Platelet antithrombin defect in malignancy: platelet protein alterations

Sixty-eight patients with malignant disease were divided into two groups based on the results of the platelet antithrombin test (PAT). The normal group had a PAT clotting time ranging from 21.4 to 29.8 seconds, which was equivalent to 25% to 65% inactivation of the 2 U of thrombin added to the test system. The other group showed abnormal PAT clotting time, less than 21.4 seconds or less than 25% thrombin inactivation. The polypeptide composition of platelets from the two patient groups was analyzed by sodium dodecyl sulfate (SDS)- electrophoresis on 7.5% polyacrylamide gels. A polypeptide of 180,000 apparent mol wt was decreased or absent in both Coomassie blue- and Alcian blue-stained gels of the platelets from patients whose PAT was abnormal; this polypeptide comigrated with purified platelet thrombospondin. Tritium labeling of platelet surface glycoproteins by the periodate-borohydride method followed by two-dimensional electrophoresis was performed on platelets of seven patients with abnormal PAT. When they were compared with ten patients with normal PAT, a glycoprotein of 140,000 apparent mol wt with a pl of 4.5 to 5.2 was decreased in platelets of all seven patients with abnormal PAT. Nitrocellulose replicas of one-dimensional gels of platelets from 13 of 14 patients with abnormal PAT showed decreased reaction with an anti- human platelet glycocalicin antiserum. Platelets of these same patients also showed a decreased or absent platelet agglutination induced by ristocetin. Patients with normal PAT had a mean agglutination slope of 1.25 +/- 0.6 (n = 26) as compared with 0.37 +/- 0.34 (n = 26) for the abnormal PAT group (P less than .001). Results indicate that platelets from a subpopulation of tumor patients characterized by decreased platelet antithrombin activity have alterations in two platelet glycoproteins, identified as GPIb and thrombospondin.     

大鼠蛛网膜下腔联合注射kappa受体激动剂和NMDA受体拮抗剂协同镇痛

以大鼠热辐射甩尾潜伏期为测痛指标,蛛网膜下腔(it)联合注射非镇痛剂量的kappa阿片受体激动剂强啡肽(dynorphin,Dyn)A-(1-13)5nmol或U50488H(trans-(±)-3,4-dichloro-N-methyl-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide)100nmol和N-methyl-D-aspartate(NMDA)受体拮抗剂DL-2-amino-5-phosphonovalericacid(APv)10 nmol 或 kynurenicacid (KYN) 50 nmol 有显著的协同镇痛效应,其效应与NMDA受体拮抗剂呈一定量效关系。Kappa阿片受体特异性拮抗剂nor-binaltorphi-mine(nor-BNI)15nmolit可完全翻转Dyn A-(1-13)5nmol和APv10nmol及U50488H100nmol和KYN50nmol的协同镇痛。说明协同作用是通过kappa受体和谷氨酸能神经元之间的相互作用实现的。     

Severe necrotizing stomatitis and osteomyelitis after chemotherapy for acute leukaemia

Background:  Leukaemia is a malignant neoplasm characterized by clonal proliferation of white blood cells within the bone marrow. Despite an increase in the white blood cell count, the leukaemic leukocytes are non-functional. The oral complications arising in leukaemic patients can be attributed to the direct and indirect effects of immunosuppressive chemotherapy.
Methods:  This case report describes severe maxillary and mandibular necrotizing stomatitis and osteomyelitis in a young female patient after chemotherapy for acute leukaemia. On physical examination, the patient presented malnourished with pale skin, cervical lymphadenitis, frequent fever and generalized pain. The intra-oral clinical examination found halitosis, multiple ulcers, necrotizing stomatitis and osteomyelitis located in the maxillary and mandibular regions. The necrotizing stomatitis and osteomyelitis were treated locally with atraumatic removal of the necrotized tissues. The patient received a daily preventive protocol consisting of oral hygiene care, including twice daily brushing, and mouthrinses with a solution of chlorhexidine. She was also treated with systemic metronidazole and amoxicillin for 21 days.
Results:  During the course of management the patient's oral condition improved with some re-epithelialization being noted. However, severe alveolar bone destruction remained evident. Thirty-two months after presentation of the initial symptoms, the patient died due to complications related to leukaemia recurrence (haemorrhage, sepsis and respiratory distress syndrome).
Conclusions:  Dental monitoring during cancer treatment is imperative in order to emphasize the importance of dental plaque control and the maintenance of a healthy periodontal condition throughout medical treatment.     

Ultrasonographic evidence of Gatekeeper™ prosthesis migration in patients treated for faecal incontinence: a case series

Background

Faecal incontinence (FI) is both a medical and social problem, with an underestimated incidence. For patients with internal anal sphincter damage, implantation of biomaterial in the anal canal is a recognised treatment option. One such material, Gatekeeper?, has previously shown promising short- and medium-term results without any major complications, including displacement. The main aim of the present study is to assess the degree to which displacement of Gatekeeper prostheses may occur and to determine whether this is associated with patient outcomes.

Methods

Seven patients (six females) with a mean age of 55.6 years [50.5–57.2] and a mean FI duration of 6 ± 2 years were prospectively enrolled in the study. Each subject was anaesthetised and underwent implantation of six prostheses in the intersphincteric region, guided by endoanal 3D ultrasound (3D-EAU). Follow-up was performed at post-interventional months 1, 3, and 12 (median 12 ± 4 months), during which data were obtained from a defaecation diary, Wexner scale assessment, anorectal manometry (ARM), 3D-EAU, and a health status and quality of life questionnaire (FIQL).

Results

At 3-month follow-up, 3D-EAU revealed displacement of 24/42 prostheses in 5/7 patients. Of these, 15 had migrated to the lower portion and 9 to the upper portion of the anal canal and rectum. Despite this migration, treatment was considered successful in 3/7 patients. In one patient, it was necessary to remove a prosthesis due to spontaneous extrusion.

Conclusions

We have shown that displacement of the Gatekeeper? prosthesis occurs, but is not associated with poorer clinical outcomes.

     

Labile Plasma Iron Generation After Intravenous Iron is Time-dependent and Transitory in Patients Undergoing Chronic Hemodialysis

Iron supplementation in hemodialysis patients is fundamental to erythropoiesis, but may cause harmful effects. We measured oxidative stress using labile plasma iron (LPI) after parenteral iron replacement in chronic hemodialysis patients. Intravenous iron saccharate (100 mg) was administered in patients undergoing chronic hemodialysis (N = 20). LPI was measured by an oxidant-sensitive fluorescent probe at the beginning of dialysis session (T0), at 10 min (T1), 20 min (T2), and 30 min (T3) after the infusion of iron and at the subsequent session; P < 0.05 was significant. The LPI values were significantly raised according to the time of administration and were transitory: −0.02 ± 0.20 µmol/L at the beginning of the first session, 0.01 ± 0.26 µmol/L at T0, 0.03 ± 0.23 µmol/L at T1, 0.09 ± 0.28 µmol/L at T2, 0.18 ± 0.52 µmol/L at T3, and −0.02 ± 0.16 µmol/L (P = 0.001 to 0.041) at the beginning of the second session. The LPI level in patients without iron supplementation was −0.06 ± 0.16 µmol/L. Correlations of LPI according to time were T1, T2, and T3 vs. serum iron (P = 0.01, P = 0.007, and P = 0.0025, respectively), and T2 and T3 vs. transferrin saturation (P = 0.001 and P = 0.0003, respectively). LPI generation after intravenous saccharate administration is time-dependent and transitorily detected during hemodialysis. The LPI increment had a positive correlation to iron and transferrin saturation.