Significant association of anti-platelet factor 4/heparin antibody with cardiovascular disease in hemodialysis patients: a longitudinal 7-year study.

BACKGROUND: Hemodialysis patients have a high incidence of anti-platelet factor 4/heparin antibody (PF4-H Ab) and are at a high risk of cardiovascular disease. This study determines the association between PF4-H Ab and cardiovascular events including coronary artery disease (CAD), ischemic stroke (IS), and native arteriovenous fistula thrombosis (AVFT), in a longitudinal 7-year follow-up. PATIENTS AND METHODS: 84 hemodialysis patients were enrolled. Data collection included chart reviews and assessments of laboratory records. PF4-H Ab was evaluated by ELISA and a titer ≥ 0.4 was defined to have PF4-H Ab. RESULTS: 30 patients were PF4-H Ab positive, 30 patients had CAD, 29 patients had IS, and 43 patients had AVFT. In Cox proportional hazard regression analysis, PF4-H Ab (HR 2.72, p = 0.01) was a significant risk factor for CAD. Age (HR 1.06, p = 0.003), PF4-H Ab (HR 4.53, p < 0.001), 7-year averaged serum phosphate levels (HR 0.53, p = 0.012), and 7-year averaged blood platelet count (HR 1.01, p = 0.029) were risk factors for IS. Age (HR 1.03, p = 0.047), PF4-H Ab (HR 3.57, p < 0.001), and 7-year averaged serum triglyceride levels (HR 1.01, p = 0.005) were risk factors for AVFT. In PF4-H Ab-positive groups, thrombocytopenia was not associated with CAD, IS, and AVFT by Fisher's test analysis. CONCLUSION: This study reveals that PF4-H Ab is a risk factor for developing CAD, IS, and AVFT among hemodialysis patients.

Anti-Platelet Factor 4/Heparin Antibody Plays a Significant Role in Progression of Arterial Stiffness among Hemodialysis Patients.

BACKGROUND: Arterial stiffness is a determinant of cardiovascular disease in end stage renal disease. Hemodialysis patients may develop anti-platelet factor 4/heparin antibody (PF4-H Ab) because of heparin treatment in dialysis. We tested whether PF4-H Ab was associated with progression of arterial stiffness in a 3-year follow-up. METHODS: We enrolled 74 hemodialysis patients and studied their clinical, biochemical and arterial stiffness measurement with brachial-ankle pulse wave velocity (baPWV) over 3 years. Baseline and changes in baPWV after 3 years (ΔbaPWV) were collected and compared with related clinical and biochemical parameters. PF4-H Ab was evaluated by the enzyme-linked immunosorbent assay and titer ≥ 0.4 was defined to have PF4-H Ab. RESULTS: We found a positive PF4-H Ab status in 25 of 74 patients. Mean baPWV was 16.1 ± 3.8 (m/s) at baseline and 17.6 ± 4.0 (m/s) after 3 years. Mean ΔbaPWV was 3.4 ± 2.2 (m/s) in the PF4-H Ab positive group, and 0.6 ± 1.2 (m/s) in the PF4-H Ab negative group. Baseline baPWV was only significantly associated with age (ß = 0.49, p < 0.01). ΔbaPWV was significantly different between the PF4-H Ab positive and negative groups (p < 0.01). In multivariate regression analysis, only PF4-H Ab was positively associated with ΔbaPWV (ß = 0.71, p < 0.01). CONCLUSIONS: Our study concluded that PF4-H Ab was associated with progression of arterial stiffness in hemodialysis patients.

Anti-platelet factor 4/heparin antibody is associated with progression of peripheral arterial disease in hemodialysis patients.

BACKGROUND: Heparin therapy may induce anti-platelet factor 4/heparin antibody (PF4-H Ab). Hemodialysis patients receive scheduled heparin and are at a risk of developing PF4-H Ab. Hemodialysis patients are also at a high risk of peripheral arterial disease (PAD). This study examines whether chronic PF4-H Ab exposure contributes to the progression of PAD measured by ankle brachial index (ABI) in hemodialysis patients. MATERIALS AND METHODS: A total of 71 hemodialysis patients were enrolled, and the association between clinical, biochemical parameters and ABI after 3 years was studied. PF4-H Ab was evaluated by ELISA, and patients with titer ≥ 0.4 were taken as having PF4-H Ab. RESULTS: Mean ABI was 1.04 ± 0.18 at baseline and 1.01 ± 0.17 after 3 years. Mean ΔABI (change in ABI after 3 years) was -0.04 ± 0.13. PF4-H Ab was positive in 26 patients. PF4-H Ab was not related to hemodialysis duration, DM history, smoking and age. Platelet count showed no correlation with PF4-H Ab. However, there was significance in ΔABI between PF4-H Ab-positive and PF4-H Ab-negative patients (p = 0.002). ΔABI was negatively correlated with PF4-H Ab and 3-year averaged serum Ca × P only (ß = -0.378, p = 0.001; ß = -0.263, p = 0.018, respectively). However, in PF4-H Ab-positive patients, the extent of ΔABI did not correlate with PF4-H Ab titers (r = -0.021, p = 0.921). CONCLUSIONS: PF4-H Ab positivity, along with high levels of serum Ca × P, played a potential role in the progression of PAD over time.

