Pancreatic Fat Necrosis Research Articles

Effects of curcumin on oxidative stress, inflammation and apoptosis in L-arginine induced acute pancreatitis in mice

Background and purposeCurcumin, an active constituent of rhizomes of Curcuma longa Linn, exhibits a variety of biological activities such as anti-inflammation and anti-oxidant. The present study aims to examine the effects of curcumin on oxidative stress, inflammation and apoptosis in L-arginine induced acute pancreatitis (AP) in mice. MethodsMale ICR mice were randomly divided into 4 groups. Control group received intraperitoneal injection (i.p.) of 1% DMSO as a vehicle. AP group received two doses of i.p. L-arginine (L-Arg) 450 mg/100 g body weight (BW) at 1-hour interval. AP plus low-dose curcumin group received i.p. curcumin 50 mg/kg BW 1 hour before L-Arg injection and then once daily for 3 days. AP plus high-dose curcumin group received i.p. curcumin 200 mg/kg BW 1 hour before L-Arg injection and then once daily for 3 days. All mice were sacrificed at 72 hours. Pancreatic tissue was obtained for histological evaluation, immunohistochemical studies for nuclear factor-kappa beta (NF-kβ), apoptosis and myeloperoxidase (MPO), and Western blot analyses for 4-Hydroxynonenal (4-HNE). Blood samples were collected for amylase analysis. ResultsMean body weight was significantly lower in AP group than in control group, while in curcumin group, body weight was maintained. The serum amylase, number of MPO positive cells, NF-kB positive cells, TUNEL positive cells, and 4-HNE expression significantly increased in AP group when compared with control group, but decreased in low and high-dose curcumin groups. Mice in AP group developed severe pancreatic inflammation, edema and fat necrosis. While mice in low and high-dose curcumin groups showed a significant improvement in histopathological scores. There was no significant difference between low and high doses of curcumin. ConclusionCurcumin could attenuate acute pancreatitis via anti-oxidant, anti-inflammation and anti-apoptosis property leading to the improvement in pancreatic damage.

Cutaneous paraneoplastic syndromes

A variety of cutaneous abnormalities can be seen in patients with malignant diseases, some of which are infectious, with others representing direct involvement of the skin by the underlying disorder. Yet another group of lesions can be regarded as associated markers of the malignant process, and, as such, are termed "paraneoplastic." This review considers the latter collection of conditions, grouping them by the generic type of malignancy that is usually linked to the paraneoplasia. Some of the processes show a predominant association with alimentary tract malignancies (acanthosis nigricans, acrodermatitis paraneoplastica, florid cutaneous papillomatosis, necrolytic migratory erythema, palmoplantar keratoderma, pancreatic fat necrosis, and pityriasis rotunda). Others are usually linked to a hematolymphoid malignancy (acquired ichthyosis, exfoliative erythroderma, necrobiotic xanthogranuloma, pemphigus paraneoplastica, plane xanthoma, pyoderma gangrenosum, scleromyxedema, Sweet syndrome, and leukocytoclastic vasculitis). Finally, yet another collection of paraneoplastic skin disorders can associate themselves with anatomically-diverse malignancies (Leser-Trelat syndrome, Trousseau syndrome, dermatomyositis, erythema gyratum repens, hypertrichosis lanuginosa acquisita, papuloerythroderma of Ofuji, tripe palms, and multicentric reticulohistiocytosis). Recognition of these processes by the pathologist can be a valuable step in the characterization of underlying malignant diseases.

