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Recent eLetters

Displaying 11-20 letters out of 389 published

  1. A Canadian continued care prescription

    The paper by Morecraft et al. on the emergency supply of prescription medications provides a number of important insights into issues with continuity of prescribed medication in an ambulatory population. The legislative framework in England appears to allow the provision of prescription only medications in an emergency but seems to stop short of a truly satisfactory solution to this important public health issue. In Manitoba, Canada we have created a legislative framework that slightly extends the provisions allowed in England and solves many, but not all, of the problems raised in the paper. In 2002 Manitoba was the first jurisdiction in Canada to formally address the issue of prescriber inaccessibility by establishing a collaborative agreement between the regulatory bodies for pharmacy and medicine to allow pharmacists to refill these prescriptions. These "continued care" provisions were expanded to include nurse prescribers in 2006 [1] and further entrenched in the Pharmaceutical Act (2006) and the Manitoba Pharmaceutical Regulations (2013).[2,3] These regulations now authorize pharmacists to continue chronic prescriptions by acting as prescriber in urgent situations to meet the care and medication needs of the patient. The prescription can then be filled in an amount that is not in excess of the original fill. To ensure appropriate feedback, the original prescriber must be notified of this action. Manitoba has a universal insurance program for prescription medication and all pharmacies have access to the complete prescribing history of all prescriptions filled in the province. Even broader provisions are also in place in true emergencies such as when natural disasters occur.[3] Unfortunately, compensation for all these services is limited to the normal product based fees for providing prescriptions but does avoid the "loaning" situation described by Morecraft et al. We watch with interest for further developments and approaches to ensuring that the pharmacotherapeutic health needs of patients are met in the most seamless and efficient way possible. Clearly on both sides of the ocean, community pharmacists have a key role in achieving this goal.

    1. The College of Physicians and Surgeons of Manitoba, The College of Registered Nurses of Manitoba and The Manitoba Pharmaceutical Association Joint Statement: Continued Care Prescriptions from Practitioners. April 2006. Available online at: http://mpha.in1touch.org/uploaded/web/Legislation/Continued-Care- Joint-Statement-April-2006-09.pdf (accessed 30th July 2015).

    2. The Pharmaceutical Act. December 2006. Available online at: http://web2.gov.mb.ca/laws/statutes/2006/c03706e.php (accessed 30th July 2015)

    3. Manitoba Pharmaceutical Regulations. July 2013. Available online at: http://mpha.in1touch.org/uploaded/web/New%20Pharmaceutical%20Act/July%203,%202013%20Pharmaceutical%20Regulations.pdf (accessed 30th July 2015)

    Conflict of Interest:

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  2. Harmful consumption of alcohol among people aged 50 or over in England

    Dear Sir,

    I read with interest the paper on socioeconomic determinants of risk of harmful alcohol drinking among people aged 50 or over in England [1]. The study found that "harmful drinking in later life is more prevalent among people who exhibit a lifestyle associated with affluence" and suggests that harmful drinking may constitute a hidden problem. It should be noted that harmful drinking was defined only in terms of alcohol consumption above a certain threshold [2].

    Coincidentally, another study using the same dataset was also published recently [3]. This study followed a cohort over a 10 year period and did not find an association between any pattern of current alcohol consumption and poor self-rated health. Drinking above recommended guidelines is more prevalent among affluent people aged 50 or over but this does not predict poor self-rated health 10 years later.

    Yours sincerely

    Martin Frisher, Reader in Health Services Research, School of Pharmacy, Keele University, Staffs ST5 5BG Email:m.frisher@keele.ac.uk

    References

    1 Iparraguirre J. Socioeconomic determinants of risk of harmful alcohol drinking among people aged 50 or over in England. BMJ Open 2015;5:e007684. doi:10.1136/bmjopen-2015-007684

    2. Department of Health. Sensible drinking: report of an inter- departmental working group. London, UK, 1995.

    3. Frisher M, Mendonca M, Shelton N, Pikhart H, de Oliveira C, Holdsworth C. Is alcohol consumption in older adults associated with poor self-rated health? Cross-sectional and longitudinal analyses from the English longitudinal study of ageing. BMC Public Health BMC Public Health (2015) 15:703 DOI 10.1186/s12889-015-1993-x

    Conflict of Interest:

