Somatosensory evoked potentials are abnormal with plagiocephaly.

BACKGROUND: Deformational plagiocephaly is usually managed conservatively, as it tends to improve over time and with the use of conservative measures. However, before the year 2017 we operated on patients with severe plagiocephaly and neurological symptoms at the Helsinki Cleft Palate and Craniofacial Center. METHODS: Of the 20 infants with severe deformational plagiocephaly and neurological symptoms referred to us between 2014 and 2016, 10 underwent cranioplasty open reshaping of the posterior cranial vault. The parents of the last 10 patients were given information on the natural history of the condition and the patients were followed up with an outpatient protocol. The aim of this study was to gain information on the brain electrophysiology and recovery of patients after total cranial vault reconstruction by measuring the electroencephalogram (EEG) somatosensory evoked potentials (SEP; median nerve). RESULTS: Of the 10 participants in the operation arm, six had abnormal SEP at least on the affected cerebral hemisphere and all SEPs were recorded as normal when controlled postoperatively. In the follow-up arm, eight out of 10 participants had abnormal SEP at the age of approximately 24 months, and all had normalized SEPs at control visits. CONCLUSION: Our data suggest that cranioplasty open reshaping of the posterior cranial vault did not affect abnormal SEP-EEG recordings. We have abandoned the operations in deformational plagiocephaly patients due to findings suggesting that expanding cranioplasty is not beneficial for brain function in this patient group.

Contralateral prophylactic mastectomy at the time of delayed microvascular breast reconstruction adversely affects patient-reported outcomes: A retrospective cohort study.

PURPOSE: An increasing number of women with unilateral breast cancer are seeking bilateral mastectomies and reconstruction. At our centre, many women who have undergone previous unilateral therapeutic mastectomy request contralateral prophylactic mastectomy (CPM) at the time of delayed reconstruction. These mixed timing reconstructions are particularly challenging as patients have an immediate reconstruction on one side and delayed reconstruction on the other, which may result in asymmetry. This retrospective cohort study evaluates patient-reported satisfaction following mixed timing breast reconstruction and compares them to unilateral delayed reconstruction. METHODS: One hundred and forty-one patients who underwent successful deep inferior epigastric artery perforator (DIEP) flap breast reconstruction and completed baseline and 12-month BREAST-Qs were included in the study. Patient-reported outcomes following bilateral mixed timing reconstruction (n = 56) were compared to those of unilateral delayed reconstruction (UDR) without CPM (n = 85). RESULTS: Women who sought CPM were significantly younger and had lower annual incomes when compared with those who underwent unilateral reconstruction. Mixed timing reconstruction was associated with significantly lower levels of breast satisfaction and psychosocial function as compared to UDR at 12 months post-operatively. BREAST-Q scores (18 months) were available for 75 patients in the cohort and indicated that this decreased breast satisfaction and psychosocial impairment was sustained in the longer-term. CONCLUSIONS: Patients who seek CPM at the time of delayed reconstruction should be advised that this is associated with lower levels of breast satisfaction and psychosocial well-being as compared to unilateral delayed breast reconstruction.

HHV-6 and HHV-7 antigenemia related to CMV infection after liver transplantation.

BACKGROUND: Betaherpesviruses human herpesvirus-6 and -7 (HHV-6, HHV-7), which are closely related to cytomegalovirus (CMV), have been reported in transplant patients. In this retrospective study, we investigated the occurrence of HHV-6 and HHV-7 antigenemia in relation to symptomatic CMV infection after liver transplantation. METHODS: Sample material from 64 adult liver transplant recipients was included in the study. The patients were monitored weekly for CMV, HHV-6, and HHV-7. CMV infections were diagnosed by pp65-antigenemia and viral cultures. Concomitantly HHV-6 and HHV-7 antigens were demonstrated in peripheral blood mononuclear cells by monoclonal antibodies against both variants A and B and immunoperoxidase staining. Altogether 540 post-transplant blood specimens were analyzed. RESULTS: Nineteen patients (30%) developed symptomatic CMV pp65 antigenemia during the first 3 months (mean 33 days, range 5-62 days) post-transplantation and were treated with intravenous ganciclovir. Concurrent HHV-6 antigenemia was detected in 16/19 (median 9 days, range 6-24 days) and HHV-7 antigenemia 15/19 patients (median 17 days, range 5-58 days) after transplantation. HHV-6 appeared before CMV in most cases (12/16), HHV-7 usually together with CMV. In those cases that HHV-6 preceded CMV antigenemia, it also was a possible cause of graft dysfunction. HHV-7 and CMV were so closely overlapping, that no symptoms could solely be linked with HHV-7. CONCLUSION: HHV-6 and HHV-7 antigenemia usually occurred together with symptomatic CMV infection after liver transplantation. HHV-6 preceded CMV, but HHV-7 appeared together with CMV. Further investigation of the clinical significance of HHV-6 and HHV-7 antigenemia in organ transplant patients is necessary.

Pretransplant human herpesvirus 6 infection of patients with acute liver failure is a risk factor for posttransplant human herpesvirus 6 infection of the liver.