Últimos avances en pancreatitis aguda

The present article analyses the main presentations on acute pancreatitis at Digestive Disease Week 2015. Arterial pseudoaneurysm is an uncommon complication of acute pancreatitis (incidence 0.7%) and mortality from this cause is currently anecdotal. Diabetes mellitus has little impact on the clinical course of acute pancreatitis, unlike cirrhosis, which doubles the risk of mortality. Intake of unsaturated fat could be associated with an increased severity of acute pancreatitis and is a confounding factor in studies evaluating the relationship between obesity and morbidity and mortality. PET-CT (positron emission tomography-computed tomography) could be a non-invasive tool to detect infection of collections in acute pancreatitis. Peripancreatic fat necrosis is less frequent than pancreatic fat necrosis and is associated with a better clinical course. If the clinical course is poor, increasing the calibre of the percutaneous drains used in the treatment of infected necrosis can avoid surgery in 20% of patients. The use of low molecular-weight heparin in moderate or severe pancreatitis could be associated with a better clinical course, specifically with a lower incidence of necrosis. In acute recurrent pancreatitis, simvastatin is a promising drug for prophylaxis of new episodes of acute pancreatitis. Nutritional support through a nasogastric tube does not improve clinical course compared with oral nutrition.

Erythema ab igne

A 25-year-old woman was found dead in bed. She had a past history of seizures, alcohol and substance abuse, pancreatitis, psoriasis, pelvic inflammatory disease, hypertension, and depression. Previous admissions to hospital had been for chronic abdominal pain which was eased by holding a hot water bottle to her abdomen and back. At autopsy the major findings were limited to the brain which was swollen with flattening of gyri. There was no extradural or subdural hemorrhage. Subarachnoid hemorrhage was noted over the left temporal pole, with extension over the left frontal region and inferior surface of the left occipital lobe. This was associated with a ruptured saccular aneurysm of the left middle cerebral artery and adjacent intracerebral hemorrhage. The aneurysm was confirmed microscopically with reactive changes around the site of rupture at the apex of the lesion and at the margins of the intracerebral hematoma anteriorly suggesting that there had been an element of sentinel hemorrhage a few days prior to death. The pancreas had been completely effaced by firm, white, fibrous tissue containing calcific debris. At the tail of the pancreas, there was a 5 cm cyst with a smooth wall that contained white fluid with no evidence of infection. No other underlying organic diseases were present which could have caused or contributed to death. There was no evidence of a connective tissue disorder. There were no significant injuries and toxicology revealed therapeutic levels of quetiapine and temazepam, with tetrahydrocannabinol, but no alcohol or other common drugs. The other finding of note was the presence of areas of variegated pigmented skin with an arborescent pattern on the abdomen (Fig. 1) and to a lesser extent on the back. Microscopically the overlying epidermis was undulating with a basket-weave pattern of surface keratinization that ranged from a normal thickness to slight atrophy. The latter appeared due to a lichenoid reaction with foci of basal vacuolar change resulting in small numbers of apoptotic keratinocytes and papillary dermal colloid bodies. The papillary dermis showed a loose architecture from increased deposition of acid mucopolysaccharides. There was also a low grade lymphocytic inflammatory infiltrate with basal layer melanin pigmentation and moderate numbers of melanophages (Fig. 2). There was no epidermal basement membrane thickening or deep dermal inflammatory cell component, nor was there sweat gland necrosis, vasculitis, deep vaso-occlusive lesions, or pancreatic fat necrosis. There were no skin changes suggestive of psoriasis (which had been noted on the extensor surface of larger joints). Death was due to intracerebral and subarachnoid hemorrhage arising from a ruptured aneurysm of left middle cerebral artery. The striking skin lesions of a pigmented reticulate erythema on the abdominal wall were due to erythema ab igne caused by the recurrent application of a hot water bottle to the skin surface because of pain from chronic pancreatitis. & Roger W. Byard roger.byard@sa.gov.au

Pancreatitis In Patients Treated With Brentuximab Vedotin: A Previously Unrecognized Serious Adverse Event

