Nonmelanoma Skin Cancer

A metastatic malignancy of the umbilicus is commonly termed Sister Mary Joseph nodule (SMJN). It is a rare occurrence but may represent the first sign of a visceral malignancy and therefore should prompt a thorough search for the primary tumor. Typically, the most common origin of an umbilical metastasis is an adenocarcinoma from a gastrointestinal or gynecologic primary malignancy. The presence of SMJN carries a poor prognosis with the average survival time at the appearance of an umbilical metastasis being 10 months. We report a case of a 66-year-old man who was referred for evaluation of an enlarging umbilical lesion. Histopathology revealed adenocarcinoma. After a full metastatic workup, the tumor of origin was identified as adenocarcinoma of the sigmoid colon. Benign tumors of the umbilicus are uncommon. This case report serves to emphasize the importance of obtaining a histologic diagnosis when any new lesion presents in the umbilical region.

Case Report
A 66-year-old white man presented for evaluation of an umbilical lesion of 3 weeks' duration. The lesion was asymptomatic and nontender but was bleeding and oozing. The lesion, diagnosed by the patient's primary care physician as an infected pyogenic granuloma, was treated with oral antibiotics, without relief. His past medical history was unremarkable. He took no medications at that time and had an allergy to quinolones. His dermatologic history was positive for numerous actinic keratoses and a basal cell carcinoma on the forehead. Physical examination upon presentation revealed a 3-cm fungating polypoid umbilical mass with copious purulent exudates similar to Figure 1.1 The clinical differential diagnosis at that time included a pyogenic granuloma versus a Sister Mary Joseph nodule (SMJN). A shave biopsy was performed. Histopathology revealed multiple cystic and ductal spaces lined by atypical epithelial cells with numerous mitotic figures in the dermis (Figures 2 and 3). These changes favored a gastrointestinal primary lesion, supporting the clinical diagnosis of SMJN. The patient subsequently underwent a full metastatic workup. A computed tomographic scan of the abdomen and pelvis demonstrated no definite metastases to the lungs or liver but suggested a near-obstructing distal bowel primary tumor. A colonoscopy demonstrated a near-obstructing sigmoid colon carcinoma. The patient subsequently underwent an exploratory laparotomy, sigmoid resection, and primary colonic reanastomosis. Liver biopsies and resection of the omentum and the periumbilical abdominal wall including the eroding metastasis were performed as well as multiple peritoneal biopsies. Pathologic evaluation confirmed the presence of extensive carcinomatosis. The primary tumor was a 5.0X3.0-cm moderately differentiated adenocarcinoma of the sigmoid colon with extension through the bowel wall. Biopsies of the liver, lymph nodes, periumbilical soft tissue, omentum, and peritoneum were all positive for metastatic carcinoma. Postoperatively, the patient was started on the FOLFOX regimen incorporating folinic acid, 5-fluorouracil, and oxaliplatin. Currently, the patient remains clinically stable and without evidence of progressive sigmoid colon carcinoma.

Comment
SMJN is the term applied to an uncommon metastatic malignancy of the umbilicus. This eponym, coined by Sir Hamilton Bailey in his book Physical Signs in Clinical Surgery,2 honors Sister Mary Joseph Dempsey, a nun in the Franciscan order who was the first surgical assistant to Dr. William J. Mayo at St. Mary's Hospital in Rochester, Minnesota.3,4 Sister Mary Joseph made the astute observation that patients with gastrointestinal and gynecologic tumors may have involvement of the umbilicus; if there is involvement of the umbilicus, the prognosis is poor.5 Although Dr. Mayo gives credit to Sister Mary Joseph, contrary to what some believe, he is not responsible for the eponym. Dr. Mayo used the term pants button umbilicus in his article; Sir Bailey definitively coined the term SMJN. Some authors argue that the correct name is Sister Joseph's nodule; however, SMJN remains the more commonly used term.6 Frequency—Cutaneous metastasis, in and of itself, is a rare feature of visceral malignancy, occurring in about 1% to 2% of cases, with umbilical metastasis occurring even less frequently. There are approximately 265 cases of SMJN reported in the literature up to 1990, emphasizing its infrequency. The most common origin of an umbilical metastasis is an adenocarcinoma from a gastrointestinal or gynecologic primary malignancy. In a review of the world literature on metastatic umbilical tumors, Barrow7 found that the most common primary tumor identified was carcinoma of the stomach. The second most common was ovarian tumor,7 with colon, rectal, and pancreatic cancers following in descending order of frequency.8 In very rare cases, the primary tumor involved the breast, cervix, endometrium, small bowel, liver, gallbladder, lung, prostate, kidney, fallopian tube, appendix, and penis.9 In approximately 20% to 30% of cases, the primary tumor could not be identified.9 Umbilical Anatomy—A neoplasm may metastasize to the umbilicus by one of many mechanisms, most commonly direct extension from the anterior peritoneal surface from adjacent organs. Other mechanisms of metastasis include vascular spread via arterial and venous channels, lymphatic spread, and umbilical ligamentous spread. The rich vascular supply to the anterior abdominal wall facilitates metastasis of a neoplasm. The main arteries supplying the umbilical region are the inferior epigastric, deep circumflex iliac, and superior epigastric arteries. Venous drainage of the umbilical region stems from a network of veins radiating from the umbilicus, including the axillary vein above and the femoral vein below the umbilicus. There also are small paraumbilical veins that connect with the portal system along the ligamentum teres hepatis, the superior portion of the falciform ligament.10 The superficial lymphatic drainage of the periumbilical region leads to axillary lymph nodes above and inguinal lymph nodes below the periumbilical region. The deep lymphatic drainage runs along the falciform ligament of the liver and then enters the anterior mediastinum by traversing the diaphragm. Inferiorly, the deep lymphatics communicate by coursing to the lymph nodes of the iliac arteries. Because the lymphatic channels of the periumbilical region communicate with the deep inguinal, axillary, deep femoral, and periaortic lymph nodes, once a neoplasm is established at the umbilicus, it can metastasize to any part of the body,8 supporting the notion that the presence of SMJN portends a poor prognosis. In the fetus, the umbilicus serves as the opening for the umbilical vessels. In the adult, there are several ligaments that contain remnants of obliterated fetal structures and connect to the umbilicus. For example, the median umbilical ligament, also known as the urachus, represents the obliterated umbilical arteries that formerly connected the umbilicus to the bladder. The falciform ligament in the adult contains the obliterated umbilical vein and runs along the hepatic surface. Therefore, a firm command of the anatomy and embryology of the periumbilical region is essential for an accurate clinical workup once the diagnosis of SMJN has been established. Physical Examination—Clinically, SMJN usually presents as a firm indurated plaque or nodule that is 0.5 to 2 cm in size, though lesions up to 10 cm have been reported. The lesion is occasionally painful and may have a fibrous consistency with irregular edges that are attached to the anterior abdominal wall. It tends to have a vascular appearance and can be fissured, ulcerated, or necrotic. Purulent discharge may be present if it is secondarily infected. Typically, there are no gross features to distinguish between a primary and secondary umbilical tumor. Differential Diagnosis—The differential diagnosis of SMJN includes a primary carcinoma of the umbilicus, a benign umbilical lesion, and a metastatic lesion of the umbilicus. Primary umbilical carcinomas are rare and include malignant melanoma, basal cell carcinoma, and omphalomesenteric duct carcinoma. Endometriosis is the most common benign lesion of the umbilicus. Other benign umbilical lesions include papillomas, epidermal/inclusion cysts, seborrheic keratoses, dermal nevi, polyps, congenital malformations, foreign bodies, talc granulomas, angiomas, pyogenic and pilonidal granulomas, keloids, incarcerated hernias, angiokeratomas, and lymphangiomas.11 Histopathology—In general, the histology of a cutaneous metastatic lesion is of finite value in determining the site of the primary malignancy. In contrast, when speaking of an umbilical metastasis, histologic sampling more often aids in determining the derivation.11 The histopathology is dependent on the primary tumor and is most often adenocarcinoma, which was the case with our patient. Prognosis—Although the presence of umbilical disease indicates metastasis, it does not suggest unresectability and, in fact, may be the first sign of a recurrence.11 However, in general, SMJN portends a poor prognosis and is considered an ominous sign. The presence of SMJN should prompt a thorough metastatic workup and appropriate clinical staging. Survival time in untreated patients ranges from 2 to 11 months, with 10 months as the average survival time from the appearance of an umbilical metastasis.6,9 This rapid deterioration may be, in part, caused by the rich lymphatic network in the abdominal wall providing communication with the deep inguinal, axillary, deep femoral, and periaortic lymph nodes. Therefore, from the umbilicus, a tumor may spread to many parts of the body.

