Barlow and Nathwani[1] reviewed medico legal and allied
aspects of restraints encountered by clinicians in teaching hospital based
units in recommending intravenous and broad-spectrum antibiotics. While
the local epidemiological resistance patterns would be an asset,
clinicians would desire for a rapid response from the local clinical
microbiologist. Recently marketed automated devices might not be perfect...
Barlow and Nathwani[1] reviewed medico legal and allied
aspects of restraints encountered by clinicians in teaching hospital based
units in recommending intravenous and broad-spectrum antibiotics. While
the local epidemiological resistance patterns would be an asset,
clinicians would desire for a rapid response from the local clinical
microbiologist. Recently marketed automated devices might not be perfect
as evident in the recent controlled investigations on clinical outcome of
morbidity, mortality and cost on utility of Vitek 2 system. In the
Netherlands, in the 1,1000-bed tertiary care teaching hospital, there was
little utility of Vitek 2 as against the conventional overnight methods.[2]
Round the clock functioning of microbiology laboratory and frequent
dialogues with health care personnel looking after the hospitalized cases
would enhance the clinical utility of any conventional or automated
reporting system. That has been evident with extended clinical
microbiology activity in a tertiary care hospital in the Indian capital.
Sant Parmanand Hospital, a private sector 140-bed hospital is managed by a
benevolent organization that aims to impart first-rate medical care at a
rational and reasonably priced expenditure. Microbiology personnel are
available round the clock.
Rather than vouching for Vitek 2 or other system, a reduction with
the turnaround time for microbiology reporting has been attempted. Instead
of the conventional overnight gap between the inoculation of culture media
and recording the growth characters, there is a 6-8 hours gap for reading
inoculated plates. The antibiotics susceptibility profiles are
communicated verbally to nurses, residents or the consultants charged with
care of patents in the wards. Round-the-clock activities reduced the
turnaround by at least one day. There has been no fiscal cost on the
organization or the patient.
Utility of the above exercise towards appropriate chemotherapy was
evident in two cases with MRSA. A shift from cephalosporin recipe to
vancomycin was effective in recovery of two MRSA patients in the surgical
intensive care unit3. While no systematic evaluation has been made on the
clinical impact, clinicians have appreciated the reduced turnaround time.
Clinicians have been rather incredulous about the utility of the
automation in microbiology. Although automation might be of significant
benefit within the laboratory itself, communication with those directly
responsible for patient care is vital towards an improvement of the
quality of healthcare4. Surely, improvised rapid turnaround time for
antibiotics susceptibility profiles and quicker response by clinicians
would avoid medico legal litigations1 in Courts.
ARYA, Subhash C.
AGARWAL, Nirmala
AGARWAL, Shekhar
Sant Parmanand Hospital
18 Alipore Road
Delhi-110054, India
Email: subhashji@hotmail.com
References:
1. Barlow G, Nathwani D. Is antibiotic resistance a problem? A
practical
guide for hospital clinicians. Postgrad Med J 2005; 81: 680-692.
2. Bruins M, Oord H, Bloembergen P, et al. Lack of effect of shorted
turnaround time of microbiological procedures on clinical outcomes: a
randomized controlled trial among hospitalized patients in the
Netherlands. Eur J Clin Microbiol Infect Dis 2005; 24:305-311.
3. Arya SC, Kapoor S, Agarwal N, Bhasin R, George S. Re: Evaluation of
a
disk diffusion method with cefoxitin (30lG) for detection of Methicillin-
resistant Staphylococcus aureus. Eur J Clinical Micro Infect Dis 2004;
23(11): 867-868.
4. Dupont PF. Automation in microbiology: a physician_s viewpoint. Am J
Med Technol 1983; 49(5): 323-325.
We thank Dr. Singh for his interest in our review. Excellent reviews
are available that focus exclusively on the role of amyloid degrading
enzymes in aging and neurodegeneration and we would like to refer the
interested readers to these reviews (Turner, Fisk et al. 2004; Hama and
Saido 2005).
