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Year : 2017  |  Volume : 60  |  Issue : 1  |  Page : 135-137
Pancreatic lipomatosis in a pregnant diabetic patient

Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

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Date of Web Publication14-Feb-2017

How to cite this article:
Bhagat P, Vaiphei K. Pancreatic lipomatosis in a pregnant diabetic patient. Indian J Pathol Microbiol 2017;60:135-7

How to cite this URL:
Bhagat P, Vaiphei K. Pancreatic lipomatosis in a pregnant diabetic patient. Indian J Pathol Microbiol [serial online] 2017 [cited 2020 Jul 11];60:135-7. Available from: http://www.ijpmonline.org/text.asp?2017/60/1/135/200035


Pancreatic lipomatosis (PL) is characterized by fat replacement of the pancreatic parenchyma. It may be congenital or may coexist with morbid obesity, diabetes mellitus (DM), chronic pancreatitis, hereditary pancreatitis, pancreatic duct obstruction by calculus or tumor, and cystic fibrosis.[1] Here, we report such a rare case in a young female who had gestational DM and died of renal failure and septicemia following spontaneous abortion.

A 30-year-old female presented to us with fever following spontaneous abortion at 5 months of her second pregnancy. She had a history of fever of 5 days duration associated with cough, progressive breathlessness, right-sided chest pain, and lower back ache. In her first pregnancy, she was detected to have an intrauterine fetal death due to congenital heart block at 37 weeks of gestation 4 years back. During routine investigations, she was detected to have gestational DM with no record of the level of blood sugar available, and was treated with insulin during the hospital stay. At the time of discharge, she was put on oral hypoglycemic drugs, which she had taken only for a few weeks. During the routine check-up in the second pregnancy, she was detected to have random blood sugar of 320 mg/dl at 5 months of pregnancy. Her fasting blood sugar was 230 mg/dl, and she was treated with insulin. She was nonalcoholic and nontobacco user. There was no history that might be associated with malabsorption and no family history of DM or hypertension. On examination, she was found to be thin built and pale, no jaundice or cyanosis or pedal edema. Laboratory investigations revealed hemoglobin of 6.9 g/dL with hypochromic micro- and macro-cytes, and occasional ovalocytes. Total leukocyte count was 12,100/cumm with neutrophilia. She had normal platelets and erythrocyte sedimentation rate. Her serum electrolytes were within normal range. Her peripheral blood smear was negative for malarial parasite. She had normal liver function test. Her renal function test showed urea of 25 mg/dl and creatinine of 1.8 mg/dl. The venereal disease research laboratory test and rapid test for human immunodeficient virus were nonreactive. Urine examination showed 4+ sugar, ketone bodies, pus, and red blood cells. Her blood culture was sterile in three different samples. Ultrasonography of the kidneys showed hypoechoic cortex and loss of demarcation between outer cortex and pyramids suggesting a diagnosis of pyelonephritis. The findings of the ultrasound were further confirmed by computerized tomography of the abdomen, which also revealed the presence of multiple stones within pancreas [Figure 1]a. Her blood sugar normalized with insulin. She was also given antibiotics for the underlying sepsis. She had responded initially but towards the end, i.e., on the 13th day of the hospital stay, she again developed fever and radiological evidence of bronchopneumonia. Ultimately, she succumbed to her illness after 15 days of hospital stay.
Figure 1: (a) Computerized tomography highlighted radio-opaque multiple stones within pancreas. (b) Gross photograph of the cut surface of the whole pancreas to show the yellow colored fat replacing the pancreatic parenchyma diffusely. (c) Medium power photomicrograph of the pancreas to show the mature fat cells entrapping the residual pancreatic tissue comprising only of  Islets of Langerhans More Details (H and E, ×250). (d) Low power photomicrograph of the kidney to show diffuse infiltration of the renal parenchyma by inflammatory cells entrapping the renal glomeruli (H and E, ×100)

