A. S. W. Yong

Follicular porokeratosis of Mibelli on the buttocks

We report a case of follicular porokeratosis of Mibelli affecting the natal cleft in a 42‐year‐old white man. To our knowledge, this is the first report in the English‐language literature of follicular porokeratosis of Mibelli limited to the genitogluteal area.

British Association of Dermatologists’ guidelines for the investigation and management of generalized pruritus in adults without an underlying dermatosis, 2018

G.W.M. Millington iD , A. Collins, C.R. Lovell, T.A. Leslie, A.S.W. Yong, J.D. Morgan, T. Ajithkumar, M.J. Andrews, S.M. Rushbook, R.R. Coelho, S.J. Catten, K.Y.C. Lee, A.M. Skellett, A.G. Affleck, L.S. Exton, M.F. Mohd Mustapa and N.J. Levell Dermatology Department, Haematology Department, Nephrology Department and Hepatology Unit, Norfolk and Norwich University Hospital, Colney Lane, Norwich NR4 7UY, U.K. Dermatology Department, Royal United Hospital, Combe Park, Bath BA1 3NG, U.K. Dermatology Department, Royal Free Hospital, Pond Street, London NW3 2QG, U.K. General Practitioner, Chet Valley Medical Practice, 40–48 George Lane, London NR14 6QH, U.K. Oncology Department, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, U.K. Dermatology Department, St George’s Hospital, Blackshaw Road, London SW17 0QT, U.K. Dermatology Department, Ninewells Hospital, Dundee DD1 9SY, U.K. British Association of Dermatologists, Willan House, 4 Fitzroy Square, London W1T 5HQ, U.K.

Uremic pruritus is improved by gabapentin.

encompass obsessive thoughts. Stressful events prior to the onset of the condition may act as triggering or aggravating factors. Young women comprise the majority of patients. The present case demonstrates the importance of acquiring a complete history and a review of systems analysis, including psychological aspects of the patient’s condition. It also demonstrates how interdisciplinary collaboration among dermatologists, psychologists, and psychiatrists is important in managing these cases in order to achieve optimal results.

Nodular localized cutaneous amyloidosis in an immunosuppressed patient

A 77-year-old man presented with a 3-month history of an asymptomatic, firm nodule on his right oral commissure in 2011. He had undergone a renal transplant in 2006 for end-stage renal failure caused by immunoglobulin A (IgA) nephropathy. Since the transplant, the patient had been maintained on cyclosporine, azathioprine, and prednisolone. He had experienced significant sun exposure; he had lived in Africa for three years and was a keen golfer. Examination revealed a 1.5 9 1.0-cm, firm, pink, pearly nodule on his right oral commissure (Fig. 1). The patients tongue was of normal size, and he showed no other lesions elsewhere. Biopsy of the nodule revealed an amorphous eosinophilic deposit extending to the deep dermis and surrounded by a plasma cell infiltrate (Fig. 2). Congo red staining viewed under polarized light revealed a green birefringence of the eosinophilic material (Fig. 3). Cytokeratin stain of the eosinophilic deposit was negative. Kappa and lambda light chain analysis using immunohistochemistry confirmed a polyclonal population. Full blood count, urea and electrolytes, liver function tests, serum and urinary protein electrophoresis, serum b2-microglobulin, 24-hour urinary protein, and chest radiograph were all normal. An autoimmune screen including antinuclear antibody, extractable nuclear antigens (including anti-Ro and anti-La antibodies), and rheumatoid factor was unremarkable. An abdominal fat pad biopsy viewed after Congo red staining under polarized light was negative. (This technique has been shown to have sensitivity of 57% and specificity of 100% in a case series of over 70 patients.) Nodular localized cutaneous amyloidosis was diagnosed. Figure 1 Clinical examination shows a pearly nodule on the right oral commissure in a 77-year-old renal transplant recipient

Acute febrile neutrophilic dermatosis(Sweet's syndrome) in a patient with biliary sepsis.

Robert Sweet first described acute febrile neutrophilic dermatosis (Sweets syndrome (SS)) in 1964 affecting eight women. They had four cardinal features: fever, neutrophilia, tender plaques and dermal infiltrate of neutrophils histologically.1 SS is rare and occurs worldwide with no racial predilection.2 Associations include infections, drugs, malignancy, inflammatory bowel disease and pregnancy.2 We present a case of SS in a patient with biliary sepsis. A 54-year-old Caucasian man developed pyrexia, leukocytosis with neutrophilia and raised C-reactive protein one day after transhepatic biliary stent insertion. Intravenous piperacillin/tazobactam (Tazocin, Pfizer, USA) was started for presumed biliary sepsis. He remained pyrexial 2 days later. The antibiotic was changed to meropenem. He remained unwell with swinging pyrexia while his leucocytosis, neutrophilia and C-reactive protein worsened over the following 5 days. Two days after he became unwell, …

Superior vena cava obstruction presenting as acute allergy.

