Myelomatous pleural effusion in a patient with plasmablastic myeloma: A case report

Myelomatous pleural effusion is an unusual clinical condition associated with poor outcomes. We report a case with myelomatous pleural effusion upon the presentation of the disease. The patient had multiple risk factors for inferior prognosis of multiple myeloma, including old age, immunoglobulin D (IgD) isotype, high lactate dehydrogenase, C‐reactive protein, β2‐microglogulin levels, and a high myeloma cell burden in the bone marrow. The myeloma cells in both bone marrow and pleural effusion had characteristic features of plasmablasts, including gigantic size, large and eccentrically placed nuclei, fine cytoplasm, and prominent nucleoli. Immunophenotypical analysis showed the plasmablastic cells in the pleural effusion were positive for surface CD38, cytoplasmic immunoglobulin, both κ and λ light chains but negative for surface CD19 or CD79a. Our experience suggests that the diagnosis of myelomatous pleural effusion should be made with clinical alertness and careful cytological examination, preferably supplemented by immunophenotypical analysis. Diagn. Cytopathol. 2009. © 2009 Wiley‐Liss, Inc.     

Expression of amyloid beta peptide in human platelets: pivotal role of the phospholipase Cgamma2-protein kinase C pathway in platelet activation.

The amyloid beta peptide (Abeta), a mediator of neuronal and vascular degeneration in the pathogenesis of Alzheimer's disease and cerebral amyloid angiopathy may have peripheral actions. Platelets are enriched with Abeta and have been shown to enhance platelet actions. However, the detailed signaling pathways through which Abeta activates platelets have not been previously explored. In this study, we examined the intra-platelet Abeta distribution using a gold labeling technique and noted that Abeta was predominantly localized in the cytoplasm of resting platelets. A marked increase in Abeta-gold labeling in an open canalicular system was observed in collagen-activated platelets. Exogenous Abeta (2-10 microM) stimulated platelet aggregation accompanied by phospholipase Cgamma2 (PLCgamma2) phosphorylation, phosphoinositide breakdown, and [Ca(2+)]i mobilization as well as protein kinase C (PKC) activation. Ro318220, an inhibitor of PKC, suppressed Abeta-induced platelet aggregation, PKC activation, and [Ca(2+)]i mobilization in platelets, suggesting that the PLCgamma2-PKC pathway is involved in Abeta-induced platelet aggregation. In the electron spin resonance study, Abeta (2 and 10 microM) markedly triggered hydroxyl radical formation in platelets. In an in vivo study, Abeta (2mg/kg) significantly shortened the latency for inducing platelet plug formation in the mesenteric venules of mice. In conclusion, we are the first to demonstrate (1) the distribution of Abeta in human platelets; and that (2) Abeta activation of platelets is mediated, at least partially, by the PLCgamma2-PKC pathway; and (3) Abeta triggers thrombus formation in vivo.     

The occurrence and clinical significance of antibodies to type II collagen in sera and synovial fluid of Chinese patients with rheumatoid arthritis

Antibodies to type II collagen (Col II) in sera and synovial fluid (SF) were measured with an enzyme linked immunosorbent assay (ELISA) using a solid phase sandwich method. The subjects included: 42 patients with rheumatoid arthritis (RA); 31 cases of osteoarthritis (OA); 10 cases of gouty arthritis; 4 cases of ankylosing spondylitis (AS); 5 cases of systemic lupus erythematosus (SLE); and 44 normal controls. The antigens used to detect antibodies against Col II were in native and heat-treated denatured forms, both of which were purified from chicken sternal cartilage by limited enzyme digestion and differential precipitation with salt. The reactivity to native type II collagen was generally higher than the reaction to the denatured collagen. In sera, significant higher levels of Col II were detected in the different arthritis groups when compared with the normal control group, with the exception of AS. In SF, the Col II was significantly higher in RA than it was in OA (p less than 0.001), while no difference was present between gout and OA (p less than 0.05). When native Col II was simultaneously measured in sera and SF among arthritics, positive rates were both higher among RA (65% and 58%, respectively). Positive rates were only higher in sera among OA (59% in sera and 3% in SF) and were both lower among gouty arthritis. The above findings show that the measurement of Col II is more important in SF than in sera.     