BackgroundBrentuximab vedotin (BV) is a novel antibody drug conjugate consisting of an anti- CD30 IgG1 antibody, cAC10, linked to monomethylauristatin E, a potent inhibitor of microtubule polymerization. It is approved for treatment of relapsed classical Hodgkin lymphoma (cHL) and anaplastic large cell lymphoma (ALCL) in the US (FDA; 8/2011) and Europe (EMA; 10/2012). Peripheral neuropathy was the most frequent treatment-related adverse event (AE) in phase II trials, and the most common Grade 3 or higher toxicity apart from cytopenias. Although abdominal pain has been observed in up to 25% of all patients, pancreatitis is a previously unrecognized AE. We now report 8 cases of BV-associated pancreatitis, 2 of them fatal. MethodsFollowing a grade 5 AE from pancreatitis in a patient receiving single-agent BV on an ongoing clinical trial (NCT01476410), collaborating investigators examined their collective cases of pancreatitis associated with BV. Lymphoma specialists at other centers were solicited for additional events. IRB or Ethics Committee approval as required was obtained in all cases. AE's reported to the FDA Adverse Event Report Systems (FAERS) from 6/2011-7/2013 were also examined. Data was collected and analyzed through the Research on Adverse Drug Events and Reports Project. Immunohistochemical staining with the anti-CD30 antibody BER-H2 (DAKO) was performed on residual normal pancreas from one of the fatal cases and normal control pancreas. ResultsEight cases of BV-associated pancreatitis were identified by collaborators, and one additional report with limited information was listed in FAERS. Demographic, treatment and AE information for the eight complete cases is detailed in Table 1. In all cases, BV was administered as a single agent. In seven cases, the dosing was 1.8 mg/kg every 21 days with a maximum of 180 mg; in one case, BV was administered weekly at 1.2 mg/kg (days 1,8,15, q 28). Two patients were retreated with BV after resolution of pancreatitis; one had no further evidence of pancreatitis and proceeded to a stem cell transplant, whereas the other patient, having recovered from Grade 4 pancreatitis, experienced a second episode (Grade 3). All patients demonstrated clinical evidence of pancreatitis as manifested by severe abdominal pain and nausea. In addition, all patients had biochemical and radiologic evidence of pancreatitis. Notably, no patient had an antecedent history of excess alcohol use or radiologic evidence of biliary pathology. Two patients developed progressive and fatal multiorgan dysfunction as a consequence of acute pancreatitis. An autopsy performed on one of the two fatalities showed evidence of acute necrotizing pancreatitis as the cause of death; diffuse pancreatic parenchymal necrosis and fat necrosis were seen but no cholelithiasis. Although the anti-CD30 antibody BER-H2 was previously reported to stain normal pancreas (BLOOD 1989 74:1678), routine immunohistochemical staining for CD30 on both the patient pancreas and normal pancreas controls were negative. ConclusionThis is the first series describing pancreatitis as a rare, but serious and potentially fatal toxicity related to BV. Pancreatitis has been previously reported with other microtubule inhibitors such as taxanes and vinca alkaloids, but the mechanism, as with BV, remains unclear. Genetic factors that predispose to both acute and chronic pancreatitis have been reported and may underlie a susceptibility to this uncommon complication of treatment with BV. Clinicians prescribing BV should evaluate patients who present with abdominal pain for pancreatitis, and should consider pre-treatment biochemical assessments with serum lipase and/or amylase. Disclosures:Off Label Use: Brentuximab Vedotin is approved for relapsed, refractory Hodgkin Lymphoma in patients who have already had a transplant or are ineligible for one, or for patients with relapsed, refractory anaplastic large cell lymphoma. Patients treated on clinical trials or off label will be included in this presentation. Evens:Seattle Genetics : Consultancy, Honoraria. Fenske:Seattle Genetics: Consultancy. Hamlin:Seattle Genetics : Consultancy, Honoraria. Coiffier:Millennium Pharmaceuticals : Consultancy. Engert:Millennium Pharmaceuticals : Consultancy. Moskowitz:Seattle Genetics : Research Funding. Ghosh:Millennium Pharmaceuticals : Membership on an entity's Board of Directors or advisory committees. Petrich:Seattle Genetics : Consultancy, Honoraria, Research Funding. Gordon:Seattle Genetics : Research Funding. Winter:Seattle Genetics : Research Funding.

