Letters to Editor
any alarming signs, evaluation by imaging modalities complemented by angiographic studies, and timely intervention, either medical or surgical, can be life saving in this clinical scenario. S. A. George, I. Francis Department of Histopathology, Mubarak Al Kabir Hospital, Jabriya, Kuwait Address for correspondence: Dr. Smiley Annie George, Department of Histopathology, Mubarak Al Kabir Hospital, P. O. Box 43787, 32052 Jabriya, Kuwait. E‑mail: [email protected]
References 1.
2.
3.
4.
Arlet JB, Le ThiHuong D, Marinho A, Cluzel P, Wechsler B, Piette JC. Arterial aneurysms in Wegener’s granulomatosis: Case report and literature review. Semin Arthritis Rheum 2008;37:265‑8. Ohta N, Waki T, Fukase S, Suzuki Y, Kurakami K, Aoyagi M, et al. Aortic aneurysm rupture as a rare complication of granulomatosis with poyangiitis: A case report. J Med Case Rep 2013;7:202. Senf R, Jürgensen JS, Teichgräber U, Kampf D, Schindler R. Ruptured arterial aneurysm of the kidney in a patient with Wegener’s granulomatosis. Nephrol Dial Transplant 2003;18:2671‑3. Durai R, Agrawal R, Piper K, Brohi K. Wegener’s granulomatosis presenting as an abdominal aortic aneurysm: A case report. Cases J 2009;2:9346. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.127923
She was found to have multiple myeloma and was started on bortezomib and dexamethasone. Each cycle consist of 4 doses on 0, 4, 11, 14th day. During the 1st and 2nd cycle, she was asymptomatic and responded well to treatment. During the 3rd cycle, after 1st dose of bortezomib, she developed abdominal pain localized in the epigastrium and mild distension of abdomen. There was mild epigastric tenderness and decreased bowel sounds. There was no rigidity or guarding. A laboratory work‑up did not demonstrate hypertriglyceridemia or hypercalcemia. The serum lipase and amylase were high (233 IU/L and 126 IU/L respectively). Ultrasound abdomen revealed heterogeneous and bulky distal body and tail of pancreas, there were no peripancreatic fluid collections, no biliary dilatation or gallstones. A diagnosis of AP was made. An endoscopic ultrasound did not reveal any evidence of microlithiasis, pancreas divisum or any change suggestive of underlying chronic pancreatitis. Her lipase level 2 days after the 1st dose decreased to 193 IU/L. On day 4, 2nd dose of bortezomib given, but her epigastric pain increased and serum lipase increased to 361 IU/L, which started resolving after few days and the patient became asymptomatic. In view of resolving pancreatitis, 3rd dose of bortezomib was given on day 11. After the 3rd dose, her symptoms again aggravated and lipase increased to 353 IU/L as shown in Figure 1. Concomitant medications including dexamethasone had not been stopped. In view of suspicion of bortezomib induced pancreatitis, 4th dose of 3rd cycle was withheld. Her symptoms subsided and she discharged with advice to follow‑up after 7 days. According to the Naranjo probability scale, bortezomib‑induced AP was probable.[4] A retrospective study conducted in Germany concluded that the incidence of drug‑induced AP is 1.4%.[5] Other
An unusual complication of bortezomib therapy: Acute pancreatitis Sir, Bortezomib is recommended as a primary induction therapy for patients with multiple myeloma who are not candidates for bone marrow transplantation. There are few case reports of bortezomib‑induced acute pancreatitis (AP).[1‑3] A 58‑year‑old female presented with fever and vomiting of 2‑month duration with rapidly progressive renal failure. In view of nephrotic range proteinuria and normal kidney size, kidney biopsy was done, which revealed cast nephropathy. Indian Journal of Nephrology
Figure 1: Line diagram showing relationship between dose of Inj. bortezomib with serum lipase levels during 3rd cycle of chemotherapy. Inj. bortezomib was given on day 1, 4 and 11 March 2014 / Vol 24 / Issue 2
135
Letters to Editor
mechanisms for drug‑induced AP have been associated with adverse effects of drugs, such as hypertriglyceridemia or chronic hypercalcemia, which are risk factors for AP. In our case, the diagnosis was based on the exclusion of other causes and the resolution of clinical and biological signs when the bortezomib was withdrawn and evidence of a positive rechallenge. In conclusion, clinicians should be aware that AP may occur in patients taking bortezomib. H. Gupta, R. Bansal, S. Khanna1, S. Saxena Departments of Nephrology, and 1Gastroenterology, PSRI Hospital, New Delhi, India Address for correspondence: Dr. Hitesh Gupta, Department of Nephrology, PSRI Hospital, New Delhi ‑ 110 017, India. E‑mail: [email protected]
References 1. 2.
