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An air crescent sign describes the crescent of air that can be seen in invasive aspergillosis, or other processes that cause pulmonary necrosis.It should not to be confused with the Monad sign which describes the air that surrounds an aspergilloma. Unfortunately, the air around the fungal ball is also crescent shaped and the term air crescent sign is often used interchangeably as in this case report
An air crescent sign describes the crescent of air that can be seen in invasive aspergillosis, or other processes that cause pulmonary necrosis.It should not to be confused with the Monad sign which describes the air that surrounds an aspergilloma. Unfortunately, the air around the fungal ball is also crescent shaped and the term air crescent sign is often used interchangeably as in this case report
Kushwaha et al (1) make the rather positive assertion, regarding the
cause of their patient's symptoms and a possible role of L-DOPA in their
genesis, that it is 'fact that levodopa can contribute to [ST]
occurrence.' Their writing seems to convey an unwarranted confidence in
the strength of this possible, but only remotely possible, association.
I remind readers that the definition of serotonin syndrome (a.k.a....
Kushwaha et al (1) make the rather positive assertion, regarding the
cause of their patient's symptoms and a possible role of L-DOPA in their
genesis, that it is 'fact that levodopa can contribute to [ST]
occurrence.' Their writing seems to convey an unwarranted confidence in
the strength of this possible, but only remotely possible, association.
I remind readers that the definition of serotonin syndrome (a.k.a.
serotonin toxicity) has always been that it is a prerequisite (included in
the benchmark 'Hunter" criteria (2)) that a known (potent) serotonergic
drug must have been administered shortly before symptoms emerge. This
definition became universally accepted ab initio because the
characteristic picture of ST has only ever been reliably described (in
'normal' subjects) following the ingestion of potently serotonergic drugs.
L-dopa is not a 'known serotonergic' drug and there is no evidence that it
produces significant release of serotonin in the human brain. Thus, their
case fails to qualify as ST by the very first criterion of the Hunter
system (Fig 1, (2)).
The authors have failed to adduce any evidence to support the
mechanism they speculate about because the 'supporting' reference they
quote (3) is a letter to a journal which reports no original scientific
data to support their contention: it is an evidence-poor speculation. It
is merely a hypothetical notion that might just possibly warrant
investigation. However it is noteworthy that in the ensuing four decades
no researchers appear to have found it worthy of pursuit and no other
evidence has emerged to support it. Furthermore, of the huge number of
patients (probably many millions) similarly treated over many decades
there are only a couple of rather doubtful case reports. That alone
strongly suggests that the picture reported owes more to the state of
those patients than to L-DOPA.
As a writer involved with many publications on this subject (as both
an author, advisor and referee) it is my common experience that authors
who do not have extensive familiarity with this subject frequently quote
sources which do not contain original data and are frequently speculations
and opinions propounded by people with modest experience or knowledge of
the topic. Such opinions are then reproduced by subsequent writers who
elevate the perception of their status by citing them without critical
comment and without noting that they constitute speculations that have a
scientific foundation that is non-existent or weak. Thus the literature
becomes populated by contributions that are most appropriately described
as rumours: they do not constitute science and have no place in a
'scientific' journal. In my experience there is a widespread failure by
referees to prevent authors from mis-representing references which do not
support the statements concerning which they are cited (or, worse still,
are completely irrelevant). Indeed, Kushwaha et al. mis-cite their two key
ST references, my own review paper (4) and the seminal paper of Dunkerley
et al. There is a widespread failure to recognise that these practices are
a serious academic failing, confuse and impoverish the literature and on
occasions can segue into academic fraud.
A comparable, relevant and topical example of this same type of
careless mis-citation error is the advice/warning about ondansetron (and
related drugs) issued by various regulatory agencies/authorities
(including the WHO, FDA, Health Canada and the Australian TGA). These
warnings are based on similar misconceptions and poor quality mis-quoted
and mis-understood second-hand evidence, as enumerated by Rojas-Fernandes
(5).
I suspect many experienced practitioners who treat organic brain
disease and dementia would agree that atypical side-effects are much more
frequent in this group compared to normal subjects (i.e. those without
organic brain disease). However, it is exceedingly doubtful that
extrapolating to the general population, from rare and unusual reactions
occurring in such cases, is a either a valid or a useful activity. I
suggest it is unlikely to inform us about patho-physiology or treatment:
but it is likely to cause confusion, especially among non-experts and less
critical readers.
