From: "Clifford G. Miller"
|Subject:||Letters to the Editor - Barbara Ellen: All that smooching was far too cordiale|
|Date:||Tue, 15 Apr 2008 06:29:28 +0100|
|From:||Clifford G. Miller <email@example.com>|
|CC:||Barbara Ellen, Denis Campbell, Jamie Doward|
"The Science Media Centre actually praised Barbara's piece for being was 'extremely balanced' adding 'she clearly concedes that this issue can be seen from both sides'."This is part of what I had to say in reply to you:-
"Your comment that "The Science Media Centre actually praised Barbara's piece" (3rd April - on 'All that smooching was far too cordiale') will concern many people. They have good cause to be concerned. May I suggest you take some time out to read George Monbiot's Guardian story "Invasion of the entryists" on Fiona Fox, The Science Media Centre and Sense About Science. You might then want to take a look here:-The New York Times' piece is about Hannah Poling and her autism being admitted by US government experts to have been caused by vaccines (and not simply by MMR but by vaccines in general). They conceded her case in the Federal Court rather than fight it and have a court decision. This story has been reported over many weeks and on numerous mainstream print and broadcast media in the US including the popular Larry King Live, which I am sure people in the UK have heard of. It is also reported that the Hannah Poling case is not isolated and that similar cases could be common, with as many as 1 in 60 sharing the same predisposition to react adversely to vaccines.
"The investigation has found that when [Wakefield] warned parents to avoid MMR, and published research claiming a link with autism, he did not disclose he was being funded through solicitors seeking evidence to use against vaccine manufacturers. "Now we know from this that Horton's claims do not stand up and with them, those of The Sunday Times fall as well. But of course, not a word in The Observer, which is in thrall to The Science Media Centre, as you have so ably demonstrated.
"Young children who have dysfunctional cellular energy metabolism therefore might be more prone to undergo autistic regression between 18 and 30 months of age if they also have infections or immunizations at the same time. Although patterns of regression can be genetically and prenatally determined, it is possible that underlying mitochondrial dysfunction can either exacerbate or affect the severity of regression. Abnormalities of oxidative phosphorylation can be developmental and age related and can normalize with time."If you look at the other 9 cases cited below and take for example of Banks v HHS, you will see that he was diagnosed as PDD-NOS which is also called "atypical autism", and that it was described as "pervasive developmental delay".
[In the US the official diagnostic definition of what we call "Autism Spectrum Disorders" or ASD are instead called "Pervasive Development Disorders" or PDD for short. That is under the ""Diagnostic and Statistical Manual of Mental Disorders (4th edn)" or "DSM IV" for short.]Some of the US press is hard hitting:-
["Autistic Spectrum Disorder" is the term applied internationally under the "ICD" or "International Classification of Disease"]
Banks v. HHS (Case 02-0738V, 2007 U.S. Claims LEXIS 254, July 20, 2007)
MMR vaccine administered in March 2000.
The child was diagnosed with PDD secondary to acute disseminated encephalomyelitis (ADEM).
Michael McLaren, counsel for petitioner; Richard Abell, Special Master
Noel v. HHS (Case 99-538V, 2004 U.S. Claims LEXIS 354, December 14, 2004)
DPaT and HiB vaccines administered in March 1997.
Seizure disorder in a child diagnosed with autism.
Clifford Shoemaker, counsel for petitioner; Laura Millman, Special Master
Freeman v. HHS (Case 01-390V, 2003 U.S. Claims LEXIS 285, September 25, 2003)
MMR vaccine administered in July 1999.
Seizure disorder in a child displaying features of “atypical autism.”
Ronald Homer and Sylvia Chin-Caplan, counsel for petitioner; George L. Hastings, Special Master
Suel v. HHS (Case 90-935V, 1997 U.S. Claims LEXIS 210, September 22, 1997)
DPT vaccine administered in the 1980’s.
Aggravation of tuberous sclerosis in a child diagnosed with autism.
Richard Gage, counsel for petitioner; Laura Millman, Special Master
Kleinert v. HHS (Case 90-211V, 1991 U.S. Cl. Ct. LEXIS 69, February 20, 1991)
DPT vaccine administered in February 1981.