Pancreatic Fat Necrosis and Hemorrhagic Necrosis as Separate Morphological and Functional Entities

Peculiarities of pathomorphogenesis of two destructive forms of acute pancreatitis were compared using three experimental models. We have shown that the direction of the pathological process is determined by specific combinations of pathogenic factors. Pathological processes caused by common bile duct ligation (ductal hypertension) alone and in combination with injection of phospholipase A2 are characterized by mixed pattern with strong predominance of fat necrosis symptoms (coagulative acinar necrosis, inflammatory demarcation, and sites of lipolysis) and hemorrhagic necrosis, respectively. Trypsin injection into the pancreatic tissue induces rapidly progressing hemorrhagic pancreatic necrosis with massive hemorrhages, extensive acinar necrosis, and weak cell reaction. Considerable differences in pathomorphogenesis and outcome of the pathological process allow us to consider pancreatic fat necrosis and hemorrhagic necrosis as separate morphological and functional entities, which is essential for the prognosis and treatment strategy.

Chronic pancreatitis in dogs: A retrospective study of clinical, clinicopathological, and histopathological findings in 61 cases

The objective of this study was to characterize the clinical, clinicopathological, and histopathological findings of dogs with chronic pancreatitis. The necropsy database at Texas A&M University was searched for reports of dogs with histological evidence of chronic pancreatitis defined as irreversible histologic changes of the pancreas (i.e. fibrosis or atrophy). A reference necropsy population of 100 randomly selected dogs was used for signalment and concurrent disease comparisons. Cases were categorized as clinical or incidental chronic pancreatitis based on the presence of vomiting, decreased appetite, or both vs. neither of these signs. All archived pancreas samples were scored histologically using a published scoring system. Sixty-one dogs with chronic pancreatitis were included. The most frequent clinical signs were lethargy, decreased appetite, vomiting, and diarrhea. Compared to the reference necropsy population, chronic pancreatitis cases were more likely to be older, neutered, of the non-sporting/toy breed group, and to have concurrent endocrine, hepatobiliary, or neurological disease. Clinical cases had significantly higher histological scores for pancreatic necrosis and peripancreatic fat necrosis, and were significantly more likely to have hepatobiliary or endocrine disease as well as increased liver enzyme activities, or elevated cholesterol and bilirubin concentrations. In conclusion, clinical disease resulting from chronic pancreatitis might be related to the presence of pancreatic necrosis and pancreatic fat necrosis. The signalment, presentation, and concurrent diseases of dogs with chronic pancreatitis are similar to those previously reported for dogs with acute pancreatitis.

Panniculitis: clinical overlap and the significance of biopsy findings

Panniculitides are well-recognized clinicopathologic entities but the non-specificity of their clinical and pathological features often troubles the diagnostician. This study retrospectively evaluates the clinical overlaps and the significance of histological findings among various panniculitides. The clinical evaluation in 55 panniculitides cases suggested the diagnosis of typical erythema nodosum (EN) in 26 cases, atypical EN in 17 cases, atypical nodular vasculitis (NV) in two cases, soft tissue infection in five cases and five cases remained unclassified. Skin biopsy evaluation provided definite panniculitis diagnosis in 53 cases including EN (28 cases), leukocytoclastic vasculitis (seven cases), NV (four cases), superficial thrombophlebitis (ST) (two cases), eosinophillic panniculitis (EP) (three cases), infection-related panniculitis (five cases), and one case each of erythema nodosum leprosum (ENL), lupus panniculitis (LP), pancreatic fat necrosis and acne conglobata with two cases remaining unclassified. Histologically, 'predominantly septal' and 'mixed panniculitis' were the chief inflammatory patterns in EN cases, while mixed panniculitis was seen in most LCV cases and predominantly lobular and mixed panniculitis in NV cases. Biopsy evaluation of a panniculitis lesion is usually significant, and the application of a combination of histologic features rather than of a single biopsy finding or an inflammatory pattern is helpful in the diagnosis of panniculitis.