3.
4.
5.
Elouni B, Ben Salem C, Zamy M, Sakhri J, Bouraoui K, Biour M. Bortezomib‑induced acute pancreatitis. JOP 2010;11:275‑6. Li Destri G, Innao V, Petrillo G, Di Cataldo A. A rare pancreatic pseudoaneurysm in patient with acute pancreatitis and multiple myeloma. Ann Ital Chir 2011;82:301‑4. Solakoglu T, Akyol P, Guney T, Dilek I, Atalay R, Koseoglu H, et al. Acute pancreatitis caused by bortezomib. Pancreatology 2013;13:189‑90. Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981;30:239‑45. Lankisch PG, Dröge M, Gottesleben F. Drug induced acute pancreatitis: Incidence and severity. Gut 1995;37:565‑7. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.127928
and blood pressure of 80/60 mmHg. Abdomen was distended and tender with sluggish peristaltic sounds. Patient had a past history of nephrotic syndrome during childhood for which he was treated with steroids and he had frequent relapses. He was treated with cyclophosphamide at the age of 17 years, after which he remained asymptomatic. The straight X‑ray abdomen showed distended small bowel loops. He was managed conservatively with intravenous crystalloids, Ryle’s tube aspiration and antibiotics. He had Hemoglobin of 10.9 g/dl, normal liver function test and urea: 53 mg/dl, creatinine: 1.9 mg/dl. Blood triglyceride and cholesterol level were: 872 mg/dl and 345 mg/dl respectively. His serum albumin was: 1.8 g/dl and urine for Albumin creatinine ratio was 1072 mg/dl. Serum amylase and lipase were within the normal limits. Autoimmune serology was negative and complement level was normal. Ultrasonography showed distended small bowel loops, normal pancreas, normal renal size and echotexture and normal renal vein. The findings were suggestive of intussussception of the bowel with a typical “crescent in doughnut” sign [Figure 1]. This is formed by hypoechoiec intussusceptum surrounding hyperechoiec mesenteric fat. [1] Percutaneous renal biopsy demonstrated features consistent with minimal change disease. Patient improved with conservative management. Nephrotic syndrome may be associated with gastrointestinal disturbances. The differential diagnosis considered in this setting is renal vein thrombosis, peptic ulcer disease and sub‑acute bowel obstruction. Ultrasonography is the diagnostic tool of choice to detect intussusception. In our case, presence of hypertriglyceridemia initially tempted us to make pancreatitis as a provisional diagnosis. Intussusception has been reported frequently in pediatric
Small bowel intussusception in an adult with nephrotic syndrome Sir, A 27‑year‑old male was admitted to our hospital with acute colicky pain abdomen, abdominal distention for 4 days with no passage of stool for the same duration. He also had swelling of bilateral lower limbs for a week. Examination showed mild pallor, tachycardia 136
March 2014 / Vol 24 / Issue 2
Figure 1: Transverse view of intussusception in ultrasonography producing the “crescent in doughnut”sign (white arrow)
Indian Journal of Nephrology
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
any alarming signs, evaluation by imaging modalities complemented by angiographic studies, and timely intervention, either medical or surgical, can be life saving in this clinical scenario. S. A. George, I. Francis Department of Histopathology, Mubarak Al Kabir Hospital, Jabriya, Kuwait Address for correspondence: Dr. Smiley Annie George, Department of Histopathology, Mubarak Al Kabir Hospital, P. O. Box 43787, 32052 Jabriya, Kuwait. E‑mail: [email protected]
References 1.
