Cotyledonoid-dissecting leiomyoma, a very unusual form of uterine leiomyoma, often leads to misdiagnosis as a malignant tumor. Here, we describe a case of a 45-year-old nulliparous woman who underwent a laparoscopic biopsy of a large pelvic mass consisting of multiple flaps. Histologically, the mass was composed of smooth muscle fascicle nodules separated by hydropic connective tissue, and exhibited extensive stromal hyalinization. The tumor was diagnosed as a cotyledonoid-dissecting leiomyoma based on the laparoscopic, pathological, and image findings. Prior to performing radical laparotomy, two courses of leuprorelin were administered in anticipation of tumor reduction and hypoperfusion, and the tumor size reduced remarkably. We demonstrated the utility of laparoscopic biopsy, considering its minimal invasiveness and diagnostic accuracy. Furthermore, the preoperative use of Gonadotropin-releasing hormone (GnRH) analogs to reduce surgical stress may be useful for treating cotyledonoid-dissecting leiomyomas.

Interface dermatitis or lichenoid interface dermatitis refers to a cutaneous inflammatory pattern in which keratinocyte cell death is the essential feature. These terms have evolved from the originally described lichenoid tissue reaction. These lesions are the basis for an important group of skin diseases in animals and people where cytotoxic T-cell-mediated epidermal damage is a major pathomechanism. Yet, for largely historical reasons these commonly used morphological diagnostic terms do not reflect the essential nature of the lesion. An emphasis on subsidiary lesions, such as the presence of a lichenoid band, and definitions based on anatomical features, such as location at the dermo-epidermal location, may cause confusion and even misdiagnosis. This review covers historical aspects of the terminology, including the origin of terms such as \"lichenoid.\" The types of cell death involved and the histopathologic lesions are described. Etiopathogenesis is discussed in terms of aberrations of immune/inflammatory mechanisms focusing on cutaneous lupus erythematosus, erythema multiforme, and Stevens-Johnson syndrome/toxic epidermal necrolysis. Mechanisms have most extensively been studied in humans and laboratory animals and the discussion is centered on these species. As interface dermatitis is firmly entrenched in dermatological parlance, rather than using \"cytotoxic\" as its substitute, the terminologies \"interface cytotoxic dermatitis\" and \"panepidermal cytotoxic dermatitis\" are recommended, based on location and extent of epithelium affected.

BACKGROUND: Favipiravir is very effective in the treatment of many viral infections, especially at high doses. It was used at such doses to treat coronavirus disease 2019 (COVID-19) during the pandemic. However, liver damage was reported in patients undergoing such treatment.
OBJECTIVE: This study aimed to investigate the effects of low and high doses of favipiravir on the liver of rats, using biochemical and histopathological methods.
METHODS: Wistar albino rats were allocated to one of 3 groups, namely a healthy group (HG), a 100 mg/kg favipiravir (FAV-100) group and a 400 mg/kg favipiravir (FAV-400) group. Favipiravir was administered orally at 100 mg/kg and 400 mg/kg doses to the FAV-100 (n = 6) and FAV-400 (n = 6) groups, respectively. Distilled water was administered orally (1 mL) using the same method to the HG (n = 6). This procedure was repeated twice a day for 1 week. At the end of this period, the animals were euthanized with a high dose of thiopental anesthesia (50 mg/kg) and their liver tissues were removed.
RESULTS: Favipiravir caused an increase in malondialdehyde (MDA), nuclear factor kappa B (NF-κB) and interleukin 6 (IL-6) levels in the liver tissue, as well as elevated alanine aminotransaminase (ALT) and aspartate aminotransferase (AST) levels in the blood. Moreover, favipiravir caused a decrease in total glutathione (tGSH), superoxide dismutase (SOD) and catalase (CAT) levels. In addition, severe edema, lymphocyte infiltration and hydropic degeneration were observed in the liver tissue of the FAV-400.
CONCLUSIONS: High-dose favipiravir caused more significant oxidative and inflammatory damage in the liver tissue of rats than low-dose favipiravir.

We induced experimental nephrolithiasis in female rats using ethylene glycol (EG) and ammonium chloride (AC). We investigated the effects of carvacrol, an essential oil with antioxidant and anti-inflammatory properties, on nephrolithiasis using histopathology, immunohistochemistry and biochemistry. We used 40 female rats divided into four equal groups: control group, administered olive oil; carvacrol group, administered carvacrol in olive oil; nephrolithiasis group, administered EG and AC to induce experimental nephrolithiasis; treatment group with induced nephrolithiasis and administered carvacrol in olive oil. We observed no significant difference in crystal accumulation in the treatment group compared to the nephrolithiasis group. We found a significant reduction in hydropic degeneration of tubules and degree of inflammatory cell infiltration of intertubule areas. We also found a significant reduction in immunohistochemical staining of macrophage- and monocyte-specific antigens. Carvacrol treatment reversed the induced nephrolithiasis, increased malondialdehyde and urea, and decreased levels of glutathione peroxidase and catalase. Although carvacrol did not decrease crystal accumulation, it reduced pathological and biochemical damage, and improved kidney function by lowering the serum urea level.

