Journal of Pathology and Translational Medicine

Case Report

Childhood Asymmetry Labium Majus Enlargement.: Mi Jin Gu, Sang Yoon Kim; Korean J Pathol. 2011;45(5):529-531.; DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.5.529

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Childhood asymmetry labium majus enlargement (CALME) is a disctinctive clinicopathologic entity of pre- and early puberty first described in 2005. It is defined as an expansion of normal soft tissues of the vulva. Although CALME is not a rare lesion, it has been called lipoma, fibroma, hamartoma, and fibrous hyperplasia. CALME is not a true neoplasm and is a physiologic growth in response to hormone. It may tend to resolve spontaneously and recur after surgical resection. We report four cases of CALME with a review of the literature. To the best of the knowledge, this is the first Korean report.

Citations

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Keep CALME (childhood asymmetry labium majus enlargement) and follow up
Andrea Sechi, Annalisa Patrizi, Giulio Vara, Rita Golfieri, Iria Neri
JDDG: Journal der Deutschen Dermatologischen Gesellschaft.2021; 19(9): 1276. CrossRef
Bei CALME (childhood asymmetry labium majus enlargement): die Ruhe bewahren und nachverfolgen
Andrea Sechi, Annalisa Patrizi, Giulio Vara, Rita Golfieri, Iria Neri
JDDG: Journal der Deutschen Dermatologischen Gesellschaft.2021; 19(9): 1276. CrossRef
Childhood Asymmetry Labium Majus Enlargement (CALME): Description of Two Cases
Cristina Salvatori, Ilaria Testa, Marco Prestipino, Maria Elena Laurenti, Sara Riccioni, Giuseppe Di Cara, Nicola Principi, Susanna Esposito, Mirko Bertozzi
International Journal of Environmental Research and Public Health.2018; 15(7): 1525. CrossRef
Childhood asymmetrical labium majus enlargement sonographic and MR imaging appearances
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Original Articles

Glomerular Hypertrophy in Focal Segmental Glomerulosclerosis.: So Dug Lim, Tae Sook Kim, Hyun Soon Lee; Korean J Pathol. 1995;29(4):423-430.

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Abstract PDF: It is not clear whether glomerular hypertrophy is related to the pathogenesis of focal segmental glomerulosclerosis (FSGS). We analyzed renal biopsies from 20 adults with FSGS by morphometry, and the data were compared with those from age- and sex-matched patients with minimal lesion. Mean glomerular volume in the FSGS group was significantly larger than that in the minimal lesion group[(3.4 + 1.1 vs 2.5 0.5)x10(6) micrometer3, P<0.01]. The percentage of glomeruli with global and segmental sclerosis in FSGS group was significantly correlated with the mean glomerular volume (r=+0.66, P<0.001). Relative interstitial volume of renal cortex in the FSGS group was correlated with the serum creatinine concentration(r=+0.5, P<0.05). These results suggest that glomerular hypertrophy observed in our patients with FSGS was related to nephron loss caused by glomerulosclerosis. The interstitial fibrosis may lead to obliteration of postglomerular interstitial capillary network with secondary elevation of glomerular capillary pressure resulting in progressive loss of renal function.

Comparison of Glomerular Size between Focal Segmental Glomerulosclerosis and Minimal Lesion in Children.: Jung Yeon Kim, Hyun Soon Lee; Korean J Pathol. 1996;30(10):903-911.