    None declared

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  3. Provision of iron to COPD patients

    Nickol et al. presents an interesting study examining the prevalence of iron deficiency in chronic obstructive pulmonary disease (COPD) and its associations with clinical phenotypes.1 Iron deficiency was observed in 18% of COPD patients and 5% of controls. Extrapolating from other chronic diseases, Nickol et al. suggests that intravenous iron therapy should be explored as a novel therapeutic option in COPD. Prior investigation advises restraint on clinicians in the actual adoption of this potential therapy. Iron metabolism is recognized to participate in the pathogenesis of cancer.2 The supplementation of iron can impact carcinogenesis by reversing host defenses which limit iron required for the growth and replication of neoplastic cells.3,4 An increased availability of iron to cells following supplementation accordingly increases the incidence of cancers. The overwhelming majority of COPD patients are either ex-smokers or current smokers. This population is defined to be at increased risk for numerous cancers.5 Independent of smoking, COPD also is a risk factor for lung cancer.6 Iron supplementation in this population would potentially increase the incidence of all neoplasms associated with smoking but particularly lung cancer. Further research is absolutely essential prior to any use of iron as a treatment in COPD.

    References 1. Nickol AH, Frise MC, Cheng HY, et al. A cross-sectional study of the prevalence and associations of iron deficiency in a cohort of patients with chronic obstructive pulmonary disease. BMJ Open 2015; 5:e007911 2. Stevens RG, Cologne JB, Nakachi K, et al. Body iron stores and breast cancer risk in female atomic bomb survivors. Cancer Sci 2011; 102:2236-40 3. Yano T, Obata Y, Yano Y, et al. Stimulating effect of excess iron feeding on spontaneous lung tumor promotion in mice. Int J Vitam Nutr Res 1995; 65:127-31 4. Ilsley JN, Belinsky GS, Guda K, et al. Dietary iron promotes azoxymethane-induced colon tumors in mice. Nutr Cancer 2004; 49:162-9 5. Carter BD1, Abnet CC, Feskanich D, et al. Smoking and mortality-- beyond established causes. N Engl J Med 2015; 372:631-40 6. Houghton AM. Mechanistic links between COPD and lung cancer. Nat Rev Cancer 2013; 13:233-45.

    Conflict of Interest:

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  4. Under-use of Statins is also linked with duration of therapy and the use of concomitant drugs.

    It is well-known that the statin use, even for secondary prevention decreases over time; at the end of 5 years the compliance is less than 50%. Moreover, as the number of drugs a patient should take increases, the number of drugs the patient actually takes decreases.

    It would have been very informative/interesting to report (In the elegant longitudinal study by Catriona Murphy et al.), the correlation between the use of statin and the duration of the disease (duration of the use of statin) and the number of concomitant drugs used by the patients.

    The authors need to be congratulated for documenting the poor use of evidence-based therapy (with cheap and well-tolerated drug) even in the rich-economy country.

    Conflict of Interest:

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  5. Burning incense stick is equally pernicious

    Like second hand smoke, burning the incense ( a common practice in India, particularly as a ritual at temples and at religious ceremonies) is also a source of indoor pollution. It is documented to cause inflammation of the human lung cells ( A study from University of North Carolina, USA, 2013). In the past, already respiratory symptoms, headaches, exacerbation of the cardiovascular diseases and changes in the lung-cell functions are well documented.It is timely that ban on incense production and its use be enforced.

    Conflict of Interest:

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  6. Letter to the Editor: The need for and provision of intrathecal baclofen therapy for the management of spasticity in England: an assessment of the Hospital Episode Statistics database

    Letter to the Editor: The need for and provision of intrathecal baclofen therapy for the management of spasticity in England: an assessment of the Hospital Episode Statistics database

    Xiulu Ruan, MD, Adjunct Clinical Associate Professor of Anesthesia (corresponding author) Dept. of Anesthesiology, Louisiana State University Health Science Center 1542 Tulane Ave. New Orleans, LA 70112

    Alan David Kaye, MD, Ph.D., Professor and Chairman of Anesthesia Dept. of Anesthesiology, Louisiana State University Health Science Center 1542 Tulane Ave. New Orleans, LA 70112

    Word Count Without References: 695

    We read with interest the article by Narendran and colleagues, "The need for and provision of intrathecal baclofen therapy for the management of spasticity in England: an assessment of the Hospital Episode Statistics database" published on June 30, 2015 in BMJ Open (1).