OBJECTIVE: Based on the modified diagnostic criteria for oral lichen planus (OLP) proposed by Van der Meij and Van der Waal, the objective of the current investigation was to demonstrate a clinicohistopathological association in the diagnosis of OLP.
METHODS: Data were retrieved from 250 individuals who visited the Department of Oral Medicine and Radiology and were diagnosed with OLP between September 2018 and December 2021. Upon completion of the histopathological analysis, the precise diagnosis of OLP was made. Repeat biopsies were performed in the cases suspecting malignant transformation during the follow-up phase. The data were analyzed using SPSS software. The Fisher\'s exact test and chi-square test of association were used to establish the significant differences between the variables at a 5% significance level.
RESULTS: Of the 250 patients, 48% and 52% were males and females, respectively. The two clinical manifestations observed were reticular (n=145, 58%) and erosive types (n=105, 42%). The most frequently impacted locations were the buccal mucosa (n=150, 60%) and labial mucosa (n=100, 40%). Fourteen individuals (two with reticular form and 12 with erosive form) later during follow-up showed dysplasia, with moderate (n=2) to mild (n=12) dysplastic alterations. Koilocytes were reported in 84 cases (34%), which included 35 (24%) reticular cases and 49 (47%) erosive lesions. The histopathological features such as acanthosis, epithelial atrophy, hyperkeratosis, presence of neutrophils, koilocytes, and epithelial dysplasia were shown to be statistically significant between the clinical forms (p<0.001).
CONCLUSIONS: The results of the current study highlight the concordance of histopathological and clinical diagnoses, especially for early definitive diagnosis of OLP. More research studies are warranted to validate the trend of epithelial dysplasia in OLP associated with human papillomavirus (HPV) and to explore the course of the lesions that might be affected by this trait.

OBJECTIVE: Hepatic changes have been described during the refeeding syndrome due to increase in enzymes and hepatomegaly; however, they have not been properly described. Thus, the objective of this study was to investigate the hepatic histological characteristics and biochemical markers of hepatic steatosis in Wistar rats with refeeding syndrome.
METHODS: Thirty male Wistar rats were allocated to one of three groups: C, F or R. The animals from group C received an AIN-93 diet for 96 hours, and were then sacrificed. Animals allocated to group F were fasted for 48 hours and sacrificed. Animals from group R were also fasted for 48 hours, but were refed for another 48 hours, with AIN-93. The liver, blood and epididymal and retroperitoneal fats were collected.
RESULTS: Data obtained in groups F and R show the changes observed in refeeding syndrome, during starvation and refeeding. The serum glucose, magnesium, potassium and phosphorus, in group F, decreased. There was no evidence of hepatic steatosis. Hypophosphatemia, hypomagnesemia and hypokalemia were also observed in group R, confirming refeeding syndrome. The main histological characteristic, in this group, was the extensive presence of ballooning degeneration. This is the first article that has detected such change in liver structure, due to refeeding syndrome. The possible causes are: retention of sodium, causing whole body edema; and/or dysfunction of the sodium/potassium pump of the hepatocytes, as a result of hypophosphatemia.
CONCLUSIONS: This is the first description of an animal model of hepatic severe ballooning degeneration induced due to refeeding syndrome.

BACKGROUND: Copper is an essential microelement for animals and has been used at pharmacological doses in weaned piglets to improve growth performance. However, it also induces systemic oxidative stress after short-term feeding. The aim of this study was to investigate the effects of dose and duration of dietary copper on lipid peroxidation and oxidative stress status in model of weaned piglets.
METHODS: A total of 48 crossbred piglets (weaned at 21d, weight ∼8.2 kg) were randomly assigned into 4 groups of 12 in each. The control group and 3 treatment groups fed with basal diet supplemented with 20, 100 and 200 mg/kg copper as copper sulfate for 3 and 6 weeks, respectively.
RESULTS: Dietary copper supplementation significantly affected the activities of ALP, LDH, LIPC and the levels of Ca and TG in serum as well as the copper and zinc deposition in liver. Increased MDA concentrations, and decreased GPX, CP and CAT concentrations in serum were found in 0, 100 and 200 mg Cu/kg diet groups at 3 weeks post weaning. Hepatic lipid peroxidation was also induced in these groups indicated from hepatic SOD1, GPX1, CAT, CP, MT1A and MT2A transcriptional levels. Those adverse symptoms were alleviative at 6 weeks post weaning. The hepatic Cu and Zn concentrations, serum MDA concentrations, and serum CAT and GPX activities were significantly correlated with Actinobacillus, Lactobacillus, Sarcina, Helicobacter, Campylobacterales, which could affect the intestinal health further.
CONCLUSIONS: These results indicated that copper deficiency or over supplementation would affect the systemic lipid peroxidation. These adverse changes were not observed when the dietary copper concentration at 20 mg Cu/kg diet. The results suggested the appropriate dietary copper concentration is around 20 mg Cu/kg diet, and its range might be much stricter than we thought.