Iwata (Iwata, Takaki et al. 2002) demonstrated a statistically significant
decrease of NE in the hi...
We thank Dr. Singh for his interest in our review. Excellent reviews
are available that focus exclusively on the role of amyloid degrading
enzymes in aging and neurodegeneration and we would like to refer the
interested readers to these reviews (Turner, Fisk et al. 2004; Hama and
Saido 2005).
Iwata (Iwata, Takaki et al. 2002) demonstrated a statistically significant
decrease of NE in the hippocampal formation of aged mice and hypothesized
that this might be associated with the neuropathology in AD patients or
Abeta production of normal aging.
In our review we mentioned that the relationship between region-dependent
decreases of neprilysin, aging and AD was not yet fully elucidated mainly
because of the two following reasons. First, in mice NE levels are not
altered in other brain areas (e.g. cortex) where Abeta pathology is
nevertheless observed (Apelt, Ach et al. 2003; Caccamo, Oddo et al. 2005).
Second, in humans, the regional age-dependent changes in NE have not
always been consistent between studies. A decrease of hippocampal but not
cortical NE levels was reported (Caccamo, Oddo et al. 2005), a more
uniform decrease by (Russo, Borghi et al. 2005), and unaltered
immonureactivity of NE in cortex of normal and pathological aged human
brains by Wang et al. (Wang, Lipton et al. 2005).
We agree with Dr. Singh that the role of neprilysin in aging and AD is a
very exciting and promising field of research. Unfortunately it is not
possible within the scope of our clinical review to do full justice to
each of the important molecular biological topics we touched upon. We do
not have a strong position in favour of or against the neprilysin
hypothesis and we would like to refer interested readers to expert reviews
that focus exclusively on the role of amyloid degrading enzymes in aging
and neurodegeneration (Turner, Fisk et al. 2004; Hama and Saido 2005).
References:
Apelt, J., K. Ach, et al. (2003). "Aging-related down-regulation of
neprilysin, a putative beta-amyloid-degrading enzyme, in transgenic Tg2576
Alzheimer-like mouse brain is accompanied by an astroglial upregulation in
the vicinity of beta-amyloid plaques." Neurosci Lett 339(3): 183-6.
Caccamo, A., S. Oddo, et al. (2005). "Age- and region-dependent
alterations in Abeta-degrading enzymes: implications for Abeta-induced
disorders." Neurobiol Aging 26(5): 645-54.
Hama, E. and T. C. Saido (2005). "Etiology of sporadic Alzheimer's
disease: somatostatin, neprilysin, and amyloid beta peptide." Med
Hypotheses 65(3): 498-500.
Iwata, N., Y. Takaki, et al. (2002). "Region-specific reduction of A beta-
degrading endopeptidase, neprilysin, in mouse hippocampus upon aging." J
Neurosci Res 70(3): 493-500.
Russo, R., R. Borghi, et al. (2005). "Neprylisin decreases uniformly
in Alzheimer's disease and in normal aging." FEBS Lett 579(27): 6027-30.
Turner, A. J., L. Fisk, et al. (2004). "Targeting amyloid-degrading
enzymes as therapeutic strategies in neurodegeneration." Ann N Y Acad Sci
1035: 1-20.
Wang, D. S., R. B. Lipton, et al. (2005). "Decreased neprilysin
immunoreactivity in Alzheimer disease, but not in pathological aging." J
Neuropathol Exp Neurol 64(5): 378-85.
I read with interest Sorabjee and Garje’s recent article
on reactivation of old scars[1] I feel that some points must be
clarified.
Sorabjee and Garje state that histopathological demonstration of non-caseating granulomas on scar tissue obtained by biopsy in a patient presented with multiple mediastinal lymph nodes
accompanied with numerious old scars is sufficient for diagnosis of
sarcoidosi...
I read with interest Sorabjee and Garje’s recent article
on reactivation of old scars[1] I feel that some points must be
clarified.
Sorabjee and Garje state that histopathological demonstration of non-caseating granulomas on scar tissue obtained by biopsy in a patient presented with multiple mediastinal lymph nodes
accompanied with numerious old scars is sufficient for diagnosis of
sarcoidosis.