    First, we would like to point out that the statement, "Baclofen is well absorbed orally, but because of its hydrophilic nature, it crosses the blood-brain barrier poorly." is somewhat inaccurate. It is believed that the transport of baclofen may be carrier mediated (2, 3). Therefore, despite its unfavorable physicochemical properties, baclofen is therapeutically active following oral administration. In this regard, it is true that intrathecal baclofen therapy (ITB) has evolved into an effective alternative treatment for severe spasticity, especially in patients with spinal cord injury and multiple sclerosis, as Narendran et al. have suggested.

    We believe the reason for the observed gap between the need for and provision of ITB is multifactorial. Our speculation is that the challenging and tedious IT baclofen trial protocols can be one of the reasons. It is well accepted that prior to permanent ITB pump placement, a trial should be performed to document efficacy of spinal baclofen (4, 5).

    Usually, the candidate is admitted inpatient to the hospital, an intrathecal bolus injection of a dose of baclofen between 50 mcg and 100 mcg is given (6), a physician or physical therapist performs focused serial neuromuscular examinations, using commonly accepted spasticity rating scale, i.e., the Ashworth Scale, or the Modified Ashworth Scale (7), to assess the reduction of spasticity, following the IT baclofen bolus. Trialing for baclofen is usually performed as a single shot bolus. However, in patients with severe hemiparetic spasticity or in patients where weakness in the unaffected limb might significantly affect quality of life, single shot bolus trialing technique may be inadequate. In these patients, placement of a temporary intrathecal catheter and inpatient admission may be a more effective trial method (4).

    One of the authors (XR) has performed an outpatient baclofen epidural infusion trial with significant positive result (5). We believe such a trialing method offers the patients and their caregivers the opportunity to experience and to observe the therapeutic change from a functional point of view, i.e., how they perform with their activities of daily living (ADL). There were reported cases of worsening ambulation or transfers following permanent ITB pump placement following ITB bolus trial, as some of the tonicity were used by patients to perform pivot transfer or assist ambulation, when their lower extremities became totally flaccid with ITB infusion, they lost their ambulating abilities (8). This underscores the importance of performing a thorough evaluation, including functional improvement during a patients' ADL, rather than a mere reduction of Ashworth score.

    Regardless what trialing method, it will require a team effort of the treating physician, physical therapist, implanting physician, the patient, and the patient's family members to conduct such a trial before deciding on the candidacy for the patient to receive a permanent ITB pump. Therefore, it is highly likely that because there are so many stakeholders involved in the trialing process, this has, in part, resulted in limited growth in ITB in recent years despite its demonstrated efficacy.

    Another reason we believe which might explain the observed gap aforementioned is the special skill and expertise in managing patients with indwelling ITB pumps. ITB overdose or withdrawal, either due to pump failure or refill error, can be fatal. Unlike spinal cord stimulator therapy, which does not involve IT infusion of medication, a malfunctioning device can be easily adjusted by turning the stimulator off, without the concern of worrying about potential medication delivery to the IT space and its related adverse effects, which can include overdose or withdrawal. Thus, the treating physician has to be willing to take the extra responsibility and liability of managing patients with ITB pumps.

    Lastly, reimbursement charges to the hospital, anesthesiologist, or the implanting physician may be another area of consideration as to explain limited growth in ITB pump placement. In the USA, we have encountered some hospitals refusing to allow physician implantation of IT pumps for spasticity or pain control related to reimbursement cuts to the hospitals.

    References:

