis may be clinically defined as: (i) extensive erythematous plaques on buttocks appearing 10 to 15 days after the onset of AP and fading with the amelioration of SAP; (ii) the exclusion of cellulitis; and (iii) a presence of fever or ascites. Accordingly, extensive erythematous plaques on the buttocks in the present
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
NM/NM 16/NM 17/NM 12/36 10/45 NM/NM 7/NM 9/NM NM/NM 14/NM 10/NM
12/27 NM/NM
6/M 57/F 41/F 45/M 27/F 41/M 25/F 49/F 50/M 7/M 45/M
29/M 17/F
Appeared/ subsided (d)
Lower legs Lower legs
Forearms, abdomen, buttocks, legs Legs, right arm, buttocks Lower extremies Legs Abdominal wall Lower legs
Thorax, buttocks, back and extremities Both hips, upper thighs, buttocks Flanks, buttocks, upper thighs Left flank, left buttock, outer left thigh Buttocks, perianal region
Location
Fat necrosis Fat necrosis
Fat necrosis Fat necrosis Lipocyte necrosis Fat necrosis Fat necrosis Fat necrosis
Fat necrosis Fat necrosis Fat necrosis Fat necrosis NM
Biopsy
Yes Yes
Yes Yes No NM Yes NM
No NM NM NM Yes
Fever
No NM
NM NM NM Yes Yes NM
Yes NM Yes NM Yes
Ascites
M-SAP SAP
SAP M-SAP MAP SAP MAP MAP
SAP SAP SAP NM SAP
Severity
Alive Alive
Death NM Alive Death Alive Alive
Death Death Death Alive Alive
Outcome
d, days (from the clinical onset of acute pancreatitis); F, female; M, male; MAP, mild acute pancreatitis; M-SAP, moderately severe acute pancreatitis; NM, not mentioned; SAP, severe acute pancreatitis.
Erythematous plaques 19676 19981 19981 19981 Present case Nodular fat necrosis 19957 19958 20069 200710 200911 201012 Mixture of erythematous plaques and nodular fat necrosis 200513 201114
Age (years)/gender
The characteristics of 13 cases with acute pancreatitis panniculitis
Case report (publication year)
Table 1.
Journal of Digestive Diseases 2014; 15; 327–330 SAP with pancreatic panniculitis 329
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
330
ZZ Guo et al.
case were clinically classified as pancreatic panniculitis without biopsy. The pathogenesis of pancreatic panniculitis in AP remains unclear. The release of pancreatic enzymes may induce permeability of microcirculation and cause fat necrosis. Severe systemic inflammation may also involve subcutaneous fat tissues. Therefore, an efficient anti-inflammatory regimen, such as octreotide therapy used in the present case, may be helpful for treating pancreatic panniculitis during AP. The length of hospital stay for patients with SAP usually varies due to diverse complications. Because we had no experience in the treatment for pancreatic panniculitis, we deliberately prolonged the patient’s hospital stay to ensure her recovery from this complication. This case suggests that the fading of the erythematous plaques combined with a return to normal body temperature may be an indication for hospital discharge for patients with SAP complicated with pancreatic panniculitis. REFERENCES 1 Bem J, Bradley EL 3rd. Subcutaneous manifestations of severe acute pancreatitis. Pancreas 1998; 16: 551–5. 2 Tomasini C, Lentini F, Borroni G. The role of skin biopsy in diagnosis of panniculitides. G Ital Dermatol Venereol 2013; 148: 335–49. 3 Tenner S, Baillie J, DeWitt J, Vege SS; American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108: 1400–15.
