Anaerobic mediastinitis complicating median sternotomy

Two cases of mediastinitis and bacteremia caused by Bacteroides species following median sternotomy are described. In both patients, purulent sternal drainage and signs of systemic toxicity led to the diagnosis. Surgical reexploration and administration of appropriate antibiotics effected clinical cure. Although there is only a single previous case of anaerobic mediastinitis following median sternotomy incision reported, these two cases suggest that this unusual infection may not be so rare as previously thought.     

The course of diabetic retinopathy following cataract surgery in eyes previously treated by laser photocoagulation.

The course of diabetic retinopathy following extracapsular cataract extraction with posterior chamber lens implantation in eyes previously treated by laser photocoagulation for diabetic retinopathy was retrospectively studied in 33 eyes (33 patients). In 20 eyes (61%) there was no change in the retinal status postoperatively. In 13 (39%) there was postoperative progression of diabetic retinopathy compared with the fellow non-operated eye, in which progression occurred in nine eyes (27%). The severity of the preoperative status affected the incidence of progression. Four eyes (12%) developed complications of diabetic retinopathy--that is, rubeosis iridis and vitreous haemorrhage--which regressed after lasering. Cystoid macular oedema developed in 13 eyes (39%) and its incidence varied according to the postoperative course of diabetic retinopathy. The majority of the eyes showed a postoperative improvement in vision.     

Destructive arthritis in a patient with Haim-munk syndrome

Haim-Munk and Papillon-Lefèvre are 2 closely related syndromes, inherited in an autosomal recessive pattern, manifested by palmoplantar keratoderma and early, destructive periodontitis. Recently, mutations in the cathepsin C gene have been recognized in both syndromes. We describe a patient with Haim-Munk syndrome (palmar plantar keratosis and periodontitis) and destructive arthritis of the wrists and shoulder joints, an association that has not been previously described.     

The prodrome: a prominent yet overlooked pre-attack manifestation of familial Mediterranean fever

OBJECTIVE: To identify and characterize pre-attack symptoms (prodrome) in patients with familial Mediterranean fever (FMF). METHODS: Forty-eight patients with FMF whose attacks are preceded by a prodromal period composed the study population. Clinical, demographic, and genetic characteristics of the study group were compared to those of a control group of 48 patients with FMF whose attacks begin without a premonitory phase. Patients of both groups were recruited consecutively, during their routine followup visit to the FMF clinic. RESULTS: A prodrome was found to be a common manifestation of FMF, experienced by about 50% of the patients. Overall, demographic, clinical, and genetic variables were comparable between study and control groups. In affected patients prodrome recurs in most attacks, lasts a mean of 20 hours, and manifests with either a mildly unpleasant sensation at the site of the forthcoming spell (discomfort prodrome), or with a spectrum of physical, emotional, and neuropsychological complaints (variant prodrome). The 2 types of prodromata are frequently accompanied by a host of constitutional symptoms. CONCLUSIONS: A prodromal period heralding attacks is a newly defined and reliable FMF manifestation that reproducibly predicts attacks and may help prevent attacks and elucidate the pathogenesis of the disease.     

Halofuginone inhibits NF-kappaB and p38 MAPK in activated T cells

Halofuginone, a low molecular weight plant alkaloid, inhibits collagen alpha1 (I) gene expression in several animal models and in patients with fibrotic disease, including scleroderma and graft-versus-host disease. In addition, halofuginone has been shown to inhibit angiogenesis and tumor progression. It was demonstrated recently that halofuginone inhibits transforming growth factor-beta (TGF-beta), an important immunomodulator. The present study was undertaken to explore the effects of halofuginone on activated T cells. Peripheral blood T cells were activated by anti-CD3 monoclonal antibodies in the absence and presence of halofuginone and assessed for nuclear factor (NF)-kappaB activity, production of tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma), T cell apoptosis, chemotaxis, and phosphorylation of p38 mitogen-activated protein kinase (MAPK). A delayed-type hypersensitivity (DTH) model was applied to investigate the effect of halofuginone on T cells in vivo. Preincubation of activated peripheral blood T cells with 10-40 ng/ml halofuginone resulted in a significant dose-dependent decrease in NF-kappaB activity (80% inhibition following incubation with 40 ng halofuginone, P = 0.002). In addition, 40 ng/ml halofuginone inhibited secretion of TNF-alpha, IFN-gamma, interleukin (IL)-4, IL-13, and TGF-beta (P < 0.005). Similarly, halofuginone inhibited the phosphorylation of p38 MAPK and apoptosis in activated T cells (P = 0.0001 and 0.005, respectively). In contrast, T cell chemotaxis was not affected. Halofuginone inhibited DTH response in mice, indicating suppression of T cell-mediated inflammation in vivo. Halofuginone inhibits activated peripheral blood T cell functions and proinflammatory cytokine production through inhibition of NF-kappaB activation and p38 MAPK phosphorylation. It also inhibited DTH response in vivo, making it an attractive immunomodulator and anti-inflammatory agent.     

