Evaluation of argon laser surgery in children under 13 years of age

Argon laser surgery is an effective treatment for ectasias and congenital port-wine stains; however, its use in children under the age of 13 is controversial. This paper reviews 202 children under the age of 13 who underwent argon laser treatments for congenital port-wine stains, spider angiomas, epidermal nevi, and lentigines. The clinical characteristics of port-wine stains in 170 children are discussed. Good to excellent results (moderate to complete clearing) in port-wine stains were obtained in 60 percent of patients and seemed to correlate best with lack of blanchability on pressure. Hypertrophic scarring was seen in only 7 children, all of whom had undressed wounds; no significant scarring has been seen in any subsequent child who had maintained a dressed wound postoperatively.     

Trigger finger secondary to anomalous lumbrical insertion: a case report and review of the literature

Trigger finger is a relatively common clinical entity, most frequently caused by stenosing tenosynovitis. Several other conditions not related to tenosynovitis also have been described as a cause of triggering, and these have been reviewed. We present a rare anomaly of the fourth lumbrical muscle insertion as a cause of triggering of the right little finger. This was completely relieved following excision of the anomalous muscle. This rare anatomic variant should be added to the list of potential causes of trigger finger.     

Metabolic pathways involved in the oxidation of isopropanol into acetone by the intact rat

Isopropanol administered in a large (6 g/kg, orally) as well as in a lower dose (1 g/kg, I.P.) is slowly oxidized into acetone by the intact rat. Using two inhibitors, 3 amino-1,2,4-triazole and pyrazole, investigations on the hepatic enzymatic system involved in the oxidation of isopropanol show that catalase does not play an important part in this pathway, contrary to alcohol dehydrogenase which is the major enzyme responsible for this oxidation. Although isopropanol oxidation is mainly catalysed in the liver through alcohol dehydrogenase, no alteration of the hepatic extramitochondrial redox state occurs after the administration of a large as well as of a lower dose of isopropanol. From these experiments it may be concluded that alterations of the liver NAD⁺/NADH ratio, which seem to play an important part in the ethanol induced fatty liver, are not involved in the isopropanol induced one.