References
1. Kushwaha, S, Panda, AK, Malhotra, HS, and Kaur, M, Serotonin
syndrome following levodopa treatment in diffuse Lewy body disease. BMJ
Case Rep, 2014. 2014.
2. Dunkley, EJC, Isbister, GK, Sibbritt, D, Dawson, AH, et al., Hunter
Serotonin Toxicity Criteria: a simple and accurate diagnostic decision
rule for serotonin toxicity. Q. J. Med., 2003. 96: p. 635-642.
3. Sandyk, R, L-Dopa induced "serotonin syndrome" in a parkinsonian
patient on bromocriptine. J Clin Psychopharmacol, 1986. 6([letter]): p.
194-195.
4. Gillman, PK, A review of serotonin toxicity data: implications for the
mechanisms of antidepressant drug action. Biol Psychiatry, 2006. 59(11):
p. 1046-51.
5. Rojas-Fernandes, C, Can 5-HT3 antagonists really contribute to
serotonin toxicity? A call for clarity and pharmacological law and order.
Drugs - Real World Outcomes, 2014: p. [in press].
Very interesting case with complex and expert care. Wondered why
repeated courses off co-amoxiclav were given when it is associated with
cholestatic jaundice which while usually self-limiting can be fatal. Do
you have IgG4 levels on patient and did patient have eosinophilia at any
time?
I have 2 points to make here, and i also agree whether this patient
had ischemia in the first place.
1)In case of ischemia it is known that the Echo shows regional wall
motion abnormalities in 1 to 2 minutes, and much earlier than the ECG
changes, but in this case, patient had no regional wall motion
abnormalities and normal LV function.
2) This patient might be having a NSTEMI with a preexisting RBBB...
I have 2 points to make here, and i also agree whether this patient
had ischemia in the first place.
1)In case of ischemia it is known that the Echo shows regional wall
motion abnormalities in 1 to 2 minutes, and much earlier than the ECG
changes, but in this case, patient had no regional wall motion
abnormalities and normal LV function.
2) This patient might be having a NSTEMI with a preexisting RBBB.
I would like to raise two specific questions with regard to the RBBB
seen in this patient. Firstly, how are the authors certain that this
patient did not have a pre-existing benign RBBB with a superimposed
NSTEMI? Did they have an older ECG for comparison? Secondly, in addition
to the presence of RBBB, this ECG also shows an S1Q3T3 pattern suggestive
of RV volume overload, although the tachycardia seen in PE is absent. D...
I would like to raise two specific questions with regard to the RBBB
seen in this patient. Firstly, how are the authors certain that this
patient did not have a pre-existing benign RBBB with a superimposed
NSTEMI? Did they have an older ECG for comparison? Secondly, in addition
to the presence of RBBB, this ECG also shows an S1Q3T3 pattern suggestive
of RV volume overload, although the tachycardia seen in PE is absent. Did
echocardiography show any evidence of RV dysfunction?
I thank Dr. Veloso for his comments regarding our case report [1].
Directly from the consensus statement he cites [2], his opinion is
valuable, but feel that aborted sudden death conveys a better picture due
to successful resuscitation with CPR and defibrillation, a description
already used by other authors [3].
Rienzi A Diaz, MD, FACC, EACVI,
Professor of Cardiology
I thank Dr. Veloso for his comments regarding our case report [1].
Directly from the consensus statement he cites [2], his opinion is
valuable, but feel that aborted sudden death conveys a better picture due
to successful resuscitation with CPR and defibrillation, a description
already used by other authors [3].
Rienzi A Diaz, MD, FACC, EACVI,
Professor of Cardiology
References: 1) Diaz RA, Valdes J. Aborted sudden cardiac death
associated with an anomalous right coronary artery. BMJ Case Rep 2015;
doi: 10.1136/bcr-2015- 210850. 2) Buxton AE, Calkins H, Callans DJ, et al.