Recognition of Toxoplasma gondii by TLR11 Prevents Parasite-Induced Immunopathology

TLRs are thought to play a critical role in self/non-self discrimination by sensing microbial infections and initiating both innate and adaptive immunity. In this study, we demonstrate that in the absence of TLR11, a major TLR involved in recognition of Toxoplasma gondii, infection with this protozoan parasite induces an abnormal immunopathological response consisting of pancreatic tissue destruction, fat necrosis, and systemic elevations in inflammatory reactants. We further show that this immunopathology is the result of non-TLR dependent activation of IFN-gamma secretion by NK cells in response to the infection. These findings reveal that in addition to triggering host resistance to infection, TLR recognition can be critical for the prevention of pathogen-induced immune destruction of self tissue.

Histologic Assessment and Grading of the Exocrine Pancreas in the Dog

Histologic grading schemes for canine inflammatory conditions are sparse, and in the case of the canine pancreas, have not been previously described. In a previous study, we determined that histologic lesions of the exocrine pancreas occurred much more frequently than gross lesions. The intention of the current study was to develop a histologic grading scheme for nonneoplastic lesions following extensive assessment of the exocrine pancreas from dogs presented for necropsy examination. The parameters of the proposed scheme include neutrophilic inflammation, lymphocytic inflammation, pancreatic necrosis, pancreatic fat necrosis, edema, fibrosis, atrophy, and hyperplastic nodules. In this case series, the most common lesion was pancreatic hyperplastic nodules (80.2%), followed by lymphocytic inflammation (52.5%), fibrosis (49.5%), atrophy (46.5%), neutrophilic inflammation (31.7%), pancreatic fat necrosis (25.7%), pancreatic necrosis (16.8%), and edema (9.9%). Only 8 of the 101 animals had no evidence of any of the lesions in any of the sections examined. Fibrosis, atrophy, and/or lymphocytic infiltration most commonly accompanied nodules. Neutrophilic inflammation, when present, was often associated with necrosis (pancreatic necrosis, pancreatic fat necrosis, or both) and occasionally with hyperplastic nodules. The utilization of a grading scheme for exocrine pancreatic lesions will be useful in advancing the classification of exocrine pancreatic disease in the dog, which may lead to multicenter studies of exocrine pancreatic disorders in the dog and in other species.

Pancreatic Panniculitis Due to Pancreatic Carcinoma

A 52-year-old woman had a 3-month history of multiple red-brown, tender subcutaneous nodules confined to the lower extremities and associated with a 15-kg weight loss. A skin incisional biopsy specimen revealed lymphocytic panniculitis with necrosis of fat cells, some appearing as ghostlike cells, consistent with pancreatic panniculitis. The serum lipase level was 2910 U/L. Computed tomography of the abdomen showed what appeared to be a tumor thrombus in the portal vein. On the basis of additional laboratory test results and fine-needle aspiration of the mass, the likely primary source for the malignancy was determined to be the pancreas, with secondary spread into the portal venous system. The patient underwent palliative chemotherapy and died within 3 months. This rare form of panniculitis typically presents as tender, dull red lower extremity nodules that may ulcerate.1Dahl PR Su WP Cullimore KC Dicken CH Pancreatic panniculitis.J Am Acad Dermatol. 1995; 33: 413-417Abstract Full Text PDF PubMed Scopus (155) Google Scholar The characteristic histological finding is the “ghost cell,” representing a necrotic, partially calcified adipocyte.1Dahl PR Su WP Cullimore KC Dicken CH Pancreatic panniculitis.J Am Acad Dermatol. 1995; 33: 413-417Abstract Full Text PDF PubMed Scopus (155) Google Scholar, 2Ball NJ Adams SP Marx LH Enta T Possible origin of pancreatic fat necrosis as a septal panniculitis.J Am Acad Dermatol. 1996; 34: 362-364Abstract Full Text PDF PubMed Google Scholar Pancreatitis and pancreatic carcinoma are the most frequently encountered precipitating conditions for pancreatic panniculitis.1Dahl PR Su WP Cullimore KC Dicken CH Pancreatic panniculitis.J Am Acad Dermatol. 1995; 33: 413-417Abstract Full Text PDF PubMed Scopus (155) Google Scholar Several other factors have been implicated as causes, including pancreatic pseudocysts, congenital anomalies of the pancreas, and blunt abdominal trauma.1Dahl PR Su WP Cullimore KC Dicken CH Pancreatic panniculitis.J Am Acad Dermatol. 1995; 33: 413-417Abstract Full Text PDF PubMed Scopus (155) Google Scholar, 2Ball NJ Adams SP Marx LH Enta T Possible origin of pancreatic fat necrosis as a septal panniculitis.J Am Acad Dermatol. 1996; 34: 362-364Abstract Full Text PDF PubMed Google Scholar When possible, correction of the underlying abnormality may lead to resolution of the panniculitis.1Dahl PR Su WP Cullimore KC Dicken CH Pancreatic panniculitis.J Am Acad Dermatol. 1995; 33: 413-417Abstract Full Text PDF PubMed Scopus (155) Google Scholar