Before a final comment like this, it should be remembered that scar
sarcoidosis is most likely to be associated with severe systemic
lesions,but it may also be the only manifestation of sarcoidosis.[2] On
the other hand, the occurence of sarcoidosis associated with Hodgkin
disease or tuberculosis are infrequent but well described events.[3]
If there had been no improvement with steroids in this case, one might have
easily suggested a similar association mentioned above. Since India is
considered to be an endemic country of tuberculosis[4] the diagnosis of
sarcoidosis in this case requires to be supported by additional
histopathological and microbiological evaluation of lymph nodes as well.
This approach may be useful in clinical practise , its reliability is
indeterminate. Certainly this is a single case and larger series are
needed to make an algorithm of diagnostic steps in sarcoidosis.
References
1.Sorabjee JS,Garje R.Reactivation of old scars:inevitably sarcoid.
Postgrad Med J 2005 Jan;81(951):60-1.
2.Veien NK, Stahl D,BrodthagenH. Cutaneous sarcoidosis in
caucasions.J Am Acad Dermatol 1987;16:534-540.
4.Gopi PG,Subramani R,Santha T, Chandrasekarran V,et al. Estimation
of burden of tuberculosis in India for the year 2000. Indian J Med Res
2005 Sep;122(3):243-8.
Article by Vandenberghe R and Tournoy J. entitled “Cognitive aging
and Alzheimer’s disease” tells a story of Alzheimer’s disease and its
cognitive relation with aging. As reported in this review that there is
age related changes in the amyloid degrading enzymes, IDE and Neprilysin,
differs between regions and no clear picture has been emerged.
But researchers from RIKEN brain Institute demons...
Article by Vandenberghe R and Tournoy J. entitled “Cognitive aging
and Alzheimer’s disease” tells a story of Alzheimer’s disease and its
cognitive relation with aging. As reported in this review that there is
age related changes in the amyloid degrading enzymes, IDE and Neprilysin,
differs between regions and no clear picture has been emerged.
But researchers from RIKEN brain Institute demonstrated about region
specific and age related reduction in neprilysin expression in year 2001-
2002.[1,2,3]The authors show that there is more reduction in neprilysin
expression in hippocampus and cerebral cortex. This is hypothesized that
this reduction might be involved in region specific brain impairments in
Alzheimer’s disease.
References:
1. Iwata N, Tsubuki S, Takaki Y, Shirotani K, Lu B, Gerard NP, Gerard
C, Hama E, Lee HJ, Saido TC.(2001) Metabolic regulation of brain Abeta by
neprilysin. Science. 292(5521):1550-2.
2. Iwata N, Takaki Y, Fukami S, Tsubuki S, Saido TC.(2002) Region-
specific reduction of A-beta-degrading endopeptidase, neprilysin, in mouse
hippocampus upon aging. J Neurosci Res. 70(3):493-500.
3. Fukami S, Watanabe K, Iwata N, Haraoka J, Lu B, Gerard NP, Gerard
C, Fraser P, Westaway D, St George-Hyslop P, Saido TC. (2002).Abeta-
degrading endopeptidase, neprilysin, in mouse brain: synaptic and axonal
localization inversely correlating with Abeta pathology. Neurosci. Res.
43(1):39-56.
We read with great interest the editorial by Dr Rajagopal concerning
the clinical implications of ethnic benign neutropenia in patients
receiving clozapine treatment.[1)
It is noteworthy that clozapine itself may induce transient and
harmless neutropenia, and that such phenomenon are not restricted to
certain ethnic groups. Transient neutropenia (defined as a return of the
neutrophil count t...
