The Bartholin's glands are located symmetrically at the posterior region of the vaginal opening and play an important role in the female reproductive system. These two pea-sized glands are involved in mucus secretion and vaginal lubrication. Cyst formation in the glands is common and results from mucus build-up in gland ducts. It is important to monitor such cysts because they may occur in the form of carcinomas. Larger cysts and abscesses are found in the lower vestibular region and typically present with erythema and edema. Biopsy is an effective method for distinguishing between Bartholin's gland cysts and differential diagnosis. While smaller cysts may be asymptomatic and may be left untreated, larger cysts require medical attention. Several treatment options are available, including marsupialization and CO2 laser. Healing and recovery depend on the severity of infection and course of treatment.
ABSTRACT:Dichloromethane (DCM) is metabolically converted to carbon monoxide mostly by CYP2E1 in liver, resulting in elevation of blood carboxyhemoglobin (COHb) levels. We investigated the effects of a subtoxic dose of acetaminophen (APAP) on the metabolic elimination of DCM and COHb elevation in adult female rats. APAP, at 500 mg/kg i.p., was not hepatotoxic as measured by a lack of change in serum aspartate aminotransferase, alanine aminotransferase, and sorbitol dehydrogenase activities. In rats pretreated with APAP at this dose, the COHb elevation resulting from administration of DCM (3 mmol/kg i.p.) was enhanced significantly. Also blood DCM levels were reduced, and its disappearance from blood appeared to be increased. Hepatic CYP2E1-mediated activities measured with chlorzoxazone, p-nitrophenol, and p-nitroanisole as substrates were all induced markedly in microsomes of rats treated with APAP. Aminopyrine N-demethylase activity was also increased slightly, but significantly. Western blot analysis showed that APAP treatment induced the expression of CYP2E1 and CYP3A proteins. Neither hepatic glutathione contents nor glutathione S-transferase activity was changed by the dose of APAP used. The results indicate that, contrary to the well known hepatotoxic effects of this drug at large doses, a subtoxic dose of APAP may induce CYP2E1, and to a lesser degree, CYP3A expression. This is the first report that APAP can increase cytochrome P450 (P450)-mediated hepatic metabolism and the resulting toxicity of a xenobiotic in the whole animal. The pharmacological/toxicological significance of induction of P450s by a subtoxic dose of APAP is discussed.Acetaminophen (APAP), a widely used analgesic-antipyretic, may cause severe liver and kidney injuries at large or chronic doses. The APAP-mediated cellular injury is primarily initiated by metabolic conversion of this drug into a reactive intermediate, N-acetyl-p-benzoquinoneimine. It has been demonstrated that multiple forms of cytochrome P450 (P450) including CYP2E1, 1A2, and 3A4 are implicated in the activation of APAP to the reactive metabolite (Raucy et al., 1989;Patten et al., 1993;Zaher et al., 1998), but most investigators accept the fact that CYP2E1 has a principal role in the oxidative metabolism of this drug both in humans and rodents. The reactive metabolite is normally detoxified by conjugation with glutathione (GSH). Therefore, the hepatotoxicity of APAP is mainly dependent on the metabolic activities responsible for the activation of this drug and the effectiveness of GSH conjugation reaction.Dichloromethane (DCM, CH 2 Cl 2 ) is widely used in industry as a degreaser, as a solvent, as an extraction medium, and also as an important constituent of paint removers. Unlike its chemical congeners, such as carbon tetrachloride and chloroform, that are potent hepatotoxins, the liver toxicity of this substance is negligible (Nitschke et al., 1988). Instead, DCM is metabolically converted to carbon monoxide (CO) by CYP2E1 (Guengerich et al., 1991;Kim and Kim, 1996;Wi...
Abstract. Our previous studies showed that administration of a subtoxic dose of acetaminophen (APAP) to female rats increased generation of carbon monoxide from dichloromethane, a metabolic reaction catalyzed mainly by cytochrome P450 (CYP) 2E1. In this study we examined the changes in metabolism and toxicity of APAP upon repeated administration. An intraperitoneal dose of APAP (500 mg/kg) alone did not increase aspartate aminotransferase, alanine aminotransferase, or sorbitol dehydrogenase activity in serum, but was significantly hepatotoxic when the rats had been pretreated with an identical dose of APAP 18 h earlier. The concentrations and disappearance of APAP and its metabolites in plasma were monitored for 8 h after the treatment. APAP pretreatment reduced the elevation of APAP-sulfate, but increased APAP-cysteine concentrations in plasma. APAP or APAP-glucuronide concentrations were not altered. Administration of a single dose of APAP 18 h before sacrifice increased microsomal CYP activities measured with p-nitrophenol, p-nitroanisole, and aminopyrine as probes. Expression of CYP2E1, CYP3A, and CYP1A proteins in the liver was also elevated significantly. The results suggest that administration of APAP at a subtoxic dose may result in an induction of hepatic CYP enzymes, thereby altering metabolism and toxicological consequences of various chemical substances that are substrates for the same enzyme system.
Introduction: Pneumoscrotum is a critical, physical finding that may indicate significant morbidity and mortality. Accumulation of gas in the scrotum can be primary or secondary. Objective: This paper discusses rapid diagnosis and treatment options. Material and Methods: PubMed searches for pneumoscrotum, etiology, diagnosis, and treatment. Results: We review the historical perspective, classification, etiology, diagnosis, and treatment options of pneumoscrotum, as well as the presentation of pneumoscrotum in neonates/infants. Conclusion: It is crucial to diagnose the etiology pneumoscrotum and designing a treatment option based off that.
These results suggest that the CWT and TS of the CCA are associated with the severity of carotid atherosclerosis in untreated hypertensive patients. Hence, the hemodynamics of vessels may contribute to the plaque burden of low-resistance arteries.
Although RI indirectly reflected the atherosclerotic process, the correlation between RI and CHD risk was comparable to the well-known correlation between cardiovascular event and carotid IMT. Hence, carotid RI can be used as a tool for risk stratification in Taiwanese patients with essential hypertension.
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