Successful treatment of a common hepatic artery pseudoaneurysm using a coronary covered stent following pancreatoduodenectomy: report of a case.

This report presents the case of a common hepatic artery (CHA) pseudoaneurysm secondary to postoperative pancreatic fistula (POPF) after pancreatoduodenectomy (PD), which was successfully treated using a coronary covered stent. A 70-year-old female underwent subtotal stomach-preserving PD for middle cholangiocarcinoma. POPF was identified on postoperative day (POD) 7, and the patient suddenly lost 500 ml of blood via the abdominal drain on POD 19. Urgent celiac arteriography revealed a CHA pseudoaneurysm. A coronary covered stent was placed to prevent rupture of the pseudoaneurysm and to maintain hepatic arterial flow, instead of performing transarterial embolization. No vascular adverse events were encountered during or after the procedure. Computed tomography and angiography showed a patent stent graft and good hepatic arterial flow 9 months after placement of the stent. Endovascular stent-graft placement not only treated the pseudoaneurysm, but also preserved the arterial blood flow. This report describes the placement of a covered stent graft for delayed hemorrhage after PD.

Risk factors for conversion of laparoscopic cholecystectomy to open surgery associated with the severity characteristics according to the Tokyo guidelines.

PURPOSE: The aim of this retrospective study was to identify the risk factors associated with the severity characteristics in the Tokyo guidelines for conversion to open surgery in patients with acute cholecystitis (AC) who underwent laparoscopic cholecystectomy. METHODS: A total of 225 patients were enrolled in the study. The patients were classified into two groups: a conversion group and a no-conversion group. The preoperative characteristics and therapeutic strategy were analyzed as risk factors for conversion to open surgery. The postoperative outcomes were also analyzed. RESULTS: Conversion to open surgery occurred in 29 patients (12.9%), including seven patients (6.7%) with mild AC and 22 patients (18.5%) with moderate AC. A univariate analysis showed that the risk factors for conversion to open surgery included a duration of symptoms longer than 72 h, an elevated C-reactive protein (CRP) value and the Tokyo guidelines 2013 (TG 13) severity classification. The multivariate analysis showed that the risk factors for conversion to open surgery included a duration of symptoms longer than 72 h and a CRP value >11.5 mg/dl. CONCLUSIONS: A duration of symptoms longer than 72 h, which is included in the criterion for moderate AC severity in the TG 13, was an independent risk factor for conversion to open surgery. In addition, adoption of a high CRP value as an additional criterion for moderate AC may increase the utility of the TG 13.

Neonatal lupus erythematosus in identical twins, showing transient bullous lesions.

One of identical twin girls was born with ulcers on her leg, and shortly after birth developed a flaccid blister on the leg. Subepidermal blister with vacuolar degeneration of basal cell layer and the heavy infiltration of mononuclear cells in the upper dermis were observed in the blister lesion. She also had generalized livedo. Her identical twin sister did not exhibit ulcers or blisters, but was born with milia on her limbs. Their mother was found to have lupus erythematosus with positive anti-Ro/SSA antibodies and developed Sjögren syndrome. We emphasize neonatal blistering and congenital milia unique manifestations of neonatal lupus erythematosus.

Erdheim-Chester disease: report of a case with PCR-based analysis of the expression of osteopontin and survivin in Xanthogranulomas following glucocorticoid treatment.

Erdheim-Chester disease (ECD) is a form of non-Langerhans histiocytosis. In this report, we show a case of ECD presenting diabetes insipidus and multiple xanthogranulomas received glucocorticoid treatment over a year. During this period, xanthogranulomas improved in response to the glucocorticoid therapy. Furthermore, the expression of osteopontin in xanthogranulomatous tissues significantly decreased following the treatment. Our data show the expression of osteopontin in xanthogranulomatous tissues of ECD. Furthermore, the osteopontin mRNA decreased following glucocorticoid therapy with xanthogranuloma regression, suggesting that the expression level of osteopontin could be a marker of the disease activity of ECD.

Transition of psoriasiform drug eruption to psoriasis de novo evidenced by histopathology.

Drug reaction can be one of the triggering factors either for exacerbation of pre-existing psoriasis or precipitation of psoriasis de novo. Herein, we report a case with psoriasiform drug eruption due to pravastatin, but it relapsed after discontinuance of the drug. Serial investigation of the histopathology and immunohistochemistry with anti-signal transducer and activator of transcription 3 (STAT3) revealed drug reaction-associated lesions intermingled with psoriasiform changes, which later predominated, suggesting a conversion into psoriasis de novo.

