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Panniculitis
Kinds of Panniculitis Selected AbstractsDermatomyositis presenting as panniculitisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2000Yen-Yu Chao MD A 44-year-old obese woman was transferred to our clinic with a diagnosis of panniculitis. Examination showed multiple, indurated, erythematous, painful nodules and plaques distributed on the shoulders, back, forechest, abdomen, buttock, and bilateral thighs. These skin lesions appeared 2 months previously, measured 5,8 cm, and were tender on palpation. No obvious inducing factor was traced. The lesions seemed unresponsive to treatment with nonsteroidal anti-inflammatory drugs (ibuprofen, 400 mg three times a day) as similar lesions appeared in subsequent visits. Progressive proximal muscle weakness was found 1 month later. She was then admitted via the emergency room because of extensive painful skin plaques and abdominal pain. Diffuse erythematous to violaceous swelling of the face, neck, and shoulder was noted at about the same time ( Fig. 1). A skin biopsy specimen from the nodular lesion showed poikilomatous epidermal changes ( Fig. 2), and marked mononuclear cell infiltration in the dermis and subcutaneous fat ( Fig. 3). Dermatomyositis was considered as the diffuse violaceous facial erythema could be a form of heliotrope eruption, but Gottron's papule was not found. At admission, serum creatinine phosphokinase (CPK) was mildly elevated (436 IU/L; normal range, 20,170 IU/L), but serum asparagine transaminase (AST) and lactate dehydrogenase (LDH) levels were within normal limits (36 IU/L; normal, 11,47 IU/L; and 108 IU/L; normal, 90,280 IU/L, respectively). Antinuclear antibody was 1 : 80 positive with an atypical speckled pattern. Muscle strength was weakest during the first 2 days, about grade 3 by the Medical Research Council (MRC) of Great Britain scale. Gower's sign was positive. An electromyogram showed myopathic changes and a nerve conduction velocity study was normal. Serum enzymes were elevated further on the third day: AST, 55 IU/L; CPK, 783 IU/L with 100% MM form. The diagnosis of dermatomyositis was established. As for the work-up result, anti-dsDNA antibody, anti-ENA antibody, and anti-Jo1 antibody were negative. Tumor marker screen (,-HCG, AFP, CEA, and CA-125), was negative, and rhinolaryngopharyngoscope examination and gynecologic sonography were normal. Figure 1. Diffuse erythematous swelling with subtle violaceous hue extending from the temporal area to the cheeks, neck, and shoulders. The crusted lip ulcers of herpes simplex were also noted Figure 2. Basketweave hyperkeratosis, mild acanthosis, subtle vacuolar degeneration of the basal cells, and melanin incontinence (hematoxylin and eosin, ×400) Figure 3. Heavy mononuclear cells infiltrated in the subcutaneous fat tissue (hematoxylin and eosin, ×100) Pancreatitis was initially suspected because of epigastric pain and tenderness, elevated serum lipase (382 U/L; normal, 23,200 U/L), and amylase (145 U/L; normal, 35,118 U/L). No evidence of pancreatitis could be found in abdominal sonography and abdominal computed tomography (CT), however. The epigastric pain and tenderness subsided soon after admission and the serum pancreatic enzyme level declined on the second day (amylase 69 U/L; lipase, 276 U/L). The patient was then diagnosed with dermatomyositis and treated with prednisolone (120 mg/day). CPK dropped dramatically from 3286 IU/L the day before treatment to 1197 IU/L 3 days after. Panniculitis lessened and the muscle power improved after 1 week of treatment. The disease activity fluctuated even with treatment with prednisolone and the patient often felt listless and weak. The muscle weakness sometimes deteriorated to affect the patient's mobility. Facial erythema and panniculitis-like lesions were found during the worse times. Methotrexate and azathioprine were then added (7.5 mg and 250 mg per week, respectively), but CPK was still mildly elevated (189 IU/L), and the patient still felt ill. Human immune globulin (5%, 500 mL per day, 5 days per month) intravenous infusion was initiated thereafter. There was a dramatic response. Full muscle strength was retained and CPK was within the normal range in the following 6 months with only immune globulin therapy. [source] Lipoatrophic Connective Tissue PanniculitisPEDIATRIC DERMATOLOGY, Issue 1 2010Myriam Marque M.D. Among them, an autoimmune process involving the subcutaneous fat without criteria for another defined disorder coined "connective tissue panniculitis" by Winckelman et al in 1980 has been described. We describe this disease in a 4-year-old boy who presented with multiple subcutaneous inflammatory nodules that extended in an annular fashion, resolved leaving lipoatrophy, with recurrence 8 years later. The histologic findings were consistent with a granulomatous lipophagic panniculitis. We review previous reports and emphasize the limited therapeutic options, chronic evolution, severe esthetic sequelae and possible association with other autoimmune disorders of this uncommon condition. [source] Panniculitis in a patient with chronic myelogenous leukaemia treated with imatinibBRITISH JOURNAL OF DERMATOLOGY, Issue 3 2003S. Ugurel No abstract is available for this article. [source] Erythema nodosum and erythema induratum (nodular vasculitis): diagnosis and managementDERMATOLOGIC THERAPY, Issue 4 2010Heidi Gilchrist ABSTRACT Erythema nodosum is the most common type of panniculitis; it may be due to a variety of underlying infectious or otherwise antigenic stimuli. The pathogenesis remains to be elucidated, but both neutrophilic inflammation and granulomatous inflammation are implicated. Beyond treating underlying triggers, therapeutic options consist mainly of nonsteroidal anti-inflammatory drugs, symptomatic care, potassium iodide, and colchicine. Erythema induratum (nodular vasculitis) is a related but distinctly different clinicopathologic reaction pattern of the subcutaneous fat. It is classically caused by an antigenic stimulus from Mycobacterium tuberculosis but may be associated with several other underlying disorders. After appropriate antimicrobial