Nonsteroidal anti-inflammatory drugs and necrotising fasciitis. An update.

Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen and others are the treatment of choice for mild to moderate pain. Because of the relative safety and efficacy of NSAIDs, many of the agents are now available in the US and in other parts of the world without a physician prescription. While these drugs are relatively well tolerated, adverse effects resulting from their use can occur. One such adverse effect recently linked to NSAID use is necrotising fasciitis. Reports of necrotising fasciitis possibly associated with NSAID use have been published in both the medical and lay literature. Several hypotheses regarding a possible association between NSAIDs and the development of necrotising fasciitis have appeared in the literature. One hypothesis is a simple masking of the signs and symptoms of an existing infection, leading to a delay in diagnosis. Some authors have speculated that in certain skin and soft-tissue infections, particularly those caused by group A beta-haemolytic streptococci, this delay in diagnosis may have allowed a simple infection to progress to necrotising fasciitis. Other postulated mechanisms of NSAID involvement in the development of necrotising fasciitis include an impairment of natural host defense mechanisms. A review of the medical literature for reports of possible NSAID-associated necrotising fasciitis revealed that the events were rare, but clinically significant. From the available evidence, a causal relationship between NSAIDs and necrotising fasciitis cannot be established.

Rapid eye movement sleep periodic leg movements in patients with spinal cord injury.

We describe three spinal cord injury cases exhibiting periodic leg movements (PLMs) in both rapid eye movement (REM) and nonrapid eye movement (NREM) sleep. The difference in the average periodicity in REM and NREM sleep was modest, but was generally shorter in REM than in NREM sleep. However, the variability associated with the PLMs was nearly three to six times smaller in REM than in NREM sleep, suggesting that the periodicity of the PLMs in REM sleep was more precise than in NREM sleep. The finding of PLMs in these patients suggests that a spinal cord injury may permit the expression of a spinal PLM generator, which may be an unusual presentation of a spinal locomotor generator. The PLM generator would be displayed when the descending inhibitory spinal pathways are interrupted by a spinal injury. The rapid periodicity of the PLM generator in REM sleep, compared with NREM sleep, may result from an increase in sympathetic activity normally accompanying this sleep state. Alternative explanations for the occurrence of PLMs in spinal injury are the influence of adverse sleeping position, age, an increase in circulating catecholamines and peripheral perfusion. We conclude that the presence of PLMs may be an important, but neglected, sleep disorder in spinal cord patients. Therefore, health care professionals should be aware of the possibility of sleep-related PLMs when these patients have sleep and/or waking complaints.

Coaxial percutaneous biopsy technique with automated biopsy devices: value in improving accuracy and negative predictive value.

Three hundred percutaneous biopsies were performed in 267 consecutive patients by means of a coaxial technique with use of 18- and 20-gauge automated cutting biopsy devices and 22-gauge aspiration needles. Thoracic, hepatic, renal, pancreatic, adrenal, splenic, retroperitoneal, and musculoskeletal soft-tissue masses were sampled. For malignant masses (229 cases), the sensitivity was 79% for cytologic analysis, 88% for histologic analysis, and 92% for both combined. In benign disease (71 cases), a correct specific diagnosis was made with cytologic analysis in 38%, with histologic analysis in 97%, and with both combined in 97%. The negative predictive value was 60% for cytologic analysis, 72% for histologic analysis, and 80% for both combined. When only cancer-negative results in which a specific benign diagnosis was made were considered, the negative predictive value was 100% for cytologic analysis, 97% for histologic analysis, and 97% for both combined. The positive predictive value was 100% for both cytologic and histologic analysis. Bleeding complications occurred in 3% of biopsies, including in one patient who died.

Type II hyperprolinaemia in a pedigree of Irish travellers (nomads).

We describe a study of 312 subjects in 71 families near related to a proband with type II hyperprolinaemia. The subjects were Irish travellers (nomads) among whom consanguineous marriage and high fertility are common. Thirteen additional cases of type II hyperprolinaemia were discovered; all were offspring of consanguineous unions. A further 50 subjects were found to have mild hyperprolinaemia. We found a strong association between type II hyperprolinaemia and seizures during childhood but no significant association with mental handicap. Most adults with type II hyperprolinaemia enjoyed normal health and there was no evidence that maternal hyperprolinaemia compromised fetal development. The documented association between type II hyperprolinaemia and seizures may be related to the neuromodulatory or reducing-oxidising effects of proline and pyrroline-5-carboxylate, respectively, that has been shown in vitro. Alternatively, another genetic defect closely linked to the type II hyperprolinaemia allele could be the explanation.

Treatment of loculated pleural effusions with transcatheter intracavitary urokinase.

Surgical thoracostomy tube placement and radiologically guided catheter drainage are standard therapy for loculated pleural fluid collections. Treatment may fail if the catheter is not placed optimally within the loculation or if the fluid is hemorrhagic or fibrinous. We studied the value of transcatheter urokinase instillation in facilitating drainage of hemorrhagic or fibrinous nonhemorrhagic loculated pleural collections in 11 patients with 13 loculated pleural collections. Eight of the fluid collections were hemorrhagic, five were nonhemorrhagic. Five patients had had a thoracostomy tube placed surgically and all had had radiologically guided placement of single lumen drainage catheters managed with suction, saline irrigation, and mechanical guidewire manipulation. This therapy had failed to drain the loculations completely over an average of 10 days (range, 1-22 days). Urokinase (1000 units/ml) was instilled into the drainage catheters in 80- to 150-ml aliquots. After 1-2 hr, suction was reinstituted and the procedure was repeated. Twelve (92%) of the 13 collections were drained completely after an average of 4.3 instillations (range, three to eight instillations). Successful urokinase therapy required an average of 28 hr (range, 8-75 hr). In one case, therapy was discontinued after partial resolution for unrelated clinical reasons. There were no complications. These results suggest that transcatheter intracavitary urokinase therapy is a safe and effective method to facilitate drainage of loculated hemorrhagic or fibrinous nonhemorrhagic pleural fluid collections.

Immunohistochemical localization of human immunodeficiency viral antigens in formalin-fixed spinal cords with AIDS myelopathy.

Some patients with the acquired immunodeficiency syndrome (AIDS) have long-tract degeneration in the spinal cord. Spinal-cord sections showing degeneration were immunoreactive in 13 of 17 AIDS patients using rabbit antiserum to whole disrupted human immunodeficiency virus (HIV) or a mouse monoclonal antibody to HIV core protein p24. The immunostaining was in a few macrophages, multinucleated cells, gliomesenchymal-cells nodules, glial cells and vascular endothelial cells. Eleven of the positive cases had histopathologic evidence of long-tract vacuolar alterations associated with this immunoreactivity, and the two cases without vacuolar alterations had immunoreactive multinucleated cells and gliomesenchymal-cell nodules. Immunolocalization of HIV in the spinal cord correlated well with clinical signs and symptoms, although concomitant cerebral and systemic infections often obscured the significance of the spinal-cord findings in the clinical setting. HIV vasculitis could lead to myelitis and to the clinical appearance of long-tract signs and symptoms.