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PubMed1991

Panniculitis: a report of four cases and literature review.

Panniculitis is a disease with many causes and associations. The classification of clinical subtypes is unsatisfactory and hampered by the use of eponyms. Four children with recurring panniculitis are described and their histology presented. Three had subcutaneous fat atrophy with lobular panniculitis on biopsy; all responded well to corticosteroids. The fourth child had a septal panniculitis with no atrophy of subcutaneous tissues and only a partial response to treatment with corticosteroids. A widely accepted precise histological classification of panniculitis is needed to enable accurate predictions of the outcome of this serious disorder.

Adipose Tissue↗
PubMed2002

Pancreatic panniculitis in an 88-year-old man with neuroendocrine carcinoma.

Pancreatic panniculitis is a rare complication that occurs in 0.3-3% of patients with pancreatic diseases. Most of the cases reported to date were associated with adenocarcinoma and acute or chronic pancreatitis. We here present an 88-year-old man who was admitted to our institution with a nonfunctional neuroendocrine carcinoma of the pancreas. He subsequently developed pancreatic panniculitis and arthritis. Treatment with octreotide did not have an effect neither on progression of the carcinoma nor on development of new skin lesions. Two months after the diagnosis of pancreatic panniculitis had been made, the patient died from progressing carcinoma. A review of the literature shows that there is no congruent hypothesis for the pathogenesis of pancreatic panniculitis. Vascular damage seems to induce lipolysis by pancreatic enzymes. This eventually leads to fat necrosis. The diversity of disorders that can go along with pancreatic panniculitis suggests an unspecific damage of pancreatic tissue as a first step in the chain of events.

Aged↗
PubMed2002

[Case of subcutaneous and mesenteric acute panniculitis with Sjögren's syndrome].

We report a case of a 27-year-old Japanese female with Sjogren's syndrome (SS), who suffered from several episodes of subcutaneous and mesenteric panniculitis with a recurrence within one year. After a history of fever and skin rash, the patient underwent surgery at a local hospital with a diagnosis of acute appendicitis complicated with an ileocecal abscess. She was also diagnosed as having SS. After the operation, the fever and skin rash persisted. She was treated with prednisolone (PSL), and her symptoms resolved. A recurrent bout of abdominal pain with fever, annular erythema on the trunk and a nodular erythematous rash on the lower extremities occurred six months after the operation. A skin biopsy from the lower extremities showed findings that were compatible with panniculitis. Abdominal computer tomography (CT) showed a diffuse swelling with soft tissue density in the intestinal mesenterium and para aortic area. A retrospective examination of the operative specimen obtained from the local hospital revealed centrilobular infiltration of neutrophils in the mesenteric adipose tissue with fat necrosis, which is compatible with mesenteric panniculitis. Twenty mg/day of PSL was successful in treating the systemic panniculitis, and the abnormal diffuse soft tissue density on the abdominal CT disappeared after three weeks of PSL administration. Systemic panniculitis is a rare complication in SS, and the pathogenesis is unclear.

Acute Disease↗
PubMedDate not supplied

Update on panniculitis.

There is considerable confusion regarding the pathogenesis, nosology and treatment of panniculitis. This paper examines newer concepts in five types of panniculitis: i.e., histiocytic cytophagic panniculitis, erythema induratum, lipodermatosclerosis, pancreatic panniculitis and alpha-1-antitrypsin deficiency panniculitis. Recent developments in etiology, pathogenesis, molecular techniques, and therapy are discussed.

Erythema Induratum↗
PubMed2001

Treatment of alpha1-antitrypsin-deficiency panniculitis with minocycline.

A small proportion of patients with alpha1-antitrypsin (alpha1AT) deficiency experience recurrent ulcerating panniculitis. Studies suggest that alpha1AT-deficiency panniculitis reflects an uncontrolled inflammatory process because of the serum's incapacity to neutralize proteolytic enzymes released by leukocytes in the skin. Dapsone is considered the treatment of choice for this entity, but it is limited by its side effects, especially hematologic ones. Tetracyclines have anticollagenase and anti-inflammatory activity and have been used successfully to treat this type of panniculitis. We report the case of a 42-year-old woman with recurrent alpha1AT-deficiency panniculitis who did not tolerate the side effects of dapsone or systemic corticosteroid. Minocycline treatment led to disappearance of lesions, and long-term administration prevented recurrences without evident negative side effects. We consider minocycline a safe treatment that allows control of alpha1AT-deficiency panniculitis.

Anti-Bacterial Agents↗
PubMed2001

[Auto-induced eosinophilic panniculitis: a diagnostic dilemma].