ACC/AHA/HRS 2006 key data elements and definitions for
electrophysiological studies and procedures: a report of the American
College of Cardiology/American Heart Association Task Force on Clinical
Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on
Electrophysiology). Circulation 2006; 114(23):2534-70. 3) Kaushik S,
Subramanian SR, Rafii S, Castillo R. Aborted sudden cardiac death (SCD) in
a patient with hypertrophic cardiomyopathy (HCM) with low-risk factors for
SCD. BMJ Case Reports 2013; doi: 10.1136/bcr-2012-006459
I read with interest the case reported by Diaz and Valdez (1)
regarding a patient who was successfully resuscitated from ventricular
fibrillation cardiac arrest while running in a marathon race. The patient
had a posterior diagnosis of anomalous right coronary artery arising from
the aorta above the left sinus of Valsalva that subsequently runs between
the aorta and the pulmonary artery, discovered by a 64-slice multidet...
I read with interest the case reported by Diaz and Valdez (1)
regarding a patient who was successfully resuscitated from ventricular
fibrillation cardiac arrest while running in a marathon race. The patient
had a posterior diagnosis of anomalous right coronary artery arising from
the aorta above the left sinus of Valsalva that subsequently runs between
the aorta and the pulmonary artery, discovered by a 64-slice multidetector
coronary computerized tomography. However, the title of this article is
not in accordance with current standards defined by the American College
of Cardiology, the American Heart Journal, and the Heart Rhythm Society
(2). In this document, it was postulated that "sudden cardiac death should
not be used to describe events that are not fatal", restricting the use of
this term only to the events directly resulting in death, in order to
avoid misinterpretations. Thus, I do believe that the best title for this
interesting report would be: 'Cardiac arrest associated with an anomalous
right coronary artery'.
References:
1) Diaz RA, Vald?s J. Aborted sudden cardiac death associated with an
anomalous right coronary artery. BMJ Case Rep 2015; doi:10.1136/bcr-2015-
210850.
2) Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data
elements and definitions for electrophysiological studies and procedures:
a report of the American College of Cardiology/American Heart Association
Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to
Develop Data Standards on Electrophysiology). Circulation
2006;114(23):2534-70.
Thank you very much Mr M.A Warner for reviewing our article and
sharing your views from the same. We do agree with your suggestion that,
there in no 'strong' correlation between the use of peripheral nerve
blockage and delay in diagnosis of acute compartment syndrome following
surgical procedures on extremities. Among the reported cases of peripheral
nerve blockage use in extremity surgeries and where the compartment
syn...
Thank you very much Mr M.A Warner for reviewing our article and
sharing your views from the same. We do agree with your suggestion that,
there in no 'strong' correlation between the use of peripheral nerve
blockage and delay in diagnosis of acute compartment syndrome following
surgical procedures on extremities. Among the reported cases of peripheral
nerve blockage use in extremity surgeries and where the compartment
syndrome was diagnosed and prompt fasciotomy preformed, all the patients
were within the "hospital or clinical setting". The clinicians were
vigilant with high index of suspension of acute compartment syndrome hence
there were no delays in making the diagnosis nor in performing the
fasciotomy surgery to adequately decompress the compartments, thus avoided
the potential long-term complications and disabilities.
Our patient received 10mls of 0.25% Chirocaine and 13mls of 2%
lignocaine with adrenaline 1:200000 strength, in total for his left
axillary nerve block. The procedure was performed with ultrasound guidance
and confirmed with nerve stimulator of adequate block in Radial, Ulnar,
Median and Musculoskeletal nerve. He was discharged 8 hours following his
surgery as he was quite comfortable with no pain in the operated limb and
unfortunately there was no clear documentation with regards to distal
muscular activity, prior to discharge .
We also agree with you in that, this patient underwent a revision
procedure that would involve more soft tissue dissection and stripping,
which itself contribute to increased post operative swelling compared to
fractures with minimal displacement.
We believe, learning points in addition to aforementioned in the case
report are, clinicians and all health care professional involved in
providing care, should have awareness of compartment syndrome risk in
extremity injuries and caution with clinical vigilance is needed when
treating patients with extremity fractures and regional block is still in
effect.
[Apologies for late edits to letter submitted yesterday, please note
there are 3 new references addressing hepatotoxicity of fluoroquinolones
that were not in orginal letter].
Lugg et al (2015) reported a case study of a 16 year old girl born
who presented with signs of chronic joint pain, dizziness and non-specific
abdominal pains after consuming 3 cups per day of imported herbal green
tea (as tea bags) for a p...
[Apologies for late edits to letter submitted yesterday, please note
there are 3 new references addressing hepatotoxicity of fluoroquinolones
that were not in orginal letter].