2.
3.
4.
Arlet JB, Le ThiHuong D, Marinho A, Cluzel P, Wechsler B, Piette JC. Arterial aneurysms in Wegener’s granulomatosis: Case report and literature review. Semin Arthritis Rheum 2008;37:265‑8. Ohta N, Waki T, Fukase S, Suzuki Y, Kurakami K, Aoyagi M, et al. Aortic aneurysm rupture as a rare complication of granulomatosis with poyangiitis: A case report. J Med Case Rep 2013;7:202. Senf R, Jürgensen JS, Teichgräber U, Kampf D, Schindler R. Ruptured arterial aneurysm of the kidney in a patient with Wegener’s granulomatosis. Nephrol Dial Transplant 2003;18:2671‑3. Durai R, Agrawal R, Piper K, Brohi K. Wegener’s granulomatosis presenting as an abdominal aortic aneurysm: A case report. Cases J 2009;2:9346. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.127923
She was found to have multiple myeloma and was started on bortezomib and dexamethasone. Each cycle consist of 4 doses on 0, 4, 11, 14th day. During the 1st and 2nd cycle, she was asymptomatic and responded well to treatment. During the 3rd cycle, after 1st dose of bortezomib, she developed abdominal pain localized in the epigastrium and mild distension of abdomen. There was mild epigastric tenderness and decreased bowel sounds. There was no rigidity or guarding. A laboratory work‑up did not demonstrate hypertriglyceridemia or hypercalcemia. The serum lipase and amylase were high (233 IU/L and 126 IU/L respectively). Ultrasound abdomen revealed heterogeneous and bulky distal body and tail of pancreas, there were no peripancreatic fluid collections, no biliary dilatation or gallstones. A diagnosis of AP was made. An endoscopic ultrasound did not reveal any evidence of microlithiasis, pancreas divisum or any change suggestive of underlying chronic pancreatitis. Her lipase level 2 days after the 1st dose decreased to 193 IU/L. On day 4, 2nd dose of bortezomib given, but her epigastric pain increased and serum lipase increased to 361 IU/L, which started resolving after few days and the patient became asymptomatic. In view of resolving pancreatitis, 3rd dose of bortezomib was given on day 11. After the 3rd dose, her symptoms again aggravated and lipase increased to 353 IU/L as shown in Figure 1. Concomitant medications including dexamethasone had not been stopped. In view of suspicion of bortezomib induced pancreatitis, 4th dose of 3rd cycle was withheld. Her symptoms subsided and she discharged with advice to follow‑up after 7 days. According to the Naranjo probability scale, bortezomib‑induced AP was probable.[4] A retrospective study conducted in Germany concluded that the incidence of drug‑induced AP is 1.4%.[5] Other
An unusual complication of bortezomib therapy: Acute pancreatitis Sir, Bortezomib is recommended as a primary induction therapy for patients with multiple myeloma who are not candidates for bone marrow transplantation. There are few case reports of bortezomib‑induced acute pancreatitis (AP).[1‑3] A 58‑year‑old female presented with fever and vomiting of 2‑month duration with rapidly progressive renal failure. In view of nephrotic range proteinuria and normal kidney size, kidney biopsy was done, which revealed cast nephropathy. Indian Journal of Nephrology
Figure 1: Line diagram showing relationship between dose of Inj. bortezomib with serum lipase levels during 3rd cycle of chemotherapy. Inj. bortezomib was given on day 1, 4 and 11 March 2014 / Vol 24 / Issue 2
135
Letters to Editor
mechanisms for drug‑induced AP have been associated with adverse effects of drugs, such as hypertriglyceridemia or chronic hypercalcemia, which are risk factors for AP. In our case, the diagnosis was based on the exclusion of other causes and the resolution of clinical and biological signs when the bortezomib was withdrawn and evidence of a positive rechallenge. In conclusion, clinicians should be aware that AP may occur in patients taking bortezomib. H. Gupta, R. Bansal, S. Khanna1, S. Saxena Departments of Nephrology, and 1Gastroenterology, PSRI Hospital, New Delhi, India Address for correspondence: Dr. Hitesh Gupta, Department of Nephrology, PSRI Hospital, New Delhi ‑ 110 017, India. E‑mail: [email protected]
References 1. 2.