Community validation of the U.K. diagnostic criteria for atopic dermatitis in Japanese elementary schoolchildren.

BACKGROUND: A simple list of diagnostic criteria for atopic dermatitis for use in epidemiological studies was developed by a U.K. working party. This list served well for both hospital patients with skin diseases and in general population within the U.K. OBJECTIVES: To validate the U.K. diagnostic criteria in Japanese elementary schoolchildren, we collected the questionnaires on regular health checkups, which had been completed by parents of schoolchildren in 2001/2002 and 2004/2005. METHODS: Elementary schoolchildren were examined by dermatologists in eight areas (16,152 children) in 2001/2002 and in three areas (3849 children) in 2004/2005. The questionnaire was distributed to the parents 2 weeks before the skin examination, completed by the parents and collected after the survey. RESULTS: In 2002/2002 comparing the U.K. diagnostic criteria with the findings on clinical examination used as the reference standard, the U.K. criteria (1-year prevalence measure) showed a sensitivity of 71.8%, specificity of 89.3% and positive predictive value of 44.7%. In 2004/2005 we confirmed that the U.K. criteria for a point prevalence measure showed a higher positive predictive value (59.9%) compared with that for 1-year prevalence measure (49.3%). CONCLUSION: Now that we know the sensitivity and specificity of the U.K. criteria in the population examined in this study, we will be able in the near future to estimate the prevalence of atopic dermatitis in a similar population with reverse operation by questionnaires alone using these criteria without examination by dermatologists. Therefore, the validation study of U.K. criteria could be useful for future epidemiologic surveys.

Mast cell distribution, activation, and phenotype in xanthoma.

BACKGROUND: Activated mast cells enhance the uptake of mast cell-derived proteoglycan-low-density lipoprotein complexes by macrophages. OBJECTIVE: We sought to investigate mast cell contribution to the pathogenesis of xanthoma. METHODS: Twenty cases of xanthelasma palpebrarum and 6 cases of tuberous xanthoma lesions were analyzed using immunohistochemical staining. RESULTS: Xanthelasma lesions contained up to 5-fold more tryptase-stained mast cells than tuberous xanthoma lesions. Tuberous xanthoma lesions especially showed extensive staining of tryptase around mast cells and within some macrophages and foam cells. More than 99% of mast cells in xanthelasma lesions contained both tryptase and chymase. Approximately 60% of mast cells represented only tryptase in tuberous xanthoma lesions where the ratio of macrophages to tryptase-stained mast cells was extremely high (15:1) as compared with xanthelasma lesions (2:1). LIMITATIONS: A change in mast cell phenotype has not been necessarily proven. CONCLUSION: Mast cells are activated under the microenvironment in which macrophages predominate rather than mast cells, which thus reflects the clinical phenotypes of xanthoma lesions.

Combined Bowen disease and extramammary Paget disease.

BACKGROUND: The histological resemblance between extramammary Paget disease and Bowen disease has been described since Bowen's original article was published in 1912. METHODS: We herein describe a case of vulval primary extramammary Paget disease in a 61-year-old women with the histological features of Bowen disease. RESULTS: Histological examination of a biopsy specimen showed acanthosis with full-thickness cellular atypia, focal hyperkeratosis and parakeratosis in the epidermis, and no characteristic Paget cells were observed. However, histological examination of an operative specimen revealed areas characteristic of Paget disease and Bowen disease. Overall, the areas characteristic of Bowen disease and Paget disease occupied 6% and 32% of the total operative specimen, respectively. The two areas were sharply separated. Immunohistochemical findings showed carcinoembryonic antigen to be expressed in areas containing Paget cells, but not in the areas characteristic of Bowen disease. Cytokeratin 7 (CK7) (OV-TL 12/30) and CK8 (35betaH11) were strongly expressed in both of these areas. The staining for high-molecular-weight cytokeratins was negative in both of these areas. CONCLUSIONS: Our findings indicated that primary extramammary Paget disease and squamous cell carcinoma in situ arose multifocally from a common cell in the epidermis.

Plane xanthoma associated with multiple mastocytoma.