Lugg et al (2015) reported a case study of a 16 year old girl born
who presented with signs of chronic joint pain, dizziness and non-specific
abdominal pains after consuming 3 cups per day of imported herbal green
tea (as tea bags) for a period of 3 months [1]. There are a number of
interesting points not addressed in the case study which physicians may
not be aware of that are of clinical significance.
Firstly, the description of the ailments which the subject presented
with strongly suggest chronic fluoride intoxication. Hallanger et al
(2007) reported that the clinical features associated with fluoride
intoxication resulting from habitual tea consumption can include joint
pain and gastrointestinal complaints and that fluoride toxicity is often
overlooked by clinicians [2]. Despite the publication of a large number of
reports addressing fluoride intoxication from habitual tea drinking [3]
many health care professionals remain unaware of the risk of fluoride
intoxication from tea and lack an understanding of the pathophysiology of
fluoride toxicosis. The United States National Academy, National Research
Council (2006) reported that excessive intake of fluoride will manifest
itself in a musculoskeletal disease with associated symptoms including
chronic joint pain and arthritic symptoms [4]. However, perhaps one the
most detailed explanations of the pathophysiology of fluoride toxicosis is
provided by Professor Alexander V. Akleyev [5]. In addition to
musculoskeletal disorders, Akleyev reported that stage 2 fluorosis, the
following symptoms are observed: subatrophic and atrophic rhinitis,
pharyngitis, laryngitis, chronic conjunctivitis, retinal degeneration with
visual impairment, hearing loss, increasing impairment of bronchial
patency, and pulmonary insufficiency; mycrodial dystrophy with reduced
contractility, chronic gastritis mainly with the reduction of secretory
and acid forming function of the stomach, and chronic hepatitis with
persistent liver failure; distinct astheno-vegetative syndrome, toxic
polyneuritis and decrease in glucocorticoid function of adrenal cortex;
and microhematuria and proteinura [4]. Kessabi et al (1986) also reported
that acute hepatitis and degeneration in the liver develop following
chronic fluoride intake [6]. Other studies have also found that fluoride
toxicosis can induce hepatotoxicity and oxidative stress in humans [7-8]
and animals [9].
In the case study described by Lugg and associates [1], the fluoride
concentration in the tea samples ingested by the patient are unknown, as
they were not tested. Chan et al (2013) reported high fluoride levels in
tea infusions in the United Kingdom including green tea leaves which were
found to contained up to 6.67mg/L when made with deionized water [10]. The
European Food Safety Authority (EFSA) have reported that drinking just 2
cups of tea per day (with a fluoride content of 5mg/l), combined with an
average consumption of fluoridated drinking water and use of fluoridated
tap water in the preparation of food, but excluding all other sources
(including solid foods, toothpaste and dental products), would provide a
daily dietary intake of 6 mg per day [11]. The EFSA have established
daily recommended intake levels (AI) and Tolerable Upper Intake Levels
(ULs) for fluoride. For an adult female the AI is 2.9mg per day while the
UL is 7mg per day [11-12]. Birmingham is the largest city in the England
with artificially fluoridated water. Thus, the patient having consumed 3
cups of tea per day, is likely to have exceeded the recommended UL for
fluoride, thereby increasing the risk of chronic fluoride intoxication.
Secondly, Lugg and associates noted that the condition of the subject
worsened following prescribing of amoxicillin [1]. Amoxicillin is a
fluoroquinolone. The name fluoroquinolone comes from the presence of
fluorine which is found in all fluoroquinolones. Hong et al (2005)
reported that amoxicillin was associated with dental fluorosis in children
[13]. Thus, it is likely that administration of amoxicillin resulted in
further contributing to chronic fluoride intoxication of the subject and a
worsening of her condition. Other fluoroquinolones such as ciprofloxacin
have been found to significantly increase plasma fluoride levels in
individuals [14]. Fluoroquinolones have also been found to be associated
with severe hepatotoxicity [15-18]. It is likely that the toxicity of
fluoroquinolones would be more immediate in persons with elevated
background plasma fluoride levels.
Thirdly, on cessation of the herbal tea and treatment with
intravenous fluids and N-acetylcysteine, her condition resolved [1]. N-
acetylcysteine is known to protect against fluoride-induced oxidative
damage [19].
Overall the evidence indicates the symptoms reported may be due
fluoride toxicosis caused by high fluoride intake from tea, combined with
other fluoride sources such as fluoridated drinking water and medications.