Conclusion
Cutaneous metastasis is a rare occurrence, making SMJN exceptionally infrequent. The finding of SMJN should prompt a thorough search for the primary malignancy. As demonstrated by our patient, SMJN may be the first sign of a visceral malignancy, making proper and timely diagnosis lifesaving.

A metastatic malignancy of the umbilicus is commonly termed Sister Mary Joseph nodule (SMJN). It is a rare occurrence but may represent the first sign of a visceral malignancy and therefore should prompt a thorough search for the primary tumor. Typically, the most common origin of an umbilical metastasis is an adenocarcinoma from a gastrointestinal or gynecologic primary malignancy. The presence of SMJN carries a poor prognosis with the average survival time at the appearance of an umbilical metastasis being 10 months. We report a case of a 66-year-old man who was referred for evaluation of an enlarging umbilical lesion. Histopathology revealed adenocarcinoma. After a full metastatic workup, the tumor of origin was identified as adenocarcinoma of the sigmoid colon. Benign tumors of the umbilicus are uncommon. This case report serves to emphasize the importance of obtaining a histologic diagnosis when any new lesion presents in the umbilical region.

Case Report
A 66-year-old white man presented for evaluation of an umbilical lesion of 3 weeks' duration. The lesion was asymptomatic and nontender but was bleeding and oozing. The lesion, diagnosed by the patient's primary care physician as an infected pyogenic granuloma, was treated with oral antibiotics, without relief. His past medical history was unremarkable. He took no medications at that time and had an allergy to quinolones. His dermatologic history was positive for numerous actinic keratoses and a basal cell carcinoma on the forehead. Physical examination upon presentation revealed a 3-cm fungating polypoid umbilical mass with copious purulent exudates similar to Figure 1.1 The clinical differential diagnosis at that time included a pyogenic granuloma versus a Sister Mary Joseph nodule (SMJN). A shave biopsy was performed. Histopathology revealed multiple cystic and ductal spaces lined by atypical epithelial cells with numerous mitotic figures in the dermis (Figures 2 and 3). These changes favored a gastrointestinal primary lesion, supporting the clinical diagnosis of SMJN. The patient subsequently underwent a full metastatic workup. A computed tomographic scan of the abdomen and pelvis demonstrated no definite metastases to the lungs or liver but suggested a near-obstructing distal bowel primary tumor. A colonoscopy demonstrated a near-obstructing sigmoid colon carcinoma. The patient subsequently underwent an exploratory laparotomy, sigmoid resection, and primary colonic reanastomosis. Liver biopsies and resection of the omentum and the periumbilical abdominal wall including the eroding metastasis were performed as well as multiple peritoneal biopsies. Pathologic evaluation confirmed the presence of extensive carcinomatosis. The primary tumor was a 5.0X3.0-cm moderately differentiated adenocarcinoma of the sigmoid colon with extension through the bowel wall. Biopsies of the liver, lymph nodes, periumbilical soft tissue, omentum, and peritoneum were all positive for metastatic carcinoma. Postoperatively, the patient was started on the FOLFOX regimen incorporating folinic acid, 5-fluorouracil, and oxaliplatin. Currently, the patient remains clinically stable and without evidence of progressive sigmoid colon carcinoma.

