[Injury of the long thoracic nerve after LRA, which etiology? Clinical case]. / Danno del nervo toracico lungo dopo ALR: quale eziologia? Caso clinico.

The long thoracic nerve supplies the serratus magnus muscle. Its injury causes "winging" of the scapula and functional limitation of the upper limb. Such lesion is mostly due to chronic trauma, occasionally iatrogenic. This case report presents a case of serratus magnus muscle paralysis following an anesthetic block of the brachial plexus performed at the time of a minor orthopedic surgery of the wrist, in a young healthy woman who was a tennis player. The observed lesion seemed to have been caused by the anesthetic technique employed, but, at the same time, it is impossible to rule out, in the etiology of the disease, a role of other predisposing factors, such as the intense sport activity above mentioned, or of concurrent factors, such as an incorrect position in the immediate postoperative period.

Role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ("statins") in familial combined hyperlipidemia.

Familial combined hyperlipidemia (FCHL) is a heterogeneous genetic disorder characterized by multiple lipoprotein phenotypes. The genetic defect is unknown, although linkage to the region of the apolipoprotein (apo) A-I-apoC-III-apo A-IV gene cluster on chromosome 11 has been suggested. The metabolic abnormality in many affected individuals is overproduction of apoB-containing lipoproteins causing elevated levels of plasma cholesterol, triglycerides, or both. Low levels of high-density lipoprotein (HDL) cholesterol and an abundance of dense low-density lipoprotein (LDL) particles are other features contributing to the high association of this disorder with premature coronary artery disease. Many affected individuals need drug therapy to lower their lipid levels. The hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or "statins," offer a potent therapeutic option in patients with FCHL. These drugs significantly decrease levels of total cholesterol, LDL cholesterol, and apoB, although their effects on HDL cholesterol and triglycerides are limited. The mechanisms by which statins exert their beneficial effects in patients with FCHL remain controversial. We studied 7 patients with FCHL and 5 genetically uncharacterized patients with mixed lipemia during treatment with pravastatin 20 mg/day. Metabolic parameters of very-low-density lipoprotein (VLDL)-apoB and LDL-apoB were studied using endogenous labeling with stable isotopes. In all patients pravastatin caused an increase in fractional catabolic rates of LDL-apoB without a significant effect on the production rates of apoB-containing lipoproteins. We cannot exclude the possibility that higher doses of statins may decrease VLDL and LDL production.