A 5-month-old boy was noted to have brown macules with palpable infiltration on the head, trunk, and extremities a few weeks after birth, with recurrent episodes of generalized flushing and blistering in some of the macules. These lesions developed into yellowish plaques after 1 year of topical treatment with clobetasol propionate. Serum lipid levels were within normal limits. The appearance of the yellowish lesions was similar to that of the xanthelasmoid type of cutaneous mastocytosis. The brown macules showed infiltration of a large number of mast cells and a small number of scattered foam cells, whereas in the yellowish plaques, the number of foam cells was greatly increased. The yellowish plaques regressed spontaneously within a year after cessation of topical corticosteroid treatment. Immunohistochemical analysis found that the foam cells were stained with monocyte/macrophage markers including HAM56, and with SRA-C6, a monoclonal antibody to macrophage scavenger receptor class A (CD204). Therefore, the yellowish plaques were considered to be plane xanthoma associated with cutaneous mastocytoma.

Treatment of pseudoxanthoma elasticum with tocopherol acetate and ascorbic acid.

Pseudoxanthoma elasticum is an inherited systemic disorder of connective tissue characterized by fragmentation of elastic fibers and calcification in cutaneous, ocular, and cardiovascular systems. Mutation in the ATP-binding cassette subfamily C member 6 gene has recently been found in people with pseudoxanthoma elasticum. However, the precise mechanisms of elastic fiber fragmentation and calcification remain obscure. Recently, it has been reported that mild chronic oxidative stress affects pseudoxanthoma elasticum fibroblasts. This suggests that reactive oxygen scavengers might improve this disorder.

IgG/IgA pemphigus with dyskeratotic acantholysis and intraepidermal neutrophilic microabscesses.

Herpetiform vesicles and erythema with erosion developed on the trunk of a 48-year-old Japanese man. Acantholysis was observed in the spinous layer of the lesional epidermis and direct immunofluorescence revealed cell surface deposition of immunoglobulin IgG and C3. Indirect immunofluorescence could not detect circulating anti-cell surface antibodies. Immunoblot analysis detected neither anti-desmoglein (Dsg)1 antibody nor anti-Dsg3 antibody. Enzyme-linked immunosorbent assay could detect IgG and IgA anti-Dsg1 antibodies and IgA anti-Dsg3 antibody, in addition to a gray zone titer of IgG anti-Dsg3 antibody. Intraepidermal neutrophilic infiltration with neutrophilic microabscesses and intense dyskeratotic cells were histopathologically characteristic in this case. Skin lesions improved within 1 month and remission has continued for 9 years under oral administration of dapsone.

Hyaluronan forms complexes with low density lipoprotein while also inducing foam cell infiltration in the dermis.

BACKGROUND: Xanthoma is a foam cell infiltrating lesion similar to atherosclerosis. Glycosaminoglycans and proteoglycans have long been considered to play a role in atherogenesis. OBJECTIVE: The purpose of this study is to investigate the role of hyaluronan, the main dermal glycosaminoglycan, in xanthoma formation. METHODS: The complex formation of low density lipoprotein (LDL) with hyaluronan was investigated by assaying the cholesterol level of precipitates that were formed by incubating LDL, hyaluronan and cetylpyridinium chloride in the presence of Ca2+. The uptake of LDL by mouse peritoneal macrophages was studied by assaying the cellular cholesterol esterification activity. The responsible receptor for the LDL internalization was examined by saturating hyaluronan receptor and blocking class A macrophage scavenger receptor (CD204). Hyaluronan was injected into the dorsal skin of diet-induced hypercholesterolemic rabbits to reveal the xanthoma inducing activity of hyaluronan. RESULTS: Cetylpyridinium chloride precipitated hyaluronan, which had formed complexes with LDL. The macrophages incorporated hyaluronan-LDL complexes and oxidized LDL via CD204. Foam cell infiltration and cholesterol accumulation were induced by intradermal injections of hyaluronan in diet-induced hypercholesterolemic rabbits. CONCLUSION: Hyaluronan, like other sulfated glycosaminoglycans, retains LDL by forming a complex. Via macrophage scavenger receptors, macrophages incorporate not only LDL-hyaluronan complexes, but also oxidized LDL, which has been oxidized during the retention time.

Contribution of xanthoma tissue-derived LDL density substances in the transformation of macrophages to foam cells.