Comment
SMJN is the term applied to an uncommon metastatic malignancy of the umbilicus. This eponym, coined by Sir Hamilton Bailey in his book Physical Signs in Clinical Surgery,2 honors Sister Mary Joseph Dempsey, a nun in the Franciscan order who was the first surgical assistant to Dr. William J. Mayo at St. Mary's Hospital in Rochester, Minnesota.3,4 Sister Mary Joseph made the astute observation that patients with gastrointestinal and gynecologic tumors may have involvement of the umbilicus; if there is involvement of the umbilicus, the prognosis is poor.5 Although Dr. Mayo gives credit to Sister Mary Joseph, contrary to what some believe, he is not responsible for the eponym. Dr. Mayo used the term pants button umbilicus in his article; Sir Bailey definitively coined the term SMJN. Some authors argue that the correct name is Sister Joseph's nodule; however, SMJN remains the more commonly used term.6 Frequency—Cutaneous metastasis, in and of itself, is a rare feature of visceral malignancy, occurring in about 1% to 2% of cases, with umbilical metastasis occurring even less frequently. There are approximately 265 cases of SMJN reported in the literature up to 1990, emphasizing its infrequency. The most common origin of an umbilical metastasis is an adenocarcinoma from a gastrointestinal or gynecologic primary malignancy. In a review of the world literature on metastatic umbilical tumors, Barrow7 found that the most common primary tumor identified was carcinoma of the stomach. The second most common was ovarian tumor,7 with colon, rectal, and pancreatic cancers following in descending order of frequency.8 In very rare cases, the primary tumor involved the breast, cervix, endometrium, small bowel, liver, gallbladder, lung, prostate, kidney, fallopian tube, appendix, and penis.9 In approximately 20% to 30% of cases, the primary tumor could not be identified.9 Umbilical Anatomy—A neoplasm may metastasize to the umbilicus by one of many mechanisms, most commonly direct extension from the anterior peritoneal surface from adjacent organs. Other mechanisms of metastasis include vascular spread via arterial and venous channels, lymphatic spread, and umbilical ligamentous spread. The rich vascular supply to the anterior abdominal wall facilitates metastasis of a neoplasm. The main arteries supplying the umbilical region are the inferior epigastric, deep circumflex iliac, and superior epigastric arteries. Venous drainage of the umbilical region stems from a network of veins radiating from the umbilicus, including the axillary vein above and the femoral vein below the umbilicus. There also are small paraumbilical veins that connect with the portal system along the ligamentum teres hepatis, the superior portion of the falciform ligament.10 The superficial lymphatic drainage of the periumbilical region leads to axillary lymph nodes above and inguinal lymph nodes below the periumbilical region. The deep lymphatic drainage runs along the falciform ligament of the liver and then enters the anterior mediastinum by traversing the diaphragm. Inferiorly, the deep lymphatics communicate by coursing to the lymph nodes of the iliac arteries. Because the lymphatic channels of the periumbilical region communicate with the deep inguinal, axillary, deep femoral, and periaortic lymph nodes, once a neoplasm is established at the umbilicus, it can metastasize to any part of the body,8 supporting the notion that the presence of SMJN portends a poor prognosis. In the fetus, the umbilicus serves as the opening for the umbilical vessels. In the adult, there are several ligaments that contain remnants of obliterated fetal structures and connect to the umbilicus. For example, the median umbilical ligament, also known as the urachus, represents the obliterated umbilical arteries that formerly connected the umbilicus to the bladder. The falciform ligament in the adult contains the obliterated umbilical vein and runs along the hepatic surface. Therefore, a firm command of the anatomy and embryology of the periumbilical region is essential for an accurate clinical workup once the diagnosis of SMJN has been established. Physical Examination—Clinically, SMJN usually presents as a firm indurated plaque or nodule that is 0.5 to 2 cm in size, though lesions up to 10 cm have been reported. The lesion is occasionally painful and may have a fibrous consistency with irregular edges that are attached to the anterior abdominal wall. It tends to have a vascular appearance and can be fissured, ulcerated, or necrotic. Purulent discharge may be present if it is secondarily infected. Typically, there are no gross features to distinguish between a primary and secondary umbilical tumor. Differential Diagnosis—The differential diagnosis of SMJN includes a primary carcinoma of the umbilicus, a benign umbilical lesion, and a metastatic lesion of the umbilicus. Primary umbilical carcinomas are rare and include malignant melanoma, basal cell carcinoma, and omphalomesenteric duct carcinoma. Endometriosis is the most common benign lesion of the umbilicus. Other benign umbilical lesions include papillomas, epidermal/inclusion cysts, seborrheic keratoses, dermal nevi, polyps, congenital malformations, foreign bodies, talc granulomas, angiomas, pyogenic and pilonidal granulomas, keloids, incarcerated hernias, angiokeratomas, and lymphangiomas.11 Histopathology—In general, the histology of a cutaneous metastatic lesion is of finite value in determining the site of the primary malignancy. In contrast, when speaking of an umbilical metastasis, histologic sampling more often aids in determining the derivation.11 The histopathology is dependent on the primary tumor and is most often adenocarcinoma, which was the case with our patient. Prognosis—Although the presence of umbilical disease indicates metastasis, it does not suggest unresectability and, in fact, may be the first sign of a recurrence.11 However, in general, SMJN portends a poor prognosis and is considered an ominous sign. The presence of SMJN should prompt a thorough metastatic workup and appropriate clinical staging. Survival time in untreated patients ranges from 2 to 11 months, with 10 months as the average survival time from the appearance of an umbilical metastasis.6,9 This rapid deterioration may be, in part, caused by the rich lymphatic network in the abdominal wall providing communication with the deep inguinal, axillary, deep femoral, and periaortic lymph nodes. Therefore, from the umbilicus, a tumor may spread to many parts of the body.

Conclusion
Cutaneous metastasis is a rare occurrence, making SMJN exceptionally infrequent. The finding of SMJN should prompt a thorough search for the primary malignancy. As demonstrated by our patient, SMJN may be the first sign of a visceral malignancy, making proper and timely diagnosis lifesaving.

A metastatic malignancy of the umbilicus is commonly termed Sister Mary Joseph nodule (SMJN). It is a rare occurrence but may represent the first sign of a visceral malignancy and therefore should prompt a thorough search for the primary tumor. Typically, the most common origin of an umbilical metastasis is an adenocarcinoma from a gastrointestinal or gynecologic primary malignancy. The presence of SMJN carries a poor prognosis with the average survival time at the appearance of an umbilical metastasis being 10 months. We report a case of a 66-year-old man who was referred for evaluation of an enlarging umbilical lesion. Histopathology revealed adenocarcinoma. After a full metastatic workup, the tumor of origin was identified as adenocarcinoma of the sigmoid colon. Benign tumors of the umbilicus are uncommon. This case report serves to emphasize the importance of obtaining a histologic diagnosis when any new lesion presents in the umbilical region.

