Use of antimicrobials for acne treatment is correlated with an increased occurrence of antimicrobial‐resistant Cutibacterium acnes. To clarify the role of antimicrobial use on the resistance and to investigate the characteristics of resistant strains, we conducted a multicenter study in dermatological clinics frequently visited by new patients with acne vulgaris. We collected specimens in 264 acne patients and tested 164 C. acnes strains isolated from 164 patients visiting 13 dermatological clinics. Antimicrobial susceptibility testing showed that the rates of resistance for tetracyclines, macrolides and clindamycin were significantly higher in C. acnes strains isolated from patients using antimicrobials for acne treatment than patients not using them. In particular, clindamycin‐resistant strains were frequently isolated from patients with older median age (≥24 years) and severe/moderate acne. After investigating the resistance mechanism of 15 high‐level clindamycin‐resistant strains, the transposable clindamycin resistance genes, erm(X) or erm(50), were detected in 14 strains. Using single‐locus sequence typing for C. acnes, the strains with erm(X) or multidrug resistance plasmid pTZC1 coding erm(50) and tetracycline resistance gene tet(W) were classified into clade F, which were specifically isolated from Japanese patients with acne, except for one strain. Our data showed that patients’ information, such as antimicrobial use, age and acne severity, are valuable in estimating whether a patient carries antimicrobial‐resistant C. acnes. Additionally, our results suggest that the clade F strains have a high risk of acquiring multidrug resistance.
Background: Although it is known that renal amyloidosis may complicate several dermatoses, recessive dystrophic epidermolysis bullosa (RDEB) complicated by nephropathy has been thought to be rare. We, however, had seen a young adult with RDEB who died of renal failure due to systemic amyloidosis. Objective: A retrospective study was performed in order to investigate the incidence and etiology of renal amyloidosis in RDEB. Methods: Routine urinalysis, serum amyloid A protein (SAA) and creatinine levels were repeatedly determined in 11 patients with RDEB (mean age 17.7 years, range 5–28, 7 males, 4 females). Nephropathy was defined as the presence of both proteinuria and hematuria with red blood cell casts. Results: Seven out of 9 generalized RDEB patients had nephropathy including 3 cases with end-stage renal disease (2 died within 2 years from the onset of nephropathy), while 2 patients with localized RDEB did not. Levels of SAA were significantly higher in patients with nephropathy than those in patients without nephropathy (p < 0.05). Conclusion: Nephropathy is a common and serious complication of RDEB. Renal amyloidosis may play an important role in its etiology. We recommend that patients with RDEB should be periodically screened for nephropathy due to amyloidosis by urinalysis and measuring SAA levels.
A 35-year-old male with lepromatous leprosy showed significant pro gression of the disease on initial examination. Along with typical lepromatous skin lesions, many scar-forming lesions were present, mainly on his extremities. Some lesions showed erosive surfaces. From clinicopathological findings, these lesions were suspected to be due to the partial excretion of intradermal lepromatous granulomata by 'transepidermal elimination'. Increased local volume, which might be due mainly to rapidly growing lepromatous infiltration before chemotherapy, is suspected of triggering this phenomenon. There is no doubt that many fresh Mycobacterium leprae were included in these excretions. After the initiation of chemotherapy, no new scar-forming lesions were observed.
Cathepsin L, a cysteine proteinase, and cystatin A, an inhibitor of cysteine proteinases, are thought to regulate the invasion and metastasis of malignant cells. In this study, the expression of cathepsin L and cystatin A in skin tumors was investigated immunohistochemically in order to examine the relationship between these two enzymes in the pathophysiology of malignant cells. Formalin-fixed and paraffin embedded specimens from normal skin, seborrheic keratoses, and squamous cell carcinomas were reacted with polyclonal antibodies against rat cathepsin L or cystatin a which cross-react to human cathepsin L and cystatin A, respectively. The consequent immunostaining of these enzymes was observed to be strong in normal skin (4 cases) and seborrheic keratosis (6 cases). In well-differentiated squamous cell carcinoma (SCC) (9 cases), staining for cathepsin L and cystatin A was moderately positive in differentiated tumor cells and negative in undifferentiated SCC (5 cases). The degree of staining of these enzymes was inversely correlated with the differentiation of the malignant cells. These results suggest that the immunohistochemical analysis of cathepsin L and cystatin A is a useful indicator for an aspect of malignancy in human epidermal keratinocytes.
A 35-year-old Japanese man consulted our clinic with an eight year history of a 6 cm diameter subcutaneous tumor on the left cheek. Hematoxylin and eosin staining of the resected section showed histology corresponding to a benign chondroid syringoma. Keratin was positive in most of the constituent cells, and S-100 protein was positive in the cells distant from the lumens and in myxomatous cells. A benign chondroid syringoma of this size has only been very rarely reported in the literature.
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