We report a case of apparent acute allergy, the underlying cause of which was found to be superior vena cava obstruction (SVCO). A 57-year-old woman presented to an allergy clinic with a 4-month history of persistent facial swelling, which she reported had started after a ‘flu-like’ illness and nasal congestion. No improvement had occurred despite six courses of oral antibiotics. Blood tests had shown eosinophilia, leading her general practitioner to start the patient on fexofenadine and prednisolone for presumed ‘allergy’. Owing to her persistent facial swelling, the patient attributed her ‘reactions’ to a number of food types. Despite her avoidance of dairy products, fish and eggs, there was no improvement in her symptoms. She was a life-long smoker, and her medical history included chronic obstructive pulmonary disease and osteoporosis. Her regular medications included codydramol, lansoprazole and alendronate. The patient was referred to a dermatologist, but 1 month before this appointment was due, she presented to the accident and emergency department with acute breathlessness and swelling of her face and arms. She was given intravenous hydrocortisone and chlorphenamine. The trigger for this episode was unclear, but blood tests (full blood count, renal and liver function) and chest radiograph were reported as normal. She had a plethoric complexion with facial swelling and marked bilateral infraorbital oedema (Fig. 1a). There were prominent veins on her chest wall and flanks, with a raised jugular venous pressure (Fig. 2b–d). Her right arm was more swollen than the left, with finger clubbing and nicotine staining of all fingernails (Fig. 2a). The differential diagnosis included dermatomyositis and SVCO.

Resin lacquer: a cheaper alternative to amorolfine for onychomycosis?

inumab and other psoriasis treatments from the Psoriasis Longitudinal Assessment and Registry (PSOLAR). J Drugs Dermatol 2015; 14:706–14. 7 Leonardi CL, Kimball AB, Papp KA et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 1). Lancet 2008; 371:1665–74. 8 Papp KA, Langley RG, Lebwohl M et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2). Lancet 2008; 371:1675–84. 9 Langley RG, Papp K, Gottlieb AB et al. Safety results from a pooled analysis of randomized, controlled phase II and III clinical trials and interim data from an open-label extension trial of the interleukin-12/23 monoclonal antibody, briakinumab, in moderate to severe psoriasis. J Eur Acad Dermatol Venereol 2013; 27:1252–61. 10 Kavanaugh A, Ritchlin C, Rahman P et al. Ustekinumab, an anti-IL12/23 p40 monoclonal antibody, inhibits radiographic progression in patients with active psoriatic arthritis: results of an integrated analysis of radiographic data from the phase 3, multicentre, randomised, double-blind, placebo-controlled PSUMMIT-1 and PSUMMIT-2 trials. Ann Rheum Dis 2014; 73:1000–6.

Cutaneous leishmaniasis in a returning UK traveller

The Leishmaniases are diseases caused by protozoan parasites from more than 20 Leishmania (L.) species (order Kinetoplastida ) that are transmitted to humans by the bites of infected female Phlebotomine and Lutzomyia sandflies. There are three main forms of the disease: cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis and visceral leishmaniasis or kala-azar.1 It is estimated that 0.7–1.2 million of new CL cases and 0.2–0.4 million of new visceral leishmaniasis cases occur each year worldwide.1 CL is classified into Old and New World Cutaneous Leishmaniasis (NWCL) depending on the geographical region where the infection was acquired. NWCL is commonly caused by the L. mexicana complex and L . Viannia subgenus. The majority of CL cases occur in Afghanistan, Algeria, Brazil, Colombia, the Islamic Republic of Iran, Pakistan, Peru, Saudi …

Cold-induced rashes.

A 56-year-old woman presented with a 4-month history of arthralgia, purpura and leg ulceration. She experienced transient painful and pruritic weals on her neck, thighs and upper arms, precipitated by cold exposure, on rewarming. There were palpable purpura and healed ulcerations on her lower legs, with livedo reticularis and perniotic discolouration over her thighs (Fig. 1). An ice-cube test was positive after 5 min, producing a transient weal. IgG(k) monoclonal paraprotein was detected (11.1 g/L; normal range 5.9–15.6 g/L) consisting mainly of cryoglobulin. C3 and C4 complement were reduced due to consumption by immune complexes. Bone marrow and skeletal survey did not show myeloma.

An unusual cause of ulcer.

An 82-year-old Caucasian man was referred to respiratory medicine with a three-month history of dry cough, lethargy, and weight loss. He was previously well with no significant medical history. His general practitioner had treated him with two courses of oral amoxicillin and one course of oral clarithromycin, both producing dramatic but transient improvement in his symptoms. He was a retired electrician but denies any exposure to asbestos and never smoked. He denied recent or past exposure to tuberculosis. A chest radiograph performed after his first respiratory team consultation showed right basal shadowing. A computed tomography scan of his chest subsequently showed right-sided bulky hilar nodes and ipsilateral calcified pleural plaques suggestive of mesothelioma (Fig. 1). With a working diagnosis of mesothelioma, he underwent a computed tomography-guided pleural biopsy. The pleural tissue histology consisted of a chronic inflammatory, fibrotic process with no evidence of malignancy. Bacterial and fungal cultures from pleural sampling were all negative. Three weeks after the pleural biopsy, he developed an 8 · 2 cm non-tender cutaneous ulcer around the biopsy entry site (Fig. 2). Fine needle aspirate of the ulcer showed a mixed inflammatory cell infiltrate. Ultrasound of surrounding tissues showed a strand of hypoechoic chord from an ulcer on the right, in continuation with the 12th rib, which has a connection to fibrotic pleura. A dermatological opinion was sought at this time. Four punch biopsies were taken from each quadrant of the ulcer, and the debrided curettings of the ulcer’s central portion were all sent for histological analysis. Multiple swabs from the surface of the ulcer were sent. All the wound swabs were negative for organisms. The punch biopsies all showed inflamed granulation tissue. Curettings from the central portion of the ulcer revealed necrotic, inflamed granulation tissue with collagen deposition, which was positive for both periodic acid-Schiff and Grocott stains, suggestive of actinomycosis (Fig. 3).