Figure 2. A) Many well differentiated plasmocytes and a few mastocytes were infiltrated in the superficial and middle layers of dermis. HE, ×400. B) Positive CD38 staining. ×400. C) Partially positive CD117 staining. ×400. D) Toluidine blue staining showing small purple heterophilic granules distributed in the cytoplasm of a few cells infiltrating of the dermis. ×400.
A case of cutaneous plasmacytosis with mast cell inﬁltration In this patient, slightly itchy brown plaques with positive Darier’s sign were observed, initially suggestive of UP. As signs of mastocytosis are unspecific and may often overlap with other diseases , to confirm the diagnosis, some examinations are required as follows [2, 3]. Regular tests of peripheral blood, CT, and abdomen ultrasound exam showed no obvious abnormalities. Kappa light chain was 3160 mg/dL (normal range 629-1350 mg/dL) and Lambda 1260 mg/dL (313-723 mg/dL). Bone marrow biopsy showed no active myeloproliferation, although with a high rate of mature plasma cells exhibiting no atypia. Histology showed many well differentiated plasmocytes and a few mastocytes infiltrating in the superficial and middle dermis. Immunohistochemistry showed CD117(+), CD38(+), CD138(+), Kappa and Lambda partially (+), Ki67 (5%+). Toluidine blue staining partially (+) (ﬁgure 2).
Residents’corner February 2015. DeRmpath & Clinic – Leukocytoclastic vasculitis Justyn M. THOMAS, Alana DURACK, George MELIGONIS Dermatology Department, Addenbrooke’s Hospital, Hills Road, Cambridge, CB2 0QQ e-mail: [email protected]
Case 1: A 64 year-old female presented with a nonpalpable purpuric livedoid change on the dorsal aspects of both forearms a month after starting quadruple therapy (rifampicin, isoniazid, moxifloxacin and pyridoxine) for Mycobacterium tuberculosis infection. Case 2: A 44 year-old male presented with palpable and non-palpable purpura overlying the upper and lower limbs, in association with abdominal pain, arthralgia and acute kidney injury. Both cases shared histological features typical of leukocytoclastic vasculitis. These included: – Disruption of small vessels with infiltrating neutrophils and karyorrhectic debris (leukocytoclasia) – Fibrin deposition with necrosis – Erythrocyte extravasation – Absence of intraluminal thrombi
1. Ishida M, Iwai M, Kagotani A, Iwamoto N, Okabe H. Cutaneous mastocytosis with abundant eosinophilic inﬁltration: a case report with review of the literature. Int J Clin Exp Pathol 2014; 7: 2695-7. 2. Hartmann K, Henz BM. Mastocytosis: recent advances in deﬁning the disease. Br J Dermatol 2001; 144: 682-95. 3. Magliacane D, Parente R, Triggiani M. Current concepts on diagnosis and treatment of mastocytosis. Transl Med UniSa 2014; 4: 65-74.
Whilst direct immunofluorescence in Case 1 demonstrated granular IgG, IgA and C3 deposition, exclusive IgA deposition was evident in Case 2.
Leukocytoclastic vasculitis is a histological diagnosis (ﬁgures 1, 2). Clinical presentation is classically with
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infection. Investigations should include assessment for an underlying trigger and extra-cutaneous, particularly renal, involvement.
1. Carlson JA. The histological assessment of cutaneous vasculitis. Histopathology 2010; 56: 3-23. doi:10.1684/ejd.2015.2541
Figure 1. Histology from Case 1 demonstrates superficial perivascular neutrophilic inflammation with karyorrhectic debris. Subtle endothelial swelling, interstitial oedema and erythrocyte extravasation are also present (H&E 20×). Direct immunofluorescence revealed granular IgG, IgA and C3 deposition in superficial vessel walls (not shown).
Residents’corner February 2015. Clues in DeRmoscopy: Dermoscopy of amelanotic cutaneous melanoma metastases Franc¸ois KUONEN, Olivier GAIDE Department of Dermatology and Venereology, Hôpital de Beaumont, Lausanne University Hospital Center, CH-1011 Lausanne, Switzerland e-mail: [email protected]
Skin metastases may be the first clinical manifestation of an evolving melanoma. As they mimic primary cutaneous lesions, their diagnosis is challenging and they may easily be misdiagnosed. Dermoscopy, as an extension of the clinical examination, may help in their recognition.
Dermoscopy of amelanotic cutaneous melanoma metastases
Figure 2. Histology from Case 2 demonstrates features similar to those described in ﬁgure 1. An uninvolved arteriole can be seen in the deep dermis (H&E 20×). Direct immunofluorescence confirmed granular IgA deposition in the superficial vessel walls (not shown).
palpable purpura but, as here, non-palpable lesions can also be seen. Optimal timing for biopsy is within the first 48 hours. Beyond this period, lymphocytes and other inflammatory cells begin to replace the initial neutrophilic infiltrate . Leukocytoclastic vasculitis can be triggered by many aetiological factors. In Case 1, both infection and drug therapy were potential triggers. In Case 2, the clinical triad of purpura, abdominal pain and arthralgia, occurring with IgA deposition, points towards a diagnosis of the leukocytoclastic subtype Henoch-Schönlein purpura (HSP) – a condition often occurring after an upper respiratory tract
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The clinical presentation of cutaneous melanoma metastases (CMMs) is highly heterogeneous, depending on the primary tumor type, differentiation grade, dissemination pathway and skin depth. Dermoscopic features of CMMs vary accordingly. One of the most frequent clinical presentations of CMMs is the appearance of erythematous papules arranged linearly (ﬁgure 1A). In these cases, the partial or even total absence of pigmentation gives few dermoscopic findings and dermoscopy will have to rely mostly on the morphology of the vascular pattern. Typically, amelanotic CMMs show milky-red areas, resulting from increased vascularity (ﬁgure 1B). They also show irregular polymorphous vessels, as irregular and thick hairpin vessels (lacking the hypopigmented halo seen in seborrheic keratoses or keratinizing tumors), dotted vessels and corkscrew vessels (ﬁgure 1B). Although highly suggestive of a malignant process, these vascular patterns do not distinguish a primary from a metastatic lesion. Therefore, dermoscopic findings should always be correlated with both the clinical and histopathological presentations. Importantly, vascular