Microskin grafting of rabbits with pigskin xenograft overlay

Pigskin xenografts were used to replace allografts in microskin grafting (10: 1 expansion ratio) on 15 rabbits. Rabbits were selected randomly for the removal of the overlaid pigskin at days 7, 10 or 14 for the evaluation of the degree of epithelialization. Histological examination of the removed pigskin 7 days after application showed obvious eosinophilic changes in the epidermal cells and pyknotic changes of the nuclei, however in some areas newly formed epidermis could be found. The pigskin became an eschar or slough on day 14. The microskin autografts proliferated and expanded actively under the protection of this overlaid pigskin. The epidermis increased in thickness and with increasing differentiation. The dermal layer was well vascularized with a large number of capillaries and fibroblasts. The wound was covered by the neoepithelium with almost normal skin texture on day 14, by which time the overlaid pigskin became a dry eschar. In areas where the overlaid pigskin was sloughing, the epithelialization of the underlying microskin grafts was not complete at the same time. In these animal studies of microskin grafting, these overlaid pigskin xenografts showed the same effects as those of allografts.     

A phase I trial of recombinant interleukin-2 combined with recombinant interferon-gamma in patients with cancer

Twenty-six patients with metastatic cancer were entered into a phase I trial of concurrent recombinant interleukin-2 (IL-2) and recombinant interferon-gamma (IFN-gamma). IL-2 was administered as a continuous intravenous infusion for 5 days. IFN-gamma was administered by a daily intramuscular (IM) injection during the 5 days of IL-2 administration. Treatment was repeated twice after 9-day rest periods. After a 2-week rest, patients without evidence of tumor progression were retreated. Natural killer (NK)- and lymphokine-activated killer (LAK)-cell activity were assayed in each patient before treatment, on day 1, and on day 5 of each cycle. Constitutional symptoms occurred in most patients but were not dose-limiting. Other toxicities included hypotension responsive to fluids, transient elevations in liver function tests, erythema/pruritus, eosinophilia, and transient leukopenia/thrombocytopenia. The maximum-tolerated dose (MTD) of the combination was 1 x 10(6) U/m2/d of IL-2 combined with 0.50 mg/m2/d of IFN-gamma. The dose-limiting toxicity was pulmonary manifesting as rales and shortness of breath. The dose of the combination that resulted in the optimal generation of in vivo LAK-cell activity was a dose of at least 0.25 mg/m2/d of IFN-gamma combined with 1 x 10(6) U/m2/d of IL-2. Objective clinical responses were seen in five of 26 patients. These included a partial response of 2 months duration in a patient with non-Hodgkin's lymphoma (NHL), mixed responses in a patient with NHL and two patients with renal cell carcinoma (RCC), and an ongoing assessable response in a patient with bone metastases from RCC. The recommended dose for phase II trials of this combination is 0.50 mg/m2 of IFN-gamma and 1 x 10(6) U of IL-2.     

Prenatal diagnosis of intrahepatic arteriovenous shunts.

A case of mixed intrahepatic arteriovenous shunts in a fetus diagnosed at 35 weeks' gestation is presented. Color Doppler ultrasonography in the fetal liver demonstrated complicated vascular connections fed by the hepatic arterial branches and drained into the portal and middle hepatic veins. Pulsed Doppler ultrasonography identified a high cardiac output state by the detection of increased flow velocities of the great vessels. The contribution of Doppler ultrasonography to hemodynamic changes is highlighted. The management is briefly discussed.     

Reducing limping by tibial lengthening along nails in adult unilateral developmental dysplasia of the hip with high dislocation

Background/Purpose: Treatment of adult neglected developmental dysplasia of the hip (DDH) with high dislocation is still not established. The main concern of young patients is leg-length discrepancy (LLD), which leads to limping gait and impaired body image. Such patients usually ask for a minimally invasive treatment that can improve the LLD. Methods: Between 1993 and 2003, 17 patients with neglected DDH with high dislocation (mean age, 22.8 years) were treated by tibial lengthening using the Ilizarov external fixator over an intramedullary nail. The inclusion criteria were unmarried young adults, unilateral lesion, significant limping or unsightly gait with psychologic discomfort, marked shortening > 4 cm with the block test, and benefit from a shoe-lift. Exclusion criteria were patients older than 30 years, hip pain as the chief complaint, and compensated low hip dislocation without significant limping. Results: All 17 patients had eventual bone consolidation without further operation. The mean external fixation index was 14.2 day/cm. Bone formation was good in all patients with a mean consolidation index of 57.7 day/cm. At an average follow-up period of 7.8 years, the limping was much improved from a moderate or severe degree to a mild degree in all patients. No patients had equinus contracture. All patients were satisfied with their treatment results. There were two complications: transient loss of big toe extension and mild wound infection. Conclusion: Tibial lengthening can improve limping in adult patients with neglected DDH and high dislocation with a low morbidity. Lengthening along intramedullary nails can effectively reduce the external fixation time, improve bone formation, and prevent complications.