Eosinophilic panniculitis is characterized by a prominent infiltration of subcutaneous fat with eosinophils. The clinical spectrum of lesions that display pathologic changes of eosinophilic panniculitis is diverse, but nodular lesions are the most common. The factitial eosinophilic panniculitis are exceptional, show a pleomorphic pattern of findings and are associated with personality disorders. Its main challenge is to establish the correct diagnostic. We report an unusual case of factitial nodular febrile panniculitis of the left forearm and proximal arm in an 16 year-old girl. She admitted that the lesions were self-inflicted by autoinjection of several farming products as attempted suicide. We describe the clinical, radiological and histopathological features as well as the differential diagnosis of this type of panniculitis.

Adolescent↗
PubMed1993

Panniculitis as the first manifestation of systemic lupus erythematosus: description of two cases.

Two patients are described in whom panniculitis proved to be the first symptom of the disease systemic lupus erythematosus (SLE). Histological examination of a painless solitary cutaneous lesion in the otherwise asymptomatic first patient showed a nonspecific nodular panniculitis; 1 yr later a definite diagnosis of SLE was made. In the second patient panniculitis had the clinical appearance of erythema nodosum and was one of several presenting symptoms of SLE. These patients were part of a group of 68 newly diagnosed patients with SLE, indicating a 3% prevalence of panniculitis in SLE. These cases illustrate that SLE should always be considered as an underlying disease in young female patients presenting with nodular panniculitis, which may mimic the clinical picture of erythema nodosum.

Adult↗
PubMed1993

Periparotid lupus erythematosus panniculitis. Clinicopathologic correlation of two cases presenting as primary parotid disease.

Lupus erythematosus (LE) panniculitis, also called lupus profundus, is an uncommon but well-established manifestation of both chronic cutaneous (discoid) LE and systemic LE. Although LE panniculitis characteristically may involve the face, specific parotid and periparotid involvement has not, to the best of our knowledge, been previously reported. We describe the clinicopathologic correlation of two cases of LE panniculitis that presented as apparent primary parotid parenchymal disease; one as a neoplasm, the other as parotiditis. Failure to recognize LE panniculitis resulted in prolonged periods of inappropriate therapy and significant morbidity, including an unnecessary parotidectomy. Lupus erythematosus panniculitis has well-established histologic criteria that should be considered in the differential diagnosis of an unexplained parotid mass.

Adult↗
PubMed1997

[Histiocytic cytophagic panniculitis].

A HISTOPATHOLOGICAL DIAGNOSIS: Histiocytic cytophagic panniculitis is the specific skin finding in the reactive hemophagocytic syndrome. It is a feverish nodular eruption which accompanies the other clinical and biological features of the reactive hemophagocytic syndrome. Histopathologic changes are diagnostic and consist in a lobular panniculitis characterized by the presence of a histiocytic infiltration of the fat. Histiocytes are benign in appearance and show variable degree of phagocytosis. INFECTION AND IMMUNE ANOMALIES: In more than 50% of the cases, the disease is triggered by an infection (mainly a viral infection from the herpes-virus family) in a patient with altered immune function (immunodeficiency, autoimmune disease, hematological disease). Search for subcutaneous T-cell lymphoma is mandatory, but is a diagnostic challenge. Such lymphomas are associated with histologic features of histiocytic cytophagic panniculitis. PATHOPHYSIOLOGY: Histiocytes in the histiocytic cytophagic panniculitis are activated by an abnormal cytokine secretion (interferon gamma, granulocyte/macrophage colony stimulating factor, phagocytosis inducing factor, ...) from neoplastic or reactive T cells. CLINICAL TRIALS: Untreated, the course of the disease is usually lethal. Etiologic treatment should be provided whenever possible. Symptomatic treatment consists in transfusion and corticosteroid therapy. Etoposide, and sometimes cyclosporin, have been reported to be efficient. Some authors recommend that histiocytic cytophagic panniculitis should always be treated with a CHOP-like polychemotherapy. More recently, good results were obtained with high dose intravenous immunoglobulin and this treatment therefore deserves further evaluation.

Diagnosis, Differential↗
PubMed1996

Panniculitis: recent developments and observations.

Dermatopathologists rarely greet a biopsy of panniculitis with total confidence that a specific, definitive diagnosis will be rendered. As with many other areas in dermatopathology, our understanding of the pathogenesis of many forms of panniculitis is incomplete. This article examines a subset of panniculitis primarily from a pathogenetic standpoint, with the intention of providing a differential diagnosis for those cases in which ischemic changes are seen in the subcutis. The diverse group of conditions evoked by this approach also shares the distinction of having been the focus of nosologic and causative controversy, both historically and currently. In particular, stasis-associated sclerosing panniculitis, vascular calcification-cutaneous necrosis syndrome (calciphylaxis), oxalosis, and nodular vasculitis-erythema induratum are examined in depth. Erythema nodosum and variants, other granulomatous panniculitides, and panniculitides showing cytophagocytosis are also discussed with current perspectives.