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Abstract PDF: The pathogenetic mechanism of focal segmental glomerulosclerosis (FSGS) is not known. Some authors suggest glomerular hypertrophy may precede the development of FSGS in patients with minimal lesion. It was recently reported that the size of nonsclerotic glomeruli in adults with FSGS is significantly larger than that of cases with minimal lesion. It is not clear whether glomerular hypertrophy observed in adults with FSGS is also seen in children with FSGS. Thus, we have analyzed 37 renal biopsies from children with FSGS by morphometry and the data were compared with 37 renal biopsies from age- and sex-matched patients with minimal lesion. The number of glomeruli submitted for morphometric analysis was 22.6+/-14.2 in cases with FSGS and 30.9+/-11.4 in cases with minimal lesion. Mean glomerular volume (MGV) in FSGS group was significantly larger than that of minimal lesion [(13.1+/-3.9) x10(5) microm3 vs. (10.1+/-1.9) x10(5) microm3, p<0.001]. The relative interstitial volume of renal cortex in patients with FSGS was significantly larger than that of minimal lesion [(0.106+/-0.051) microm3/microm3 vs. (0.029+/-0.012) microm3/microm3, p<0.0001]. In FSGS, the percentage of glomeruli with FSGS was significantly correlated with relative interstitial volume of renal cortex (r=0.79, p<0.0001). As is the case for adult FSGS, MGV of children with FSGS is significantly larger than that of minimal lesion. Thus, the presence of glomerular hypertrophy observed in biopsies with minimal lesion nephropathy seems to be an indication that the coexistent FSGS lesions are undetected due to sampling problems.

Structural-Functional Relationships in Renal Amyloidosis.: Myeong Cherl Kook, Hyun Soon Lee; Korean J Pathol. 1997;31(11):1190-1199.

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Abstract: The pathogenetic mechanism of renal dysfunction in renal amyloidosis is poorly understood. To evaluate the morphologic parameters which are correlated with renal function in this disorder, we have examined renal biopsies from 14 patients with renal amyloidosis by morphometry. Of the 14 patients, 8 were male and 6 were female. They were between 41 and 70 years of age. The serum concentration of albumin and creatinine were 2.1+/-0.7 mg/dl and 1.1+/-0.5 mg/dl, respectively. The 24-hour excretion of urinary protein was 7.9+/-5.2 g. Creatinine clearance was 62+/-23 ml/min/1.73m2. The mean glomerular volume (MGV) was (2.2+/-1.3) 10(6) micrometer3. The surface density of peripheral glomerular basement membrane [Sv (PGBM/glom)] was 0.049+/-0.027 (micrometer3/micrometer3). Volume density of mesangium [Vv (mes/glom)] was 0.31+/-0.14 (micrometer3/micrometer3) and volume density of glomerular amyloid deposition [Vv (amyl/glom)] was 0.21+/-0.14 (micrometer3/micrometer3). The volume density of cortical interstitium [Vv (int/cortex)] was 0.14+/-0.09 (micrometer3/micrometer3). The serum creatinine concentration was significantly correlated with Vv (int/cortex) (r=+0.66, p<0.05). MGV was correlated with Vv (mes/glom) (r=+0.75, p<0.01) and Vv (amyl/glom) (r= +0.68, p<0.05) but showed negative correlation with Sv (PGBM/glom) (r=-0.79, p<0.01). Sv (PGBM/glom) showed negative correlation with Vv (mes/glom) (r=-0.77, p<0.01) and with Vv (amyl/glom) (r=-0.87, p<0.01). Positive correlation was observed between Vv (mes/glom) and Vv (amyl/glom) (r=+0.95, p<0.01). These results suggest that the decreased renal function in patients with amyloidosis is related to interstitial fibrosis rather than glomerular lesions. In addition, glomerular hypertrophy in these patients is related to amyloid deposition in the mesangium and peripheral glomerular basement membrane.

Cardiac Myocyte Cell Death in Isoproterenol-Induced Cardiac Hypertrophy in Rats.: Soo Kyung Kim, Eun Sook Chang, Gee Youn Kwon; Korean J Pathol. 2001;35(3):189-195.