Seizure disorder in a child diagnosed with “overfocussing,” “similar in some respects to autism.”
Michael Hugo, counsel for petitioner; Denis J. Hauptly, Special Master
Underwood v. HHS (Case 90-719V, 1991 U.S. Cl. Ct. LEXIS 373, July 31, 1991)
DPT vaccine administered in 1974.
Seizure disorder in a child diagnosed with autism.
Curtis Webb, counsel for petitioner; Elizabeth Wright, Special Master
Sanford v. HHS (Case 90-2760V, 1993 U.S. Claims LEXIS 49, May 10, 1993)
DPT vaccine administered in September 1979.
Seizure disorder in a child with “autistic tendencies.”
Mari Bush, counsel for petitioner; LaVon French, Special Master
Bastian v. HHS (Case 90-1161V, 1994 U.S. Claims LEXIS 196, September 22, 1994)
DPT administered in December 1984.
Seizure disorder in a child diagnosed with autism. Testifying doctors for petitioners and HHS all agreed that while he “exhibits some autistic symptomatology, [he] is not autistic.”
Boyd McDowell, counsel for petitioner; Richard Abell, Special Master
Lassiter v. HHS (Case 90-2036V, 1996 U.S. Claims LEXIS 216, December 17, 1996)
DPT vaccine administered in 1972.
Seizure disorder in an young man diagnosed with autism. The court ruled that a diagnosis of idiopathic autism (i.e., autism of unknown origin) was not sufficient to establish a “factor unrelated” that might result in the dismissal of a claim.
Clifford Shoemaker, counsel for petitioner; LaVon French, Special Master
The Vaccine-Autism Court Document Every American Should Read
FULL TEXT OF THE US GOVERNMENT'S CONCESSION OF THE HANNAH POLING CASE:-
IN THE UNITED STATES COURT OF FEDERAL CLAIMSOn Friday, February 22, HHS conceded that this child's complex partial seizure disorder was also caused by her vaccines. Now US taxpayers will award this family compensation to finance her seizure medication.
OFFICE OF SPECIAL MASTERS
CHILD, a minor,
by her Parents and Natural Guardians,
SECRETARY OF HEALTH AND HUMAN SERVICES,
RESPONDENT'S RULE 4(c) REPORT
In accordance with RCFC, Appendix B, Vaccine Rule 4(c), the Secretary of Health and Human Services submits the following response to the petition for compensation filed in this case.
CHILD ("CHILD") was born on December --, 1998, and weighed eight pounds, ten ounces. Petitioners' Exhibit ("Pet. Ex.") 54 at 13. The pregnancy was complicated by gestational diabetes. Id. at 13. CHILD received her first Hepatitis B immunization on December 27, 1998. Pet. Ex. 31 at 2.
From January 26, 1999 through June 28, 1999, CHILD visited the Pediatric Center, in Catonsville, Maryland, for well-child examinations and minor complaints, including fever and eczema. Pet. Ex. 31 at 5-10, 19. During this time period, she received the following pediatric vaccinations, without incident:
Vaccine Dates Administered
Hep B 12/27/98; 1/26/99
IPV 3/12/99; 4/27/99
Hib 3/12/99; 4/27/99; 6/28/99
DTaP 3/12/99; 4/27/99; 6/28/99
Id. at 2.
At seven months of age, CHILD was diagnosed with bilateral otitis media. Pet. Ex. 31 at 20. In the subsequent months between July 1999 and January 2000, she had frequent bouts of otitis media, which doctors treated with multiple antibiotics. Pet. Ex. 2 at 4. On December 3,1999, CHILD was seen by Karl Diehn, M.D., at Ear, Nose, and Throat Associates of the Greater Baltimore Medical Center ("ENT Associates"). Pet. Ex. 31 at 44. Dr. Diehn recommend that CHILD receive PE tubes for her "recurrent otitis media and serious otitis." Id. CHILD received PE tubes in January 2000. Pet. Ex. 24 at 7. Due to CHILD's otitis media, her mother did not allow CHILD to receive the standard 12 and 15 month childhood immunizations. Pet. Ex. 2 at 4.