Serum ferritin is associated with progression of peripheral arterial disease in hemodialysis patients.

BACKGROUND: Dialysis patients received intravenous iron to treat anemia and had high prevalence of peripheral artery disease (PAD). We hypothesized that high iron status might associate with the progression of PAD among hemodialysis patients. Therefore, we evaluated the relationship between iron status and progression of PAD. METHODS: We measured iron status in 74 hemodialysis patients and studied the association with clinical, biochemical, and vascular parameters including progression of PAD measured by ankle-brachial index (ABI) over 3 years. RESULTS: Mean baseline ABI was 1.03 ± 0.18. Mean ABI at 3 years was 0.95 ± 0.20. Mean ∆ABI (change in ABI after 3 years) was -0.08 ± 0.14. Serum ferritin was negatively correlated with baseline ABI (r = -0.232, p = 0.046). After 3 years, ∆ABI was negatively associated with 3-year averaged serum ferritin, phosphorus, and calcium-phosphate product (Ca × P) (r = -0.253, p = 0.029; r = -0.278, p = 0.016; r = -0.288, p = 0.013; respectively). After an adjusted model, 3-year averaged serum ferritin and Ca × P remained the significant determinants of ∆ABI (ß = -0.234, p = 0.038; ß = -0.271, p = 0.017; respectively). ∆ABI was significantly different between 3-year averaged serum ferritin level ≥600 and <600 ng/mL (p = 0.032). CONCLUSIONS: In hemodialysis patients, high serum ferritin associates with progression of PAD, especially among those with high Ca x P level.

Necrotizing pneumonia: a rare complication of pneumonia requiring special consideration.

PURPOSE OF REVIEW: Necrotizing pneumonia is a rare complication of bacterial lung infection. Its cause is owing to either a virulence factor of the microorganism or a predisposing factor of the host. This disease may cause devastating complications such as diffuse pulmonary inflammation, septic shock, and respiratory failure, making treatment more difficult. In the recent decade, the cause of necrotizing pneumonia and the role of surgical treatment have raised considerable attention, leading to therapeutically specific suggestions. RECENT FINDINGS: Staphylococcus aureus strains that produce Panton-Valentine leukocidin have been reported to cause rapidly progressive necrosis of the lung tissue in young immunocompetent patients. Furthermore, recent studies have showed the risk of disease progression is associated with underlying medical conditions. Although antibiotics are the first choice of treatment for necrotizing pneumonia, it has been emphasized that surgical treatment is a feasible alternative option in patients who fail to respond to antibiotics and develop continued deterioration and complications. SUMMARY: The current knowledge of cause, clinical features, diagnosis, treatment, and prognosis of necrotizing pneumonia are summarized. Antibiotics remain the mainstay of treatment. Lung resection can be considered an alternative treatment option in patients who are unresponsive to antibiotic therapy and develop parenchymal complications. Outcome is affected by the degree of disease progression and comorbidities.

Anti-PF4/heparin antibodies are associated with arteriovenous fistula thrombosis in non-diabetic hemodialysis patients.

AIM: Anti-platelet factor 4/heparin complex antibodies (anti-PF4/heparin Ab) have been found to cause heparin-induced thrombocytopenia (HIT), a clinical syndrome thrombocytopenia and thrombosis. There is still controversy as to whether the presence of anti-PF4/heparin antibodies in hemodialysis patients augments clot formation in access fistula thrombosis, peripheral artery disease (PAD), and coronary heart disease (CHD). METHODS: We enrolled 111 non-diabetic hemodialysis patients without liver cirrhosis and without an ankle-brachial index (ABI) ≥1.3 (arterial calcification). ABI measurements were performed and patients with an ABI ≤0.9 were defined as having PAD and included in the PAD group. ELISA was used for determination of anti-PF4/heparin Ab. Correlation factors include PAD, native arteriovenous fistula (AVF) thrombosis, platelet count, and CHD. RESULTS: Thirty-seven of 111 patients (33.3%) presented with anti-PF4/heparin Ab. Thirty-eight of 111 patients (34%) had PAD; fourteen of these patients (36.8%) and 23/73 of patients without PAD (31.5%) were anti-PF4/heparin Ab-positive (P = 0.57). Fifty-two of 111 patients (46.8%) had AVF thrombosis; twenty-three of these patients (44.2%) and 14/59 of patients without AVF thrombosis (23.7%) were anti-PF4/heparin Ab-positive (P = 0.02). The odds ratio for AVF thrombosis was 2.55 (95% CI 1.14-5.71) for anti-PF4/heparin Ab-positive patients. Thirty-two of 111 patients (28.8%) had thrombocytopenia (platelet count <140 × 10(3)/µL); eleven of these patients (34.3%) and 26/79 patients without thrombocytopenia (32.9%) were anti-PF4/heparin Ab-positive (P = 0.88). Ten of 111 patients (9%) had CHD; two of these patients (20%) and 35/101 patients without CHD (34.6%) were anti-PF4/heparin Ab-positive (P = 0.49). CONCLUSIONS: We found that anti-PF4/heparin Ab may contribute to an increased risk of AVF thrombosis in non-diabetic hemodialysis patients.