treatment in tuberculous cases, therapy for erythema induratum is similar to options for erythema nodosum. [source] Cellulite: nature and aetiopathogenesisINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 3 2006F. Terranova Abstract Only a limited number of studies on cellulite have been published in the international literature and many of them reach somewhat antithetical conclusions. Consequently, it is not yet possible to reconcile the extreme differences of opinion which have lingered on for years concerning the nature of this disorder, as well as its origin and even the most basic aspects of its histopathological classification. It does not even have a recognized name: in fact, the term ,cellulitis' is used in scientific English to indicate a spreading gangrenous infection of the subcutaneous cellular tissue. The other terms used from time to time [panniculitis, lipodystrophy, edematofibrosclerotic panniculitis (EFP), liposclerosis, lipoedema, etc.] have quite different morphological and pathogenetic connotations in general. Over the last few decades, three major conflicting theories have emerged in relation to the ethiopathogenesis of cellulite. These indicate, respectively, the following causes: 1. Oedema caused by excessive hydrophilia of the intercellular matrix. 2. A homeostatic alteration on a regional microcirculatory level; this pathogenetic theory is summarized in a synthetic and self-explanatory denomination: EFP. 3. A peculiar anatomical conformation of the subcutaneous tissue of women, different from male morphology. These theories must all now be updated in the light of recent advances on the sophisticated and composite physiopathology of the adipose organ , which acts not only as a control device which regulates the systematic equilibrium of energy and modulates the food intake and the metabolism of other tissue substrate through a multiple glandular secretion of hormones and parahormones. Résumé Seulement un nombre limité d'études sur la cellulite a été publié dans la littérature internationale et beaucoup de ces articles arrivent à des conclusions plutôt antithétiques. Par conséquent, actuellement il est impossible de reconcilier les opinions extrèmement différentes concernant la nature de ce désordre, ainsi que son origine, de même que les aspects les plus basilaires de sa classification histopathologique. Le nom même de cette affection n'est pas reconnu: en fait le terme ,, cellulite ''est utilisé dans le language scientifique pour indiquer une inflammation du tissu cellulaire sous-cutané, d'origine infectieuse. Les autres termes employés de temps an temps tels que panniculopathie, lipodystrophie, panniculopathie oedémato-fibroscléreuse, liposclérose, lipoedème etc. ont en general des connotations morphologiques e pathogénétiques tout à fait différentes. Au cours des dernières décennies, trois principales théories contradictoires ont émergé pour ce qui concerne l'etiopathologie dela cellulite. Chacune théorie indique respectivement les suivantes causes: 1. Oedème causé par excessive hydrophilie de la matrice intercellulaire. 2. Altération parcellaire de l'homeostase au niveau microcirculatoire ; cette théorie pathogénétique est résumée à l'intérieur de la synthétique et explicite dénomination: panniculopathie oedémato-fibroscléreuse. 3. Particulière conformation anatomique du tissu sous-cutané chez la femme, différente par rapport à l'homme. Ces théories doivent toutes être mises à jour, à la lumière des recents développements concernant la sophistiquée et composée physiopathologie de l'adipocyte, qui n'agit pas seulement comme entrepôt de stockage du matériel calorique en excès mais aussi comme dispositif de régulation de l'équilibre énergetique systémique, avec la capacitè de moduler l'ingestion d'aliments et le métabolisme d'autres substrats tissutaires. La révision de ces théories doit être faite aussi sur la base des nouvelles acquisitions concernant la modalitè attravers laquelle cet organe règle les multiples sécrétions hormonales et parahormonales. [source] A case with two unusual findings: cutaneous leishmaniasis presenting as panniculitis and pericarditis after antimony therapyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2010Aydolu Ery, lmaz MD Background, Cutaneous leishmaniasis is a parasitic disease caused by a Protozoan. Clinically and histopathologically, it can be confused with various dermatologic diseases. Methods, We report a case of cutaneous leishmaniasis (CL) with two unusual findings. A 49-year-old male patient presented to our clinic with a 3-month history of multiple nodules exhibiting arciform arrangement on the lateral side of the left leg. Results, Histopathologic examination revealed it as nodular vasculitis. Leishmania smear showed suspicious parasites. Although leishmania culture was negative, PCR was positive for Leishmania. The patient was considered to have CL and was treated with systemic meglumine antimoniate for 14 d. Three days after the end of the treatment, the patient presented to emergency room with a sharp, pleuritic chest pain. He was diagnosed with pericarditis based on clinical and electrocardiogram findings. As other causes of pericarditis were absent, it was thought to be related to antimony therapy. Conclusion, The histopathologic presentation of CL as panniculitis is a very rare and this is the first case of pericarditis after the antimony treatment. [source] Intravascular large B-cell lymphoma presenting in subcutaneous fat tissue and simulating panniculitis clinicallyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 12 2009Pei-Hsuan Lu MD First page of article [source] ,1-Antitrypsin deficiency presenting with panniculitis and incidental discovery of chronic obstructive pulmonary diseaseINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 10 2007Gretchen Korver MD A 60-year-old man presented to the Emergency Department (ED) with large, painful, indurated plaques on the right thigh, left abdomen, left chest, and right chest, which began without any preceding trauma on the right thigh 3 weeks prior to presentation in the ED. He was initially treated with cefazolin 1 g three times daily as home infusions. When