We read with great interest the editorial by Dr Rajagopal concerning
the clinical implications of ethnic benign neutropenia in patients
receiving clozapine treatment.[1)
It is noteworthy that clozapine itself may induce transient and
harmless neutropenia, and that such phenomenon are not restricted to
certain ethnic groups. Transient neutropenia (defined as a return of the
neutrophil count to normal values without changing the clozapine dosage)
has been shown to occur in 22% of 68 Caucasians patients treated with
clozapine for the first time.[2] Neutropenia of short duration (2-5 days)
and weekly benign variations of the neutrophil count, not necessitating
the discontinuation of clozapine treatment, have been reported in five
Asian patients.[3] Circadian variations in the number of circulating
neutrophils, i.e. morning pseudoneutropenia, have also been described in
several non-Jewish Caucasians.[4,5] Therefore, some clozapine-treated
patients may unnecessarily be denied effective treatment.
The question arises why some patients treated with clozapine develop
only transient neutropenia while others go forward to a progressive
disorder. It has been hypothesized that successful compensatory mechanisms
by cytokines, such as the production of granulocyte colony-stimulating
factor (G-CSF), may stimulate granulopoiesis sufficiently in the case of
benign neutropenia. If the cytokine compensation is insufficient,
neutropenia may become apparent and at times progressive.[2]
It seems essential, before interrupting clozapine treatment, to
determine whether drug-induced neutropenia is benign or malignant. As
patients with benign neutropenia are not systematically predisposed to
agranulocytosis, interruption of clozapine can be avoided. Laboratory
screening tests are being devised to make such a distinction. These tests
could include monitoring of endogenous G-CSF levels or the use of a
hydrocortisone test.[6,7] Until these tests become available for routine
use, it is necessary to increase the frequency with which white blood cell
counts are determined in patients with clozapine-associated neutropenia.
Funding : none.
Competing interests : none.
References
1. Rajagopal S. Clozapine, agranulocytosis, and benign ethnic
neutropenia. Postgrad Med J 2005;81:545-6.
2. Hummer M, Kurz M, Barnas C, et al. Clozapine-induced transient
white blood count disorders. J Clin Psychiatry 1994;55:429-32.
3. Ahn YM, Jeong SH, Jang HS, et al. Experience of maintaining
clozapine medication in patients with ‘red-alert zone’ neutropenia: long-
term follow-up results. Int Clin Psychopharmacology 2004;19:97-101.
4. Esposito D, Aouillé J, Rouillon F, et al. Two year follow-up of a
patient with successful continuation of clozapine treatment despite
morning pseudoneutropenia. J Clin Psychiatry 2004;65:1281.
5. Esposito D, Corruble E, Hardy P, et al. Risperidone-induced
morning pseudoneutropenia. Am J Psychiatry 2005;162:397.
6. Jauss M, Pantel J, Werle E, et al. G-CSF plasma levels in
clozapine-induced neutropenia. Biol Psychiatry 2000;48:1113-5.
7. Murry P, Laurent A. Is it possible to distinguish between benign
and malignant neutropenia in clozapine-treated patients by means of a
hydrocortisone test? Psychopharmacology 2001;158:329-30.
David Esposito, Emmanuelle Corruble, Patrick Hardy
I read with interest the recent report by Menon and colleagues in the
Journal.[1] The explanations regarding the anatomy underpinning occurrences of crossed
aphasia, i.e. transcallosal diaschisis (p. 342), does not hold since no
such events occur in the vast majority of behavioral right-handers who
sustained similar injuries to the temporoparietal lobe of the minor
hemisphere as because there is no mot...
I read with interest the recent report by Menon and colleagues in the
Journal.[1] The explanations regarding the anatomy underpinning occurrences of crossed
aphasia, i.e. transcallosal diaschisis (p. 342), does not hold since no
such events occur in the vast majority of behavioral right-handers who
sustained similar injuries to the temporoparietal lobe of the minor
hemisphere as because there is no motor communication from the minor to
the major hemisphere (see below for the newly discovered anatomical
definitions of these terms).
The problem relates to the laterality of the command center which may
or may not coincide with the behavioural handedness of the patient. Thus,
it has been shown that behavioural handedness relates to neural handedness
in a statistical manner, not biological.
Neural handedness is determined by the proximity of the dominant side
of the body to the command centre (major hemisphere, the one with which we
speak) by a callosum width, providing for a quick determination of the
same with a reaction time test. The latter is longer on the entire
nondominant side of the body by an interhemispheric transfer time (IHTT).
