Jasleen Kaur

Comparison of the efficacy of psoralen ultraviolet A with narrowband ultraviolet B phototherapy for the treatment of chronic plaque psoriasis in patients with skin types IV and V

1 Cascajo CD, Reichel M, Sanchez JL. Malignant neoplasms associated with seborrhoeic keratoses. An analysis of 54 cases. Am J Dermatopathol 1996; 18: 278–82. 2 Thomas I, Kihiczak NI, Rothenberg J et al. Melanoma within the seborrhoeic keratosis. Dermatol Surg 2004; 30: 559–61. 3 Yakar JB, Sagi A, Mahler D, Zirkin H. Malignant melanoma appearing in seborrhoeic keratosis. J Dermatol Surg Oncol 1984; 10: 382–3. 4 Jones-Cabellero M, Penas PF, Buezo GF et al. Malignant melanoma appearing in a seborrhoeic keratosis. Br J Dermatol 1995; 133: 1016–18. 5 Zabel RJ, Vinson RP, McCollough ML. Malignant melanoma arising in a seborrhoeic keratosis. J Am Acad Dermatol 2000; 42: 831–3.

Adenocarcinoma of the gall bladder presenting with a cutaneous metastasis

1. O’Brien SG, Guilhot F, Larson RA, Gathmann I, Baccarani M, Cervantes F, et al. Imatinib compared with interferon and lowdose cytarabine for newly diagnosed chronic phase chronic myeloid leukemia. N Engl J Med 2003;348:994–1004. 2. Valeyrie L, Bastuji-Garin S, Revuz J, Bachot N, Wechsler J, Berthaud P, et al. Adverse cutaneous reactions to imatinib (STI-571) in Philadelphia chromosome positive leukemias: a prospective study of 54 patients. J Am Acad Dermatol 2003;48:201–6. 3. Arora B, Kumar L, Sharma, Wadhwa J, Kochupillai V. Pigmentary changes in chronic myeloid leukemia patients treated with imatinib mesylate. Ann Oncol 2004;15:358-9. 4. Schaich M, Schakel K, Illmer T, Ehninger G, Bornhauser M. Severe epidermal necrolysis after treatment with imatinib and consecutive allogeneic hematopoietic stem cell transplant. Ann Hematol 2003;82:303-4. 5. Schwarz M, Kreuzer KA, Baskaynak G, Dorken B, le Coutre P. Imatinib induces acute generalized exanthematous pustulosis in two patients with chronic myeloid leukemia. Eur J Hematol 2002;69:254–6. 6. Tsao AS, Kantarjian H, Cortes J, O ’ Brien S, Talpaz M. Imatinib mesylate causes hypopigmentation in the skin. Cancer 2003;98:2483–7.

Symmetrical scrofuloderma with tuberculosis verrucosa cutis

range 4.0–9.0) and elevated serum C-reactive protein level, 69.0 mg ⁄ L (normal range 0–10), which were speculated to reflect bacterial infection of the subcutaneous shunt for haemodialysis on her left arm, and intravenous antibiotics were effective. She also had hypocalcaemia, hyperphosphataemia, and an elevated parathyroid hormone level of 17.2 pmol ⁄ L (normal range 1.05–6.84). Calcium-phosphate product was slightly elevated to 4.46mmol ⁄ L (< 4.44 mmol ⁄ L). She was not obese, did not have diabetes, and was not on any anticoagulant therapy. Histopathologically, the specimen from abdominal nodule showed calcium deposits within the medium-sized vessels in the subcutaneous fat and inside walls of the fat cells (Fig. 1b). A diagnosis of calcific uraemic arteriolopathy (CUA) was made. Surgical debridement was perfomed after the patient’s general state had been improved. A wide and deep excision was made, down to the fascia level. The wounds were successfully closed without using a graft. After surgery, the patient had no pain, and made a good recovery without new lesions (Fig. 2). CUA was first described as calciphylaxis by Hans Selye in 1962; the term calcific uraemic arteriolopathy is now preferred. CUA is mainly seen in patients with endstage renal disease, and manifests as a rapidly developing purpuric patch or plaque. Although a high mortality rate of 30–80% has been reported, a recent report showed that CUA has several clinical presentations, including a more indolent variant. Patients with proximal lesions tend to have a poorer prognosis because of secondary infection. Kang et al. reported a better prognosis in patients who underwent skin debridement than patients who did not. Calcium-phosphate product deposits into adipose cells may contribute to the pain experienced. The areas of vascular calcification often extend past the clinical boundary of the CUA plaques, so a wide excision containing peripheral grossly normal skin is needed. Other treatment options have been reported, including diet, binding agents, and vitamin D analogues. Parathyroidectomy is recommended only if severe hyperparathyroidism persists despite these therapies. Some reports suggest the efficacy of hyperbaric oxygen and corticotherapy for local wound care. We propose that wide local excision should be taken into consideration as the first-line treatment of CUA. It will decrease the intractable pain of CUA and the possibility of secondary infection, contributing to better prognosis.

Nicotinamide: Mechanism of action and indications in dermatology

Introduction Nicotinamide aka Vitamin B3 (niacinamide, nicotinic acid amide) is the pyridine 3 carboxylic acid amide form of niacin [Figure 1]. It is a water‐soluble vitamin that is not stored in the body. The main source of vitamin in diet is in the form of nicotinamide, nicotinic acid, and tryptophan.1 The main source of niacin include meat, liver, green leafy vegetables, wheat, oat, palm kernel oil, legumes, yeast, mushrooms, nuts, milk, fish, tea, and coffee.2,3 The recommended daily dose of vitamin B3 in niacin equivalent is given in Table 1.4

Response by authors

We would like to thank the editors and the commentators for their comments and the opportunity to respond. We greatly appreciate the time and effort that such experienced and expert practitioners have taken to read our paper. We think the Istanbul Protocol is a crucially important document in the struggle against torture, and it is therefore very important to think about the ways in which it is used in practice as part of a wider campaign to prevent torture and provide survivors with redress. More broadly, our general aim is to participate in a wider debate about the ways in which human rights organizations can produce effective evidence in the struggle to end impunity and provide justice. We welcome this opportunity to clear up some misunderstandings that may have arisen. We do not say in the article that the IP requires comprehensive documentation. Indeed we say early on in the paper that it is designed as a flexible protocol. It is all the more important therefore to think about how the IP can be best used in practice, given the range of potential options it presents. The article therefore sets out to see if, how and when human rights practitioners use the IP in the context of wider human rights processes. Our conclusion is not that the IP is inapplicable to Low-Income Countries, but the much more limited claim that more comprehensive forms of forensic documentation , as set out in the IP, will be limited to a small, albeit, important number of cases. The commentators are concerned that we have included the opinions of non-clini-cians in our study. We did this deliberately. Our aim was to examine how documentation is used as part of human rights work. Journalists and lawyers are certainly not qualified to carry out forensic documentation. However, they are often the ones who use such documentation as part of wider attempts to seek justice. To end the discussion of the IP at what clinicians think would be to ignore the ways in which the IP should be seen as a tool in these broader struggles. The three countries in which we carried out the study can all be classified as Low-Income. We do not make any causal inferences about the ways in which Low-Income status impacts on human rights work. We of course recognize that impunity is a problem all over the world. At the same …