Amiodarone-Induced Epididymitis: A Case Report and Review of the Literature.

Amiodarone is commonly used to prevent and treat life-threatening cardiac arrhythmias. However, it is also known to have an extensive side effect profile. A rare adverse effect of amiodarone is epididymitis. Epididymitis is inflammation of the epididymis that causes moderate pain in the posterior scrotum. The patient, in this case, developed left scrotal pain seven months after starting amiodarone and presented with symptoms consistent with epididymitis. The patient's work-up included urinalysis with culture, treatment with antibiotics, and testicular ultrasound before being diagnosed with amiodarone-induced epididymitis. This diagnosis led to the discontinuation of amiodarone, which resulted in the complete resolution of the patient's symptoms within two weeks. This case report is intended to increase awareness of epididymitis as a possible adverse effect of amiodarone and to stress the importance of considering this when there are no apparent anatomical or infectious causes of epididymitis.

Metastatic lung adenocarcinoma to the kidney diagnosed by urine cytology: a case report.

BACKGROUND: Although lung cancer is the solid tumor which most frequently metastasizes to the kidney, metastatic pulmonary adenocarcinoma detected by urine cytology examination is exceedingly rare. CASE: A 52-year-old woman presented with gross hematuria. Urine cytology revealed numerous crowded, overlapped 3-dimensional clusters with occasional papillary and luminal formations. The tumor nuclei were uniformly enlarged with smooth oval contours, regular nuclear membranes, finely granular chromatin, and prominent nucleoli. Numerous clear, intracytoplasmic vacuoles were noted. Urine fluorescence in situ hybridization (FISH) examination was abnormal. Positive immunohistochemical thyroglobulin transcription factor-1 and Napsin-A staining of a renal calyx biopsy confirmed the diagnosis of metastatic lung cancer. CONCLUSION: Although rare, metastatic lung adenocarcinoma in urine has characteristic cytomorphologic findings which appear distinct from the more commonly encountered urothelial carcinoma. Differentiation from other metastatic malignancies may be more problematic and will likely require immunohistochemical confirmation. Metastatic lung cancer may also cause abnormal urine FISH results and thus may be misdiagnosed as urothelial cancer. Therefore, this ancillary testing modality must be employed with caution in the setting of metastatic disease.

Nonphotochemical base-catalyzed hydroxylation of 2,6-dichloroquinone by H2O2 occurs by a radical mechanism.

Kinetic and structural studies have shown that peroxidases are capable of the oxidation of 2,4,6-trichlorophenol (2,4,6-TCP) to 2,6-dichloro-1,4-benzoquinone (2,6-DCQ). Further reactions of 2,6-DCQ in the presence of H(2)O(2) and OH(-) yield 2,6-dichloro-3-hydroxy-1,4-benzoquinone (2,6-DCQOH). The reactions of 2,6-DCQ have been monitored spectroscopically [UV-visible and electron spin resonance (ESR)] and chromatographically. The hydroxylation product, 2,6-DCQOH, has been observed by UV-visible and characterized structurally by (1)H and (13)C NMR spectroscopy. The results are consistent with a nonphotochemical base-catalyzed oxidation of 2,6-DCQ at pH > 7. Because H(2)O(2) is present in peroxidase reaction mixtures, there is also a potential role for the hydrogen peroxide anion (HOO(-)). However, in agreement with previous work, we observe that the nonphotochemical epoxidation by H(2)O(2) at pH < 7 is immeasurably slow. Both room-temperature ESR and rapid-freeze-quench ESR methods were used to establish that the dominant nonphotochemical mechanism involves formation of a semiquinone radical (base -catalyzed pathway), rather than epoxidation (direct attack by H(2)O(2) at low pH). Analysis of the kinetics using an Arrhenius model permits determination of the activation energy of hydroxylation (E(a) = 36 kJ/mol), which is significantly lower than the activation energy of the peroxidase-catalyzed oxidation of 2,4,6-TCP (E(a) = 56 kJ/mol). However, the reaction is second order in both 2,6-DCQ and OH(-) so that its rate becomes significant above 25 °C due to the increased rate of formation of 2,6-DCQ that feeds the second-order process. The peroxidase used in this study is the dehaloperoxidase-hemoglobin (DHP A) from Amphitrite ornata , which is used to study the effect of a catalyst on the reactions. The control experiments and precedents in studies of other peroxidases lead to the conclusion that hydroxylation will be observed following any process that leads to the formation of the 2,6-DCQ at pH > 7, regardless of the catalyst used in the 2,4,6-TCP oxidation reaction.

Revisiting the peroxidase oxidation of 2,4,6-trihalophenols: ESR detection of radical intermediates.

The peroxidase oxidation of 2,4,6-trichlorophenol (TCP) has been clearly shown to result in 2,6-dichloro-1,4-benzoquinone (DCQ). DCQ is a 2-electron oxidation product of TCP that has undergone para dechlorination. Many peroxidases show similar oxidation of the substrate, TCP, to yield the quinone, DCQ. Depending on the substrate, peroxidases are thought to carry out both 1- and 2-electron oxidations; the mechanism can be confirmed by the detection of both enzyme and substrate intermediates. This article presents ESR evidence for the transient 2,4,6-trichlorophenoxyl radical intermediate (TCP•), which exists free in solution, i.e., is not enzyme associated. These data are best explained as a 1-electron peroxidase oxidation of TCP to form TCP•, followed by enzyme-independent radical reactions leading to the 2-electron oxidized product. Also presented are data for the peroxidase oxidation of 2,4,6-trifluorophenol and 2,6-dichloro-4-fluorophenol.