    1. Narendran RC, Duarte RV, Valyi A, Eldabe S. The need for and provision of intrathecal baclofen therapy for the management of spasticity in England: an assessment of the Hospital Episode Statistics database. BMJ Open. 2015;5(6):e007517. 2. Zhang H, Schmidt M, Murry DJ, Donovan MD. Permeation and systemic absorption of R?and S?baclofen across the nasal mucosa. Journal of pharmaceutical sciences. 2011;100(7):2717-23. 3. van Bree JB, Heijligers-Feijen CD, de Boer AG, Danhof M, Breimer DD. Stereoselective transport of baclofen across the blood-brain barrier in rats as determined by the unit impulse response methodology. Pharmaceutical research. 1991;8(2):259-62. 4. Harned ME, Salles SS, Grider JS. An introduction to trialing intrathecal baclofen in patients with hemiparetic spasticity: A description of 3 cases. Pain physician. 2011;14(5):483-9. 5. Ruan X, Chen T, GW B, Hamilton J, Peavy A, Harville S, et al. Novel Epidural Baclofen Infusion Trial for Intractable Spasticity with Long-Term Follow-Up Observation and a Focused Review of the Literature. Journal of Pain & Relief. 2013;2(2). 6. Rawicki B. Treatment of cerebral origin spasticity with continuous intrathecal baclofen delivered via an implantable pump: long-term follow- up review of 18 patients. Journal of neurosurgery. 1999;91(5):733-6. 7. Damiano DL, Quinlivan JM, Owen BF, Payne P, Nelson KC, Abel MF. What does the Ashworth scale really measure and are instrumented measures more valid and precise? Developmental medicine & child Neurology. 2002;44(02):112-8. 8. Pin TW, Mccartney L, Lewis J, WAUGH MC. Use of intrathecal baclofen therapy in ambulant children and adolescents with spasticity and dystonia of cerebral origin: a systematic review. Developmental Medicine & Child Neurology. 2011;53(10):885-95.

    Conflict of Interest:

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  7. A Possible Cause of SIDS is Found in SIDS Data of Carpenter et al., BMJO 2013, Figure 1 and Table 1

    SIDS is characterized and diagnosed by exclusion, especially when expert pediatric pathologists, trained forensic investigators, and learned epidemiologists are unable to find a sufficient cause of infant death at autopsy, at the scene, or in the data, respectively. Therefore the cause of SIDS may be invisible or immeasurable. Furthermore, SIDS is characterized by the fact that in every such case that the parents had no premonition that their infant was at imminent risk of death and "there was a complete absence of prodromal symptoms or any departure from the normal sufficient to justify the parent in seeking medical advice (1)." Therefore, most authors now look at risk factors that are not causes of death (prone sleep position, maternal smoking, etc.) However, they overlook three possible causal factors that alone might be insufficient to cause SIDS, but may act simultaneously in order to do so, that appear in this paper, as follows:

    1) An unknown X-linked recessive allele for SIDS susceptibility with frequency q = 2/3, in Hardy-Weinberg-Equilibrium (HWE), that predicts the 50% male excess of SIDS for equal numbers of males and females at risk. The XY male is at risk with q = 2/3 and the XX female is at risk with q x q = 4/9, a 50% male excess. Given a nominal 5% male excess birth rate the expected male fraction is 0.612 for 60 x 1.05 males per 40 females (2). Table 1 reports 898 male and 578 female SIDS, for male fraction = 0.613;

    2) Physiological anemia (3) causing the lognormal-type age distribution of SIDS in their Figure 1 that is its most unique characteristic. Unfortunately, "cases and controls over 1 year of age were excluded", which is like 'throwing the baby out with the bathwater.' The upper 1-year limit for SIDS is an artifact of the perception that SIDS over 1 year may include more false positives, so they should not be included in research studies.(4) Physiological anemia occurs when fetal hemoglobin (HbF) decays rapidly after birth while adult hemoglobin (HbA) slowly begins to replace the HbF. The term infant has its lifetime maximal total Hb at birth and it rapidly falls to their lifetime minimal Hb at or about 2-months of life, and then it follows a slow increase until a new equilibrium Hb concentration is established [we neglect here the different binding strengths of oxygen molecules to HbF and HbA, and pre-term Hb relations]. We estimated 19 as the missing number over 1-year that the authors excluded, by fitting an exponential decay curve to the numbers of SIDS from 8 weeks to 52 weeks in Figure 1 and extrapolating it to 178 weeks as determined previously as the upper limit for SIDS.(5) We then fit these weekly data (w) by the Johnson SB transformation that y = Log[(w + 1.343)/(178 - w)] where y = mu + sigma z, and mu = -1.025, sigma = 0.3, w is age in weeks, and z is a standard normal deviate. We interpret this Figure 1 as the number of the most anemic genetically susceptible infants whose total mix of Hb = HbF + HbA falls below some critical threshold, and therefore cannot survive a respiratory infection (see below) that reduces blood oxygenation in the lungs sufficiently to create an acute anoxic encephalopathy resulting in neuronal death. Hemoglobin concentration cannot be measured accurately at autopsy because of the gravitational settling of red blood cells during hemostasis leading to lividity so it is missing in virtually all SIDS autopsy studies (6); and