BACKGROUND: Acute liver failure (ALF) is a significant cause of liver transplantation. We have previously reported that human herpesvirus-6 (HHV-6) was found in most livers of patients with ALF of unknown origin ending up with liver transplantation. In this study, we investigated the posttransplant HHV-6 infection of the liver graft in these patients. METHODS: Thirty-two patients transplanted due to ALF were included in this retrospective study. Twelve of the 15 patients with unknown cause and four of 17 patients with a known cause of ALF had HHV-6 antigens in the explanted liver. Altogether, 18 patients had some pretransplant evidence of HHV-6. After transplantation, the patients were frequently monitored for the viruses, and biopsy histology was performed in every case of graft dysfunction. HHV-6 was demonstrated in liver tissue by immunohistochemistry. RESULTS: During the follow-up of 6 months, hepatic HHV-6 infection was demonstrated in 9 of the 18 patients, at a mean 19 days (6-38 days) after transplantation. All patients with posttransplant HHV-6 showed graft dysfunction. In biopsy histology, seven out of these nine patients demonstrated viral infection, one of them also having CMV antigens in the liver. None of those patients without evidence of pretransplant HHV-6 showed HHV-6 in the posttransplant biopsies. Posttransplant HHV-6 was not treated and the virus had no effect on 1-year patient or graft survivals. CONCLUSION: Pretransplant hepatic HHV-6 infection of patients with ALF is a risk factor for posttransplant HHV-6 infection and liver dysfunction, but has no effect on 1-year graft or patient survival.

HHV-6 DNA in peripheral blood mononuclear cells after liver transplantation.

BACKGROUND: Human herpesvirus-6 (HHV-6) infections have been reported after liver transplantation. In this study, the detection of HHV-6 DNA in peripheral blood mononuclear cells (PBMC) was compared with HHV-6 antigenemia in liver transplant patients. OBJECTIVES: Forty-three adult liver recipients were frequently monitored by HHV-6 antigenemia test, which detects the viral antigens in PBMC, but is rather qualitative than quantitative. STUDY DESIGN: From the same PBMC specimens HHV-6 DNA was demonstrated by in situ hybridization using a biotinylated probe and quantified as positive cells/10, 000 PBMC. Altogether 330 blood specimens were analyzed. RESULTS: During the first 6 months (mean 12 days) after transplantation, 35/43 patients developed HHV-6 antigenemia. Concurrently, HHV-6 DNA-positive cells with mean peak number of 661(+/-574)/10, 000 were detected in 33/35 patients. Seven patients received ganciclovir treatment because of concurrent CMV infection with mean peak number of HHV-6 DNA-positive cells 381(+/-336) before and 34(+/-59)/10, 000 after the treatment (p = 0.03). All CMV infections responded to ganciclovir, but HHV-6 DNAemia disappeared slowly, within 79 days (mean 36 days). Without antivirals, HHV-6 DNAemia/antigenemia lasted usually longer. CONCLUSIONS: Detection of HHV-6 DNA in PBMC correlated well with HHV-6 antigenemia, and may be used in the monitoring of transplant patients.

Human herpesvirus-6 and acute liver failure.

BACKGROUND: In patients with acute liver failure (ALF) of unknown cause, viral infections are believed to be involved. This study investigates the involvement of human herpesvirus-6 (HHV-6). METHODS: Thirty-two patients with ALF who underwent transplantations during a 6-year period were studied for viruses in biopsies from their explanted livers. Non-A to non-E hepatitis (unknown) ALF was the reason for transplantation in 15 patients, and another 17 patients with a known disease from the same time period served as controls. The explanted livers were examined for hepatitis viruses and other possible viral agents. HHV-6 antigens were demonstrated in the livers and blood mononuclear cells by immunoperoxidase staining. RESULTS: Of the 15 patients with ALF of unknown cause, 12 (80%) demonstrated HHV-6 antigens in the liver. Most of these patients (10/12) also demonstrated HHV-6 antigenemia. The predominant histologic finding of HHV-6 infection was moderate to severe portal lymphocytic infiltration. HHV-6 was found in 4 of 17 control patients, and cytomegalovirus was found in 2 of 17 control patients (in the blood and explanted liver). No other viruses were found in the livers of the patients with ALF. CONCLUSIONS: HHV-6 was found in most explanted livers of patients with ALF of unknown cause. HHV-6 antigenemia was associated with HHV-6 antigens in the liver. Only a few control patients displayed HHV-6 in the liver. These observations indicate that HHV-6 may be one of the causes of ALF.

Human herpesvirus-6 infection is associated with adhesion molecule induction and lymphocyte infiltration in liver allografts.

BACKGROUND/AIMS: Human herpesvirus-6 (HHV-6) infection has been recently described in liver transplants. HHV-6 may infect the transplant and cause graft dysfunction. Some association between HHV-6 and rejection has also been recorded. We have now investigated the possible involvement of HHV-6 in the intragraft immunological processes, adhesion molecules induction and lymphocyte activation. METHODS: HHV-6 was detected in liver biopsies of 19 patients transplanted in the period from 1996 to 2000. Patients with other infections or rejection were excluded from the study. Finally, 19 biopsies of eight allografts with pure HHV-6 infection were available. Adhesion molecules (ICAM-1, VCAM-1, ELAM-1) and their ligands (LFA-1, VLA-4, sLeX) and lymphoid activation markers (MHC class II, IL-2R) were demonstrated in liver biopsies by immunohistochemistry. Five biopsies from patients with normal graft function and without rejection or infection were used as controls for immune staining, and ten biopsies with acute rejection but without infection were used as positive controls. RESULTS: Biopsy histology demonstrated mild to moderate lymphocyte infiltration associated with HHV-6 infection. HHV-6 significantly (P < or = 0.05) increased the vascular expression of ICAM-1 and VCAM-1, and the number of graft infiltrating lymphocytes positive for LFA-1, VLA-4 and class II antigens. A total of 3/8 grafts developed chronic rejection. CONCLUSIONS: HHV-6 infection increased adhesion molecule expression and lymphocyte infiltration in liver allografts.