Does less surgical trauma result in better outcome in management of iatrogenic tracheobronchial laceration?

BACKGROUND: Iatrogenic tracheobronchial injury is a rare, but severe complication of endotracheal intubation. Risk factors are emergency intubation, percutaneous dilatational tracheostomy and intubation with double lumen tube. Regarding these procedures, underlying patients often suffer from severe comorbidities. The aim of this study was to evaluate the results of a standardized treatment algorithm in a referral center with focus on the surgical approach. METHODS: Sixty-four patients with iatrogenic tracheal lesion were treated in our department by standardized management adopted to clinical findings between 2003 and 2019. Patients with superficial laceration were treated conservatively. In the case of transmural injury of the tracheal wall and necessity of mechanical ventilation, patients underwent surgery. We decided on a cervical surgical approach for lesions limited to the trachea. In case of involvement of a main bronchus we performed thoracotomy. Data were evaluated retrospectively. RESULTS: In 19 patients the tracheal lesion occurred in elective intubation and in 17 patients during emergency intubation. In 23 cases a tracheal tear occurred during percutaneous dilatational tracheostomy and in three patients at replacement of a tracheostomy tube. Two patients received laceration during bronchoscopy. Twenty-nine patients underwent surgery with cervical approach and 14 underwent thoracotomy. There was no difference in the mortality of these groups. Treatment of tracheal tear was successful in 62 individuals. Nine patients died of multi organ dysfunction syndrome (MODS), two of them during surgery. CONCLUSIONS: Iatrogenic tracheal laceration is a life-threatening complication and the mortality after tracheal injury is high, even in a specialized thoracic unit. Conservative management in patients with superficial tracheal lesion is a feasible procedure. In case of complete laceration of tracheal wall, surgical therapy is recommendable, whereby several approaches of surgical management seem to be equivalent.

Role of BK polyomavirus (BKV) and Torque teno virus (TTV) in liver transplant recipients with renal impairment.

PURPOSE: Renal impairment is a common complication after liver transplantation (LT). While BK polyomavirus (BKV) has been linked to renal failure in kidney transplant recipients, Torque teno virus (TTV) is a surrogate marker for immunosuppression that does not have a clear association with any human disease. The impact of BKV and TTV on renal impairment after LT is unknown. METHODOLOGY: In this retrospective study, urine and serum samples from 136 liver transplant recipients were screened for BKV and TTV by quantitative PCR. In addition, serum was screened for BKV-specific antibodies and the VP1 typing region was sequenced for BKV genotyping. All parameters were correlated with clinical data.Results/Key findings. BK viruria was detected up to 21 years after transplantation in 16.9 % of cases. BK viraemia was detected in 8.7 % of patients with BK viruria up to 4 years after LT. BKV-specific antibodies were detected in 93.6 % of all LT recipients and correlated with BKV viral load in urine. There was no correlation between renal impairment and the detection of BK DNA in urine (OR 0.983). TTV DNA was detected in 84.6 % of serum samples and in 66.6 % of urine samples. The TTV viral load in serum correlated with the BKV viral load but had no impact on renal impairment. CONCLUSION: Our data indicate that the detection of BKV and TTV is not a risk factor for renal impairment after LT. A correlation of TTV and BKV viral load seems to be an indicator for the immune status of the host.

HBV reactivation in allogeneic stem cell transplant recipients: Risk factors, outcome, and role of hepatitis B virus mutations.

Hepatitis B virus (HBV) reactivation (HBVr) in recipients of allogeneic hematopoetic stem cells (aHSCs) appears heterogeneously with respect to its frequency, manifestation, and outcome. The aim of this study was to present data from a large German cohort of recipients of aHSC transplantation (aHSCT), focusing on the incidence of HBVr in antibody to hepatitis B core antigen (anti-HBc)-positive aHSCT recipients, its clinical outcome, and the role of mutations in HBV. Between 2005 and 2015, 1,871 patients received aHSCT at University Hospital Essen. A follow-up of at least 6 months after transplant was available in 55 patients who were anti-HBc-positive; clinical and virologic data were analyzed. The HBV genome was sequenced with next generation technology from serum samples of 8 patients with HBVr. Thirteen out of 55 (23.6%) patients developed HBVr at a median of 26 months after aHSCT. After initiation of antiviral treatment, complete HBV DNA suppression was achieved in 7/10 (70%) patients 1 to 40 months after HBVr. Nine of 13 patients had increased alanine aminotransferase; 3 patients had compromised coagulation and model for end-stage liver disease scores of 18-27, and 1 of these patients died due to liver failure 5 weeks after HBVr. As a risk factor for HBVr, we identified anti-HBc signal to cut-off ration (S/CO) ≥7.5 before transplantation. Complete HBV DNA suppression was achieved in 7/10 patients; therapy-relevant mutations were found in 1 patient. In 4/8 patients, immune escape mutations were detected either as majority or minority variants. Conclusion: HBVr is common in anti-HBc-positive aHRCT recipients and can lead to severe hepatitis with compromised coagulation. The level of anti-HBc S/CO before transplantation is a risk factor for HBVr. Complete virologic response under adequate antiviral treatment could not be achieved in all patients. (Hepatology Communications 2017;1:1014-1023).

GRO-alpha: a potential marker for cancer and aging silenced by RNA interference.

Age-regulated genes may serve as markers of aging, enabling assessment of physiological aging independent of chronological age. One gene with transcripts that increase in abundance with age in human organs, inter alia in epithelial skin cells, is the chemokine growth-regulated protein alpha (GRO-alpha). When chemokines, such as GRO-alpha, become disregulated so that they are chronically expressed, tissue damage, angiogenesis, and tumorigenesis can follow. To consider the role of GRO-alpha as a potential marker for aging and cancer, we compared the transient knockdown of GRO-alpha by RNA interference in the human sebaceous gland cell line SZ95, which behaves like normal human sebocytes, and in the melanoma cell line A375, which originates from a primary human tumor. The reduced GRO-alpha RNA expression, of about 75% in SZ95 sebocytes and 58% in A375 melanoma cells, has functional consequences in normal aged cells and in cancer cells. Silencing of the proangiogenic chemokine GRO-alpha is proportionally correlated with interleukin-6 (IL-6), IL-8 and vascular endothelial growth factor secretion in both cell types. Thus, GRO-alpha may be a novel diagnostic marker for age-related pathology, including cancer.

[Two cases of frontal fibrosing alopecia in postmenopausal women]. / Zwei Fälle einer Frontalen fibrosierenden Alopezie in der Postmenopause.

Frontal fibrosing alopecia (FFA) is an uncommon, slowly progressive, cicatricial alopecia which mainly affects postmenopausal women. It is considered to be a variant of lichen planopilaris. We describe two postmenopausal women who developed over 11 and 24 months an asymptomatic atrophic alopecia, restricted to the frontal hairline. The diagnosis of FFA was confirmed by biopsy showing a perifollicular lymphocytic infiltrate with fibrosis. Topical corticosteroids, in one case combined with minoxidil, administered for 3 months arrested the hair loss. The treatment of FFA is often difficult. In most cases, the disease resolves spontaneously after several years. Immunomodulators such as corticosteroids and calcineurin antagonists should be tried in the early stage of FFA (frontal effluvium with perifollicular erythema) in order to arrest the disease in its inflammatory phase.