Pancreatic Carcinoma‐Associated Subcutaneous Fat Necrosis Improved by Palliative Surgery

The Journal of DermatologyVolume 31, Issue 7 p. 584-586 Letter to the Editor Pancreatic Carcinoma-Associated Subcutaneous Fat Necrosis Improved by Palliative Surgery Hye-Jin Choi, Hye-Jin Choi Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorKyoung-Jin Kim, Corresponding Author Kyoung-Jin Kim Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, Korea Correspondence to: Kyoung-Jin Kim, M.D. Department of Dermatology Asan Medical Center University of Ulsan College of Medicine 388-1 Poongnap-dong, Songpa-gu Seoul 138-736, KoreaSearch for more papers by this authorMi-Woo Lee, Mi-Woo Lee Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorJee-Ho Choi, Jee-Ho Choi Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorKee-Chan Moon, Kee-Chan Moon Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorJai-Kyoung Koh, Jai-Kyoung Koh Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this author Hye-Jin Choi, Hye-Jin Choi Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorKyoung-Jin Kim, Corresponding Author Kyoung-Jin Kim Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, Korea Correspondence to: Kyoung-Jin Kim, M.D. Department of Dermatology Asan Medical Center University of Ulsan College of Medicine 388-1 Poongnap-dong, Songpa-gu Seoul 138-736, KoreaSearch for more papers by this authorMi-Woo Lee, Mi-Woo Lee Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorJee-Ho Choi, Jee-Ho Choi Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorKee-Chan Moon, Kee-Chan Moon Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this authorJai-Kyoung Koh, Jai-Kyoung Koh Department of Dermatology, Asan Medical Center University of Ulsan College of Medicine, KoreaSearch for more papers by this author First published: 22 July 2014 https://doi.org/10.1111/j.1346-8138.2004.tb00562.xCitations: 3Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume31, Issue7July 2004Pages 584-586 RelatedInformation

An Unusual Case of Cutaneous Pancreatic Fat Necrosis

Background: Cutaneous pancreatic fat necrosis is a pathognomonic sign for pancreatic disease and usually presents as subcutaneous nodules in the pretibial region. Objective: A case of cutaneous pancreatic fat necrosis is presented in which the clinical presentation of diffuse erythema was unusual. This disease is discussed and its possible etiologies are reviewed. Methods: A MEDLINE search for cases of cutaneous pancreatic fat necrosis presenting as diffuse erythema without nodules was conducted. Results: Diffuse erythema is an unusual presentation of cutaneous pancreatic fat necrosis. Conclusion: This may be the first case of cutaneous pancreatic fat necrosis presenting as diffuse erythema.

