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Öğe Barraquer-Simons syndrome with benign infundibulocystic proliferation(Wiley, 2003) Tüzün, B; Kirçuval, D; Demirkesen, C; Göksügür, N; Ünal, G; Tüzün, YA white man attended our outpatient clinic because of soft papules on the second finger of the left hand. They were livid red-colored, warty surfaced cysts, 1-2 cm in diameter, arranged in an annular configuration (Fig. 1). The patient showed prominent zygomatic bones and symmetric loss of buccal fat pads (Bichat's fats), leading to sunken cheeks (Fig. 2). The history of the patient could not be taken because of his debility. Laboratory findings included: hemoglobin, 14.5 g/dL; Htc, 41.6%; red blood cells (RBC), 4.67/muL; white blood cells (WBC), 10.3 x 10(3) /muL; Plt, 274 x 10(3) /muL; mean corpuscular volume (MCV), 89.1 fL; mean corpuscular hemoglobin (MCH), 31.0 pg; mean corpuscular hemoglobin concentration (MCHC), 34.8 g/dL; blood urea nitrogen, 33 mg/dL; creatinine, 0.7 mg/dL; cholesterol, 152 mg/dL; total protein, 8.1 g/dL; albumin, 4.6 g/dL; total bilirubin, 0.5 mg/dL; direct bilirubin, 0.1 mg/dL; calcium, 8.8 mg/dL; erythrocyte sedimentation rate, 6 mm/h; urinalysis, normal - there was no anomaly in the urine in 24 h. The patient was negative for antinuclear antibody (ANA), anti-DNA, anticentromer antibody, Scl 70 antibody, hepatitis B surface antigen (HBsAg), and human immunodeficiency virus (HIV). Chest X-ray was normal. Hand X-ray showed bone cysts on the distal phalanx of the second finger of the left hand. Histologic examination of the papules on the second finger of the left hand revealed multilobulated or, in other words, proliferating cystic structures lined by epithelium similar to the infundibular epithelium of the hair follicle. The cysts were connected with the surface of the skin and were filled with cornified cells in a basket-weave array (Fig. 3). The IQ was measured as 50 indicating mental retardation. Audiogram could not be performed, but sensory neural hearing loss was suspected. After 1.5 months of pimozide therapy (Norofren, 2.5 mg/day), hearing loss was measured as 50% and a diagnosis of otosclerosis was made. The cystic lesions resolved completely and Bichat's fats regenerated partially.Öğe Familial erythromelanosis follicularis and chromosomal instability(European Acad Dermatology & Venereology, 2001) Tüzün, Y; Wolf, R; Tüzün, B; Özdemir, M; Demirkesen, C; Deviren, A; Kotogyan, AWe report a 17-year-old male patient with erythromelanosis follicularis faciei et colli (EFFC), oral leucokeratosis and diabetes mellitus without islet cell antibody. His sister also had minimal findings of EFFC and minimal follicular papules on her shoulders and extensor surfaces of the arms. The father had only fine follicular papules, but no erythromelanosis. Skin and mucous membrane lesions of the proband were investigated histopathologically. Interestingly, in peripheral lymphocyte cultures of the family members, chromosomal breakage was not observed spontaneously, but it was seen with nitrogen mustard, although this disease may be of autosomal recessive inheritance. Thus, we suggest that EFFC may be a poly-aetiological disorder (i.e. familial and environmental) and might be considered one of the chromosomal instability syndromes.Öğe Wolf's isotopic response(Wiley, 2000) Tüzün, Y; Isçimen, A; Göksügür, N; Demirkesen, C; Tüzün, BA 37-year-old man was first seen in November 1998 with a unilateral painful eruption of grouped small vesicles at the right side of his thorax. His general health was good. He was diagnosed as having herpes tester, which was successfully, treated with oral acyclovir 800 mg, five times a day. Five months later, and after complete resolution of the herpes tester, he developed a pustular eruption on exactly the same area of his first herpetic lesion. There was a diffuse distribution of pustules on the dorsal part of the dermatome, and a grouped pattern on the ventral side (Fig. 1). A punch biopsy was performed for differential diagnosis of recurrent herpes tester and folliculitis. Methicillin-resistant Staphylococcus aureus colonies were isolated from the bacterial culture of the pustular content. Cefadroxil monohydrate 500 mg twice a day and the application of fucidic acid ointment were prescribed. There was no improvement at the end of the second week of therapy. A histopathologic study demonstrated hyperkeratosis, acanthosis, focal accumulation of neutrophils and bacteria in the epidermis, and a perivascular and perifollicular infiltration of eosinophils, lymphocytes, and histiocytes in the dermis (Fig. 2). After the diagnosis of eosinophilic pustular dermatosis was histopathologically confirmed, fungal folliculitis and immunosuppressive conditions were investigated. Routine blood tests were within the normal ranges. The human immunodeficiency virus (HIV), hepatitis C virus (HCV), and anti-hepatitis B surface antibody (anti-HBs) tests were negative, but the hepatitis B surface antigen (HBsAg) test was positive. Abundant fungal hyphae were seen in potassium hydroxide under direct microscopic examination of the pustule content, and a fungal culture was performed. Although no evidence of fungal infection was demonstrated in repeated periodic acid-Schiff (PAS) staining of punch biopsy specimens, Trichophyton rubrum was isolated from fungal culture. The patient was then given a regimen of itraconazole pulse therapy (400 mg/day, for 7 days a month, repeating the monthly cycle three times) and cycloproxolamine cream. Two months later, at the end of therapy, only a few pustules remained, and these completely disappeared after another 5 months.