Case Report
A 66-year-old white man presented for evaluation of an umbilical lesion of 3 weeks' duration. The lesion was asymptomatic and nontender but was bleeding and oozing. The lesion, diagnosed by the patient's primary care physician as an infected pyogenic granuloma, was treated with oral antibiotics, without relief. His past medical history was unremarkable. He took no medications at that time and had an allergy to quinolones. His dermatologic history was positive for numerous actinic keratoses and a basal cell carcinoma on the forehead. Physical examination upon presentation revealed a 3-cm fungating polypoid umbilical mass with copious purulent exudates similar to Figure 1.1 The clinical differential diagnosis at that time included a pyogenic granuloma versus a Sister Mary Joseph nodule (SMJN). A shave biopsy was performed. Histopathology revealed multiple cystic and ductal spaces lined by atypical epithelial cells with numerous mitotic figures in the dermis (Figures 2 and 3). These changes favored a gastrointestinal primary lesion, supporting the clinical diagnosis of SMJN. The patient subsequently underwent a full metastatic workup. A computed tomographic scan of the abdomen and pelvis demonstrated no definite metastases to the lungs or liver but suggested a near-obstructing distal bowel primary tumor. A colonoscopy demonstrated a near-obstructing sigmoid colon carcinoma. The patient subsequently underwent an exploratory laparotomy, sigmoid resection, and primary colonic reanastomosis. Liver biopsies and resection of the omentum and the periumbilical abdominal wall including the eroding metastasis were performed as well as multiple peritoneal biopsies. Pathologic evaluation confirmed the presence of extensive carcinomatosis. The primary tumor was a 5.0X3.0-cm moderately differentiated adenocarcinoma of the sigmoid colon with extension through the bowel wall. Biopsies of the liver, lymph nodes, periumbilical soft tissue, omentum, and peritoneum were all positive for metastatic carcinoma. Postoperatively, the patient was started on the FOLFOX regimen incorporating folinic acid, 5-fluorouracil, and oxaliplatin. Currently, the patient remains clinically stable and without evidence of progressive sigmoid colon carcinoma.

Comment
SMJN is the term applied to an uncommon metastatic malignancy of the umbilicus. This eponym, coined by Sir Hamilton Bailey in his book Physical Signs in Clinical Surgery,2 honors Sister Mary Joseph Dempsey, a nun in the Franciscan order who was the first surgical assistant to Dr. William J. Mayo at St. Mary's Hospital in Rochester, Minnesota.3,4 Sister Mary Joseph made the astute observation that patients with gastrointestinal and gynecologic tumors may have involvement of the umbilicus; if there is involvement of the umbilicus, the prognosis is poor.5 Although Dr. Mayo gives credit to Sister Mary Joseph, contrary to what some believe, he is not responsible for the eponym. Dr. Mayo used the term pants button umbilicus in his article; Sir Bailey definitively coined the term SMJN. Some authors argue that the correct name is Sister Joseph's nodule; however, SMJN remains the more commonly used term.6 Frequency—Cutaneous metastasis, in and of itself, is a rare feature of visceral malignancy, occurring in about 1% to 2% of cases, with umbilical metastasis occurring even less frequently. There are approximately 265 cases of SMJN reported in the literature up to 1990, emphasizing its infrequency. The most common origin of an umbilical metastasis is an adenocarcinoma from a gastrointestinal or gynecologic primary malignancy. In a review of the world literature on metastatic umbilical tumors, Barrow7 found that the most common primary tumor identified was carcinoma of the stomach. The second most common was ovarian tumor,7 with colon, rectal, and pancreatic cancers following in descending order of frequency.8 In very rare cases, the primary tumor involved the breast, cervix, endometrium, small bowel, liver, gallbladder, lung, prostate, kidney, fallopian tube, appendix, and penis.9 In approximately 20% to 30% of cases, the primary tumor could not be identified.9 Umbilical Anatomy—A neoplasm may metastasize to the umbilicus by one of many mechanisms, most commonly direct extension from the anterior peritoneal surface from adjacent organs. Other mechanisms of metastasis include vascular spread via arterial and venous channels, lymphatic spread, and umbilical ligamentous spread. The rich vascular supply to the anterior abdominal wall facilitates metastasis of a neoplasm. The main arteries supplying the umbilical region are the inferior epigastric, deep circumflex iliac, and superior epigastric arteries. Venous drainage of the umbilical region stems from a network of veins radiating from the umbilicus, including the axillary vein above and the femoral vein below the umbilicus. There also are small paraumbilical veins that connect with the portal system along the ligamentum teres hepatis, the superior portion of the falciform ligament.10 The superficial lymphatic drainage of the periumbilical region leads to axillary lymph nodes above and inguinal lymph nodes below the periumbilical region. The deep lymphatic drainage runs along the falciform ligament of the liver and then enters the anterior mediastinum by traversing the diaphragm. Inferiorly, the deep lymphatics communicate by coursing to the lymph nodes of the iliac arteries. Because the lymphatic channels of the periumbilical region communicate with the deep inguinal, axillary, deep femoral, and periaortic lymph nodes, once a neoplasm is established at the umbilicus, it can metastasize to any part of the body,8 supporting the notion that the presence of SMJN portends a poor prognosis. In the fetus, the umbilicus serves as the opening for the umbilical vessels. In the adult, there are several ligaments that contain remnants of obliterated fetal structures and connect to the umbilicus. For example, the median umbilical ligament, also known as the urachus, represents the obliterated umbilical arteries that formerly connected the umbilicus to the bladder. The falciform ligament in the adult contains the obliterated umbilical vein and runs along the hepatic surface. Therefore, a firm command of the anatomy and embryology of the periumbilical region is essential for an accurate clinical workup once the diagnosis of SMJN has been established. Physical Examination—Clinically, SMJN usually presents as a firm indurated plaque or nodule that is 0.5 to 2 cm in size, though lesions up to 10 cm have been reported. The lesion is occasionally painful and may have a fibrous consistency with irregular edges that are attached to the anterior abdominal wall. It tends to have a vascular appearance and can be fissured, ulcerated, or necrotic. Purulent discharge may be present if it is secondarily infected. Typically, there are no gross features to distinguish between a primary and secondary umbilical tumor. Differential Diagnosis—The differential diagnosis of SMJN includes a primary carcinoma of the umbilicus, a benign umbilical lesion, and a metastatic lesion of the umbilicus. Primary umbilical carcinomas are rare and include malignant melanoma, basal cell carcinoma, and omphalomesenteric duct carcinoma. Endometriosis is the most common benign lesion of the umbilicus. Other benign umbilical lesions include papillomas, epidermal/inclusion cysts, seborrheic keratoses, dermal nevi, polyps, congenital malformations, foreign bodies, talc granulomas, angiomas, pyogenic and pilonidal granulomas, keloids, incarcerated hernias, angiokeratomas, and lymphangiomas.11 Histopathology—In general, the histology of a cutaneous metastatic lesion is of finite value in determining the site of the primary malignancy. In contrast, when speaking of an umbilical metastasis, histologic sampling more often aids in determining the derivation.11 The histopathology is dependent on the primary tumor and is most often adenocarcinoma, which was the case with our patient. Prognosis—Although the presence of umbilical disease indicates metastasis, it does not suggest unresectability and, in fact, may be the first sign of a recurrence.11 However, in general, SMJN portends a poor prognosis and is considered an ominous sign. The presence of SMJN should prompt a thorough metastatic workup and appropriate clinical staging. Survival time in untreated patients ranges from 2 to 11 months, with 10 months as the average survival time from the appearance of an umbilical metastasis.6,9 This rapid deterioration may be, in part, caused by the rich lymphatic network in the abdominal wall providing communication with the deep inguinal, axillary, deep femoral, and periaortic lymph nodes. Therefore, from the umbilicus, a tumor may spread to many parts of the body.