An Unusual Case of Cutaneous Pancreatic Fat Necrosis

Cutaneous pancreatic fat necrosis is a pathognomonic sign for pancreatic disease and usually presents as subcutaneous nodules in the pretibial region. A case of cutaneous pancreatic fat necrosis is presented in which the clinical presentation of diffuse erythema was unusual. This disease is discussed and its possible etiologies are reviewed. A MEDLINE search for cases of cutaneous pancreatic fat necrosis presenting as diffuse erythema without nodules was conducted. Diffuse erythema is an unusual presentation of cutaneous pancreatic fat necrosis. This may be the first case of cutaneous pancreatic fat necrosis presenting as diffuse erythema.

Relationship of Pancreatic and Peripancreatic Fat Necrosis to Organ Failure in Acute Pancreatitis

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Possible origin of pancreatic fat necrosis as a septal panniculitis

We describe pancreatic subcutaneous fat necrosis in a man with alcoholism and pancreatitis. The initial specimen, from a 2-day-old lesion, showed a septal inflammatory infiltrate in the subcutis. A second specimen, from a 5-day-old lesion, showed the lobular pattern of enzymatic fat necrosis diagnostic for pancreatic panniculitis. We suggest that the histologic appearance of subcutaneous pancreatic fat necrosis evolves from an early septal reaction to a fully developed lobular panniculitis.

FAT NECROSIS WITH FEATURES OF ERYTHEMA NODOSUM IN A PATIENT WITH METASTATIC PANCREATIC CARCINOMA

A 59-year-old man presented with painful subcutaneous nodules on the anterior surfaces of the legs. He had received oral antibiotics and supportive care for presumed cellulitis and thrombophlebitis, but had minimal improvement. Five months earlier, he had undergone pancreaticoduodenectomy for acinar pancreatic carcinoma; at that time, the serum level of amylase had been normal, but the level of lipase was elevated. The patient denied fever, rigors, arthritis/arthralgia, or pleuritic pain. His medications included aspirin, furosemide, ranitidine, and nortriptyline. He denied any allergies. Physical examination revealed numerous firm, tender, erythematous and violaceous, subcutaneous nodules on the lower extremities, with marked bilateral pitting edema (Fig. 1). Skin biopsy of a representative lesion revealed septal panniculitis, consistent with erythema nodosum (Fig. 2). None of the characteristic changes of pancreatic fat necrosis was present. The patient was treated with aspirin, 650 mg orally, q 6 h, and indomethacin, 50 mg orally, q 12 h, but he continued to develop new nodules; prednisone, 60 mg orally was begun. Although he reported improvement in symptoms, the nodules failed to respond clinically and older nodules ulcerated along the medical aspect of the right leg (Fig. 3). The complete blood count was normal, except for hemoglobin, 10.9 mg per dL. Routine serum biochemical studies were also normal, except for albumin, 3.1 mg per dL, LDH, 312 U per L, and SGOT, 51 U per L. Serum amylase was 14 U per L (normal per 30 to 115 U per L) and serum lipase was 54,160 U per L (normal 0 to 200 U per L). Chest roentgenogram and tuberculin skin test were negative. A CT scan of the abdomen revealed extensive liver metastases. A second biopsy of the skin and subcutis of a necrotic nodule revealed lobular panniculitis with the characteristic picture seen in pancreatic fat necrosis (Fig. 4). The patient was presumed to have metastatic pancreatic carcinoma and pancreatic fat necrosis. Nodules subsequently developed on the thighs, arms, hands, wrists, and fingers. He developed arthritis and arthralgias of the ankles, wrists, and hands, bilaterally, and the right knee. Aspiration of a right knee effusion revealed numerous neutrophils, but no evidence of infection. Treatment was begun with the somatostatin analog, octreotide, in increasing doses. During this therapy, the lesions did not progress and new lesions did not appear. There was no change in the lipase level. Inadvertently, octreotide was omitted at discharge, but reintroduction of octreotide was associated with lack of further progression of the nodules, according to the patient's spouse; however the patient became progressively debilitated and his abdominal pain worsened, requiring continuous sedation. His condition deteriorated and he died several weeks after hospital discharge.

