Nerve injuries of the elbow, wrist, and hand in athletes.

Upper extremity compression neuropathies are fairly rare in athletes. Initially, most can be managed conservatively. These conditions can follow direct contusion of the tissues that overlay these peripheral nerves or can result from vigorous, repetitive, athletic activity leading to tissue swelling and ischemia with nerve compression symptoms. A complete history and physical examination, including a neurologic examination, should be paramount when treating athletes with upper extremity injuries. Early diagnosis and treatment with conservative measures such as splinting, rest, activity modification, and medications can afford the athlete an earlier return to sports. Surgery can be employed when conservative treatment fails and a specific diagnosis has been ascertained.

Traumatic nerve injuries about the elbow.

Although not common, nerve injuries about the elbow occur because of the proximity of the three upper extremity nerves or because of the relationship of the median, ulnar, and radial nerves to the bony and soft-tissue structures about the elbow joint. Nerve injuries at and about the elbow joint occur more frequently with fractures than with any other kind of trauma. Nerve injuries may be found with periarticular fractures, dislocations, gunshot wounds, lacerations, and other iatrogenic causes.

Enhanced skin reactivity to platelet-derived permeability factor (PDPF) and exogenous histamine in an acute phase rabbit model.

Rabbits made acute phase by sub-cutaneous trauma with 2% croton oil (in mineral oil) were tested by intradermal (ID) injection with platelet-granule extracts containing platelet-derived permeability factor (PDPF). Compared with controls, skin reactivity to PDPF was enhanced in acute phase animals 3-7 days post-trauma, a period of acute inflammation as reflected by the occurrence in the circulation of C-reactive protein; maximal skin responses were observed 3-4 days post-trauma. Individual skin sites reached maximum intensity 15 min-1 hour post-ID injection of PDPF and were sensitive to chlorpheniramine maleate, suggesting a major role for histamine. Intradermal injection of histamine revealed that acute phase animals yielded an initially more intense skin reaction, and were markedly less capable of recovering from the effects of histamine. These data suggest that in the acute phase, there exists a heightened and prolonged sensitivity to the action of histamine which can be exploited by pro-inflammatory agents such as PDPF.

Selective inhibition of platelet activation by the amyloid P-component of serum.

One component of amyloid, protein AP, has a characteristic pentameric structure and is identical with a 9.5s serum alpha 1-globulin designated serum amyloid P-component or SAP. Another pentameric molecule, the acute-phase reactant C-reactive protein (CRP), shares major amino acid sequence homology with SAP although, in man, SAP is not an acute-phase reactant. Recently, we demonstrated that heat-aggregated CRP (H-CRP), like heat-aggregated IgG, activates platelets to reactions of aggregation, secretion, and generation of thromboxane A2. We report here that physiologic concentrations of SAP inhibit platelet aggregation stimulated by H-CRP. SAP must be present before platelet challenge with H-CRP to be effective. Native (unaggregated) CRP does not inhibit platelet activation induced by H-CRP, and the platelet inhibitory effect of SAP is restricted because platelet responses to each heat-aggregated IgG, acid-soluble collagen, DNA, ADP, and thrombin remain unaltered in the presence of SAP. Thus, human SAP seems to selectively modulate platelet reactivity to modified CRP, and as such to down-regulate at least one aspect of the biologic capacity of its acute-phase homologue.

Comparison of the enzymatic sensitivities of the platelet receptor for human C-reactive protein and its functional relationship to the platelet IgG Fc receptor.

Thermally modified human C-reactive protein (H-CRP) and IgG (AHGG) each activate isolated human platelets to reactions of aggregation and secretion. As these molecules exhibit many functional similarities, we questioned whether they might also share a receptor on the platelet membrane. Neither plasmin nor phospholipase C altered the platelet response to H-CRP or AHGG, although these reagents enhanced the platelet expression to acid soluble collagen (ASC). Conversely, chymotrypsin treatment of platelets resulted in an elevated response to each H-CRP and AHGG, but not to ASC. These data suggest that the H-CRP and AHGG platelet receptors share characteristics which contrast with those of the receptor for collagen. However, monomeric IgG, which can bind with the platelet and inhibit the response to AHGG, exerted no effect on the platelet response to H-CRP. Further, a functional receptor for thermally modified human or rabbit CRP was detected on rabbit platelets in the absence of a demonstrable Fc receptor for aggregated IgG. These data indicate that the platelet receptors for the modified forms of CRP and IgG are distinct.

Generation of thromboxane A2 and aorta-contracting activity from platelets stimulated with modified C-reactive protein.

The classical acute phase reactant, C-reactive protein (CRP), appears in markedly elevated concentration in the sera of individuals undergoing reactions of acute inflammation and tissue degradation. We previously demonstrated that like IgG, appropriately purified CRP could be thermally modified (H-CRP) such that it enhanced platelet activation in plasma and initiated platelet responses in isolated systems. We now report that this direct platelet activation by modified CRP results in the secretion of both platelet dense body and alpha-granule constituents, and is sensitive to non-steroidal anti-inflammatory drugs as well as the adenosine diphosphate (ADP)-removing enzyme system creatine phosphate/creatine phosphokinase. Thin-layer chromatographic (TLC) analysis of prostanoate endproducts following platelet activation with H-CRP revealed the formation of thromboxane B2 (the hydrated endproduct of thromboxane A2), an important endogenous platelet activator and contractor of vascular tissue; bioassay on rabbit aorta strips of supernatants obtained from platelets undergoing challenge with H-CRP supported the TLC analysis. Complexes formed between CRP and one major ligand, the polycation, were found to share certain platelet activating properties with H-CRP, as does latex-aggregated CRP. These data imply a potential agonist role for this acute phase reactant in platelet physiology and suggest that the interaction of modified forms of CRP with the platelet at sites of vascular damage could have pathological significance.