BACKGROUND: The source of accumulated lipids in the foam cells of xanthoma is primarily the lipoproteins existing in the lesional dermis. OBJECTIVE: This study was designated to clarify the contribution of low density lipoprotein (LDL) density substances existing in xanthoma tissue to foam cell formation. METHODS: An LDL density fraction was obtained from homogenized rabbit experimental xanthoma tissue. Biochemical and functional characteristics of xanthoma-extracted LDL density substance were examined. The in vivo foam cell-inducing ability of xanthoma-extracted LDL density substance was examined microscopically at the intradermal injection site. RESULTS: Xanthoma-extracted LDL density substance showed more negatively charged mobility on agarose gel electrophoresis than plasma native LDL. A small amount of aggregated material remained at the origin on agarose gel electrophoresis. Xanthoma-extracted LDL density substance contained much higher level of lipid peroxides than native LDL. Mouse peritoneal macrophages internalized xanthoma-extracted LDL density substance extensively and transformed into foam cells by incubation with xanthoma-extracted LDL density substance. Intradermal injection of the xanthoma-extracted LDL density substance induced foam cell infiltration in the skin of a normolipemic rabbit. CONCLUSION: LDL density substances prepared ex vivo from experimental xanthoma tissue contained lipid-protein complexes that have physiochemical properties of oxidized LDL. The lipid-protein complexes were incorporated into foam cells. The substances were considered to contribute to foam cell recruitment during the persistence of xanthoma lesions.

Neuronal conditions of spinal cord in dermatitis are improved by olopatadine.

Intense pruritus and cutaneous reactivity represent cardinal features of eczema. The resulting scratching behaviors alter neuronal conditions of the spinal dorsal horn where the primary sensory afferent fibers transmit cutaneous stimulation and deteriorate eczematous skin lesions. We investigated the effects of olopatadine hydrochloride (olopatadine) on alteration of neuronal conditions of the spinal dorsal horn and eczematous skin lesions induced by contact dermatitis. Eczematous lesions were induced by repeated application of diphenylcyclopropenone (DCP) in BALB/c mice. Olopatadine suppressed scratching behavior caused by repeated application of DCP in mice. Increased expressions of c-Fos and substance P in the spinal dorsal horn following DCP application were improved by olopatadine. Furthermore, olopatadine diminished the number of infiltrating cells and levels of cytokines in eczematous skin lesions resulting from DCP application. Olopatadine improves neurological conditions in the spinal cord and eczematous skin lesions in a murine contact dermatitis model.

Histamine helps development of eczematous lesions in experimental contact dermatitis in mice.

Histamine is released from mast cells in the skin, causing urticaria and itching. However, little is known about the roles of histamine in development of eczematous lesions in contact dermatitis. Effects of histamine on development of eczematous lesions in contact dermatitis were assessed using histamine-deficient mice in which contact dermatitis was developed by repeated application of diphenylcyclopropenone. Development of eczematous lesions in contact dermatitis was suppressed in histamine-deficient mice compared to wild-type mice. H(1) agonist ((6-12-(4-imidazol)ethylamino)-N-(4-trifluoro- methylphenyl)hepatanecarboxamide) promoted development of eczematous lesions in histamine-deficient mice. H(1) receptor antagonist (loratadine) suppressed development of eczematous lesions in wild-type mice, whereas H(2) agonist (dimaprit) and receptor antagonist (cimetidine) were ineffective. These results suggest that histamine facilitates the development of eczematous lesions in a murine model of contact dermatitis via H(1) receptors.

Discrete papular mucinosis on the back.

A rare case of papular mucinosis on the back of a 78-year old man is described. The patient developed approximately 20 discrete papules on the upper back. His serum glucose concentration was borderline elevated, but no other systemic symptoms or signs were apparent. A biopsy revealed mucin deposits only in the upper reticular dermis. The papules were distinctly different from lichen myxedematosus in clinical and histochemical appearance. The present case may represent very early-stage lichen myxedematosus complicated by borderline diabetes mellitus.

Spindle cell squamous cell carcinoma showing continuous mesenchymal dedifferentiation in a single tumor.

We report the case of an 85-year-old man who presented with an enlarging tumor on the right temple. Histologically, spindle-shaped cells were proliferating continuously within well-differentiated squamous cell carcinoma that was immunohistochemically negative for vimentin and alpha-smooth muscle actin (ASMA) but positive for cytokeratin (AE1/3). These spindle-shaped cells expressed vimentin and ASMA but not cytokeratin (AE1/3). Intermediate cells with round nuclei and small amounts of cytoplasm displayed slight expression of vimentin, ASMA, and cytokeratin. This case illustrated spindle cell squamous cell carcinoma with mesenchymal metaplasia of malignant epithelial cells.