This includes moving the eyes or the diaphragm in neural right handers.[2,3]
It would have been helpful to know if the patient had apraxia of the
right hand side, a finding commonly reported in crossed aphasics, where
the laterality of hemiparesis and apraxia simply switch sides, compared to
what is the case when neural and behavioural handedness of the subject does
match.[4-6]
More clinical information on the subjects of crossed aphasia and
crossed nonaphasia may be obtained in my recent articles on the laterality
of motor control in humans, the one-way callosal traffic scheme.[7-10]
References
1. Menon B, Vengamma B. A woman with language disturbance. Postgrad
Med J. 2005; 81:341-342.
2. Derakhshan I. How do the eyes move together? New understandings
help explain eye deviations in patients with stroke. CMAJ. 2005 Jan 18;
172:171-173.
3. Derakhshan I. In defense of the sinistrals: anatomy of handedness
and the safety of prenatal ultrasound. Ultrasound Obstet Gynecol. 2003;
21:209-212.
4. Marien P, Engelborghs S, Vignolo LA, De Deyn PP. The many faces of
crossed aphasia in dextrals: report of nine cases and review of the
literature. Eur J Neurol. 2001; 8:643-658. (Table 2)
5. Derakhshan I. Handedness: neural versus behavioural. Eur J Neurol.
2002; 9:701-702.
6. Derakhshan I, Franz EA, Rowse A. An exchange on Franz, Rowse, and
Ballantine (2002). Handedness, neural versus behavioral: is there a
measureable callosal difference.
J Mot Behav. 2003; 35:409-414.
7. Derakhshan I. Laterality of motor control revisited:
directionality of callosal traffic and its rehabilitative implications.
Top Stroke Rehabil. 2005; 12:76-82.
8. Derakhshan I. Handedness and macular vision: laterality of motor
control underpins both. Neurol Res. 2004; 26:331-337.
9. Derakhshan I. Kernohan notch. J Neurosurg. 2004; 100:741-742.
10. Derakhshan I. Callosum and movement control: case reports. Neurol
Res. 2003; 25:538-542.
We read with great interest the editorial by Dr Rajagopal concerning
the clinical implications of ethnic benign neutropenia in patients
receiving clozapine treatment.[1]
It is noteworthy that clozapine itself may induce transient and
harmless neutropenia, and that such phenomenon are not restricted to
certain ethnic groups. Transient neutropenia (defined as a return of the
neutrophil count...
We read with great interest the editorial by Dr Rajagopal concerning
the clinical implications of ethnic benign neutropenia in patients
receiving clozapine treatment.[1]
It is noteworthy that clozapine itself may induce transient and
harmless neutropenia, and that such phenomenon are not restricted to
certain ethnic groups. Transient neutropenia (defined as a return of the
neutrophil count to normal values without changing the clozapine dosage)
has been shown to occur in 22% of 68 Caucasians patients treated with
clozapine for the first time.[2] Neutropenia of short duration (2-5 days)
and weekly benign variations of the neutrophil count, not necessitating
the discontinuation of clozapine treatment, have been reported in five
Asian patients.[3] Circadian variations in the number of circulating
neutrophils, i.e. morning pseudoneutropenia, have also been described in
several non-Jewish Caucasians.[4,5] Therefore, some clozapine-treated
patients may unnecessarily be denied effective treatment.
The question arises why some patients treated with clozapine develop
only transient neutropenia while others go forward to a progressive
disorder. It has been hypothesized that successful compensatory mechanisms
by cytokines, such as the production of granulocyte colony-stimulating
factor (G-CSF), may stimulate granulopoiesis sufficiently in the case of
benign neutropenia. If the cytokine compensation is insufficient,
neutropenia may become apparent and at times progressive.[2]
It seems essential, before interrupting clozapine treatment, to
determine whether drug-induced neutropenia is benign or malignant. As
patients with benign neutropenia are not systematically predisposed to
agranulocytosis, interruption of clozapine can be avoided. Laboratory
screening tests are being devised to make such a distinction. These tests
could include monitoring of endogenous G-CSF levels or the use of a
hydrocortisone test.[6,7] Until these tests become available for routine
use, it is necessary to increase the frequency with which white blood cell
counts are determined in patients with clozapine-associated neutropenia.