Diagnosis, Differential↗
PubMed1987

Alpha 1-antitrypsin deficiency panniculitis: a histopathologic and immunopathologic study of four cases.

Four cases of alpha 1-antitrypsin deficiency associated with panniculitis were reviewed. The following histopathologic characteristics were typically present: (a) large areas of normal panniculus adjacent to severe necrotic panniculitis; (b) acute panniculitis--masses of neutrophils causing necrosis and replacing fat lobules; (c) chronic inflammation and hemorrhage at the periphery of acute panniculitis; (d) focal collection and proliferation of histiocytic cells and lipophages; (e) secondary leukocytoclastic vasculitis in areas of necrosis and lymphocytic vasculitis in areas of severe inflammation, but no evidence of primary vasculitis; (f) phlebothrombosis; and (g) in partial (heterozygous) deficiency, pronounced lipophages and giant-cell replacement of fat cells. Endarteritis obliterans was noted. Direct immunofluorescence study showed C3 deposition in the blood vessels of the panniculus or dermis (or both) in all four cases, and IgM was present in the blood vessels of three. Weak granular deposits of IgM or C3 were seen at the epidermal basement membrane zone in two cases. C3 in endothelial cells of the blood vessels was detected in one case. In general, the immunoreactants in the blood vessels were not dense and probably represent secondary vasculitis. We conclude that all patients with severe panniculitis and ulceration should have alpha 1-antitrypsin levels determined. A deep excisional biopsy specimen with abundant panniculus tissue is required for histopathologic diagnosis.

Adipose Tissue↗
PubMed2004

Small vessel vasculitis and relapsing panniculitis in tumour necrosis factor receptor associated periodic syndrome (TRAPS).

CASE REPORTS: A 66 year old female patient had relapsing fever and non-suppurative panniculitis suggestive of enigmatic "Weber-Christian disease" (WCD). Antineutrophil cytoplasmic antibodies with specificity for human leucocyte elastase (HLE-ANCA) were detected. A biopsy showed small vessel vasculitis and panniculitis. A 53 year old man had recurrent episodes of abdominal pain, erythematous rash, and myalgia. Fever attacks had stopped a few years ago. A biopsy showed panniculitis and fasciitis. In both patients mutations (R92Q, T50M) of the tumour necrosis factor receptor super family (TNFRSF) 1A gene were disclosed. Mutations of the TNFRSF 1A gene are the cause of tumour necrosis factor receptor associated periodic syndrome (TRAPS). Both patients responded favourably to treatment with the human soluble p75 TNF alpha receptor fusion protein etanercept (2 x 25 mg subcutaneously/week). DISCUSSION: Small vessel vasculitis and panniculitis have not been reported in TRAPS so far. The cases underline the importance of TNF alpha regulation in inflammatory processes including vasculitis. Genetically determined causes of fever may account for some cases of WCD.

Aged↗
PubMed1988

Weber-Christian panniculitis with systemic cytophagic histiocytosis.

A 49-year-old woman suffered from Weber-Christian panniculitis with a typically periodic course. Subsequently, the attacks of the disease developed to a severe state: high fever, endotoxinemia, pancytopenia, and clotting disorder, in addition to the cutaneous manifestations. One and a half years after the outbreak of the disease the patient died in a septic shock. At autopsy all three stages of Weber-Christian panniculitis were found. In addition, an immense proliferation of benign cytophagic histiocytes could be observed in the bone marrow, spleen, lymph nodes and, less distinctly, in the fatty and interstitial tissues of the visceral organs. As a nosologic entity, the Weber-Christian disease is frequently questioned. Some authors consider the lobular, histiocytic, cytophagic panniculitis a unique syndrome. On the other hand, it must be emphasized that benign, cytophagic histiocytosis may exist associated with infections or may accompany different diseases. Furthermore, the Weber-Christian panniculitis is clinically and morphologically well defined.

Female↗
PubMed2001

Mesenteric panniculitis of the colon with obstruction of the inferior mesenteric vein: report of a case.