the lesions continued to progress, he was admitted to the hospital and placed on amoxicillin/clavulanate and vancomycin. He had a single episode of fever of 102°F, but his white blood cell count and differential remained normal. An initial biopsy showed a dermal inflammatory infiltrate composed primarily of neutrophils and eosinophils with rare flame figures in the dermis. There was minimal fat seen in this biopsy. A differential diagnosis of Wells or Sweet's syndrome was entertained, and he was placed on 60 mg/day prednisone with no resolution of his symptoms. The patient's past medical history included hypertension, hyperlipidemia, peripheral neuropathy, and hiatal hernia. His family history was significant for emphysema in both parents and coronary artery disease in his father. Both of his parents smoked cigarettes. His grandfather, who was a coal miner, also had emphysema. Whilst on antibiotics and prednisone, the plaques on the patient's right thigh, right abdomen, and left chest expanded and ulcerated, draining an oily liquid (Figs 1 and 2). An incisional biopsy was obtained from his thigh. Histopathology showed a septal and lobular panniculitis with fat necrosis, neutrophils, and histiocytes (Fig. 3). Special stains for organisms were negative. Tissue sent for bacterial and fungal culture had no growth. Amylase and lipase levels were normal. Rheumatoid factor, antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), cryoglobulins, and antiphospholipid antibodies were all normal. The ,1-antitrypsin level was low at 25 mg/dL (ref. 75,135). The ,1-antitrypsin phenotype was PiZZ. Figure 1. Indurated plaques on right chest and thigh and left chest Figure 2. Ulcerated plaques on left chest Figure 3. Septal and lobular panniculitis with fat necrosis. Hematoxylin and eosin ×10 The patient had a normal glucose-6-phosphate dehydrogenase level and was placed on dapsone 200 mg/day. The inflammation resolved and, over the course of several months, the involved areas healed with scarring. The patient denied any pulmonary complaints but, during his hospitalization, was found incidentally to have an oxygen saturation of 88% on room air. He was sent for evaluation by a pulmonologist, and pulmonary function tests revealed a mixed restrictive and obstructive pattern with a forced expiratory volume in 1 to forced vital capacity (FEV1/FVC) ratio of 63% of predicted. He had never smoked. He was placed on supplemental oxygen but, as his pulmonary disease has been stable, he has not been treated with intravenous antitrypsin inhibitor. [source] Alpha-1-antitrypsin deficiency associated with panniculitis treated with plasma exchange therapyINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2004Priscila De Oliveira MD Background, Alpha-1-antitrypsin is the principal serum protease inhibitor. In addition to the well-recognized association with early-onset emphysema and cirrhosis, alpha-1-antitrypsin deficiency may be associated with panniculitis. The treatment of this type of panniculitis presents a significant challenge. Previous attempts using immunosuppressive, anti-inflammatory, and cytotoxic drugs have shown variable results. Aim, To report a case of alpha-1-antitrypsin deficiency-associated panniculitis treated with plasma exchange therapy. Methods, A 23-year-old patient developed painful red nodules on her thighs and buttocks with spontaneous ulceration and discharge of oily fluid. A skin biopsy specimen showed septal and lobular panniculitis. The serum alpha-1-antitrypsin level was 22 mg/dL. She was treated with plasma exchange therapy. Results, Treatment of this patient with plasma exchange therapy led to the control of the cutaneous lesions. Conclusions, Plasma exchange therapy represents an alternative treatment which restores serum and tissue alpha-1-antitrypsin levels. This method is proposed because of its clinical benefits and greater availability. [source] A case of necrobiotic xanthogranuloma without paraproteinemia presenting as a solitary tumor on the thighINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 6 2003Sung Eun Chang MD A 82-year-old Korean woman had had a 6-month history of an asymptomatic, flat, hard, red to brown tumor on her right thigh. This lesion had been slowly enlarging with an advancing margin. She had noted gradually developing pain associated with necrosis and ulceration on the lesion. Examination revealed a solitary, 8 × 7.5 cm, yellow to dark red, telangiectatic tumor with multiple areas of punched out ulceration and a peripheral elevated yellowish margin on the right inner upper thigh (Fig. 1). No clinically similar lesions on the periorbital area or other sites were seen. Histologic examination revealed a massive palisading granulomatous infiltration with several layers of extensive bands of necrobiotic zone in the entire dermis and deep subcutaneous tissue (Fig. 2a). In the granulomatous infiltrate in the dermis and subcutis, many various-shaped, some bizarre, angulated, foreign-body type multinucleated giant cells, many Touton giant cells, and a few Langhans giant cells were found to be scattered (Fig. 2b). There were numerous xanthomatized histiocytes. Dense infiltration of lymphoplasma cells was seen in the periphery of the granuloma and perivascularly. Conspicuous granulomatous panniculitis composed of lymphoplasma cells, polymorphonuclear cells, foam cells, and Touton and foreign-body giant cells was also seen. However, cholesterol clefts and lymphoid follicles were not seen. Subcutaneous septae were widened by necrobiotic change and fibrosis with thrombosed large vessels. Gram, Gomeri-methenamine silver and acid-fast stains were negative. The necrobiotic areas were positive to alcian blue. Laboratory investigation revealed elevated white blood cell counts, anemia and elevated erythrocyte sedimentation rate. The following parameters were within the normal range: lipids, glucose, renal and liver function tests, serum complements, serum immunoglobulins, cryoglobulins and antinuclear antibodies. The findings of chest X-ray, skull X-ray and ectorcardiography were normal. Serum electrophoresis and serum immunoelectrophoresis revealed no abnormality. The