Zinc oxide nanoparticles (ZnO NPs) are widely used in industry and cosmetic products with promising investment in medical diagnosis and treatment. However, these particles may reveal a high potential risk for human health with no information about hepatotoxicity that might be associated with their exposure. The present work was carried out to investigate the histological and histochemical alterations induced in the hepatic tissues by naked 35nm ZnO NPs. Male Wistar albino rats were exposed to ZnO NPs at a daily dose of 2mg/kg for 21days. Liver biopsies from all rats under study were subjected to histopathological examinations. In comparison with the control rats, the following histological and histochemical alterations were demonstrated in the hepatic tissues of rats exposed to ZnO NPs: sinusoidal dilatation, Kupffer cells hyperplasia, lobular and portal triads inflammatory cells infiltration, necrosis, hydropic degeneration, hepatocytes apoptosis, anisokaryosis, karyolysis, nuclear membrane irregularity, glycogen content depletion and hemosidrosis. The findings of the present work might indicate that ZnO NPs have potential oxidative stress in the hepatic tissues that may affect the function of the liver. More work is needed to elucidate the toxicity and pathogenesis of zinc oxide nanoparticles on the vital organs.

BACKGROUND: Uterine leiomyomas are common uterine tumors, and typical cases of leiomyoma are easily diagnosed by imaging study. However, uterine leiomyomas are often altered by degenerative changes, which can cause difficulty and confusion in their clinical diagnosis. We describe the 17th reported case of a uterine leiomyoma clinically diagnosed as an ovarian tumor; however, the present case shows the most detailed radiological evaluation, including contrast-enhanced magnetic resonance imaging. We first show that a uterine leiomyoma can histologically mimic an adenomatoid tumor.
METHODS: A 47-year-old premenopausal, nulliparous Japanese woman with a history of type 2 diabetes mellitus, hypertension, and hyperlipidemia had lower abdominal pain. Ultrasonography confirmed a 6-cm mass in the right-sided space of the pelvic cavity. Magnetic resonance imaging evaluation showed that a multilocular mass was present near the uterus, and a mucinous ovarian tumor was considered. Emergency surgery due to acute abdomen was performed under the diagnosis of pedicle torsion of the ovarian tumor. During surgery, a pedunculated uterine mass without stalk torsion was seen. The mass grossly contained serous and hemorrhagic fluids in the cavities, and pathology examination confirmed that the mass was a leiomyoma with hydropic and cystic degeneration. Anastomosing thin cord-like arrangements of the leiomyoma cells mimicked the architecture of adenomatoid tumors. The tumor cells were positive for the microphthalmia transcription factor but negative for other melanoma markers. Three days postoperatively, she was discharged without sequelae.
CONCLUSIONS: Marked intratumoral deposition of fluids may induce the multilocular morphology of a tumor, and the cellular arrangement of the tumor cells with hydropic degeneration mimicked an adenomatoid tumor in this case. Clinicians need to be aware that a subserosal leiomyoma with cystic and hydropic degeneration can mimic an ovarian tumor, and pathologists should be aware that such leiomyomas can mimic adenomatoid tumors. Additionally, perivascular epithelioid cell tumors should not be diagnosed only based on its immunoreactivity for the microphthalmia transcription factor.

Pseudo-Meigs\' syndrome secondary to uterine leiomyoma is a rare entity. A 50-year-old Japanese woman presented with a 3-month history of shortness of breath. Chest X-ray and magnetic resonance imaging revealed massive right pleural effusion, ascites and a large subserosal uterine myoma. She underwent a total abdominal hysterectomy with bilateral salpingo-oophorectomy. The pathology was consistent with a benign leiomyoma. The ascites and pleural effusion rapidly disappeared postoperatively. The serum interleukin-6 level was 3.9 pg/mL before surgery and declined to 1.6 pg/mL postoperatively. Previous published work has demonstrated that vascular endothelial growth factor and interleukin-6 may play a role in the pathogenesis of Meigs\' syndrome and that vascular endothelial growth factor may contribute to the development of pseudo-Meigs\' syndrome due to metastatic ovarian cancer. This is the first English-language study showing the possibility that interleukin-6 is relevant to the pathogenesis of pseudo-Meigs\' syndrome caused by degenerating uterine leiomyoma.