Mesenteric panniculitis is a rare disease characterized by nonspecific inflammation of the fat tissue of the mesentery. We present an extremely rare case of mesenteric panniculitis of the sigmoid colon, complicated by occlusion of the inferior mesenteric vein. A 75-year-old male presented with a one-month history of abdominal distention and abdominal mass without pain. Physical examination revealed a firm mass in the lower abdomen. Barium enema study demonstrated rugged mucosa and a serrated contour in the rectosigmoid colon. Computed tomography showed that the mass arose from the mesentery, which surrounded the mesenteric vessels. The density of the mass was slightly higher than that of fatty tissue. Based on these radiologic findings, the patient was diagnosed as having mesenteric panniculitis of the rectosigmoid colon. Colonoscopy showed narrowing with edematous mucosa in the rectosigmoid colon, whereas marked dilated vessels were noted in the proximal portion of the sigmoid colon. Angiography showed occlusion of the inferior mesenteric vein, with venous flow returning via a collateral vein. The patient was observed without medication because his condition was satisfactory. His symptoms subsequently disappeared during a period of several weeks. The mass in the lower abdomen gradually diminished in size, disappearing three months later. Computed tomography and barium enema showed improvement of the lesion. The favorable outcome of the present case was probably because of formation of a collateral vein. The present case suggests that aggressive therapy for mesenteric panniculitis should be avoided, because the outcome of this disorder is good, even when there is obstruction of vessels.

Abdominal Pain↗
PubMed1994

[Kaposi-Irgang lupus erythematosus profundus. Lupus erythematosus panniculitis].

Lupus panniculitis is a rare variant of cutaneous lupus erythematosus. Two typical cases demonstrate the association of lupus panniculitis with signs of discoid lupus erythematosus and systemic lupus erythematosus. Clinically it is characterised by subcutaneous nodules or plaques, which may ulcerate leaving depressed atrophic scars. Histologically the lesions show lobular panniculitis. A positive immunofluorescent band test with deposition of IgG, IgM and C3 at the dermal-epidermal junction and blood vessel walls helps to confirm the diagnosis. The knowledge of the clinical features and histopathology of the disease is important because lupus panniculitis may precede systemic lupus erythematosus by some years.

Adipose Tissue↗
PubMedDate not supplied

Mesenteric panniculitis presenting as a multilocular cystic mesenteric mass: CT and MR evaluation.

Mesenteric panniculitis is a non-neoplastic, inflammatory process affecting the adipose tissue of the mesentery in adults with slight male predilection. Typical computed tomography (CT) or magnetic resonance imaging (MRI) findings are of either diffuse mesenteric infiltration or nodular mesenteric masses. We encountered a case of mesenteric panniculitis in a 26-year-old woman with the left upper quadrant pain and fullness, in which CT and MRI disclosed a large, ill-defined, multilocular cystic mesenteric mass. After surgery, the diagnosis of mesenteric panniculitis was made. The cystic components were dilated lymphatics due to lymphatic and venous obstruction by the mesenteric panniculitis.

Adult↗
PubMed2004

Alpha-1-antitrypsin associated panniculitis: the MS variant.

Over 90 mutant alleles of the alpha-1-antitrypsin (AAT) gene are recognized and classified by mobility on an acid starch gel. The four major categories include: F=fast, M=medium, S=slow, Z=very slow. Among 41 reported cases of AAT panniculitis, most have the ZZ phenotype with AAT levels below normal. We report two cases of AAT panniculitis with MS phenotype and normal AAT levels. In addition, we review the pathophysiology, epidemiology, and extracutaneous manifestations of AAT disease and propose a diagnostic algorithm for ulcerative panniculitis. A 42-year-old man presented with a solitary plaque on the left thigh exacerbated by trauma or excessive activity. The lesion frequently suppurated with a yellowish oily material. Twenty years before, he had fractured his left femur which was repaired with a metal plate. X-rays, histology with special stains for organisms, and cultures were negative. AAT phenotype was MS and AAT value was normal. A 43-year-old woman presented with multiple plaques on the proximal extremities which suppurated with exercise or trauma. AAT phenotype was MS and AAT level was normal. Histologic exam for both patients showed a dense neutrophilic infiltrate with septal and lobular panniculitis and areas of necrobiosis in the lower reticular dermis.

Adult↗
PubMed1996

Successful treatment of severe cytophagic histiocytic panniculitis with cyclosporine A.

Cytophagic histiocytic panniculitis (CHP) can be a severe variant of Weber-Christian disease characterized by the histopathologic appearance of lobular panniculitis infiltrated by histiocytes containing blood cell fragments and by a clinical course with marked systemic features including multiorgan failure, hypertriglyceridemia, and coagulopathy, which may lead to death. Therapy of CHP includes standard treatment for panniculitis, such as antimalarials, plus immunosuppressives for more severe cases. The response to treatment, however, is unpredictable. In several recent reports, cyclosporine A has been successfully used to treat panniculitis. We report a patient and review the literature on CHP and the use of cyclosporine A as therapy. Published reports reveal that in instances of severe CHP when cyclosporine A was not given, 19 of 27 patients died (70% mortality). When severe CHP was treated with cyclosporine A, rapid remission was achieved in our patient and all five previously published cases (0% mortality). We believe cyclosporine A is the drug of choice in severe CHP and should be considered in all such patients.

Adolescent↗