patient was diagnosed as having necrobiotic xanthogranuloma without paraproteinemia. She was treated with oral steroid (0.5,0.6 mg/kg) and NSAIDS for 1 month with partial improvement of pain and the lesion ceased to enlarge. In the following 1 year of follow-up, with only intermittent NSAIDS, her lesion did not progress and there were no signs of systemic involvement or new skin lesions. Figure Figure 1 . (a) A solitary, red to brown plaque with multiple ulcerations and a peripheral elevated yellowish margin on the inner upper thigh Figure 2. (a) A dermal and subcutaneous massive xanthogranulomatous infiltrate with zonal necrobiosis of collagen (× 20). (b) Prominent infiltrate of xanthomatized histiocytes and giant cells with perivascular lymphoplasma cells (H&E, × 100) [source] Erythema induratum with pulmonary tuberculosis: histopathologic features resembling true vasculitisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 3 2001Yong Suk Lee MD A 22-year-old South Korean woman presented with a 4-month history of several nodules on both legs. She looked healthy, but suffered from tenderness and swelling of the legs. Physical examination showed multiple, nonulcerating, erythematous nodules occurring on the calves, knee joints, and thighs (Fig. 1). A biopsy specimen of the skin revealed necrotizing vasculitis of medium-sized arteries with fibrinoid necrosis at the border between the dermis and the subcutis. Dense cellular infiltrates, including numerous neutrophils and lymphocytes, presented within and around the vessel walls as in polyarteritis nodosa, with some eosinophils (Fig. 2A,B). There were no other generalized symptoms. She was diagnosed with cutaneous polyarteritis nodosa and was initially treated with systemic steroids. She was given an intravenous injection of Solu-Cortef, 60 mg/6 h for 7 days. This was replaced with oral prednisolone for 2 weeks. The skin lesions and symptoms improved. Figure 1. Small, nut-sized, erythematous, brown-colored nodules and patches on the lower extremities, even above the knee joints Figure 2. (A) Dense infiltration within and around artery (× 40). (B) Slightly expanded lobular panniculitis with vasculitis (× 100) Six months later, she complained of general weakness and recurrent skin lesions. Purified protein derivative (PPD) test gave a moderate positive reaction and chest X-ray examination showed the features of pulmonary tuberculosis: radio-opaque infiltrations in the right lower lung field. A repeated biopsy revealed mild vasculitis with more diffuse lobular infiltrations of the subcutaneous tissue compared with the former specimen. Polymerase chain reaction (PCR) and tissue culture for Mycobacterium tuberculosis were performed from a biopsy specimen. DNA was extracted from skin tissue with an AplisystemTM DNA/RNA detection kit using the resin-mediated boiling method (Stargene, Seoul, South Korea). The primers were designed on the basis of the M. tuberculosis gene IS6110 target (sense primer, 5,-CCA GAT GCA CCG TCG AAC GGC TGA T-3, antisense primer, 5,-CGC TCG CTG AAC CGG ATC GAT GTG T-3,). The amplification was performed with uracil- N -glycosylase (UNG), to prevent carry-over contamination, and internal control primers, to correct for false-negative reaction (Kox LF, Rhienthong D, Miranda AM et al. A more reliable PCR for detection of Mycobacterium tuberculosis in clinical samples. J Clin Microbiol 1994; 32: 672,678; Longo MC, Berninger MS, Hartley JL. Use of uracil DNA glycosylase to control carry-over contamination in polymerase chain reactions. Gene 1990; 93: 125,128). According to the manufacturer's instructions, amplification was carried out for 40 cycles with denaturation at 94 °C for 40 s, annealing at 70 °C for 1 min, and extension at 72 °C for 1 min in a thermal cycler (Perkin,Elmer Cetus, Norwalk, CT, USA). The results of PCR and tissue culture for M. tuberculosis using the biopsy specimen were all negative (Fig. 3). Figure 3. Negative result in PCR for M. tuberculosis (negative control is not shown; M, marker; P, positive control; I, internal control; S, specimen) The patient was finally diagnosed with erythema induratum with pulmonary tuberculosis and was started on antituberculosis medication (isoniazid 400 mg, rifampicin 600 mg, ethambutol 800 mg, and pyrazinamide 1500 mg daily). She showed prompt improvement after 2 weeks of medication. After 9 months of antituberculosis therapy, her skin lesions and chest X-ray had cleared. She was followed up for 4 months with no recurrence of skin and pulmonary lesions. [source] Dermatomyositis presenting as panniculitisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2000Yen-Yu Chao MD A 44-year-old obese woman was transferred to our clinic with a diagnosis of panniculitis. Examination showed multiple, indurated, erythematous, painful nodules and plaques distributed on the shoulders, back, forechest, abdomen, buttock, and bilateral thighs. These skin lesions appeared 2 months previously, measured 5,8 cm, and were tender on palpation. No obvious inducing factor was traced. The lesions seemed unresponsive to treatment with nonsteroidal anti-inflammatory drugs (ibuprofen, 400 mg three times a day) as similar lesions appeared in subsequent visits. Progressive proximal muscle weakness was found 1 month later. She was then admitted via the emergency room because of extensive painful skin plaques and abdominal pain. Diffuse erythematous to violaceous swelling of the face, neck, and shoulder was noted at about the same time ( Fig. 1). A skin biopsy specimen from the nodular lesion showed poikilomatous epidermal changes ( Fig. 2), and marked mononuclear cell infiltration in the dermis and subcutaneous fat ( Fig. 3). Dermatomyositis was considered as the diffuse violaceous facial erythema could be a form of heliotrope eruption, but Gottron's papule was not found. At admission, serum creatinine phosphokinase (CPK) was mildly elevated (436 IU/L; normal range, 20,170 IU/L), but serum asparagine transaminase (AST) and lactate dehydrogenase (LDH) levels were within normal limits (36 IU/L; normal, 11,47 IU/L; and 108 IU/L; normal, 90,280 IU/L, respectively). Antinuclear antibody was 1 : 80 positive with an