Journal of Digestive Diseases 2014; 15; 327–330 4 Fagenholz PJ, Castillo CF, Harris NS, Pelletier AJ, Camargo CA Jr. Increasing United States hospital admissions for acute pancreatitis, 1988–2003. Ann Epidemiol 2007; 17: 491–7. 5 Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of acute pancreatitis: a systematic review. Pancreas 2006; 33: 323–30. 6 Heuser E, Lieberman E, Donnell GN, Landing BH. Subcutaneous fat necrosis with acute hemorrhagic pancreatitis-a case in a child with steroid-resistant nephrosis treated with 6-mercaptopurine. Calif Med 1967; 106: 58–63. 7 Francombe J, Kingsnorth AN, Tunn E. Panniculitis, arthritis and pancreatitis. Br J Rheumatol 1995; 34: 680–3. 8 Lee MS, Lowe PM, Nevell DF, Fryer J, Le Guay J. Subcutaneous fat necrosis following traumatic pancreatitis. Australas J Dermatol 1995; 36: 196–8. 9 Pike JL, Rice JC, Sanchez RL, Kelly EB, Kelly BC. Pancreatic panniculitis associated with allograft pancreatitis and rejection in a simultaneous pancreas-kidney transplant recipient. Am J Transplant 2006; 6: 2502–5. 10 Lee WS, Kim MY, Kim SW, Paik CN, Kim HO, Park YM. Fatal pancreatic panniculitis associated with acute pancreatitis: a case report. J Korean Med Sci 2007; 22: 914–7. 11 Chiewchengchol D, Wananukul S, Noppakun N. Pancreatic panniculitis caused by L-asparaginase induced acute pancreatitis in a child with acute lymphoblastic leukemia. Pediatr Dermatol 2009; 26: 47–9. 12 Narváez J, Bianchi MM, Santo P et al. Pancreatitis, panniculitis, and polyarthritis. Semin Arthritis Rheum 2010; 39: 417–23. 13 Johnson MA, Kannan DG, Balachandar TG, Jeswanth S, Rajendran S, Surendran R. Acute septal panniculitis. A cutaneous marker of a very early stage of pancreatic panniculitis indicating acute pancreatitis. JOP 2005; 6: 334–8. 14 Kirkland EB, Sachdev R, Kim J, Peng D. Early pancreatic panniculitis associated with HELLP syndrome and acute fatty liver of pregnancy. J Cutan Pathol 2011; 38: 814–7.
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Journal of Digestive Diseases 2014; 15; 327–330
doi: 10.1111/1751-2980.12146
Case report
Pancreatic panniculitis in acute pancreatitis Zhen Zhen GUO, Zhi Yin HUANG, Li Bin HUANG & Cheng Wei TANG Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China
INTRODUCTION Subcutaneous manifestations of acute pancreatitis (AP), including ecchymosis and pancreatic panniculitis, are seldomly seen in clinical settings.1 Compared with ecchymosis such as Cullen’s sign and Grey Turner’s sign, pancreatic panniculitis (subcutaneous fat necrosis) is much rarer. Clinicians, especially those with less experiences, may be unable to identify pancreatic panniculitis because few photographs of the subcutaneous manifestations are available under this condition. Pancreatic panniculitis is usually confirmed by subcutaneous biopsy.2 If the typical subcutaneous manifestations are consistently related to subcutaneous fat necrosis, it would be possible for patients to avoid an invasive biopsy. In this study, we presented a case of pancreatic panniculitis with subcutaneous manifestations at the early and late stage of severe acute pancreatitis (SAP). Previous case reports on pancreatic panniculitis were also reviewed. CASE REPORT A 27-year-old woman was diagnosed with gallstoneinduced AP, presenting as acute persistent upper abdominal pain for 10 h, with plasma amylase level of > 762 U/L (reference range 60–180 U/L), and diffuse swelling of the pancreas and gallbladder stones detected by abdominal ultrasonography. After 4 days of conventional medical treatment in a local Correspondence to: Cheng Wei TANG, Department of Gastroenterology, West China Hospital, Sichuan University, No. 37 Guo Xue Xiang, Wuhou District, Chengdu, Sichuan Province 610041, China. Email: [email protected] Conflict of interest: None. © 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
hospital her symptoms did not ameliorate, and her body temperature was elevated to 39°C and dyspnea occurred, thus she was admitted to our hospital. Physical examination on admission did not inspect any ecchymosis or rash. The results of laboratory tests were as follows: white blood cell count 11.23 × 109/L with 93.8% neutrophils, serum albumin 30.7 g/L (reference range 40–55 g/L), calcium 1.44 mmol/L (reference range 2.1–2.7 mmol/L), amylase 343 U/L (reference range 25–125 U/L), lipase 402 U/L (reference range 13–60 U/L), partial pressure of oxygen 67 mmHg, C-reactive protein (CRP) 49.4 mg/L (reference range < 5 mg/L), interleukin (IL)-6 1370 pg/mL (reference range < 7 pg/mL) and IL-10 18.1 pg/mL (reference range < 9.1 pg/mL). Serum bilirubin and triglyceride levels were normal. She accepted noninvasive mechanical ventilation, oral rehydration, empirical antibiotics (moxifloxacin and tinidazole), octreotide for anti-inflammation (intravenous infusion at 50 μg/h for 3 days → 25 μg/h for 4 days → hypodermic injection at 300 μg/day for 3 days) and other supportive therapies. Her dyspnea and abdominal pain were greatly relieved after 4 days of treatment but the fever persisted (37.7– 39.2°C). Bacterial cultures of blood and ascites were negative. On the 10th day after the onset of AP, extensive erythematous plaques on the buttocks appeared but in the absence of swelling, heat or tenderness (Fig. 1a). Subsequently, contrast-enhanced computed tomography revealed necrotizing pancreatitis, peripancreatic fluid collection, massive ascites and pelvic fluid (Fig. 1b,c). After another 10 days of medical treatment, her erythematous plaques on the buttocks began to fade (Fig. 1d) and body temperature returned to normal level. She was discharged after 23 days of hospital stay as the erythematous plaques continued to fade and ultrasonography showed an almost complete disappearance of ascites and pelvic fluids.