Port-A-Cath implantation using percutaneous puncture without guidance.

BACKGROUND: The implantation of a Port-A-Cath (PAC) is a common surgical procedure usually done under guidance with techniques such as fluoroscopy, ultrasound, or intravenous electrocardiography. PAC implantation without guidance avoids radiation exposure and decreases time, expense, and complexity. The purpose of this study was to analyze the success rate, and operation-related and postoperative complications of PAC implantation without intraoperative guidance. METHODS: Between July 2004 and June 2007, 1,070 PACs were implanted in 1,025 patients receiving chemotherapy. All PACs were placed via the subclavian vein by percutaneous puncture. The catheter length was precalculated for each patient. Postoperative chest radiography was immediately performed to check the catheter position. All data on outcome of the implantations were reviewed retrospectively. RESULTS: The catheter tip was correctly placed at the cavoatrial junction without complications in 1,055/1,070 (98.6%) of the implants. Surgery-related complications occurred in 15 (1.4%) implantations: 9 malposition, 3 pneumothorax, 2 hematoma, and 1 catheter kinking. Two patients underwent PAC removal due to hematoma with subsequent wound infection in one and catheter occlusion by kinking in the other. There were 86 (8.0%) postoperative complications that resulted in PAC removal: catheter occlusion in 24 (2.2%), pocket infection in 22 (2.1%), catheter rupture in 11 (1.0%), venous thrombosis in 9 (0.8%), port exposure in 9 (0.8%), catheter fracture in 6 (0.6%), infraclavicular pain in 3 (0.3%), catheter migration in 1 (0.1%), and extraportal injection in 1 (0.1%). CONCLUSIONS: PACs can be safely and accurately placed using percutaneous puncture of the subclavian vein without intraoperative guidance.

Acid corrosive injury in patients with a history of partial gastrectomy: outcome analysis.

BACKGROUND: Our purpose was to delineate the characteristics and outcome of acid-corrosive injury in patients with a history of gastric resection. MATERIAL AND METHODS: A total of 359 patients with a history of acid-corrosive injury were retrospectively reviewed. They were grouped based on past history with group 1 consisting of 8 patients with a history of gastric surgery (6 hemigastrectomies with Billroth II gastrojejunostomy, 2 partial gastrectomies with Billroth I gastroduodenostomy) and group 2 consisting of 351 patients without a history of previous gastric surgery. Clinical data, operative findings, treatment modalities and prognoses were compared. RESULTS: Group 1 patients required significantly more emergency surgical interventions (p=0.016) and more frequent resection of alimentary necrosis (p=0.007). In the operative findings of those undergoing emergency laparotomy, group 1 had a slightly higher incidence of total gastric necrosis with or without perforation (p=0.388), and a higher incidence of jejunal resection (p=0.001). However, group 1 patients had a relatively lower operative mortality rate compared to group 2 patients (p=0.640). CONCLUSION: Acid-injured patients with a history of previous gastric surgery tended to have a higher incidence of mandatory emergency surgical exploration and resection of the alimentary tract. With early and prompt management, a good survival rate can still be anticipated.

Complete laryngotracheal disruption caused by blunt injury.

BACKGROUND: We reviewed the clinical courses and evaluated the surgical results of 7 patients with complete laryngotracheal disruption caused by blunt injury. METHODS: Seven patients with complete laryngotracheal disruption caused by blunt injury were successfully treated in a 13-year period. Six of the seven incidents involved men younger than 30 years on motorcycles. All but one had intact cutaneous tissue of the neck. Six of seven laryngotracheal disruptions were at the cricotracheal junction and the other was at the junction of second and third tracheal ring. In the emergency departments, 4 of these 7 patients underwent endotracheal intubation and three others underwent tracheostomy after failed intubation. Two of 7 patients underwent delayed surgery (posttrauma day 3 and day 5) because of delayed diagnosis. All patients underwent laryngotracheoplasty with (n = 3) or without (n = 4) concomitant tracheostomy. RESULTS: Total hospital stays ranged from 9 to 28 days (average 15 days). Intensive care unit stay ranged from 2 to 10 days (average 5.8 days). All 7 patients had paralysis of bilateral vocal cords that were revealed by postoperative bronchoscopy. In 3 patients who underwent concomitant tracheostomy, the tracheostomy tubes were removed within 3 to 5 months after surgery. In the other 4 patients who underwent laryngotracheoplasty only, the endotracheal tube was used as an airway support for 2 to 6 days (average 3.5 days). All patients had patent airways. Vocal cord function partially recovered in one side (n = 6) or both sides (n = 1). Their voices were audible but still husky 5 months or 1 year later. CONCLUSIONS: Complete laryngotracheal disruption can be treated by laryngotracheoplasty with or without concomitant tracheostomy, and phonation can be partially recovered.