There is a need for healthcare workers to be aware of the pathophysiology
of fluoride toxicosis as well as dietary fluoride sources, particularly
among habitual tea drinkers in communities with artificially fluoridated
drinking water. Urinary or blood fluoride levels should be routinely
monitored in patients with muscleoskeletal and gastrointestinal disorders.
Fasting serum fluoride concentrations ranging from 2.5 - 8.0 ?M/L can
result in chronic fluoride intoxication and stage I and stage II skeletal
fluorosis [20].
[1] Lugg ST, Menezes DB, Gompertz S. Chinese green tea and acute
hepatitis: a rare yet recurring theme. BMJ Case Rep 2015, doi:10.1136/ bcr
-2014-208534.
[2] Hallanger-Johnson JE, Kearns AE, Doran PM, Khoo TK., Wermers RA.
Fluoride-related bone disease associated with habitual tea consumption.
Mayo Clinic Proceedings 2007;82(6):719-24.
[3] Yi J, Cao J. Tea and fluorosis. Journal of Fluorine Chemistry,
2008, 129: 76-81.
[4] National Research Council, Review of Fluoride in Drinking Water,
U.S. National Research Council 2006.
[5] Neurological Disorders of Non-Radiation Nature, Fluorosis, In
Chronic Radiation Syndrome, Alexander V. Akleyev, Spriner-Verlag Berlin
Heidelberg 2014. ISBN 978-3-642-45116-4.
[6] Kessabi M, Hamliri A. Experimental fluorosis in sheep:
Alleviating effects of aluminum. Vet. Hum. Toxicol., 1986, 28: 300-304.
[7] Michael M, Barot VV, Chinoy NJ. Investigations of Soft Tissue
Functions In Fluorotic Individuals of North Gujarat. Fluoride 1996, Vol.29
No.2 63-71.
[8] Medvedeva VN. Characteristics of the course of chronic hepatitis
in workers coming in contact with flourine compounds. Gigiena Truda;
Professional'nye Zabolevaniia, Jan 1985. pg 24-6.
[9] AL-Harbia MS, Hamzaa RZ, Dwarya AA. Ameliorative effect of
selenium and curcumin on sodium fluoride induced hepatotoxicity and
oxidative stress in male mice. J Chem Pharma Res, 2014, 6(4):984-998.
[10] Chan L, Mehra A, Saikat S, Lynch P. Human exposure assessment
of fluoride from tea (Camellia sinensis L.) Food Res Internat. 2013; 51:
564-570.
[11] European Food Safety Authority, Scientific Opinion on Dietary
Reference Values for fluoride, EFSA Panel on Dietetic Products, Nutrition,
and Allergies: EFSA Journal. 2013;11(8):3332.
[12] European Food Safety Authority, Scientific Opinion of the Panel
on Dietetic Products, Nutrition, and Allergies (NDA) on the tolerable
upper intake level of fluoride. The EFSA Journal. 2005, 192, 1-65.
[13] Hong L, Levy SM, Warren JJ, Dawson DV, Bergus GR, Wefel JS.
Association of Amoxicillin Use During Early Childhood With Developmental
Tooth Enamel Defects, Arch Pediatr Adolesc Med. 2005;159:943-948, 995-996.
[14] Pradhan KM, Arora NK, Jena A, Susheela AK, Bhan MK. Safety of
ciprofloxacin therapy in children: magnetic resonance images, body fluid
levels of fluoride and linear growth. Acta Paediatr. 1995, 84:555-560.
[15] Hautekeete ML. Hepatotoxicity of antibiotics. Acta
Gastroenterol Belg. 1995 May-Aug;58(3-4):290-6.
[16] Vial T, Biour M, Descotes J, Trepo C. Antibiotic-associated
hepatitis: update from 1990. Ann Pharmacother. 1997 Feb;31(2):204-20.
[17] Thiim M, Friedman LS. Hepatotoxicity of antibiotics and
antifungals. Clin Liver Dis. 2003 May;7(2):381-99, vi-vii.
[18] Robles M, Andrade RJ. Hepatotoxicity by antibiotics: update in
2008. Rev Esp Quimioter. 2008 Dec;21(4):224-33. Article in Spanish.
[19] Paw?owska-G?ral K, Kurzeja E, Stec M. N-acetylcysteine protects
against fluoride-induced oxidative damage in primary rat hepatocytes.