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Abstract PDF: BACKGROUND
Although cardiac hypertrophy contributes to cardiac failure, the underlying mechanism has not yet been precisely determined. This study was planned in order to determine the pathogenesis of heart failure following cardiac hypertrophy induced by -adrenergic stimulation.
METHODS
The extent of cardiac hypertrophy was assessed after administrating isoproterenol (ISO, 5 mg/kg) intraperitoneally for 6 hours, 1, 3, 5, 7 and 10 days. The hematoxylin-eosin, Masson's trichrome and phosphotungstic acid hematoxylin stains along with immunohistochemical stainings for proliferating cell nuclear antigen and Ki-67 were performed in the paraffin-embedded left ventricle sections. Apoptosis was assessed by DNA laddering and terminal deoxynucleotidyl transferase TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay. TUNEL positive myocytes and some nonmyocytes appeared in the subepicardium at 6 hours after ISO administration. The localization of these cells was shifted to the subendocardium within 24 hours, and the TUNEL positive cells were seen throughout the myocardium on the 5th day after ISO treatment. Necrotic myocyte death occurred on the 3rd day of ISO administration in the subendocardium, and initial pericellular fibrosis was followed and increased thereafter, with replacement fibrosis accompanied by further necrotic myocyte cell death.
CONCLUSIONS
Our data showed that ISO treatment induced apoptotic myocyte death and superimposed necrotic myocyte death with subsequent fibrosis. The observed cardiac myocyte death may reflect myocardial dysfunction.

Image Analysis of Glomerular Changes in Patients with Post-transplant IgA Nephropathy.: Kye Won Kwon, Hyeon Joo Jeong; Korean J Pathol. 2001;35(3):206-211.

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Abstract PDF: BACKGROUND
IgA nephropathy after renal transplantation (post-transplant IgAN) may recapitulate the IgAN of native kidneys, however, little has been reported about the histologic characteristics. The aim of this study is to apply glomerular morphometry using an image analyser to examine the histologic characteristics of post-transplant IgAN.
METHODS
The outer margin of the glomerulus (Bowman's area, BA) and glomerular tuft area (GA) were traced manually. The measured area were automatically calculated by KS300 image analysis system (Kontron, Munchen, Germany). The mesangial area (MA) was calculated with a summing each manually traced mesangial area. The total number of glomerular (GC) and mesangial cells (MC) were counted. Eight cases of renal section obtained by nephrectomy due to renal cell carcinoma (normal control: N-CTRL) and nineteen cases of renal section obtained from post-transplantation patients without IgAN (transplantation control: Tx-CTRL) served as controls.
RESULTS
A total of 35 biopsies were finally selected for measurement. BA and GA of post-transplant IgAN were 1.6 and 1.4 times larger than the N-CTRL, respectively, and were not significantly different from Tx-CTRL. MA was 1.4 times significantly larger than that of the Tx-CTRL. As compared to that of the N-CTRL, it was 1.2 times larger, but this difference was not statistically significant. The GC and MC of post-transplant IgAN and the Tx-CTRL were significantly lower than the N-CTRL. There were no significant correlations between glomerular hypertrophy and duration after renal transplantation, mesangial changes, segmental sclerosis, or degree of renal cortical interstitial fibrosis in post-transplant IgAN.
CONCLUSIONS
Prominent glomerular hypertrophy and mesangial expansion suggest a hyperfiltration injury in post-transplant IgAN and a possible way to glomerulosclerosis.

Case Report

Lipomatous Hypertrophy of the Interatrial Septum: A Case Report.: Ji Eun Kwak, Han Seong Kim, Mee Joo, Sun Hee Chang, Sang Hwa Shim, Je G Chi, Wook Sung Kim; Korean J Pathol. 2007;41(3):213-215.

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Abstract PDF: Lipomatous hypertrophy of the interatrial septum is a benign cardiac mass that is characterized by excessive deposition of fat in the interatrial septum. It typically occurs in elderly, obese patients and may cause arrhythmia. We report a case of lipomatous hypertrophy of the interatrial septum. A 45-year-old man was admitted for evaluation of chest discomfort. Transthoracic echocardiography revealed a cardiac mass, which was suspected as a myxoma. A resection of the tumor was performed. Grossly, the mass was 1.3x1.2x0.8 cm, and showed yellow soft consistency and good demarcation. Microscopically, the mass consisted of mature adipose tissue, intermixed cardiac muscle fibers, entrapped nerve fibers and ganglion cells. Lipomatous hypertrophy of the interatrial septum should be differentiated pathologically from tumorous cardiac mass such as lipoma and myxoma.

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