“Osteoclastic” Giant Cell Carcinoma of the Pancreas

Osteoclastic giant cell carcinoma (OGC) is an uncommon variant of ductal carcinoma of the pancreas. It is important to differentiate this variant from other giant cell pancreatic lesions, particularly the more aggressive pleomorphic giant cell carcinoma. Aspiration cytology was performed in a case of OGC. Aspirates of OGC demonstrated three populations of discohesive cells: (1) large, bizarre, pleomorphic malignant giant cells with high nuclear/cytoplasmic ratios, irregular nuclear membranes and coarse chromatin; (2) spindle or small mononucleate cells; and (3) bland, osteoclastlike epithelial giant cells with multiple small, round, central nuclei and prominent nucleoli. Multinucleate giant cells can be seen in pancreatic abscesses, fat necrosis, pseudocysts, tuberculosis, sarcoidosis and fungal infections. When the cells are associated with malignant epithelial cells, the differential diagnosis includes metastatic carcinoma, malignant melanoma, Hodgkin's disease, large cel anaplastic lymphoma, trophoblastic tumor, epithelioid sarcoma, malignant fibrous histiocytoma, angiosarcoma and rhabdomyosarcoma. Immunohistochemical stains, such as vimentin, S-100, leukocyte common antigen, human chorionic gonadotropin, Factor VII Ag, actin and desmin play an important role in differentiating between these lesions.

Free fatty acids in serum of patients with acute necrotizing or edematous pancreatitis

Serum concentrations of free fatty acids (FFA) were assayed in 20 patients with acute necrotizing pancreatitis (ANP). Pancreatic and peripancreatic fat necrosis was verified on operation and/or by contrast-enhanced computed tomography. For comparison, 20 patients with acute edematous pancreatitis (AEP) were examined. On admission, FFA serum levels were 1.14 +/- 0.12 (SEM) mmol/L in ANP and, thus, significantly (p < 0.03) higher than in AEP (0.78 +/- 0.09 mmol/L). The two groups also differed in the later course: in ANP, the FFA values remained raised (d 5-11:0.86 +/- 0.13 mmol/L; p > 0.05 vs day 1), whereas in AEP, the FFA concentrations normalized within 1 wk (d 2-4:0.52 +/- 0.11 mmol/L; d 5-11:0.39 +/- 0.05 mmol/L; p < 0.05 vs day 1 and p < 0.01 vs ANP). Serum FFA correlated positively with C-reactive protein levels (rs = 0.42; p < 0.01), but has less discriminating potency between ANP and AEP. In AEP, the initial peak may correspond to the disease outburst itself and to unspecific stress. In ANP, the higher and sustained elevation of FFA may predominantly mirror the ongoing pancreatic parenchymal and extrapancreatic fat necrosis, and be pathophysiologically relevant, especially in view of significantly reduced serum albumin levels in ANP.

Nodular-cystic fat necrosis: A reevaluation of the so-called mobile encapsulated lipoma

We describe five patients with distinct posttraumatic subcutaneous nodules that usually evolved for several months before diagnosis. The nodules occurred in the subcutis of the elbow or hip of women, 33 to 74 years old, and in the hip of a 16-year-old boy. Histologically the fully developed lesions were totally or nearly totally encapsulated by thin, fibrous tissue. All contained well-preserved outlines of nonnucleated adipocytes; there was no inflammation or saponification. In one patient's lestion the viable subcutaneous tissue merged into several partially encapsulated necrotic nodules. In another case a smaller nodule was found within a larger, mostly calcified nodule. Names such as nodular-cystic fat necrosis, mobile encapsulated lipoma, and encapsulated necrosis have been offered to designate the lesion. Its pathogenesis seems to be related to trauma, rapid vascular insufficiency, and subsequent fibrous capsule formation. Many previously reported patients, however, had no history of trauma. The lesion must be distinguished histologically from lipoma, angiolipoma, alpha 1-antitrypsin deficiency-associated panniculitis, membranous fat necrosis, and pancreatic fat necrosis. Simple excision is the treatment of choice.