Response of Thai hospitals to the tsunami disaster

The disaster caused by the tsunami of 26 December 2004 was one of the worst that medical systems have faced. The aim of this study was to learn about the medical response of the Thai hospitals to this disaster and to establish guidelines that will help hospitals prepare for future disasters. The Israeli Defense Forces (IDF) Home Front Command (HFC) Medical Department sent a research delegation to Thai hospitals to study: (1) pre-event hospital preparedness; (2) patient evacuation and triage; (3) personnel and equipment reinforcement; (4) modes used for alarm and recruitment of hospital personnel; (5) internal reorganization of hospitals; and (6) admission, discharge, and secondary transfer (forward management) of patients. Thai hospitals were prepared for and drilled for a general mass casualty incident (MCI) involving up to 50 casualties. However, a control system to measure the success of these drills was not identified, and Thai hospitals were not prepared to deal with the unique aspects of a tsunami or to receive thousands of victims. Modes of operation differed between provinces. In Phang Nga and Krabi, many patients were treated in the field. In Phuket, most patients were evacuated early to secondary (district) and tertiary (provincial) hospitals. Hospitals recalled staff rapidly and organized the emergency department for patient triage, treatment, and transfer if needed. Although preparedness was deficient, hospital systems performed well. Disaster management should focus on field-based first aid and triage, and rapid evacuation to secondary hospitals. Additionally, disaster management should reinforce and rely on the existing and well-trusted medical system.     

Multiple branch retinal arteriolar occlusions associated with smallpox vaccination

We describe a rare combination of multiple multiple branch retinal arteriolar occlusions (BRAO) and encephalopathy, which developed in an adult male 10 days after smallpox vaccination. A 53-year-old physician presented with sudden temporal visual field loss in the left eye. Ten days earlier he had received a smallpox vaccination. Hyperbaric oxygen was administered because of suspected BRAO. Examination on day 3 revealed a decrease in visual acuity and loss of visual field. Fundoscopy of the left eye disclosed a retinal infarct in the inferior macula and multiple cotton wool spots over the entire posterior pole. Fluorescein angiography showed delayed arterial filling and multiple non-perfused areas. Magnetic resonance imaging of the brain disclosed white matter focal lesions. Neurological examination was normal. Audiological examination revealed mild hearing loss caused by an old phonic trauma. A combination of intravenous methylprednisolone and immunoglobulins, recommended for the treatment of Susac syndrome, was administered. At the follow-up visit 3 months later, visual acuity in the left eye improved, fundoscopy showed resolution of the cotton wool spots and temporal disc pallor, and the visual field was substantially restored.     

ZnT-1 protects HL-1 cells from simulated ischemia–reperfusion through activation of Ras–ERK signaling

Activation of ERK signaling may promote cardioprotection from ischemia-reperfusion (I/R) injury. ZnT-1, a protein that confers resistance from zinc toxicity, was found to interact with Raf-1 kinase through its C-terminal domain, leading to downstream activation of ERK. In the present study, we evaluated the effects of ZnT-1 in cultured murine cardiomyocytes (HL-1 cells) that were exposed to simulated-I/R. Cellular injury was evaluated by lactate dehydrogenase (LDH) release and by staining for pro-apoptotic caspase activation. Overexpression of ZnT-1 markedly reduced LDH release and caspase activation following I/R. Knockdown of endogenous ZnT-1 augmented the I/R-induced release of LDH and increased caspase activation following I/R. Phospho-ERK levels were significantly increased following I/R in cells overexpressing ZnT-1, while knockdown of ZnT-1 reduced phospho-ERK levels. Pretreatment of cells with the MEK inhibitor PD98059 abolished the protective effect of ZnT-1 following I/R. Accordingly, a truncated form of ZnT-1 lacking the C-terminal domain failed to induce ERK activation and did not protect the cells from I/R injury. In contrast, expression of the C-terminal domain by itself was sufficient to induce ERK activation and I/R protection. Interestingly, the C-terminal of the ZnT-1 did not have protective effect against the toxicity of zinc. In the isolated rat heart, global ischemic injury rapidly increased the endogenous levels of ZnT-1. However, following reperfusion ZnT-1 levels were found to be decreased. Our findings indicate that ZnT-1 may have important role in the ischemic myocardium through its ability to interact with Raf-1 kinase.