327
328
ZZ Guo et al.
Journal of Digestive Diseases 2014; 15; 327–330
a
b
c
d
Figure 1. (a) Fresh erythematous plaques on the buttocks of the patient on the 10th day after the onset of AP. Abdominal computed tomography (CT) showing (b) necrotizing pancreatitis, peripancreatic fluid collection, massive ascites and (c) pelvic fluid (contrast-enhanced CT). (d) Fading erythematous plaques.
Her erythematous plaques completely subsided one month after discharge. DISCUSSION Acute pancreatitis is a common disease with an incidence of 4.9–73.4 cases per 100 000 population.3–5 However, we found that only 12 cases of AP with panniculitis have been reported since 1967 (Table 1).1,6–14 Therefore, pancreatic panniculitis may be considered a rare condition in AP. The patient’s subcutaneous manifestations of pancreatic panniculitis were obviously different from those of cellulitis, which generally presents with swelling, tenderness and heat. Of the 13 AP patients with pancreatic panniculitis including ours, 7 (53.8%) were males and the other 6 (46.2%) were females, with a mean age of 33.8 ± 16.6 years (range 6–57 years). At least nine of those patients presented with fever or ascites. Pancreatic panniculitis usually appears 10 to 15 days after the onset of AP and may be divided into three types: (i) with extensive erythematous plaques located usually at the buttocks and trunk (38.5%, 5/13); (ii) with scattered multiple nodular fat necrosis that often appears on the lower extremities (46.1%, 6/13); and (iii) a mixture of types (i) and (ii)
(15.4%, 2/13) (Table 1). Subcutaneous signs usually subside 15 to 30 days after their appearance when the patients recover from AP. SAP occurred in at least 80% of patients with extensive erythematous plaques but in only one-third of those with nodular fat necrosis, indicating that pancreatic panniculitis with extensive erythematous plaques may be associated with the development of SAP. The clinical outcomes of SAP patients with pancreatic panniculitis may benefit from advances of supportive therapy since all SAP patients died before the year 2000, while merely one of three patients have died in the 10 years since. In previous case reports of pancreatic panniculitis, most of extensive erythematous plaques on the buttocks consistently showed subcutaneous acute inflammation with diffuse fat necrosis by histological examination. Therefore, invasive biopsy can be avoided when a clinician is able to identify the typical subcutaneous manifestations of pancreatic panniculitis. As a complication of SAP, pancreatic panniculitis may be clinically defined as: (i) extensive erythematous plaques on buttocks appearing 10 to 15 days after the onset of AP and fading with the amelioration of SAP; (ii) the exclusion of cellulitis; and (iii) a presence of fever or ascites. Accordingly, extensive erythematous plaques on the buttocks in the present
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
NM/NM 16/NM 17/NM 12/36 10/45 NM/NM 7/NM 9/NM NM/NM 14/NM 10/NM
12/27 NM/NM
6/M 57/F 41/F 45/M 27/F 41/M 25/F 49/F 50/M 7/M 45/M
29/M 17/F
Appeared/ subsided (d)
Lower legs Lower legs
Forearms, abdomen, buttocks, legs Legs, right arm, buttocks Lower extremies Legs Abdominal wall Lower legs
Thorax, buttocks, back and extremities Both hips, upper thighs, buttocks Flanks, buttocks, upper thighs Left flank, left buttock, outer left thigh Buttocks, perianal region
Location
Fat necrosis Fat necrosis
Fat necrosis Fat necrosis Lipocyte necrosis Fat necrosis Fat necrosis Fat necrosis
Fat necrosis Fat necrosis Fat necrosis Fat necrosis NM
Biopsy
Yes Yes
Yes Yes No NM Yes NM
No NM NM NM Yes
Fever
No NM
NM NM NM Yes Yes NM
Yes NM Yes NM Yes
Ascites
M-SAP SAP
SAP M-SAP MAP SAP MAP MAP
SAP SAP SAP NM SAP
Severity
Alive Alive
Death NM Alive Death Alive Alive
Death Death Death Alive Alive
Outcome
d, days (from the clinical onset of acute pancreatitis); F, female; M, male; MAP, mild acute pancreatitis; M-SAP, moderately severe acute pancreatitis; NM, not mentioned; SAP, severe acute pancreatitis.