Conclusion
Cutaneous metastasis is a rare occurrence, making SMJN exceptionally infrequent. The finding of SMJN should prompt a thorough search for the primary malignancy. As demonstrated by our patient, SMJN may be the first sign of a visceral malignancy, making proper and timely diagnosis lifesaving.

Pancreatic panniculitis represents a rare skin manifestation of underlying pancreatic pathology. The clinical presentation of the condition is remarkably consistent and privy to several unique clinical and histopathologic findings. We report a case of a 50-year-old white woman with pancreatic panniculitis and newly diagnosed pancreatic acinic cell adenocarcinoma. The clinical and histopathologic features, underlying causes, and treatments are reviewed.

Case Report
In June 2005, a 50-year-old white woman presented to the emergency department with a 6-month history of nausea, vomiting, abdominal pain, and weight loss, and a 3-week history of painful leg nodules that had been increasing in size and number in the days prior to admission. She currently was not taking any medications and was allergic to clindamycin and cefuroxime axetil. She smoked half a pack of cigarettes a day for the past 15 years and denied alcohol use. Her family history was notable for breast and colon cancer in her maternal grandmother and cervical cancer in her sister. Physical examination revealed multiple 2- to 4-cm, firm, tender, erythematous nodules on the anterior and anteromedial shins bilaterally (Figure 1). There also was mild tenderness on palpation of the abdomen in the epigastric region. The remainder of the physical examination was unremarkable. Pertinent laboratory findings included an elevated lipase level of 4000 U/L (reference range, 31–186 U/L) and a slightly elevated amylase level of 114 U/L (reference range, 27–131 U/L). A complete blood count and liver function panel were within reference range.

A 5-mm punch biopsy specimen obtained from one of the nodules revealed a predominantly septal panniculitis with some lacelike lobular infiltration of inflammatory cells (Figure 2). Lymphocytes and neutrophils were observed, and eosinophils were particularly prominent. In addition, there were small foci of lipocyte degeneration and calcification, with formation of ghost cells (Figure 3). Aggregates of granular basophilic material also were identified, particularly near the base of the specimen. Gram, Gomori methenamine-silver, and acid-fast bacilli stains were negative for organisms. A diagnosis of pancreatic panniculitis was made.

Further workup of the patient revealed a 5-cm ill-defined mass in the pancreatic head as well as a 2-cm liver mass. Biopsy specimens of the pancreatic and liver masses revealed pancreatic acinic cell adenocarcinoma with metastasis. The patient initially was started on octreotide acetate, gemcitabine hydrochloride, and nonsteroidal anti-inflammatory drugs. After 3 months of therapy, the tumor remained stable in size, but the leg nodules had begun to regress due to the octreotide acetate. Additional chemotherapeutic agents were added to her treatment, including streptozocin and doxorubicin hydrochloride liposome. In August 2005, the pancreatic carcinoma and liver metastasis had dramatically decreased in size and the panniculitis had resolved. The patient requested that the octreotide acetate and chemotherapy be discontinued. She presented again in December 2005 with the return of her panniculitis, this time involving her shins, arms, and hands. A few of the nodules on the shins were noted to express a brown-green oily fluid. Workup revealed an increase in size of her primary tumor and multiple liver masses. Octreotide acetate and chemotherapy were restarted. Two months later (February 2006), the patient's panniculitis had again regressed and her tumors slowly were decreasing in size.

Comment
Pancreatic panniculitis is a cutaneous finding marked by multiple subcutaneous, raised, firm, tender, edematous nodules varying from erythematous to violaceous to red-brown. These nodules most commonly present on the lower legs but also can involve the thighs, buttocks, trunk, and upper extremities.1-10 Individual nodules sometimes ulcerate and discharge a creamy, tan-brown, sterile, viscous substance made up of degenerated lipocytes. Lesions usually resolve with lipoatrophy and hypopigmented and/or hyperpigmented scars.1,2 Additional clinical findings can accompany the skin lesions and relate to lipocyte degeneration in other organs. Periarticular lipocyte degeneration results in a secondary acute arthritis that most frequently involves the ankles and may be migratory, intermittent, or persistent. Other joints subsequently or concurrently may be involved, including the knees, metacarpals, wrists, and elbows. Arthritis has been reported in 54% to 88% of cases.1,3 More rarely, submucosal lipocyte degeneration resulting in gastrointestinal tract bleeding can occur.1 Common laboratory abnormalities associated with pancreatic panniculitis include elevated sedimentation rates and lipase and trypsin levels (Table 1). Some cases are associated with eosinophilia and increased amylase.1-8 A differential diagnosis of panniculitides that may resemble pancreatic panniculitis could include erythema nodosum; sclerosing panniculitis (lipodermatosclerosis); α1-antitrypsin deficiency panniculitis; cutaneous polyarteritis nodosa; nodular vasculitis (erythema induratum); lupus panniculitis; and infective, traumatic, and factitial panniculitis (Table 2).2,5,11,12