    3. A prodromal respiratory infection (PRI) contracted from a family member that begins to fulminate shortly before or after the infant is placed for its final sleep. Farber (7) reported such a case where a baby was cared for by a nurse because the mother had a severe sore throat at the time. After a 2 p.m. uneventful feeding by the nurse, the baby was found dead 1.5 hours later, "lying on his back. There was no evidence of bedclothes, pillow or any other object over his face." We propose that the only thing that could have changed from the immediately previous sleep condition, sufficiently to cause death and be unnoticed, had to be a PRI that began to fulminate and cause fatal anoxic encephalopathy "before an important or appreciable amount of lung parenchyma has been involved." The author's Table 1 can provide no data on a potentially fatal respiratory infection presence in the SIDS cases, because, if such visible evidence existed at autopsy, the diagnosis by definition would not be SIDS. However, these data in Table 1 cast a visible shadow of a fulminating PRI. The authors list the SIDS and Control Live-Birth-Order (LBO) as shown below. We assume that Cohabiting Family Members (CFM) = 2 adults + (LBO - 1) Siblings = LBO + 1. We then assume that the probability of not carrying a communicable respiratory infection (CRI) (symptomatic or asymptomatic) is P so the probability of at least one CFM carrying a CRI is 1 - P^(CFM). Setting P = 0.92 by least squares gives the Model values shown. We previously fit U.S. LBO and SIDS data with P = 0.90 (8). Note that a plot of SIDS Fraction or SIDS Model vs CFM goes to the origin (0, 0) that implies that there are no SIDS cases here that are independent of CFM.

    LBO = 1, SIDS = 407, Control = 1836, SIDS Fraction = 0.181, Model = 0.152;

    LBO = 2, SIDS = 491, Control = 1566, SIDS Fraction = 0.239, Model = 0.219;

    LBO = 3, SIDS = 280, Control = 748, SIDS Fraction = 0.272, Model = 0.280;

    LBO = 4, SIDS = 149, Control = 304, SIDS Fraction = 0.329, Model = 0.337;

    LBO = 5+, SIDS = 122, Control = 200,SIDS Fraction = 0.379, Model = 0.390.

    In summary, SIDS may occur from these three causal factors (genetic susceptibility, physiological anemia, PRI) acting simultaneously that are a function of chance, age and CFM, respectively. There is no explanation we can find in the medical literature , other than an X-linkage in HWE, for a constant male fraction that is different from that of the male birth fraction. There is no explanation other than the maximum hemoglobin at birth for the virtual absence of SIDS immediately after live birth that is the most risky time for all other causes of infant death, the peak SIDS rate at or about the total Hb nadir, followed by an exponential decrease in SIDS rate as the infant's total HbA increases. We know of no other invisible cause of a sudden and unexpected infant death than a fulminating PRI that leaves no visible trace for the pathologist at autopsy or under the microscope in a genetically-susceptible physiologically-anemic infant.

    REFERENCES

    1. Davison WH. Accidental Infant Suffocation. Br Med J. 1945;2(4416):251-2.

    2. Mage DT, Donner EM. A genetic basis for the sudden infant death syndrome sex ratio. Med Hypotheses 1997;48:137-42.

    3. O'Brien RT, Pearson HA. Physiologic anemia of the newborn infant. J Pediat 1971;79:132-8.

    4. Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol. 1991;11(5):677-84.

    5. Mage DT. A probability model for the age distribution of SIDS. J Sudden Infant Death Syndrome and Infant Mortality 1996;1(1):13-31.

    6. Poets CF, Samuels MP, Wardrop CA, et al. Reduced haemoglobin levels in infants presenting with apparent life-threatening events--a retrospective investigation. Acta Paediatr. 1992;81(4):319-21.

    7. Farber S. Fulminating streptococcus infections in infancy as a cause of sudden death. NEJM 1934;211:154-9.

    8.Mage DT, Donner M, A unifying theory for SIDS. Int J Pediat 2009; 2009:368270

    Conflict of Interest:

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  8. Evaluation of a tobacco prevention programme

    We read with interest the study titled "Evaluation of a tobacco prevention programme among teenagers in Sweden". [1] This study makes a great contribution to the tobacco prevention programs. However we would like to bring out few points.

