Candida folliculitis mimicking tinea barbae

A 55-year-old man, a farmer, was referred to our dermatology department in June 1993 with inflammatory and infiltrated nodular lesions on his left cheek and neck. These nodular lesions had appeared about a month previously and had enlarged quickly. He was unaware of any antecedent trauma. Physical examination revealed a painless, slightly erythematous, soft, fluctuant plaque which measured 8 cm in diameter. It consisted of follicular papules and pustules and was partially covered with brown-black crusts (Fig. 1), Two similar plaques, 3 cm in diameter, were also detected on the neck. The regional lymph nodes were not palpable. The hair on the lesions was easily removed with a pair of forceps without causing pain. The patient had not previously had any skin disease. Laboratory investigations, including full blood count, erythrocyte sedimentation rate, serum concentrations of sodium, potassium, chloride, transaminases, alkaline phosphatase, sugar, cortisol, and renal function tests, were all normal. No fluorescence was seen on Wood's light examination. Direct microscopic examination with 15% potassium hydroxide solution revealed yeast cells and hyphae in three consecutive scrapings of the lesions. Candida albicans was isolated from the mycologic cultures; but no growth was observed in mycologic cultures of oral and anogenital mucosae swabs. Bacteriologic cultures of the lesions were also negative. A skin biopsy was performed for histologic confirmation. Examination of the biopsy specimen revealed dermal oedema and PAS(-I-) yeast cells among the infiltration of lymphocytes and plasma cells (Fig. 2). The patient was started on a regimen with fluconazole 100 mg once a day orally for a week, after which the dosage was decreased to 100 mg once every other day for a month. Also, the hair on the lesions was depilated. We noted a significant clinical improvement at the fifth week of the therapy (Fig. 3). Repeated mycologic examinations of the lesions were all negative even 1 month after the end of the therapy     

Apoptotic Vascular Smooth Muscle Cell Depletion via BCL2 Family of Proteins in Human Ascending Aortic Aneurysm and Dissection

Aims : This study investigates the expression patterns of BCL2 (B‐cell CLL/lymphoma2) family of proteins and the extent of vascular smooth muscle cell (VSMC) apoptosis in thoracic aortic aneurysms (TAA), type‐A aortic dissections (TAD), and nondilated ascending aortic samples. Methods : Aortic wall specimens were obtained from patients undergoing surgical repair for TAA (n = 24), TAD (n = 20), and normal aortic tissues from organ donors (n = 6). The expression pattern of BCL2, BCL2L1 (BCL2‐like1), BAK1 (BCL2‐antagonist/killer1), and BAX (BCL2‐associated X protein) proteins was investigated by immunohistochemistry. Furthermore, colocalization of alpha smooth muscle actin (ACTA2) and caspase3 (CASP3) in aortic VSMCs was analyzed by double‐immunofluorescence staining. Onset of DNA fragmentation was measured by TUNEL assay. Results : Apoptotic index was significantly increased in both TAD group (31.3 ± 17.2, P < 0.001) and TAA group (21.1 ± 12.7, P = 0.001) relative to control aortas (2.0 ± 1.2). Anti‐CASP3 and ACTA2 double‐immunostaining confirmed apoptosis in VSMCs in TAA and TAD groups but not in controls. Proapoptotic BAX expression was significantly elevated in VSMCs of TAA patients, compared with that of controls (OR = 20; P = 0.02; 95% CI, 16–250). In contrast, antiapoptotic BCL2L1 expression was higher in controls compared with that of TAA group (OR = 11.2; P = 0.049; 95% CI, 1.0–123.9). Furthermore, BAX/BCL2 ratio was significantly increased in both TAA (1.2 ± 0.7, P < 0.001) and TAD (0.6 ± 0.4, P = 0.05) groups relative to controls (0.2 ± 0.1, P < 0.001). Conclusions : Apoptotic VSMC depletion in human TAA/TAD is associated with disturbance of the balance between proapoptotic and antiapoptotic members of the BCL2 family proteins, which may have a role in the pathogenesis of vascular remodelling in aortic disease. In light of the future studies, targeting apoptotic pathways in TAA and TAD pathogenesis may provide therapeutic benefits to patients by slowing down the progression and even possibly preventing the TAD.     