Funding: none.
Competing interests: none.
References
1. Rajagopal S. Clozapine, agranulocytosis, and benign ethnic
neutropenia. Postgrad Med J 2005;81:545-6.
2. Hummer M, Kurz M, Barnas C, et al. Clozapine-induced transient
white blood count disorders. J Clin Psychiatry 1994;55:429-32.
3. Ahn YM, Jeong SH, Jang HS, et al. Experience of maintaining
clozapine medication in patients with ‘red-alert zone’ neutropenia: long-
term follow-up results. Int Clin Psychopharmacology 2004;19:97-101.
4. Esposito D, Aouillé J, Rouillon F, et al. Two year follow-up of a
patient with successful continuation of clozapine treatment despite
morning pseudoneutropenia. J Clin Psychiatry 2004;65:1281.
5. Esposito D, Corruble E, Hardy P, et al. Risperidone-induced
morning pseudoneutropenia. Am J Psychiatry 2005;162:397.
6. Jauss M, Pantel J, Werle E, et al. G-CSF plasma levels in
clozapine-induced neutropenia. Biol Psychiatry 2000;48:1113-5.
7. Murry P, Laurent A. Is it possible to distinguish between benign
and malignant neutropenia in clozapine-treated patients by means of a
hydrocortisone test? Psychopharmacology 2001;158:329-30.
David Esposito
Emmanuelle Corruble
Patrick Hardy
Corresponding author:
David Esposito
david.esposito@club-internet.fr Department of Psychiatry, Bicêtre Hospital
Assistance Publique - Hôpitaux de Paris
Paris XI University
INSERM U 669, France
Stebbing J et al.[1] article raises an important issue of the limited
availability of CD4 measurements in resource-scarce settings which poses a
major problem in the management of HIV infection. High cost of the
perishable reagents, technically complicated and expensive flow cytometers
remain a hurdle in developing countries where several million people are
in need of therapy. Fortunately, advances in mi...
Stebbing J et al.[1] article raises an important issue of the limited
availability of CD4 measurements in resource-scarce settings which poses a
major problem in the management of HIV infection. High cost of the
perishable reagents, technically complicated and expensive flow cytometers
remain a hurdle in developing countries where several million people are
in need of therapy. Fortunately, advances in microtechnology could soon
offer an amicable solution and make sophisticated and expensive
technologies cheaper.
Rodriguez and colleagues[2] have recently patented an electronic taste
chip (ETC) which can carry out chemical and immunological reactions on
microspheres in a small chamber through which whole blood can easily pass
through. White blood cells are captured on a membrane support and red
blood cells pass readily through pores, thus requiring no additional
sample processing like centrifugation or red blood cell lysis. The
microspheres are coated with specific lymphocyte marker fluorescent
monoclonal antibodies that attach to the surfaces of lymphocytes as they
pass through the chamber. The chip array rests on top of a fluorescent
microscope connected to a charge-coupled device (CCD). The CD4 cells
tagged with microspheres are easily distinguished via this CCD camera and
counted by a digital image analysis system.