The landmark article that first linked pancreatic disease with pancreatic panniculitis was published in 1883 by Chiari.13 Disease processes that resulted in pancreatic panniculitis included acute pancreatitis, chronic pancreatitis, pancreatic pseudocysts, pancreatic duct stenosis, abdominal trauma, and pancreatic carcinoma. A case of panniculitis associated with lupus pancreatitis also has been reported.14 Only 0.3% to 3.0% of patients with pancreatic disease develop associated panniculitis.2 Pancreatic carcinoma and pancreatitis are most intimately associated with pancreatic panniculitis.1 Specifically, acinic cell adenocarcinoma is responsible for more than 50% of all cases,4 though only 16% of acinic cell adenocarcinomas present with panniculitis.15 A small number of neuroendocrine carcinomas have been reported in the literature, as well as an isolated case of an intraductal carcinoid tumor in a pancreas divisum.2,9,10 Pancreatitis plays a role in the development of most of the remaining cases.1 Although pancreatic panniculitis only manifests in a small percentage of cases of pancreatic disease, its importance as a clinical sign should be recognized. As in our case, when panniculitis is observed, it is the presenting sign in 40% of cases of underlying pancreatic disease.16 The panniculitis usually precedes the diagnosis of pancreatic disease by an average of 13 weeks, with a reported range between 2 and 28 weeks.1 The characteristic histopathologic features of pancreatic panniculitis were first described by Szymanski and Bluefarb17 in 1961. Early lesions are nonspecific, marked by perivascular lymphocytic infiltrates that lack necrosis and may resemble erythema nodosum.4 In fact, Ball and colleagues18 have suggested that pancreatic panniculitis may begin as a septal panniculitis and only later develop lobular involvement. Biopsies performed on specimens from the nonulcerated, fully developed erythematous nodules reveal both lobular and septal panniculitis highlighted by focal areas of lipocyte degeneration populated by anucleate necrotic adipocytes surrounded by thickened acidophilic cell membranes, termed ghost cells. A unique feature, when present, is the deposition of granular or homogenous basophilic material resulting from the saponification of fat by calcium salts.12 A dense infiltration of lymphocytes, macrophages, neutrophils, and variable numbers of eosinophils exists at the periphery of the necrotic areas along with evidence of calcification. Resolution of the nodules is characterized by a granulomatous infiltrate that replaces the areas of necrotic tissue.1 The presence of numerous eosinophils was a striking feature in our case and has not been emphasized previously in the literature in this form of panniculitis. Although there is no universally accepted mechanism for the development of the skin lesions, a popular hypothesis states that a synergism exists between the elevated serum levels of lipase and trypsin. Trypsin alters the permeability of the tissue blood vessels, which allows lipase to hydrolyze lipids in the adipocyte cell membranes and interior, which leads to lipocyte degeneration of the tissue.16,19 Support for this hypothesis is garnered by the observations that more than 50% of patients with pancreatic portal fistulization develop panniculitis, and immunohistochemical analysis of the areas of lipocyte degeneration demonstrate pancreatic lipase.6,20 Potts and colleagues21 suggested a possible immunologic mechanism in a patient with pancreatic carcinoma and pancreatic panniculitis who was noted to have decreased complement levels and deposition of immunoglobulin G in the pleura. Successful treatment of pancreatic panniculitis usually requires diagnosis and treatment of the underlying pancreatic pathology. As the pancreatic enzyme levels decrease, the skin lesions usually tend to regress.3 There has been some success reported with the administration of octreotide acetate, a synthetic polypeptide that inhibits pancreatic enzyme production.1,2,4,6 In addition, general supportive measures, including rest, elevation of the legs, compression stockings, and nonsteroidal anti-inflammatory drugs, may be helpful.

Pancreatic panniculitis represents a rare skin manifestation of underlying pancreatic pathology. The clinical presentation of the condition is remarkably consistent and privy to several unique clinical and histopathologic findings. We report a case of a 50-year-old white woman with pancreatic panniculitis and newly diagnosed pancreatic acinic cell adenocarcinoma. The clinical and histopathologic features, underlying causes, and treatments are reviewed.

Case Report
In June 2005, a 50-year-old white woman presented to the emergency department with a 6-month history of nausea, vomiting, abdominal pain, and weight loss, and a 3-week history of painful leg nodules that had been increasing in size and number in the days prior to admission. She currently was not taking any medications and was allergic to clindamycin and cefuroxime axetil. She smoked half a pack of cigarettes a day for the past 15 years and denied alcohol use. Her family history was notable for breast and colon cancer in her maternal grandmother and cervical cancer in her sister. Physical examination revealed multiple 2- to 4-cm, firm, tender, erythematous nodules on the anterior and anteromedial shins bilaterally (Figure 1). There also was mild tenderness on palpation of the abdomen in the epigastric region. The remainder of the physical examination was unremarkable. Pertinent laboratory findings included an elevated lipase level of 4000 U/L (reference range, 31–186 U/L) and a slightly elevated amylase level of 114 U/L (reference range, 27–131 U/L). A complete blood count and liver function panel were within reference range.

A 5-mm punch biopsy specimen obtained from one of the nodules revealed a predominantly septal panniculitis with some lacelike lobular infiltration of inflammatory cells (Figure 2). Lymphocytes and neutrophils were observed, and eosinophils were particularly prominent. In addition, there were small foci of lipocyte degeneration and calcification, with formation of ghost cells (Figure 3). Aggregates of granular basophilic material also were identified, particularly near the base of the specimen. Gram, Gomori methenamine-silver, and acid-fast bacilli stains were negative for organisms. A diagnosis of pancreatic panniculitis was made.

Further workup of the patient revealed a 5-cm ill-defined mass in the pancreatic head as well as a 2-cm liver mass. Biopsy specimens of the pancreatic and liver masses revealed pancreatic acinic cell adenocarcinoma with metastasis. The patient initially was started on octreotide acetate, gemcitabine hydrochloride, and nonsteroidal anti-inflammatory drugs. After 3 months of therapy, the tumor remained stable in size, but the leg nodules had begun to regress due to the octreotide acetate. Additional chemotherapeutic agents were added to her treatment, including streptozocin and doxorubicin hydrochloride liposome. In August 2005, the pancreatic carcinoma and liver metastasis had dramatically decreased in size and the panniculitis had resolved. The patient requested that the octreotide acetate and chemotherapy be discontinued. She presented again in December 2005 with the return of her panniculitis, this time involving her shins, arms, and hands. A few of the nodules on the shins were noted to express a brown-green oily fluid. Workup revealed an increase in size of her primary tumor and multiple liver masses. Octreotide acetate and chemotherapy were restarted. Two months later (February 2006), the patient's panniculitis had again regressed and her tumors slowly were decreasing in size.