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Autopsy was performed to determine the underlying cause of death. At autopsy, there was 500 ml of serous fluid in peritoneal cavity, pleural and pericardial cavities did not show any excess of fluid. The pancreas was found to be grossly bulky measuring 20 cm × 5 cm × 5 cm due to gross adhesion to the surrounding soft tissue. Serial slicing of the pancreas appeared yellowish due to marked increase in adipose tissue and preservation of scanty whitish lobulated pancreatic parenchyma [Figure 1]b. There were multiple varying size brownish colored stones measuring 0.2–4.5 cm × 4.4 cm within pancreatic parenchyma and ectatic ducts. Common bile duct and gall bladder were normal. Microscopic examination showed diffuse replacement of the pancreas by mature adipose tissue, and fibrosis in and around residual lobules of pancreatic acini and periductal areas. There was minimal inflammation. Islets of Langerhans were relatively preserved and there was no amyloid deposition or evidence of inflammation [Figure 1]c. A diagnosis of PL with chronic calcific pancreatitis was considered. The kidneys were asymmetrically contracted with loss of corticomedullary distinction. Pelvicalyceal systems were distorted and contained necrotic pus-like material. The papillae were discolored and soft. Sections of the kidneys showed multiple subcapsular scars with sclerosed glomeruli. There was ulceration of the pelvicalyceal lining mucosa with exuberant inflammatory cell exudates. There was heavy diffuse inflammatory cell infiltration of the renal parenchyma [Figure 1]d with multiple microabscesses both in cortex and medulla, destruction of the tubules, patchy early collagenization, and focal lymphoid aggregate formations. There was no histological evidence of diabetic nephropathy or vasculitis. Inflammation was seen involving both ureters and urinary bladder. Lungs showed patchy bronchopneumonia and there were esophagogastric erosions. In the multiple sections studied, there was no evidence of any bacterial colony. Bone marrow section was hypercellular with erythroid hyperplasia and megaloblastosis. Rest of the organs did not show any specific finding.

PL is characterized either by a normal sized or moderately enlarged gland that maintains its shape and lobular architecture. Microscopically, the parenchyma consists of mature adipose tissue separated by fibrous septa containing isolated clusters of normal islet of Langerhans. Lipomatous infiltration of the pancreas has been reported in patients with obstruction of the pancreatic duct by an intraductal stone, carcinoma, or by cyst. There are reports of two cases in the English literature of diffuse PL; the first one was reported by Patel et al.[2] in a 59-year-old diabetic male with stones in pancreatic duct and the second one by Makay et al. in a 60-year-old male patient who had pancreatic head adenocarcinoma.[3] Haunz and Baggenstoss observed fat replacement in pancreatic tail region in a study of eighty carcinomas in pancreatic head region.[4] Patients with total PL have poor outcomes, and malabsorption has a major impact on the quality of life. Pancreatic enzyme supplementation in combination with dietary counseling is the mainstay of the treatment in these patients.

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There are no conflicts of interest.

   References Top

Soyer P, Spelle L, Pelage JP, Dufresne AC, Rondeau Y, Gouhiri M, et al. Cystic fibrosis in adolescents and adults: Fatty replacement of the pancreas – CT evaluation and functional correlation. Radiology 1999;210:611-5.  Back to cited text no. 1
Patel S, Bellon EM, Haaga J, Park CH. Fat replacement of the exocrine pancreas. AJR Am J Roentgenol 1980;135:843-5.  Back to cited text no. 2
Makay O, Kazimi M, Aydin U, Nart D, Yilmaz F, Zeytunlu M, et al. Fat replacement of the malignant pancreatic tissue after neoadjuvant therapy. Int J Clin Oncol 2010;15:88-92.  Back to cited text no. 3
Haunz EA, Baggenstoss AH. Carcinoma of head of the pancreas. Arch Pathol 1950;49:367-86.  Back to cited text no. 4

Correspondence Address:
Prof. Kim Vaiphei
Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.200035

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