The authors have tested the system by enrolling 67 HIV-positive people in
Botswana: 61 adults and 6 children. CD4 counts measured by both the
microchip system and standard flow cytometry showed excellent correlation;
sensitivity and specificity (microchip assay) at CD4 cell count of <_250 were="were" _0.86="_0.86" and="and" _0.81="_0.81" respectively.="respectively." the="the" microchip="microchip" assay="assay" requires="requires" _16.5="_16.5" xb5l="xb5l" of="of" blood="blood" provides="provides" results="results" within="within" _15="_15" minutes.="minutes." preliminary="preliminary" studies="studies" using="using" _5="_5" via="via" fingerstick="fingerstick" have="have" been="been" conducted="conducted" a="a" hand-held="hand-held" version="version" could="could" be="be" developed="developed" by="by" _2006.="_2006." estimated="estimated" cost="cost" manufactured="manufactured" machine="machine" would="would" less="less" than="than" tenth="tenth" standard="standard" flow="flow" cytometry="cytometry" expenses="expenses" can="can" operated="operated" at="at" point-of-care="point-of-care" settings.="settings." this="this" more="more" research="research" but="but" is="is" certainly="certainly" step="step" in="in" right="right" direction.="direction." p="p"/>Microtechnologies have changed the face of medical laboratories[3] and
new assays such as the micro-chip CD4 counter for the care of HIV-positive
patients merits substantial funding to address the problem more
effectively.
Competing interests: safe.
References
1. Stebbing J, Sawleshwarkar S, Michailidis C, Jones R, Bower M et al.
Assessment of the efficacy of total lymphocyte counts as predictors of
AIDS defining infections in HIV-1 infected people. Postgrad Med J 2005;
81:586-588.
2. Rodriguez WR, Christodoulides N, Floriano PN, Graham S, Mohanty S,
Dixon M, et al. A microchip CD4 counting method for HIV monitoring in
resource- poor settings. PLoS Med 2005; 2(7):e182.
3. Harris E, Tanner M. Health technology transfer. BMJ 2000; 321:817-820.
I have read Heatley et al.’s article but I have certain queries in my mind. Heatley et al.
are recommending the trial of four week therapy of proton pump
inhibitor to exclude the diagnosis of coronary artery disease. I
highly
disagree to the fact that, as we know many of the myocardial infarction
episodes, especially in elderly and diabetics, may present silently. Moreover, it is well known that with i...
I have read Heatley et al.’s article but I have certain queries in my mind. Heatley et al.
are recommending the trial of four week therapy of proton pump
inhibitor to exclude the diagnosis of coronary artery disease. I
highly
disagree to the fact that, as we know many of the myocardial infarction
episodes, especially in elderly and diabetics, may present silently. Moreover, it is well known that with inferior wall myocardial infarction
more
present with nonspecific gastointestinal symptoms.
Due to the above
described reason would Heatley et al. not think that if we rely more on 4 week
therapy of proton pump inhibitor then we will delay the management of
coronary artery disease which may have grave consequences and the patient may
lose the golden hour, which can be utilised to protect the myocardium? If we can add radionuclide scanning in our protocol then we can more
reliably exclude the diagnosis of ischemic heart disease, rather than waiting for 4 weeks to lose the golden hour which severely may affect the
prognosis.
Alok Kumar Singh
Department of Cardiology
Institute of medical sciences
B.H.U VARANASI INDIA 221005
We thank Dr Creagh-Brown for his interest in our article and
comments.
We agree with the comments about figure 2, which is maybe misleading.
The marks made by the juniors were judged with regard to the BTS
guidelines as described in the article. Figure 2 is designed to illustrate
where marks were made in relation to the triangle of safety (represented
by the centre square). We agree that fig...
We thank Dr Creagh-Brown for his interest in our article and
comments.
We agree with the comments about figure 2, which is maybe misleading.
The marks made by the juniors were judged with regard to the BTS
guidelines as described in the article. Figure 2 is designed to illustrate
where marks were made in relation to the triangle of safety (represented
by the centre square). We agree that figure 2 does not show accurate
boundaries of the safe area, but can assure Dr Creagh-Brown that the area
he refers to was included in the safe area for marking purposes. The 24%
in the lower centre square in figure 2 were all well below the nipple line
and hence outside the BTS safe area.
We also agree with the comments regarding adequate analgesia in
relation to chest drain insertion. In our experience this is poorly
performed but was not assessed in our audit. Given that many of the
juniors were unable to identify the correct anatomical landmarks, it is
unlikely they would have mastered the difficult art of infiltrating local
anaesthetic into the intercostals muscles.