    As the investigators had assigned the intervention (exposure), this study cannot be considered a cohort study and it does not have to qualities to be called a randomized controlled trial. Therefore, this study design may be most appropriately called a Quasi-experimental design with non-equivalent comparison. [2] We appraised the article based on the TREND checklist [3], which was primarily designed for reporting nonrandomized evaluations of behavioural and public health interventions. The article did not comply with many items in this checklist but we highlight a few important concerns here.

    Complete details regarding the intervention such as the actual content of intervention, deliverer, delivery method, information on unit of delivery, number of sessions delivered and length of each session, the setting were not provided. Primary outcomes of the study were not clearly defined, in that they have measured only the prevalence of tobacco use rather than comparing the reduction in the prevalence of tobacco use. This would have also taken care of baseline variations (such as differences in the living conditions) between the comparison groups. Also, the authors have mentioned that the prevalence of smoking in the study area has decreased in the last 10 years; so to rule out any secular trend in the prevalence of smoking in this area and to attribute the change in smoking to the intervention an Interrupted Time Series Analysis [4] could have been performed.

    Bivariate and multivariate analysis (Table 1) showed that there were no significant differences in the prevalence of smoking between the control group, participants, and non-participants at the end of the intervention. But the authors have mentioned that the prevalence of smoking was significantly lower among participants compared with non- participants and the control group by using Test for Trend between 3 groups at the end of intervention (Figure 2). We believed that the impact of this program could have been better estimated using baseline and follow up data and performing a Propensity Score weighted Difference-in- Difference analysis. [5] These important limitations cast a doubt over the method of analysis and the interpretations arising thereof and they have to be corrected or borne in mind to prevent wrongful conclusions.

    References

    1. Hedman L, Andersson M, Stridsman C, Ronmark E. Evaluation of a tobacco prevention programme among teenagers in Sweden. BMJ Open [Internet] 2015;5(5):e007673-e007673. Available from: http://bmjopen.bmj.com/cgi/doi/10.1136/bmjopen-2015-007673

    2. U.S. Department of Health and Human Services. Centers for Disease Control and Prevention. Office of the Director. Office of Strategy and Innovation. Introduction to Program Evaluation for Public Health Programs?: A Self-Study Guide. 2011;(October):1-100.

    3. Jarlais D, Cynthia L, Crepaz N. Improving the Reporting Quality of Nonrandomized Evaluations of Behavioral and Public Health Interventions: The TREND Statement. Am J Public Health 2004;94(3):361-6.

    4. Lagarde M. How to do ( or not to do ) . . . Assessing the impact of a policy change with routine longitudinal data. Health Policy Plan [Internet] 2012;(January 2011):76-83. Available from: http://heapol.oxfordjournals.org/content/27/1/76.full?sid=3e9e83cf-fbcc- 4140-a869-b02f14f3074c

    5. Shahidur K, Koolwal G, Samad H. Handbook on Impact Evaluation: Quantitative Methods and Practices. The World bank; 2009.

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  9. Vitamin D and endothelial function

    Dear Sirs,

    Please be aware that cytomegalovirus (CMV) has a preference for endothelial tissue.

    It has been proposed that Vitamin D may be interacting with CMV in the expression of endothelial conditions (1-5).

    Also be aware that there may be time-dependant (i.e. year the study was conducted) relationships between the outcome observed in some studies (1-11).

    References

    1. Jones R (2013) Could cytomegalovirus be causing widespread outbreaks of chronic poor health. In Hypotheses in Clinical Medicine, pp 37-79, Eds M. Shoja, et al. New York: Nova Science Publishers Inc. Available from: http://www.hcaf.biz/2013/CMV_Read.pdf

    2. Jones R (2013) Recurring outbreaks of a subtle condition leading to hospitalization and death. Epidemiology: Open access 4(3): 137.

    3. Jones R (2014) A Study of an Unexplained and Large Increase in Respiratory Deaths in England and Wales: Is the Pattern of Diagnoses Consistent with the Potential Involvement of Cytomegalovirus? British Journal of Medicine and Medical Research 4(33): 5179-5192.