atypical speckled pattern. Muscle strength was weakest during the first 2 days, about grade 3 by the Medical Research Council (MRC) of Great Britain scale. Gower's sign was positive. An electromyogram showed myopathic changes and a nerve conduction velocity study was normal. Serum enzymes were elevated further on the third day: AST, 55 IU/L; CPK, 783 IU/L with 100% MM form. The diagnosis of dermatomyositis was established. As for the work-up result, anti-dsDNA antibody, anti-ENA antibody, and anti-Jo1 antibody were negative. Tumor marker screen (,-HCG, AFP, CEA, and CA-125), was negative, and rhinolaryngopharyngoscope examination and gynecologic sonography were normal. Figure 1. Diffuse erythematous swelling with subtle violaceous hue extending from the temporal area to the cheeks, neck, and shoulders. The crusted lip ulcers of herpes simplex were also noted Figure 2. Basketweave hyperkeratosis, mild acanthosis, subtle vacuolar degeneration of the basal cells, and melanin incontinence (hematoxylin and eosin, ×400) Figure 3. Heavy mononuclear cells infiltrated in the subcutaneous fat tissue (hematoxylin and eosin, ×100) Pancreatitis was initially suspected because of epigastric pain and tenderness, elevated serum lipase (382 U/L; normal, 23,200 U/L), and amylase (145 U/L; normal, 35,118 U/L). No evidence of pancreatitis could be found in abdominal sonography and abdominal computed tomography (CT), however. The epigastric pain and tenderness subsided soon after admission and the serum pancreatic enzyme level declined on the second day (amylase 69 U/L; lipase, 276 U/L). The patient was then diagnosed with dermatomyositis and treated with prednisolone (120 mg/day). CPK dropped dramatically from 3286 IU/L the day before treatment to 1197 IU/L 3 days after. Panniculitis lessened and the muscle power improved after 1 week of treatment. The disease activity fluctuated even with treatment with prednisolone and the patient often felt listless and weak. The muscle weakness sometimes deteriorated to affect the patient's mobility. Facial erythema and panniculitis-like lesions were found during the worse times. Methotrexate and azathioprine were then added (7.5 mg and 250 mg per week, respectively), but CPK was still mildly elevated (189 IU/L), and the patient still felt ill. Human immune globulin (5%, 500 mL per day, 5 days per month) intravenous infusion was initiated thereafter. There was a dramatic response. Full muscle strength was retained and CPK was within the normal range in the following 6 months with only immune globulin therapy. [source] Intramedullary fat necrosis, polyarthritis and panniculitis with pancreatic tumor: a case reportINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 4 2010Vivek VASDEV Abstract Acute polyarthritis can occur in non-rheumatic systemic illnesses, presenting a diagnostic dilemma. We present an extremely rare case presenting as acute polyarthritis, panniculitis and medullary fat necrosis with underlying pancreatic pathology. This case report describes a young woman presenting with panniculits, pancreatic tumour, polyarthritis and intra-osseus fat necrosis with a fatal outcome. The medical fraternity needs to be aware of this potentially fatal albeit rare musculoskeletal complication secondary to a pancreatic pathology. [source] Facets of lupus erythematosus: panniculitis responding to thalidomideJOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT, Issue 3 2008Simone Wienert Summary Lupus erythematosus profundus or lupus panniculitis is a rare clinical variant of lupus erythematosus, which involves the deep dermis and subcutaneous fat. Diagnosis may be difficult in cases with isolated involvement. Further manifestations of lupus erythematosus may thus be essential for diagnosis, which depends on the clinical picture, histopathology and a positive lesional lupus band test. We report a severe, mutilating case of lupus panniculitis, which responded well to thalidomide. [source] Sonographic findings of mesenteric panniculitis: Correlation with CT and literature reviewJOURNAL OF CLINICAL ULTRASOUND, Issue 4 2006Nuria Rosón MD Abstract Purpose. To evaluate the sonographic findings of mesenteric panniculitis (MP) and correlate them with CT findings. Methods. We retrospectively evaluated the clinical, CT, and sonographic findings in 26 cases of MP in our hospital between January 1997 and July 2003. We also reviewed the sonographic features of MP previously described in the literature. Results. The sonographic findings were well correlated to CT in 24 of 26 patients (92%). In these 24 cases, abdominal sonographic examination revealed a hyperechogenic, well-defined fatty mass (corresponding to the pseudocapsule CT sign) in the root of the mesentery, displacing the bowel loops. We found a clear interface between MP and normal intra abdominal fat. Examination with color Doppler sonography revealed the nondeviated mesenteric vessels within the mass. The persence of MP improved sonographic transmission in 9 obese patients and enabled the retroperitoneal vessels to be clearly visualized. Sonography was unable to demonstrate the preservation of the fat nearest the mesenteric vessels corresponding to the "fatty halo" sign on CT. Conclusions. Sonography is useful in the diagnostic workup for MP. The characteristic sonographic features of MP (well-defined mass, homogeneous hyperechogenicity of the mass, nondeviated vessels within the mass, and displaced bowel loops) correlate well with CT findings. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:169,176, 2006 [source] Histopathology of a granulomatous lobular panniculitis in acute Q fever: a case reportJOURNAL OF CUTANEOUS PATHOLOGY, Issue 8 2010R Soulard Q fever is a zoonotic infection caused by Coxiella burnetii. Two forms of the disease have been described: an acute form with pneumonia, hepatitis or a flu-like syndrome; and a chronic form in which endocarditis is the most frequent clinical expression. We report a 77 year old male with fever and an erythematous nodule on the right leg. Biopsy revealed a granulomatous lobular panniculitis with some granulomas rimmed by an eosinophilic material, giving a "doughnut" or "fibrin-ring" appearance. Q fever serological studies were positive. Cutaneous signs, among them panniculitis, are probably underestimated during the acute phase of the disease, and recognizing different granulomatous patterns may contribute to the diagnosis. Soulard R. Histopathology of a granulomatous lobular panniculitis in acute Q fever: a case report. [source] Lobular panniculitis at the site of glatiramer acetate injections for the treatment of relapsing-remitting multiple sclerosis.JOURNAL OF CUTANEOUS PATHOLOGY, Issue 4 2008A report of two cases Lipoatrophy and localized panniculitis have been described as rare complications of daily subcutaneous glatiramer acetate injections for the treatment of relapsing-remitting multiple sclerosis (MS). We describe the biopsies from two MS patients in a single neurologist's practice who developed clinical lesions of lipoatrophy at the sites of subcutaneous glatiramer acetate injections. These biopsies showed a lobular panniculitis with lipoatrophy that more closely resembled lupus panniculitis than previous reports of localized panniculitis at glatiramer acetate injection sites. In one case, the area of clinical lipoatrophy continued to enlarge for 6 months after stopping glatiramer acetate therapy, before stabilizing at its current size for the last 8 months. Injection site reactions to glatiramer acetate should be considered in the differential diagnosis of biopsies that show a lupus panniculitis-like appearance. Our observations indicate that glatiramer acetate induced panniculitis is common and may continue to progress after therapy has stopped. In this single neurologist's practice, 64% of the patients receiving daily glatiramer acetate injections had clinical evidence of lipoatrophy or panniculitis. Of 100 consecutive patients receiving therapy for MS between February and November 2006, 14 patients were on glatiramer acetate, 9 of whom had clinical lipoatrophy. [source] Lupus erythematosus panniculitis (lupus profundus): Clinical, histopathological, and molecular analysis of nine casesJOURNAL OF CUTANEOUS PATHOLOGY, Issue 6 2005Cesare Massone Background:, The diagnosis of lupus erythematosus panniculitis (LEP) may be very difficult in cases in which involvement of the subcutaneous fat is the only manifestation of the disease. The main differential diagnosis is subcutaneous panniculitis-like T-cell lymphoma (SPTCL). Methods:, We performed a retrospective study reviewing the histopathologic features of 11 biopsy specimens from nine patients with LEP (M : F = 2 : 7; median age: 48 years; range: 20,71 years). Results:, Histopathologically, all biopsies revealed a lobular panniculitis, with concomitant septal involvement in 82% of them. Dermal changes included the presence of superficial and deep infiltrates (82%) and mucin deposition (73%). The majority of cases (73%) presented also some form of epidermal involvement. The subcutaneous infiltrate was composed of lymphocytes in all cases, admixed with plasma cells in 91% of cases. Lymphoid follicles with reactive germinal centers were detected in 45% of cases. Immunohistochemistry showed a predominance of ,/,-T-helper and cytotoxic lymphocytes in 80% of cases admixed with B lymphocytes. The polymerase chain reaction analysis of the T-cell receptor (TCR)-, gene showed a polyclonal smear in all cases. Conclusions:, Our study shows that the most useful histopathologic criteria for distinguishing LEP from SPTCL are the presence of involvement of the epidermis, lymphoid follicles with reactive germinal centers, mixed cell infiltrate with prominent plasma cells, clusters of B lymphocytes, and polyclonal TCR-, gene rearrangement. [source] Pseudoxanthoma Elasticum (PXE)-Like Fibers in Patients Without PXEJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005A.R. Bowen Pseudoxanthoma elasticum (PXE) is an inherited disorder characterised by progressive calcification of elastic fibers in the skin, eyes and cardiovascular system. Skin lesions show distinctive thickened, fragmented elastic fibers in the reticular dermis. PXE-like fibers have not been described in patients without PXE. We describe 12 patients without known PXE who demonstrated the incidental finding of small numbers of PXE-like fibers in association with the following conditions: lipodermatosclerosis, granulomatous dermatitis, lichen sclerosus, morphea profunda, erythema nodosum, septal panniculitis, basal cell carcinoma and fibrosing dermatitis NOS. The biopsies were almost exclusively from the lower extremities of elderly women (mean age 73.8). The affected gene in PXE has been recently described as ABCC6 which codes for a member of the ATP-binding cassette (ABC) family of proteins. The c.3421C>T mutation has been associated with a high risk of coronary artery disease. We describe a novel assay for this genotype employing real-time PCR of paraffin embedded skin biopsies. Four patients with PXE-like fibers were tested in this fashion and did not carry this mutation. Our series demonstrates that light microscopic findings associated with PXE are not specific, as PXE-like fibers can be observed in patients without clinical or genetic evidence of the disease. [source] More about panniculitis and lymphomaJOURNAL OF CUTANEOUS PATHOLOGY, Issue 4 2004N. Scott McNutt [source] Atypical lymphocytic lobular panniculitisJOURNAL OF CUTANEOUS PATHOLOGY, Issue 4 2004Cynthia M. Magro Background:, Although subcutaneous T-cell lymphoma (SCTCL) is considered an aggressive form of lymphoma, some patients manifest a long waxing and waning phase unaccompanied by constitutional symptoms. Methods:, Twelve patients were prospectively encountered, presenting with a lymphocytic panniculitis accompanied by lymphoid atypia, although not fulfilling criteria for SCTCL. Clinical, histologic, phenotypic, and genotypic analyses were conducted. Results:, There were five men, one boy, and six women; none had symptoms compatible with lupus erythematosus or aggressive SCTCL. All but two had a waxing and waning course of years. Four patients had periodic cytopenias accompanied by fevers. While responding somewhat to prednisone, the lesions relapsed. In one patient, treatment with alemtuzumab (CAMPATH-1) led to complete lesional resolution with no recurrence. Light microscopy showed expansion of the interstices of the fat lobule by mildly atypical lymphocytes of the CD4 subset in 10 biopsies from eight patients; in the other four patients, there was an increase in CD8 lymphocytes. There was diminished expression of CD5 and/or CD7 in the majority of biopsies. Ten of 13 biopsies showed clonal T-cell receptor-, rearrangements. Conclusions:, We apply the term atypical lymphocytic lobular panniculitis to this distinctive form of lymphocytic panniculitis manifesting this light microscopic, phenotypic, and genotypic profile. [source] The spectrum of cutaneous lesions in rheumatoid arthritis: a clinical and pathological study of 43 patientsJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2003C. M. Magro Introduction:, Rheumatoid arthritis (RA) is an idiopathic arthropathy syndrome that has a propensity to affect the small joints of the hands and feet with extra-articular manifestations comprising skin lesions, neuropathy, pericarditis, pleuritis, interstitial pulmonary fibrosis and a systemic polyarteritis nodosa (PAN)-like vasculitic syndrome. The most widely recognized skin lesion is the rheumatoid nodule. Other skin manifestations are poorly defined. Materials and methods:, Using a natural language search of the authors' outpatient dermatopathology databases, skin biopsies from 43 patients with RA were selected for retrospective analysis in an attempt to define the dermatopathological spectrum of RA and its clinical correlates. Results:, The biopsies were categorized by the dominant histologic pattern, recognizing that in most cases there were additional minor reaction patterns. Palisading and/or diffuse interstitial granulomatous inflammation was the dominant pattern seen in 21 patients; the lesions included nodules, plaques and papules with a predilection to involve skin over joints. Besides interstitial histiocytic infiltrates and variable collagen necrobiosis, these cases also showed interstitial neutrophilia, vasculitis and pauci-inflammatory vascular thrombosis. The dominant morphology in 11 other patients was vasculopathic in nature: pauci-inflammatory vascular thrombosis, glomeruloid neovascularization, a neutrophilic vasculitis of pustular, folliculocentric, leukocytoclastic or benign cutaneous PAN types, granulomatous vasculitis, and lymphocytic vasculitis and finally occlusive intravascular histiocytic foci for which the designation of ,RA-associated intravascular histiocytopathy' is proposed. Rheumatoid factor (RF) positivity and active arthritis were common in this group, with anti-Ro and anticardiolipin antibodies being co-factors contributing to vascular injury in some cases. Immunofluorescent testing in three patients revealed dominant vascular IgA deposition. In nine patients, the main pattern was one of neutrophilic dermal and/or subcuticular infiltrates manifested clinically as urticarial plaques, pyoderma gangrenosum and panniculitis. Conclusions:, The cutaneous manifestations of RA are varied and encompass a number of entities, some of which define the dominant clinical features, such as the rheumatoid papule or subcutaneous cords, while others allude to the histopathology, i.e. rheumatoid neutrophilic dermatosis. We propose a more simplified classification scheme using the adjectival modifiers of ,rheumatoid-associated' and then further categorizing the lesion according to the dominant reaction pattern. Three principal reaction patterns are recognized, namely extravascular palisading granulomatous inflammation, interstitial and/or subcuticular neutrophilia and active vasculopathy encompassing lymphocyte-dominant, neutrophil-rich and granulomatous vasculitis. In most cases, an overlap of the three reaction patterns is seen. Co-factors for the vascular injury that we believe are integral to the skin lesions of RA include RF, anti-endothelial antibodies of IgA class, anti-Ro and anticardiolipin antibodies. [source] Subcutaneous pseudomembranous fat necrosis: new observations,/linkr>JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2002Carlos Diaz-Cascajo Background: Pseudomembranous fat necrosis is a peculiar manifestation of necrosis of adipose tissue characterized by formation of pseudocystic cavities lined by crenulated membranes. The underlying mechanism for the formation of pseudomembranes is unknown and numerous hypotheses have been proposed. Despite divergent interpretations, most authors consider necrotic fat cells to be the anatomic substrate for the formation of pseudomembranes. Methods: A total of 341 panniculitides were reviewed for the presence of pseudomembranous fat necrosis. The specific diagnoses were established after correlation of all available clinical and laboratory data with the histopathology. Special attention was given to the time in the evolution of the disease when the biopsy was taken. Additional immunohistochemical studies were performed in 12 cases. Results: Thirty of 341 cases of different types of panniculitides were found to show pseudomembranous fat necrosis, namely: 10 of 15 cases of sclerosing panniculitis (lipodermatosclerosis), 6 of 95 cases of erythema nodosum, 7 of 34 cases of traumatic panniculitis, 1 of 7 cases of lupus panniculitis, 1 of 20 cases of erythema induratum Bazin (nodular vasculitis), 1 of 9 cases of necrobiosis lipoidica, 1 of 4 cases of sclerotic lipogranuloma, 1 of 9 cases of infectious panniculitis (erysipelas), 1 of 2 cases of pancreatic panniculitis, and 1 of 4 cases of subcutaneous sarcoidosis. Pseudomembranous fat necrosis labelled strongly for the histiocytic markers CD68 and lysozyme. Conclusions: Our series provides data suggesting that pseudomembranous fat necrosis represents a dynamic process that varies according to the evolution of the lesion at the time of the biopsy. In biopsies taken from early foci of panniculitides pseudomembranes show vescicular or picnotic nuclei. Later, pseudomembranes retain their crenulated appearance but lack nuclear elements. Furthermore, we present histopathologic, histochemical, and immunohistochemical evidence that pseudomembranous fat necrosis results from the