Erythematous plaques 19676 19981 19981 19981 Present case Nodular fat necrosis 19957 19958 20069 200710 200911 201012 Mixture of erythematous plaques and nodular fat necrosis 200513 201114
Age (years)/gender
The characteristics of 13 cases with acute pancreatitis panniculitis
Case report (publication year)
Table 1.
Journal of Digestive Diseases 2014; 15; 327–330 SAP with pancreatic panniculitis 329
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
330
ZZ Guo et al.
case were clinically classified as pancreatic panniculitis without biopsy. The pathogenesis of pancreatic panniculitis in AP remains unclear. The release of pancreatic enzymes may induce permeability of microcirculation and cause fat necrosis. Severe systemic inflammation may also involve subcutaneous fat tissues. Therefore, an efficient anti-inflammatory regimen, such as octreotide therapy used in the present case, may be helpful for treating pancreatic panniculitis during AP. The length of hospital stay for patients with SAP usually varies due to diverse complications. Because we had no experience in the treatment for pancreatic panniculitis, we deliberately prolonged the patient’s hospital stay to ensure her recovery from this complication. This case suggests that the fading of the erythematous plaques combined with a return to normal body temperature may be an indication for hospital discharge for patients with SAP complicated with pancreatic panniculitis. REFERENCES 1 Bem J, Bradley EL 3rd. Subcutaneous manifestations of severe acute pancreatitis. Pancreas 1998; 16: 551–5. 2 Tomasini C, Lentini F, Borroni G. The role of skin biopsy in diagnosis of panniculitides. G Ital Dermatol Venereol 2013; 148: 335–49. 3 Tenner S, Baillie J, DeWitt J, Vege SS; American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108: 1400–15.
Journal of Digestive Diseases 2014; 15; 327–330 4 Fagenholz PJ, Castillo CF, Harris NS, Pelletier AJ, Camargo CA Jr. Increasing United States hospital admissions for acute pancreatitis, 1988–2003. Ann Epidemiol 2007; 17: 491–7. 5 Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of acute pancreatitis: a systematic review. Pancreas 2006; 33: 323–30. 6 Heuser E, Lieberman E, Donnell GN, Landing BH. Subcutaneous fat necrosis with acute hemorrhagic pancreatitis-a case in a child with steroid-resistant nephrosis treated with 6-mercaptopurine. Calif Med 1967; 106: 58–63. 7 Francombe J, Kingsnorth AN, Tunn E. Panniculitis, arthritis and pancreatitis. Br J Rheumatol 1995; 34: 680–3. 8 Lee MS, Lowe PM, Nevell DF, Fryer J, Le Guay J. Subcutaneous fat necrosis following traumatic pancreatitis. Australas J Dermatol 1995; 36: 196–8. 9 Pike JL, Rice JC, Sanchez RL, Kelly EB, Kelly BC. Pancreatic panniculitis associated with allograft pancreatitis and rejection in a simultaneous pancreas-kidney transplant recipient. Am J Transplant 2006; 6: 2502–5. 10 Lee WS, Kim MY, Kim SW, Paik CN, Kim HO, Park YM. Fatal pancreatic panniculitis associated with acute pancreatitis: a case report. J Korean Med Sci 2007; 22: 914–7. 11 Chiewchengchol D, Wananukul S, Noppakun N. Pancreatic panniculitis caused by L-asparaginase induced acute pancreatitis in a child with acute lymphoblastic leukemia. Pediatr Dermatol 2009; 26: 47–9. 12 Narváez J, Bianchi MM, Santo P et al. Pancreatitis, panniculitis, and polyarthritis. Semin Arthritis Rheum 2010; 39: 417–23. 13 Johnson MA, Kannan DG, Balachandar TG, Jeswanth S, Rajendran S, Surendran R. Acute septal panniculitis. A cutaneous marker of a very early stage of pancreatic panniculitis indicating acute pancreatitis. JOP 2005; 6: 334–8. 14 Kirkland EB, Sachdev R, Kim J, Peng D. Early pancreatic panniculitis associated with HELLP syndrome and acute fatty liver of pregnancy. J Cutan Pathol 2011; 38: 814–7.
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