Vasodilatory effect of hydroxyethyl methacrylate and triethylene glycol dimethacrylate in rat aorta through calcium antagonistic action

Introduction

Resin-based dental materials contain various diluent monomers that can interfere with vascular function by causing vasodilation. In this study, we evaluated the vasoactive potential of hydroxyethyl methacrylate (HEMA) and triethylene glycol dimethacrylate (TEGDMA) and the possible mechanism of their vascular action on isolated rat aorta.

Methods

Responses of thoracic aorta rings were recorded isometrically by using force displacement transducers. After precontracting aorta rings with phenylephrine, relaxations to HEMA and TEGDMA were recorded in the absence and presence of nitric oxide synthase inhibitor N^ω-nitro-L-arginine methyl ester, cyclooxygenase inhibitor indomethacin, and K⁺ channel inhibitors tetraethylammonium, glibenclamide, and 4-aminopyridine. To investigate the Ca²⁺-channel antagonistic effect of HEMA and TEGDMA in different aorta rings, concentration-response curves to CaCl₂ were obtained in the absence and presence of the test monomers.

Results

Both HEMA and TEGDMA elicited concentration-dependent relaxations. The vasorelaxant effect of HEMA and TEGDMA was not mediated via endothelium-dependent nitric oxide and prostanoid-dependent mechanisms or by K⁺ efflux through K⁺ channels. Both monomers significantly inhibited the contractions induced by CaCl₂.

Conclusions

Our results showed that HEMA and TEGDMA induce vasodilation via Ca²⁺-antagonistic action, whereas nitric oxide and cyclooxgenase pathway and K⁺ channels were not responsible for this vasoactive effect.     

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis: report of three Turkish siblings

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), an autosomal recessive renal tubular disorder is characterized by the impaired tubular reabsorption of magnesium and calcium in the thick ascending limb of the loop of Henle. This disease is caused by mutations in the claudin-16 gene (CLDN16), which encodes the tight junction protein, claudin-16. Claudin-16 belongs to the claudin family and regulates the paracellular transport of magnesium and calcium. Here, we report on three Turkish siblings with typical clinical features of FHHNC in association with the homozygous mutation Leu151Phe.     

Giant left atrium with rheumatic mitral stenosis

A chest radiograph of a 38-year-old woman, who was diagnosed with rheumatic mitral stenosis, revealed cardiac enlargement due to a giant left atrium that was distorting the cardiac structures. The patient's cardiothoracic ratio was approximately 0.90. A giant left atrium can readily be delineated by echocardiography. Optimal timing of surgery is important in cases of mitral stenosis, because delaying mitral valve replacement can lead to fatal outcomes. To our knowledge, the left atrial diameter of 18.7 cm that we found in our patient is the largest reported to date.     

Promising utilization areas of therapeutic plasmapheresis in cardiovascular surgery practice

Objective

Apheresis is performed for treatment of numerous diseases by removing auto-antibodies, antigen-antibody complexes, allo-antibodies, paraproteins, non-Ig proteins, toxins, exogenous poisons. In current study, we present our experience of using therapeutic plasma exchange (TPE) in patients with different types of clinical scenarios.

Assessing the Effectiveness of the COPD Assessment Test (CAT) to Evaluate COPD Severity and Exacerbation Rates

Aims: The CAT is a short, simple eight-item questionnaire for assessing and monitoring COPD. It is not known how reliable the CAT scores are for COPD patients who are frequently exacerbated. The effectiveness of the CAT for assessing COPD severity and exacerbation rates was evaluated. Methods: This study enrolled 165 stable COPD patients who completed the CAT between April 2011 and February 2012. Results: Patients had a mean forced expiratory volume in one second (FEV₁) equal to 43.7% of the predicted value and a mean CAT score of 21.2 (± 7.56) units. There was a good association between the FEV₁ (percentage of predicted value) and CAT scores (p < 0.0001). Frequent exacerbators had significantly higher CAT scores than infrequent exacerbators (24.8 ± 6.7 versus 17.5 ± 6.5, p < 0.0001). Also, as the frequency of the COPD exacerbations increased, CAT scores (p < 0.0001) significantly increased. There was a significant association between the frequency of hospitalization and the CAT scores (p = 0.001). Conclusions: We observed a good relation between the CAT, FEV 1, and disease severity in patients with COPD. We found that the baseline CAT scores are elevated in frequent exacerbators.