3.
4.
5.
Elouni B, Ben Salem C, Zamy M, Sakhri J, Bouraoui K, Biour M. Bortezomib‑induced acute pancreatitis. JOP 2010;11:275‑6. Li Destri G, Innao V, Petrillo G, Di Cataldo A. A rare pancreatic pseudoaneurysm in patient with acute pancreatitis and multiple myeloma. Ann Ital Chir 2011;82:301‑4. Solakoglu T, Akyol P, Guney T, Dilek I, Atalay R, Koseoglu H, et al. Acute pancreatitis caused by bortezomib. Pancreatology 2013;13:189‑90. Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981;30:239‑45. Lankisch PG, Dröge M, Gottesleben F. Drug induced acute pancreatitis: Incidence and severity. Gut 1995;37:565‑7. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.127928
and blood pressure of 80/60 mmHg. Abdomen was distended and tender with sluggish peristaltic sounds. Patient had a past history of nephrotic syndrome during childhood for which he was treated with steroids and he had frequent relapses. He was treated with cyclophosphamide at the age of 17 years, after which he remained asymptomatic. The straight X‑ray abdomen showed distended small bowel loops. He was managed conservatively with intravenous crystalloids, Ryle’s tube aspiration and antibiotics. He had Hemoglobin of 10.9 g/dl, normal liver function test and urea: 53 mg/dl, creatinine: 1.9 mg/dl. Blood triglyceride and cholesterol level were: 872 mg/dl and 345 mg/dl respectively. His serum albumin was: 1.8 g/dl and urine for Albumin creatinine ratio was 1072 mg/dl. Serum amylase and lipase were within the normal limits. Autoimmune serology was negative and complement level was normal. Ultrasonography showed distended small bowel loops, normal pancreas, normal renal size and echotexture and normal renal vein. The findings were suggestive of intussussception of the bowel with a typical “crescent in doughnut” sign [Figure 1]. This is formed by hypoechoiec intussusceptum surrounding hyperechoiec mesenteric fat. [1] Percutaneous renal biopsy demonstrated features consistent with minimal change disease. Patient improved with conservative management. Nephrotic syndrome may be associated with gastrointestinal disturbances. The differential diagnosis considered in this setting is renal vein thrombosis, peptic ulcer disease and sub‑acute bowel obstruction. Ultrasonography is the diagnostic tool of choice to detect intussusception. In our case, presence of hypertriglyceridemia initially tempted us to make pancreatitis as a provisional diagnosis. Intussusception has been reported frequently in pediatric
Small bowel intussusception in an adult with nephrotic syndrome Sir, A 27‑year‑old male was admitted to our hospital with acute colicky pain abdomen, abdominal distention for 4 days with no passage of stool for the same duration. He also had swelling of bilateral lower limbs for a week. Examination showed mild pallor, tachycardia 136
March 2014 / Vol 24 / Issue 2
Figure 1: Transverse view of intussusception in ultrasonography producing the “crescent in doughnut”sign (white arrow)
Indian Journal of Nephrology
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