Toxicology in Vitro, December 2013, Volume 27, Issue 8, Pages 2279-2282.
doi:10.1016/j.tiv.2013.09.019.
[20] Xiang QY, Chen LS, Chen XD., Wang CS, et al. Serum Fluoride And
Skeletal Fluorosis In Two Villages In Jiangsu Province, China. 178
Fluoride 2005;38(3):178-184
I have read with surprise the case report which makes rather wide
sweeping claims about green tea being of health concern. After a quick
literature review there have been rare cases after prolonged ingestion of
green tea extract - but none ever analyzed the extract for components
besides green tea.
It is not a secret that there are problems with food safety in china,
especially pesticide use, so making claims about the p...
I have read with surprise the case report which makes rather wide
sweeping claims about green tea being of health concern. After a quick
literature review there have been rare cases after prolonged ingestion of
green tea extract - but none ever analyzed the extract for components
besides green tea.
It is not a secret that there are problems with food safety in china,
especially pesticide use, so making claims about the plant instead of
doing at least a rough test for chemicals in the extract (or in that case
the tea) seem in my opinion very much warranted prior to claims with such
impact.
Conflict of Interest:
...Kushwaha et al (1) make the rather positive assertion, regarding the cause of their patient's symptoms and a possible role of L-DOPA in their genesis, that it is 'fact that levodopa can contribute to [ST] occurrence.' Their writing seems to convey an unwarranted confidence in the strength of this possible, but only remotely possible, association.
I remind readers that the definition of serotonin syndrome (a.k.a....
Very interesting case with complex and expert care. Wondered why repeated courses off co-amoxiclav were given when it is associated with cholestatic jaundice which while usually self-limiting can be fatal. Do you have IgG4 levels on patient and did patient have eosinophilia at any time?
Conflict of Interest:
None declared
I have 2 points to make here, and i also agree whether this patient had ischemia in the first place.
1)In case of ischemia it is known that the Echo shows regional wall motion abnormalities in 1 to 2 minutes, and much earlier than the ECG changes, but in this case, patient had no regional wall motion abnormalities and normal LV function.
2) This patient might be having a NSTEMI with a preexisting RBBB...
I would like to raise two specific questions with regard to the RBBB seen in this patient. Firstly, how are the authors certain that this patient did not have a pre-existing benign RBBB with a superimposed NSTEMI? Did they have an older ECG for comparison? Secondly, in addition to the presence of RBBB, this ECG also shows an S1Q3T3 pattern suggestive of RV volume overload, although the tachycardia seen in PE is absent. D...
I thank Dr. Veloso for his comments regarding our case report [1]. Directly from the consensus statement he cites [2], his opinion is valuable, but feel that aborted sudden death conveys a better picture due to successful resuscitation with CPR and defibrillation, a description already used by other authors [3].
Rienzi A Diaz, MD, FACC, EACVI, Professor of Cardiology
References: 1) Diaz RA, Valdes J. A...
I read with interest the case reported by Diaz and Valdez (1) regarding a patient who was successfully resuscitated from ventricular fibrillation cardiac arrest while running in a marathon race. The patient had a posterior diagnosis of anomalous right coronary artery arising from the aorta above the left sinus of Valsalva that subsequently runs between the aorta and the pulmonary artery, discovered by a 64-slice multidet...
Thank you very much Mr M.A Warner for reviewing our article and sharing your views from the same. We do agree with your suggestion that, there in no 'strong' correlation between the use of peripheral nerve blockage and delay in diagnosis of acute compartment syndrome following surgical procedures on extremities. Among the reported cases of peripheral nerve blockage use in extremity surgeries and where the compartment syn...
[Apologies for late edits to letter submitted yesterday, please note there are 3 new references addressing hepatotoxicity of fluoroquinolones that were not in orginal letter].
Lugg et al (2015) reported a case study of a 16 year old girl born who presented with signs of chronic joint pain, dizziness and non-specific abdominal pains after consuming 3 cups per day of imported herbal green tea (as tea bags) for a p...
I have read with surprise the case report which makes rather wide sweeping claims about green tea being of health concern. After a quick literature review there have been rare cases after prolonged ingestion of green tea extract - but none ever analyzed the extract for components besides green tea. It is not a secret that there are problems with food safety in china, especially pesticide use, so making claims about the p...
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