Comment
Pancreatic panniculitis is a cutaneous finding marked by multiple subcutaneous, raised, firm, tender, edematous nodules varying from erythematous to violaceous to red-brown. These nodules most commonly present on the lower legs but also can involve the thighs, buttocks, trunk, and upper extremities.1-10 Individual nodules sometimes ulcerate and discharge a creamy, tan-brown, sterile, viscous substance made up of degenerated lipocytes. Lesions usually resolve with lipoatrophy and hypopigmented and/or hyperpigmented scars.1,2 Additional clinical findings can accompany the skin lesions and relate to lipocyte degeneration in other organs. Periarticular lipocyte degeneration results in a secondary acute arthritis that most frequently involves the ankles and may be migratory, intermittent, or persistent. Other joints subsequently or concurrently may be involved, including the knees, metacarpals, wrists, and elbows. Arthritis has been reported in 54% to 88% of cases.1,3 More rarely, submucosal lipocyte degeneration resulting in gastrointestinal tract bleeding can occur.1 Common laboratory abnormalities associated with pancreatic panniculitis include elevated sedimentation rates and lipase and trypsin levels (Table 1). Some cases are associated with eosinophilia and increased amylase.1-8 A differential diagnosis of panniculitides that may resemble pancreatic panniculitis could include erythema nodosum; sclerosing panniculitis (lipodermatosclerosis); α1-antitrypsin deficiency panniculitis; cutaneous polyarteritis nodosa; nodular vasculitis (erythema induratum); lupus panniculitis; and infective, traumatic, and factitial panniculitis (Table 2).2,5,11,12

The landmark article that first linked pancreatic disease with pancreatic panniculitis was published in 1883 by Chiari.13 Disease processes that resulted in pancreatic panniculitis included acute pancreatitis, chronic pancreatitis, pancreatic pseudocysts, pancreatic duct stenosis, abdominal trauma, and pancreatic carcinoma. A case of panniculitis associated with lupus pancreatitis also has been reported.14 Only 0.3% to 3.0% of patients with pancreatic disease develop associated panniculitis.2 Pancreatic carcinoma and pancreatitis are most intimately associated with pancreatic panniculitis.1 Specifically, acinic cell adenocarcinoma is responsible for more than 50% of all cases,4 though only 16% of acinic cell adenocarcinomas present with panniculitis.15 A small number of neuroendocrine carcinomas have been reported in the literature, as well as an isolated case of an intraductal carcinoid tumor in a pancreas divisum.2,9,10 Pancreatitis plays a role in the development of most of the remaining cases.1 Although pancreatic panniculitis only manifests in a small percentage of cases of pancreatic disease, its importance as a clinical sign should be recognized. As in our case, when panniculitis is observed, it is the presenting sign in 40% of cases of underlying pancreatic disease.16 The panniculitis usually precedes the diagnosis of pancreatic disease by an average of 13 weeks, with a reported range between 2 and 28 weeks.1 The characteristic histopathologic features of pancreatic panniculitis were first described by Szymanski and Bluefarb17 in 1961. Early lesions are nonspecific, marked by perivascular lymphocytic infiltrates that lack necrosis and may resemble erythema nodosum.4 In fact, Ball and colleagues18 have suggested that pancreatic panniculitis may begin as a septal panniculitis and only later develop lobular involvement. Biopsies performed on specimens from the nonulcerated, fully developed erythematous nodules reveal both lobular and septal panniculitis highlighted by focal areas of lipocyte degeneration populated by anucleate necrotic adipocytes surrounded by thickened acidophilic cell membranes, termed ghost cells. A unique feature, when present, is the deposition of granular or homogenous basophilic material resulting from the saponification of fat by calcium salts.12 A dense infiltration of lymphocytes, macrophages, neutrophils, and variable numbers of eosinophils exists at the periphery of the necrotic areas along with evidence of calcification. Resolution of the nodules is characterized by a granulomatous infiltrate that replaces the areas of necrotic tissue.1 The presence of numerous eosinophils was a striking feature in our case and has not been emphasized previously in the literature in this form of panniculitis. Although there is no universally accepted mechanism for the development of the skin lesions, a popular hypothesis states that a synergism exists between the elevated serum levels of lipase and trypsin. Trypsin alters the permeability of the tissue blood vessels, which allows lipase to hydrolyze lipids in the adipocyte cell membranes and interior, which leads to lipocyte degeneration of the tissue.16,19 Support for this hypothesis is garnered by the observations that more than 50% of patients with pancreatic portal fistulization develop panniculitis, and immunohistochemical analysis of the areas of lipocyte degeneration demonstrate pancreatic lipase.6,20 Potts and colleagues21 suggested a possible immunologic mechanism in a patient with pancreatic carcinoma and pancreatic panniculitis who was noted to have decreased complement levels and deposition of immunoglobulin G in the pleura. Successful treatment of pancreatic panniculitis usually requires diagnosis and treatment of the underlying pancreatic pathology. As the pancreatic enzyme levels decrease, the skin lesions usually tend to regress.3 There has been some success reported with the administration of octreotide acetate, a synthetic polypeptide that inhibits pancreatic enzyme production.1,2,4,6 In addition, general supportive measures, including rest, elevation of the legs, compression stockings, and nonsteroidal anti-inflammatory drugs, may be helpful.

Pancreatic panniculitis represents a rare skin manifestation of underlying pancreatic pathology. The clinical presentation of the condition is remarkably consistent and privy to several unique clinical and histopathologic findings. We report a case of a 50-year-old white woman with pancreatic panniculitis and newly diagnosed pancreatic acinic cell adenocarcinoma. The clinical and histopathologic features, underlying causes, and treatments are reviewed.

Case Report
In June 2005, a 50-year-old white woman presented to the emergency department with a 6-month history of nausea, vomiting, abdominal pain, and weight loss, and a 3-week history of painful leg nodules that had been increasing in size and number in the days prior to admission. She currently was not taking any medications and was allergic to clindamycin and cefuroxime axetil. She smoked half a pack of cigarettes a day for the past 15 years and denied alcohol use. Her family history was notable for breast and colon cancer in her maternal grandmother and cervical cancer in her sister. Physical examination revealed multiple 2- to 4-cm, firm, tender, erythematous nodules on the anterior and anteromedial shins bilaterally (Figure 1). There also was mild tenderness on palpation of the abdomen in the epigastric region. The remainder of the physical examination was unremarkable. Pertinent laboratory findings included an elevated lipase level of 4000 U/L (reference range, 31–186 U/L) and a slightly elevated amylase level of 114 U/L (reference range, 27–131 U/L). A complete blood count and liver function panel were within reference range.

A 5-mm punch biopsy specimen obtained from one of the nodules revealed a predominantly septal panniculitis with some lacelike lobular infiltration of inflammatory cells (Figure 2). Lymphocytes and neutrophils were observed, and eosinophils were particularly prominent. In addition, there were small foci of lipocyte degeneration and calcification, with formation of ghost cells (Figure 3). Aggregates of granular basophilic material also were identified, particularly near the base of the specimen. Gram, Gomori methenamine-silver, and acid-fast bacilli stains were negative for organisms. A diagnosis of pancreatic panniculitis was made.