With regards to training, we agree that respiratory physicians
usually are well experience in intercostals drain insertion and could
therefore provide local training. However, with the increased use of
Seldinger drains by physicians their expertise with formal intercostals
drains may diminish. We hope to incorporate formal teaching on the
insertion of intercostal chest drains into the SHO education programme for
both medical and surgical specialties and then repeat the survey in order
to complete the audit cycle.
Overall we thank Dr Creagh-Brown for his interest in our article
which we believe highlights an important issue in postgraduate medical
education.
Dear Editor,
Barlow and Nathwani[1] reviewed medico legal and allied aspects of restraints encountered by clinicians in teaching hospital based units in recommending intravenous and broad-spectrum antibiotics. While the local epidemiological resistance patterns would be an asset, clinicians would desire for a rapid response from the local clinical microbiologist. Recently marketed automated devices might not be perfect...
Dear Editor,
We thank Dr. Singh for his interest in our review. Excellent reviews are available that focus exclusively on the role of amyloid degrading enzymes in aging and neurodegeneration and we would like to refer the interested readers to these reviews (Turner, Fisk et al. 2004; Hama and Saido 2005).
Iwata (Iwata, Takaki et al. 2002) demonstrated a statistically significant decrease of NE in the hi...
Dear Editor,
I read with interest Sorabjee and Garje’s recent article on reactivation of old scars[1] I feel that some points must be clarified.
Sorabjee and Garje state that histopathological demonstration of non-caseating granulomas on scar tissue obtained by biopsy in a patient presented with multiple mediastinal lymph nodes accompanied with numerious old scars is sufficient for diagnosis of sarcoidosi...
Dear Editor,
Article by Vandenberghe R and Tournoy J. entitled “Cognitive aging and Alzheimer’s disease” tells a story of Alzheimer’s disease and its cognitive relation with aging. As reported in this review that there is age related changes in the amyloid degrading enzymes, IDE and Neprilysin, differs between regions and no clear picture has been emerged.
But researchers from RIKEN brain Institute demons...
Dear Editor,
We read with great interest the editorial by Dr Rajagopal concerning the clinical implications of ethnic benign neutropenia in patients receiving clozapine treatment.[1)
It is noteworthy that clozapine itself may induce transient and harmless neutropenia, and that such phenomenon are not restricted to certain ethnic groups. Transient neutropenia (defined as a return of the neutrophil count t...
Dear Editor,
I read with interest the recent report by Menon and colleagues in the Journal.[1] The explanations regarding the anatomy underpinning occurrences of crossed aphasia, i.e. transcallosal diaschisis (p. 342), does not hold since no such events occur in the vast majority of behavioral right-handers who sustained similar injuries to the temporoparietal lobe of the minor hemisphere as because there is no mot...
Dear Editor,
We read with great interest the editorial by Dr Rajagopal concerning the clinical implications of ethnic benign neutropenia in patients receiving clozapine treatment.[1]
It is noteworthy that clozapine itself may induce transient and harmless neutropenia, and that such phenomenon are not restricted to certain ethnic groups. Transient neutropenia (defined as a return of the neutrophil count...
Dear Editor,
Stebbing J et al.[1] article raises an important issue of the limited availability of CD4 measurements in resource-scarce settings which poses a major problem in the management of HIV infection. High cost of the perishable reagents, technically complicated and expensive flow cytometers remain a hurdle in developing countries where several million people are in need of therapy. Fortunately, advances in mi...
Dear Editor,
I have read Heatley et al.’s article but I have certain queries in my mind. Heatley et al. are recommending the trial of four week therapy of proton pump inhibitor to exclude the diagnosis of coronary artery disease. I highly disagree to the fact that, as we know many of the myocardial infarction episodes, especially in elderly and diabetics, may present silently. Moreover, it is well known that with i...
Dear Editor,
We thank Dr Creagh-Brown for his interest in our article and comments.
We agree with the comments about figure 2, which is maybe misleading. The marks made by the juniors were judged with regard to the BTS guidelines as described in the article. Figure 2 is designed to illustrate where marks were made in relation to the triangle of safety (represented by the centre square). We agree that fig...
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