Tuğba Oskay

Association of anticonvulsant hypersensitivity syndrome with Herpesvirus 6, 7.

BACKGROUND Anticonvulsant hypersensitivity syndrome (AHS) is one of the most severe forms of drug eruption with potentially lethal, and multiorgan involvement. Recently, it has been suggested that Human Herpesvirus (HHV) infection has been involved in this syndrome, although the pathogenesis of this syndrome remains still unclear. METHODS The objective of this study was to determine the clinical characteristics of AHS and the possible role of viral infection as a co-factor. We prospectively analyzed clinical, laboratory and virological findings for 23 cases of AHS. A viral study including viral serology and a polymerase chain reaction (PCR) was performed. RESULTS The most common anticonvulsant was carbamazepine (12) followed by phenytoin (6), phenobarbital (4) and gabapentin (1). All patients met fulfill the clinical criteria of AHS. Even though internal organ involvement such as liver (52%), kidney (34%), and lung (13%) has been observed, involvement of heart, lung, thyroid, muscle, pancreas, spleen, and brain was less frequent. We also noted two patients who died due to multiorgan failure. No association with viral infection including HSV, VZV, HHV-8, CMV, EBV, measles, rubella and parvovirus B19 was detected in the current series. Increased serum anti-HHV-6 IgG and HHV-7 titers and presence of HHV-6 and -7 DNA in serum, revealed by PCR analysis, suggested reactivation of HHV-6. In contrast to the control groups, DNA for HHV-6 was detected in serum in 5 out of the 23 patients while HHV-7 was seen in two patients. We found an evidence to link reactivation of HHV-6 or HHV-7 in the development of only carbamazepine-induced AHS. CONCLUSIONS We propose that some cases of AHS are accompanied by reactivation of not only HHV-6 but also HHV-7. HHV infection may contribute to the severity, prolongation, or relapse of AHS and may possibly have fatal consequences in some susceptible individuals receiving the anticonvulsants.

Association of psoriasis vulgaris with HLA class I and class II antigens in the Turkish population, according to the age at onset

Background Association of psoriasis vulgaris with HLA antigens reference to age at onset has been reported in different racial or ethnic populations.

Pimecrolimus 1% cream in the treatment of vulvar lichen sclerosus in postmenopausal women

Background  Vulvar lichen sclerosus (LS), a poorly recognized chronic inflammatory skin disease, may represent a therapeutic challenge. Pimecrolimus cream 1% is a nonsteroidal, selective inflammatory cytokine inhibitor that has recently been indicated for some inflammatory cutaneous diseases.

Indolent Acremonium strictum infection in an immunocompetent patient

A 35‐year‐old housewife presented with an 11‐year history of a painless lesion on the right cheek, which had enlarged over the last 2 years. She had no history of travel or trauma. Various topical and systemic antimicrobial and antifungal agents, such as fluconazole, ketoconazole, sulbactam/ampicillin, and mupirocin, had been prescribed, with a probable diagnosis of pyoderma and blastomycosis, without significant benefit. Her medical history was otherwise unremarkable. Dermatologic examination revealed a well‐circumscribed, erythematous, infiltrative, 8 × 10 cm plaque covering the right cheek and a 2 × 3.5 cm vegetative, ulcerated lesion on the chin ( Fig. 1 ). There were no sinus tracts or grains.

Juvenile colloid milium associated with conjunctival and gingival involvement

Juvenile colloid milium is an uncommon cutaneous disease characterized by translucent papules distributed on sun-exposed areas with early onset. Association of juvenile colloid milium with conjunctival and gingival deposits is uncommon and interesting. We report a case of juvenile colloid milium associated with conjunctival and gingivai deposits of an amyloid-like homogeneous eosinophilic material. It seems that all 3 of these in our patient may be different expressions of the same pathologic disease.

Evaluation of nail involvement in patients with chronic cutaneous graft versus host disease: a single-center study from Turkey.

Although graft versus host disease (GVHD) is associated with a myriad of cutaneous signs, nail involvement is rarely mentioned in the literature. This study was conducted at the Department of Dermatology and The Bone Marrow Transplantation Unit of Hematology. All patients were examined clinically for presence of nail abnormalities. Severity of nail involvement was assessed as mild or severe. Of 28 patients diagnosed with chronic cutaneous GVHD, 14 had nail manifestations. Longitudinal ridging was the most frequently observed nail change on both the fingernails and the toenails. Severe nail changes such as ptergyium and onicoatrophy were noted in a few patients. As a result we could not find any relationship between nail changes and clinical severity but there was a relationship between nail changes and duration of disease. Nail manifestations could be responsible for considerable morbidity.

Sweet's syndrome in familial Mediterranean fever: possible continuum of the neutrophilic reaction as a new cutaneous feature of FMF.

Sweet’s syndrome (SS) or acute febrile neutrophilic dermatosis is an uncommon disorder that often occurs in association with other systemic diseases. In its systemic manifestation, SS resembles familial Mediterranean fever (FMF) in many aspects. Although the exact pathogenesis of SS and FMF is not yet clear, their clinical similarities and simultaneous occurrence suggest a possible common underlying mechanism and may represent a continuum of a reactive neutrophilic condition.

Stevens–Johnson Syndrome associated with Ramipril

Stevens–Johnson Syndrome associated with Ramipril Dear Sir, An 80-year-old man was admitted to our hospital with a 10-day history of malaise and pruritic skin lesions. He complained of general fatigue, appetite loss, and oral lesions interfering with his oral nutrition. He had no known allergies to medication. He had a long history of diabetes mellitus, for which he was receiving therapy with gliclazide 150 mg once a day. He had also been suffering from hypertension for years, and one month before the eruption his antihypertensive drug regime was ceased and substituted with ramipril 5 mg daily. Dermatological examination revealed a macular and purpuric rash with erythematous, target-like lesions and multiple vesicles and bullae on the trunk, legs and arms (Fig. 1). There were also hemorrhagic bullous lesions symmetrically on his hands and soles, and blisters and erosions on his external genitalia. Oropharynx examination showed ulcers and vesicles on the hard and soft palate and epiglottis. His temperature was 38.3 ° C. The physical examination revealed no abnormality. On serial sections of the skin biopsy material, hyperkeratosis and slight acanthosis was observed. The epidermis showed subepidermal detachment from the underlying dermis to form a bullous cavity. The cavity contained fibrinoid material, erythrocytes, neutrophils, and a few eosinophils (Fig. 2). A mixed inflammatory infiltrate was also present in the dermis. Direct immunofluorescence testing was performed using IgA, IgG, IgM and C3, all of which were negative. Laboratory examinations, including complete blood count, liver and kidney function tests, electrolytes, erythrocyte sedimentation rate, urine analysis, and chest radiography, were all within normal limits. Serology for herpesvirus I and II and mycoplasma pneumonia was negative. On the basis of these findings, the diagnosis of ramiprilinduced Stevens–Johnson Syndrome (SJS) was established and ramipril was discontinued and replaced by another class of antihypertensive drug. His condition progressively resolved within 10 days after discontinuation of ramipril therapy. Appearance of the disease one month after the commencement of ramipril therapy and the lack of other etiologic factors associated with SJS indicated ramipril as the most suspicious cause of the disease. The oral rechallenge test was not clinically appropriate because of the severity of his eruptions. However, the patient developed similar eruptions following an accidental rechallenge by himself 2 weeks following cessation of ramipril, which confirmed the diagnosis of ramipril-induced SJS.