Further workup of the patient revealed a 5-cm ill-defined mass in the pancreatic head as well as a 2-cm liver mass. Biopsy specimens of the pancreatic and liver masses revealed pancreatic acinic cell adenocarcinoma with metastasis. The patient initially was started on octreotide acetate, gemcitabine hydrochloride, and nonsteroidal anti-inflammatory drugs. After 3 months of therapy, the tumor remained stable in size, but the leg nodules had begun to regress due to the octreotide acetate. Additional chemotherapeutic agents were added to her treatment, including streptozocin and doxorubicin hydrochloride liposome. In August 2005, the pancreatic carcinoma and liver metastasis had dramatically decreased in size and the panniculitis had resolved. The patient requested that the octreotide acetate and chemotherapy be discontinued. She presented again in December 2005 with the return of her panniculitis, this time involving her shins, arms, and hands. A few of the nodules on the shins were noted to express a brown-green oily fluid. Workup revealed an increase in size of her primary tumor and multiple liver masses. Octreotide acetate and chemotherapy were restarted. Two months later (February 2006), the patient's panniculitis had again regressed and her tumors slowly were decreasing in size.

Comment
Pancreatic panniculitis is a cutaneous finding marked by multiple subcutaneous, raised, firm, tender, edematous nodules varying from erythematous to violaceous to red-brown. These nodules most commonly present on the lower legs but also can involve the thighs, buttocks, trunk, and upper extremities.1-10 Individual nodules sometimes ulcerate and discharge a creamy, tan-brown, sterile, viscous substance made up of degenerated lipocytes. Lesions usually resolve with lipoatrophy and hypopigmented and/or hyperpigmented scars.1,2 Additional clinical findings can accompany the skin lesions and relate to lipocyte degeneration in other organs. Periarticular lipocyte degeneration results in a secondary acute arthritis that most frequently involves the ankles and may be migratory, intermittent, or persistent. Other joints subsequently or concurrently may be involved, including the knees, metacarpals, wrists, and elbows. Arthritis has been reported in 54% to 88% of cases.1,3 More rarely, submucosal lipocyte degeneration resulting in gastrointestinal tract bleeding can occur.1 Common laboratory abnormalities associated with pancreatic panniculitis include elevated sedimentation rates and lipase and trypsin levels (Table 1). Some cases are associated with eosinophilia and increased amylase.1-8 A differential diagnosis of panniculitides that may resemble pancreatic panniculitis could include erythema nodosum; sclerosing panniculitis (lipodermatosclerosis); α1-antitrypsin deficiency panniculitis; cutaneous polyarteritis nodosa; nodular vasculitis (erythema induratum); lupus panniculitis; and infective, traumatic, and factitial panniculitis (Table 2).2,5,11,12

The landmark article that first linked pancreatic disease with pancreatic panniculitis was published in 1883 by Chiari.13 Disease processes that resulted in pancreatic panniculitis included acute pancreatitis, chronic pancreatitis, pancreatic pseudocysts, pancreatic duct stenosis, abdominal trauma, and pancreatic carcinoma. A case of panniculitis associated with lupus pancreatitis also has been reported.14 Only 0.3% to 3.0% of patients with pancreatic disease develop associated panniculitis.2 Pancreatic carcinoma and pancreatitis are most intimately associated with pancreatic panniculitis.1 Specifically, acinic cell adenocarcinoma is responsible for more than 50% of all cases,4 though only 16% of acinic cell adenocarcinomas present with panniculitis.15 A small number of neuroendocrine carcinomas have been reported in the literature, as well as an isolated case of an intraductal carcinoid tumor in a pancreas divisum.2,9,10 Pancreatitis plays a role in the development of most of the remaining cases.1 Although pancreatic panniculitis only manifests in a small percentage of cases of pancreatic disease, its importance as a clinical sign should be recognized. As in our case, when panniculitis is observed, it is the presenting sign in 40% of cases of underlying pancreatic disease.16 The panniculitis usually precedes the diagnosis of pancreatic disease by an average of 13 weeks, with a reported range between 2 and 28 weeks.1 The characteristic histopathologic features of pancreatic panniculitis were first described by Szymanski and Bluefarb17 in 1961. Early lesions are nonspecific, marked by perivascular lymphocytic infiltrates that lack necrosis and may resemble erythema nodosum.4 In fact, Ball and colleagues18 have suggested that pancreatic panniculitis may begin as a septal panniculitis and only later develop lobular involvement. Biopsies performed on specimens from the nonulcerated, fully developed erythematous nodules reveal both lobular and septal panniculitis highlighted by focal areas of lipocyte degeneration populated by anucleate necrotic adipocytes surrounded by thickened acidophilic cell membranes, termed ghost cells. A unique feature, when present, is the deposition of granular or homogenous basophilic material resulting from the saponification of fat by calcium salts.12 A dense infiltration of lymphocytes, macrophages, neutrophils, and variable numbers of eosinophils exists at the periphery of the necrotic areas along with evidence of calcification. Resolution of the nodules is characterized by a granulomatous infiltrate that replaces the areas of necrotic tissue.1 The presence of numerous eosinophils was a striking feature in our case and has not been emphasized previously in the literature in this form of panniculitis. Although there is no universally accepted mechanism for the development of the skin lesions, a popular hypothesis states that a synergism exists between the elevated serum levels of lipase and trypsin. Trypsin alters the permeability of the tissue blood vessels, which allows lipase to hydrolyze lipids in the adipocyte cell membranes and interior, which leads to lipocyte degeneration of the tissue.16,19 Support for this hypothesis is garnered by the observations that more than 50% of patients with pancreatic portal fistulization develop panniculitis, and immunohistochemical analysis of the areas of lipocyte degeneration demonstrate pancreatic lipase.6,20 Potts and colleagues21 suggested a possible immunologic mechanism in a patient with pancreatic carcinoma and pancreatic panniculitis who was noted to have decreased complement levels and deposition of immunoglobulin G in the pleura. Successful treatment of pancreatic panniculitis usually requires diagnosis and treatment of the underlying pancreatic pathology. As the pancreatic enzyme levels decrease, the skin lesions usually tend to regress.3 There has been some success reported with the administration of octreotide acetate, a synthetic polypeptide that inhibits pancreatic enzyme production.1,2,4,6 In addition, general supportive measures, including rest, elevation of the legs, compression stockings, and nonsteroidal anti-inflammatory drugs, may be helpful.