Mucinous nevus.

A 15-year-old boy first noticed multiple firm papules on his right upper chest two years before presenting to our clinic. These papules were densely distributed and showed epidermal nevus-like linear arrangement at some sites. The number, size, and distribution of these papules remained unchanged for one year of our observation. The papules flattened leaving scars and did not recur within a year after one shaving abrasion using a scalpel. Histopathologically, epidermis of the papule displayed acanthosis with elongated rete ridges. Accumulation of mucin was apparent in the papillary and subpapillary dermis. In mucinous nevus, the origin of cells with nevoid proliferation is obscure. In contrast with common collagenous connective tissue nevus, it is hard to define the localized persistent mucin accumulation as a nevoid manifestation. The present case of mucinous nevus might be caused by significantly stimulated glycosaminoglycan synthesis in a kind of epidermal nevus without extreme hyperkeratosis.

Different mechanisms of adhesion molecule expression in human dermal microvascular endothelial cells by xanthoma tissue-mediated and copper-mediated oxidized low density lipoproteins.

BACKGROUND: Oxidation of low density lipoprotein (LDL) has been implicated in infiltration of foam cells derived from circulating monocytes. Monocyte adhesion to endothelial cells and migration into dermis are essential steps for infiltration of foam cells. OBJECTIVE: We investigated the role of adhesion molecules contributing to the process of monocyte adhesion to human dermal microvascular endothelial cells (HDMEC). Special attention was paid to the signal transduction for adhesion molecule expression induced by two distinct types of oxidized LDL. METHODS: HDMEC were incubated with xanthoma tissue-modified LDL (x-LDL), a model of extravasated LDL oxidized in xanthoma lesions, or Cu(2+)-treated LDL (Cu-LDL), a model of oxidized LDL. Adhesion of U937 cells, a human monocytic leukemia cell line, to HDMEC and expression of endothelial cell adhesion molecules on HDMEC were examined. Signal transduction pathways for the adhesion molecule expression were evaluated by employing specific inhibitors. RESULTS: x-LDL induced adhesion of U937 cells to HDMEC through vascular cell adhesion molecule-1 (VCAM-1) and E-selectin by activating tyrosine kinase pathway. Cu-LDL up-regulated the adhesion through not only VCAM-1 and E-selectin but also intercellular cell adhesion molecule-1 (ICAM-1) by activating G(i) protein pathway. CONCLUSION: Extravasated and oxidized LDL in xanthoma lesions contributes to foam cell recruitment by activating tyrosine kinase pathway and inducing adhesion of monocytes to HDMEC through VCAM-1 and E-selectin. Cu-LDL, on the other hand, activates G(i) protein pathway and induces the adhesion through ICAM-1, VCAM-1 and E-selectin.

Nuclear factor kappaB (NF-kappaB) activation by hydrogen peroxide in human epidermal keratinocytes and the restorative effect of interleukin-10.

The heterodimeric form of nuclear factor kappaB (NF-kappaB), NF-kappaB1/RelA, is one of the pluripotential transcription factors that activates various genes encoding cytokines and cell adhesion molecules. To clarify the involvement of radical oxygen species in the NF-kappaB activation pathway in keratinocytes, we examined the effect of hydrogen peroxide (H(2)O(2)) on the activation of NF-kappaB in cultured normal human epidermal keratinocytes. After the treatment of keratinocytes with 300 microM H(2)O(2), a translocation of NF-kappaB from the cytoplasm to nucleus was observed in an immunofluorescence study using anti-human NF-kappaB1 and anti-human RelA antibodies. Specific DNA binding was observed with the nuclear extract prepared from the H(2)O(2)-treated keratinocytes by the electrophoretic mobility shift assay. The presence of N-acetyl-L-cysteine or pyrrolidine dithiocarbamate during H(2)O(2) treatment prevented the nuclear localization of NF-kappaB. The involvement of radical oxygen species in the NF-kappaB activation pathway was suggested. Pretreatment of keratinocytes with 10 ng/ml of recombinant human interleukin-10 (IL-10) for 24 h suppressed the nuclear translocation of NF-kappaB induced by H(2)O(2). IL-10, which increases in ultraviolet-irradiated skin and suppresses delayed type hypersensitivity in vivo, may play an inhibitory role in cutaneous inflammation by inhibiting the NF-kappaB activation pathway in keratinocytes.