Follow-up of subjects occupationally exposed to asbestos: MRI and PET scans

MRI and PET scans are not normally used for screening and follow-up of patients following occupational exposure to asbestos. These examinations usually complement the investigation of a parenchymal mass, an effusion or pleural thickening. PET and MRI have an excellent ability to define a parenchymal lesion as malignant (cancer versus rounded atelectasis) or a pleural lesion (mesothelioma versus plaque). MRI distinguishes perfectly the involvement of sub-pleural fat by bronchial carcinoma or mesothelioma. MRI, taking account of its lack of irradiation, could be regarded as suitable for potentially repeated examinations following initial screeing by CT scan. A comparative study of multidetector scanner versus MRI, including diffusion MRI could be, nevertheless, interesting. PET cannot be proposed for the follow up or for screening on account of the irradiation induced and the difficulty of access. Pleural plaques do not take up FDG. There is no specific study of asbestos related fibrosis and there is discordance between studies of other types of pulmonary fibrosis.     

Temporal arteritis in the young

Temporal arteritis in the form of giant cell arteritis (GCA) is common in the elderly but is extremely rare in patients less than 50 years of age. We describe two male patients: one who presented at the age of 31 years with painful, nodular swellings of both temporal arteries and whose temporal artery biopsy demonstrated a non-giant cell panarteritis with mixed inflammatory cell infiltrate typical of juvenile temporal arteritis (JTA); another one, aged 40 years, who presented with headache and cerebral angiography consistent with an intracranial vasculitis and whose temporal artery biopsy confirmed an authentic multinucleated GCA. The first patient spontaneously improved after biopsy and the second patient has responded well to corticosteroid therapy. These two cases exemplify well two distinct but extremely rare forms of temporal arteritis in young patients. A 3rd subset is that associated with a systemic vasculitis. Few cases of JTA have been reported and, to our knowledge, we describe in this report one of the only cases of GCA with central nervous system involvement in the young.     

Bariatric Surgery in Obese Patients with Type 1 Diabetes: Effects on Weight Loss and Metabolic Control

Background

Type 1 diabetes patients, although typically lean, experience an increased prevalence of obesity, and bariatric surgery is considered in severe cases. Bariatric surgery in such patients leads to significant weight loss and decreased insulin requirements; however, effects on glycemic control remain discussed. We assessed, in obese patients with type 1 diabetes, the effects of bariatric surgery upon body weight, body composition, and glycemic control, including the occurrence of hypoglycemic events.

Methods

Thirteen obese patients with type 1 diabetes who underwent bariatric surgery (Roux-en-Y gastric bypass n?=?6, sleeve gastrectomy n?=?7) were matched with obese patients without diabetes and with type 2 diabetes patients during 12 months of follow-up. Outcomes included body weight, DXA-assessed body composition, HbA1c, and incidence of hypoglycemia.

Results

At 12 months, median surgery-induced weight loss was 27.9 % (21.1–33.3), 26.1 % (24.8–29.7), and 27.5 % (21.8–32.1) in patients with type 1 diabetes, type 2 diabetes, and without diabetes, respectively, with no significant differences across the groups. Similar findings were observed for body fat changes. At 12 months, median HbA1c decreased from 8.3 to 7.6 % in type 1 diabetes patients versus 8.0 to 5.9 % in type 2 diabetes patients (P?=?0.04 between the groups). In type 1 diabetes patients, the number of reported minor hypoglycemia increased transiently only at 6 months. Two patients reported severe hypoglycemia (one episode each).

Conclusions

Type 1 diabetes patients benefit from bariatric surgery in terms of weight loss and glycemic control. Close monitoring of insulin therapy appears warranted to prevent minor hypoglycemia in the first months post-surgery.

     

Patterns of arteriosclerotic lesions of the lower extremity in a West Indian population based on angiographic findings and ethnicity

Introduction

This study aimed to determine whether ethnic differences show different patterns of arterial disease in the lower limb.

Methods

A prospective analysis of 100 consecutive patients with 160 lower limb arteriograms was performed looking at the pattern of disease with relation to ethnicity in Trinidad and Tobago.

Results

There were 53 male and 47 female patients with an age range of 43–90 years (mean: 66 years). Of the 100 patients, 45 were of East Indian descent, 36 of Afro-Caribbean descent, 14 of mixed descent and 5 had other backgrounds. There were 32 smokers and 69 diabetics.The most commonly affected artery in East Indians was the anterior tibial artery (ATA, 70%) followed by the peroneal artery (60%), superficial femoral artery (SFA, 60%), posterior tibial artery (PTA, 57%) and tibioperoneal trunk (TPT, 39%). In Afro-Caribbeans, the most commonly affected artery was the ATA (79%) followed by the PTA (74%), peroneal artery (66%) and TPT (55%). The mixed group showed the PTA (85%) to be most diseased followed by the peroneal artery (75%), ATA (70%), SFA (70%), dorsalis pedis artery (DPA, 60%) and TPT (50%). Overall, the most diseased vessel in all groups was the ATA (73%) followed by the PTA (66%), peroneal artery (64%), SFA (59%), TPT (46%), DPA (38%), popliteal artery (31%) and medial plantar artery (MPA, 29%), with the proximal vessels not being affected severely.

Conclusions

Ethnic divisions were only statistically significant (p<0.05) with East Indians showing worse disease in the profunda femoris artery and Afro-Caribbeans showing worse disease in the PTA, DPA and MPA. This suggests that environmental factors may play a significant role in the disease process including smoking and dietary factors rather than purely genetics.     