    4. Jones R (2015) Roles for cytomegalovirus in infection, inflammation and autoimmunity. In Infection and Autoimmunity, 2nd Edition, Eds: N Rose, et al. Elsevier: Amsterdam. Chapter 18, pp 319-357.

    5. Jones R (2015) An unexpected increase in adult appendicitis in England (2000/01 to 2012/13): Could cytomegalovirus (CMV) be a risk factor? British Journal of Medicine and Medical Research 5(5): 579-603.

    6. Jones R (2015) A previously uncharacterized infectious-like event leading to spatial spread of deaths across England and Wales: Characteristics of the most recent event and a time series for past events. British Journal of Medicine and Medical Research 5(11): 1361- 1380.

    7. Jones R, Beauchant S (2015) Spread of a new type of infectious condition across Berkshire in England between June 2011 and March 2013:Effect on medical emergency admissions. British Journal of Medicine and Medical Research 6(1): 126-148.

    8. Jones R. (2015) Unexpected and Disruptive Changes in Admissions Associated with an Infectious-like Event Experienced at a Hospital in Berkshire, England around May of 2012. British Journal of Medicine and Medical Research 6(1): 56-76.

    9. Jones R (2015) Recurring Outbreaks of an Infection Apparently Targeting Immune Function, and Consequent Unprecedented Growth in Medical Admission and Costs in the United Kingdom: A Review. British Journal of Medicine and Medical Research 6(8): 735-770.

    10. Jones R (2015) A new type of infectious outbreak? SMU Medical Journal 2(1): 19-25.

    11. Jones R (2015) Are emergency admissions contagious? BJHCM 21(5): 227-235.

    Conflict of Interest:

    None declared

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  10. Correlation does not equal causality; selective presentation of the literature is beyond doubt

    The reply by Rachiotis et al is disappointing. The main issue I raised was on the very selective presentation of the literature, in which the authors do not really respond. The second issue is the causality question.

    As I had extensively stated in my response, our previous reports disputed a rise in suicides in Greece before 2010 and clearly reported this increase after 2010 [1-5]. I do not really follow the arguments of Rachiotis et al on this matter which is perfectly clear. The report in increased rates after 2010 was included in a letter and in an international study which is full and difficult to miss [5]. On the contrary, the authors of the paper under discussion have repeatedly suggested the increase in suicide rates had started already since 2007. It is disappointing that Rachiotis et al did not take into consideration especially our international study which was the second to mention an increase of suicides in Greece [5] and discussed the issue of suicides and economic crisis in the whole of Europe Furthermore, Since they can not explain the problematic temporal relationship between unemployment rise and increase in suicides, they change their argument from 'unemployment' to 'extreme austerity'. The discussion here is on the possible effect of unemployment. And any university student in the field knows that correlation does not imply causality unless specific properties are met.

    References

    1. Fountoulakis KN, Koupidis SA, Grammatikopoulos IA, et al. First reliable data suggest a possible increase in suicides in Greece. Bmj 2013;347:f4900 doi: 10.1136/bmj.f4900[published Online First: Epub Date]|.

    2. Fountoulakis KN, Koupidis SA, Siamouli M, et al. Suicide, recession, and unemployment. Lancet 2013;381(9868):721-2 doi: 10.1016/S0140-6736(13)60573-5[published Online First: Epub Date]|.

    3. Fountoulakis KN, Savopoulos C, Siamouli M, et al. Trends in suicidality amid the economic crisis in Greece. European archives of psychiatry and clinical neuroscience 2013;263(5):441-4 doi: 10.1007/s00406 -012-0385-9[published Online First: Epub Date]|. 4. Fountoulakis KN, Siamouli M, Grammatikopoulos IA, et al. Economic crisis-related increased suicidality in Greece and Italy: a premature overinterpretation. Journal of epidemiology and community health 2013;67(4):379-80 doi: 10.1136/jech-2012-201902[published Online First: Epub Date]|.

    5. Fountoulakis KN, Kawohl W, Theodorakis PN, et al. Relationship of suicide rates to economic variables in Europe: 2000-2011. The British journal of psychiatry : the journal of mental science 2014 doi: 10.1192/bjp.bp.114.147454[published Online First: Epub Date]|.

    Conflict of Interest:

    None declared

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