interaction of residual products of disintegrated fat cells and macrophages. Histiocytic markers such as CD68 and lysozyme may be used as reliable tools in order to detect pseudomembranes in panniculitides. [source] Eosinophilic panniculitis: a new form of local reaction with specific immunotherapyALLERGY, Issue 11 2009I. Koca Kalkan No abstract is available for this article. [source] Lipoatrophic Connective Tissue PanniculitisPEDIATRIC DERMATOLOGY, Issue 1 2010Myriam Marque M.D. Among them, an autoimmune process involving the subcutaneous fat without criteria for another defined disorder coined "connective tissue panniculitis" by Winckelman et al in 1980 has been described. We describe this disease in a 4-year-old boy who presented with multiple subcutaneous inflammatory nodules that extended in an annular fashion, resolved leaving lipoatrophy, with recurrence 8 years later. The histologic findings were consistent with a granulomatous lipophagic panniculitis. We review previous reports and emphasize the limited therapeutic options, chronic evolution, severe esthetic sequelae and possible association with other autoimmune disorders of this uncommon condition. [source] Mesenteric panniculitis: a diagnosis of exclusionANZ JOURNAL OF SURGERY, Issue 3 2010James G. Huang MBBS No abstract is available for this article. [source] Connective tissue panniculitis in a child with vitiligo and Hashimoto's thyroiditisAUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 1 2006Basit Mirza SUMMARY A 9-year-old girl presented with a 6-month history of inflamed tender nodules in the pretibial area. These eventually healed leaving depressed areas of atrophy and loss of subcutaneous tissue. Histology showed a predominantly lymphocytic lobular panniculitis, consistent with connective tissue panniculitis. Investigations revealed an elevated thyroid stimulating hormone, elevated thyroid antiperoxidase antibody and a weakly positive antinuclear antibody (titre 1 in 40). She was commenced on hydroxychloroquine 300 mg daily, which resulted in resolution of the panniculitis. She developed focal vitiligo on the thighs. This gradually improved with 0.1% mometasone furoate ointment. The hydroxychloroquine dose was tapered to 200 mg daily after 12 months, then to 100 mg daily after 18 months therapy. Her thyroid autoantibody levels continued to rise and the hydroxychloroquine was increased again to 300 mg daily. She became borderline hypothyroid. Hashimoto's thyroiditis was diagnosed. Thyroxine was instituted with a resultant improvement in her thyroid blood tests. The lipoatrophy has not developed further during 2-year follow up. [source] Unusual case of subcutaneous panniculitis-like T-cell lymphomaAUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 2 2004Jillian Wells SUMMARY An unusual case of subcutaneous panniculitis-like T-cell lymphoma is presented involving multiple organ systems, which eventually culminated in rapid demise from the haemophagocytic syndrome, after an initial protracted course. A 44-year-old man presented in April 2001 with bronchiolitis obliterans organising pneumonia that initially responded well to corticosteroids. However, the condition relapsed on attempted prednisone withdrawal in January 2002 and the patient was noted to have developed truncal subcutaneous nodules. Initial skin biopsy revealed lobular panniculitis, with negative microbiological culture. In July 2002, mononeuritis multiplex was diagnosed after the patient presented with paresthesiae and was treated with pulse cyclophosphamide therapy. By November 2002 there was ulceration of the subcutaneous nodules. Repeat skin biopsy revealed subcutaneous panniculitis-like T-cell lymphoma. The clinical manifestations were supportive of an unifying diagnosis of malignancy involving pulmonary, cutaneous and nervous systems. Combination chemotherapy with fludarabine, mitoxantrone and dexamethasone was commenced. However, the patient deteriorated, with fevers, weight loss, pancytopenia and laboratory features consistent with the haemophagocytic syndrome. Despite maximal supportive therapy the patient succumbed to his disease. [source] Inguinal panniculitis in a young Tasmanian devil (Sarcophilus harrisii) caused by Mycobacterium mageritenseAUSTRALIAN VETERINARY JOURNAL, Issue 5 2010G Reppas A 1-year-old, entire male Tasmanian devil living in captivity was presented because of a nodular inguinal lesion that subsequently developed a draining sinus tract. A second, similar lesion developed later in the ipsilateral axillary region. A deep representative biopsy specimen of abnormal subcutaneous tissue showed chronic active pyogranulomatous inflammation and beaded Gram-positive and acid-fast bacilli situated in lipid vacuoles within the lesion. A rapidly growing Mycobacterium species, shown subsequently to be M. mageritense, was grown from a swab of the primary lesion. It was susceptible to tetracyclines (including doxycycline) and moxifloxacin in vitro. The lesions resolved following treatment with doxycycline monohydrate (50 mg PO once daily) and then moxifloxacin (10 mg/kg PO for 20 days). The infection probably resulted from inoculation of subcutaneous tissues by material containing this Mycobacterium following fight or bite injuries. The presentation is reminiscent of similar lesions attributable to rapidly growing mycobacterial infections of the subcutis observed in domestic cats and quolls. [source] Panniculitis secondary to extravasation of clarithromycin in a patient with ,1-antitrypsin deficiency (phenotype PiZ)BRITISH JOURNAL OF DERMATOLOGY, Issue 2 2003D.G. Parr Summary ,1-Antitrypsin deficiency (AATD) is known to be associated with panniculitis. Although reports of this association are rare, the true incidence may be unappreciated because of underdiagnosis of AATD. We report a case of panniculitis occurring in a 34-year-old woman with severe AATD following the extravasation of clarithromycin infused intravenously for treatment of community-acquired pneumonia. Resolution occurred with conservative management. The histopathology and management of this unusual condition are discussed, with a review of the literature. [source] | ||||||||||