Idiopathic calcinosis cutis of the penis
2 Smllli I'R. UroL'kliursl K). tVlluliir bluL' IIL'\US OI Ihf scltTii. Anh OphilmhiH'! l'»7(.; 94: fil8-2(l. 3 FuU'I I>S, i!hiit;;iviin HS, Bluciicvu.s cii'lhc ulLTLii£.'(.L'rvLX. Hum I'atlwl 19SS: If): 7*J-Sfi. 4 Hasson A. (.luticrrcz \iC. Mcinn LcI ii/. Biuo iiLni on llic prcpuLXand glaniLs penis. .S'iiiii Odiccr 1990; S: 15-19. 5 Zaiiis N. T/ii' .Wii/ in livulth itiid Disfitsc. 2m\ t'tlri. Norwalk. CV: Applcton J4 LHnge. 1990.
Scrotal calcinosis: origin from dystrophic calcification of eccrine duct milia
Scrotal calcinosis is a rare benign disorder considered idiopathic by most recent authors, although an origin from dystrophic calcification of epidermoid cysts has been proposed. In 3 of 4 cases which were otherwise typical of scrotal calcinosis, there was calcification of the contents of small cysts lined by stratified squamous epithelium. These structures were identified as eccrine duct milia because some of them communicated with eccrine ducts and there were ultrastructural features of eccrine duct differentiation in one case. The eccrine nature of the milia was confirmed using the immunoperoxidase technique for the demonstration of carcitioembryonic antigen (CEA) which serves as a marker of eccrine sweat glands. Since a transition could be seen between degenerating calcified milia and typical nodules, it appeared that the calcific deposits of scrotal calcinosis result from the breakdown of such lesions. Staining of deposits unassociated with cyst walls with the technique for the demonstration of CEA supported this conclusion. An advanced stage of evolution of the disease could account for the absence of visible cysts in many cases. We propose the term “hidrocalcinosis of the scrotum” for this distinctive form of cutaneous calcification.
Electrophysiological Studies of Penticainide (CM 7857), a New Antiarrhythmic Agent, in Mammalian Myocardium
The intracellular electrophysiologic properties of a new antiarrhythmic substance, penticainide, were studied in isolated rabbit, dog, and guinea pig myocardial preparations superfused or perfused with oxygenated Tyrode's solution. “Therapeutic” concentrations of penticainide (1.5 to 3 x 10-5 M) had little effect on sinus node automaticity; sinoatrial conduction was slightly delayed. In atrial, Purkinje and ventricular fibers, amplitude, and maximal rate of rise of phase 0 (dV/dtmax) were decreased by penticainide; Purkinje-ventricle conduction velocity was depressed. Penticainide did not significantly modify action potential duration (APD) of rabbit atria and dog ventricle and reduced APD and effective refractory period (ERP) of dog Purkinje and guinea pig ventricular fibers. Penticainide reduced APD heterogeneity of Purkinje-ventricle junction with a preferential effect at the gate and decreased tension amplitude of perfused papillary muscle in dog heart. The effect of penticainide on dV/dtmax was voltage and rate dependent; the resting block was weak. Thus, penticainide is a class 1 antiarrhythmic agent with properties of class 1B agents such as APD reduction and properties of class 1C agents such as slow recovery kinetic of rate-dependent block.