Unintended consequences of policy change to watchful waiting for asymptomatic inguinal hernias

Introduction

In 2009 the Department of Health instructed McKinsey & Company to provide advice on how commissioners might achieve world class National Health Service productivity. Asymptomatic inguinal hernia repair was identified as a potentially cosmetic procedure, with limited clinical benefit. The Birmingham and Solihull primary care trust cluster introduced a policy of watchful waiting for asymptomatic inguinal hernia, which was implemented across the health economy in December 2010. This retrospective cohort study aimed to examine the effect of a change in clinical commissioning policy concerning elective surgical repair of asymptomatic inguinal hernias.

Methods

A total of 1,032 patients undergoing inguinal hernia repair in the 16 months after the policy change were compared with 978 patients in the 16 months before. The main outcome measure was relative proportion of emergency repair in groups before and after the policy change. Multivariate binary logistic regression was used to adjust the main outcome for age, sex and hernia type.

Results

The period after the policy change was associated with 59% higher odds of emergency repair (3.6% vs 5.5%, adjusted odds ratio [OR]: 1.59, 95% confidence interval [CI]: 1.03–2.47). In turn, emergency repair was associated with higher odds of adverse events (4.7% vs 18.5%, adjusted OR: 3.68, 95% CI: 2.04–6.63) and mortality (0.1% vs 5.4%, p<0.001, Fisher’s exact test).

Conclusions

Introduction of a watchful waiting policy for asymptomatic inguinal hernias was associated with a significant increase in need for emergency repair, which was in turn associated with an increased risk of adverse events. Current policies may be placing patients at risk.     

Genomic insights into abdominal aortic aneurysms

Introduction

An individual’s genetic background plays a significant role in his or her chances of developing an abdominal aortic aneurysm (AAA). This risk is likely to be due to a combination of multiple small effect genetic factors acting together, resulting in considerable difficulty in the identification of these factors.

Methods

Methods for the identification of genetic factors associated with disease are usually based on the analysis of genetic variants in case-control studies. Over the last decade, owing to advances in bioinformatics and laboratory technology, these studies have progressed from focusing on the examination of a single genetic variant in each study to the examination of many millions of variants in a single experiment. We have conducted a series of such experiments using these methods.

Results

Our original methods using candidate gene approaches led to the initial identification of a genetic variant in the interleukin-10 gene associated with AAA. However, further studies failed to confirm this association and highlighted the necessity for adequately powered studies to be conducted, as well as the need for confirmatory studies to be performed, prior to the acceptance of a variant as a risk for disease. The subsequent application of genomic techniques to our sample set, in a global collaboration, has led to the identification of three robustly verified risk loci for AAA in the LRP1, LDLR and SORT1 genes.

Conclusions

Genomic studies of AAA have led to the identification of new pathways involved in the pathogenesis of AAA. The exploration of these pathways has the potential to unlock new avenues for therapeutic intervention to prevent the development and progression of AAA.     

Neuropeptide Y Attenuates Stress‐Induced Bone Loss Through Suppression of Noradrenaline Circuits

Chronic stress and depression have adverse consequences on many organ systems, including the skeleton, but the mechanisms underlying stress‐induced bone loss remain unclear. Here we demonstrate that neuropeptide Y (NPY), centrally and peripherally, plays a critical role in protecting against stress‐induced bone loss. Mice lacking the anxiolytic factor NPY exhibit more anxious behavior and elevated corticosterone levels. Additionally, following a 6‐week restraint, or cold‐stress protocol, Npy‐null mice exhibit three‐fold greater bone loss compared to wild‐type mice, owing to suppression of osteoblast activity. This stress‐protective NPY pathway acts specifically through Y2 receptors. Centrally, Y2 receptors suppress corticotropin‐releasing factor expression and inhibit activation of noradrenergic neurons in the paraventricular nucleus. In the periphery, they act to control noradrenaline release from sympathetic neurons. Specific deletion of arcuate Y2 receptors recapitulates the Npy‐null stress response, coincident with elevated serum noradrenaline. Importantly, specific reintroduction of NPY solely in noradrenergic neurons of otherwise Npy‐null mice blocks the increase in circulating noradrenaline and the stress‐induced bone loss. Thus, NPY protects against excessive stress‐induced bone loss, through Y2 receptor‐mediated modulation of central and peripheral noradrenergic neurons. © 2014 American Society for Bone and Mineral Research.     

Computerized tomography imaging of round atelectasis. Study of a series of 21 patients

AIM: To show and compare to literature CT findings in round atelectasis. MATERIAL AND METHODS: It is a retrospective review of the clinical and radiological files of 21 patients (17 men; 4 women; Mean age: 62), having asbestos exposure (6/21) or pleural history (13/21) and in whom the diagnosis of round atelectasis was performed from 1988 to 1998. This diagnosis was based on the presence of the classical radiological triad: round mass abutting to pleurae, converging bronchovascular markings and pleural thickening adjacent to the mass associated at a one year follow up or three years radiological and clinical follow up or the association with three minors radiological signs. RESULTS: The 25 round atelectasis, 4 bilateral, were localized in the lower lobes (22/25) or upper lobes (3/25) at right (17/25) or left (8/25) side. Minor signs were found as in literature as followed: air bronchograms and centrally indistinct margin (25/25, diffused pleural thickening or pleural plaques (19/25), acute angles with the pleura (18/25), fissures displacement (18/25), main stem bronchus displacement (13/25), calcifications within the plaque (10/25), calcifications within the mass (10/25). A mean of 6.7 signs was found for each lesion. CONCLUSION: More than the major signs of round atelectasis the air bronchogram, the centrally indistinct margin and the presence of one sign of retraction were very frequent. The mean number of signs was 6.7 for every lesion.