According to the medical records, CHILD consistently met her developmental milestones during the first eighteen months of her life. The record of an October 5, 1999 visit to the Pediatric Center notes that CHILD was mimicking sounds, crawling, and sitting. Pet. Ex. 31 at 9. The record of her 12-month pediatric examination notes that she was using the words "Mom" and "Dad," pulling herself up, and cruising. Id. at 10.
At a July 19, 2000 pediatric visit, the pediatrician observed that CHILD "spoke well" and was "alert and active." Pet. Ex. 31 at 11. CHILD's mother reported that CHILD had regular bowel movements and slept through the night. Id. At the July 19, 2000 examination, CHILD received five vaccinations - DTaP, Hib, MMR, Varivax, and IPV. Id. at 2, 11.
According to her mother's affidavit, CHILD developed a fever of 102.3 degrees two days after her immunizations and was lethargic, irritable, and cried for long periods of time. Pet. Ex. 2 at 6. She exhibited intermittent, high-pitched screaming and a decreased response to stimuli. Id. MOM spoke with the pediatrician, who told her that CHILD was having a normal reaction to her immunizations. Id. According to CHILD's mother, this behavior continued over the next ten days, and CHILD also began to arch her back when she cried. Id.
On July 31, 2000, CHILD presented to the Pediatric Center with a 101-102 degree temperature, a diminished appetite, and small red dots on her chest. Pet. Ex. 31 at 28. The nurse practitioner recorded that CHILD was extremely irritable and inconsolable. Id. She was diagnosed with a post-varicella vaccination rash. Id. at 29.
Two months later, on September 26, 2000, CHILD returned to the Pediatric Center with a temperature of 102 degrees, diarrhea, nasal discharge, a reduced appetite, and pulling at her left ear. Id. at 29. Two days later, on September 28, 2000, CHILD was again seen at the Pediatric Center because her diarrhea continued, she was congested, and her mother reported that CHILD was crying during urination. Id. at 32. On November 1, 2000, CHILD received bilateral PE tubes. Id. at 38. On November 13, 2000, a physician at ENT Associates noted that CHILD was "obviously hearing better" and her audiogram was normal. Id. at 38. On November 27, 2000, CHILD was seen at the Pediatric Center with complaints of diarrhea, vomiting, diminished energy, fever, and a rash on her cheek. Id. at 33. At a follow-up visit, on December 14, 2000, the doctor noted that CHILD had a possible speech delay. Id.
CHILD was evaluated at the Howard County Infants and Toddlers Program, on November 17, 2000, and November 28, 2000, due to concerns about her language development. Pet. Ex. 19 at 2, 7. The assessment team observed deficits in CHILD's communication and social development. Id. at 6. CHILD's mother reported that CHILD had become less responsive to verbal direction in the previous four months and had lost some language skills. Id. At 2.
On December 21, 2000, CHILD returned to ENT Associates because of an obstruction in her right ear and fussiness. Pet. Ex. 31 at 39. Dr. Grace Matesic identified a middle ear effusion and recorded that CHILD was having some balance issues and not progressing with her speech. Id. On December 27, 2000, CHILD visited ENT Associates, where Dr. Grace Matesic observed that CHILD's left PE tube was obstructed with crust. Pet. Ex. 14 at 6. The tube was replaced on January 17, 2001. Id.
Dr. Andrew Zimmerman, a pediatric neurologist, evaluated CHILD at the Kennedy Krieger Children's Hospital Neurology Clinic ("Krieger Institute"), on February 8, 2001. Pet. Ex. 25 at 1. Dr. Zimmerman reported that after CHILD's immunizations of July 19, 2000, an "encephalopathy progressed to persistent loss of previously acquired language, eye contact, and relatedness." Id. He noted a disruption in CHILD's sleep patterns, persistent screaming and arching, the development of pica to foreign objects, and loose stools. Id. Dr. Zimmerman observed that CHILD watched the fluorescent lights repeatedly during the examination and
would not make eye contact. Id. He diagnosed CHILD with "regressive encephalopathy with features consistent with an autistic spectrum disorder, following normal development." Id. At 2. Dr. Zimmerman ordered genetic testing, a magnetic resonance imaging test ("MRI"), and an electroencephalogram ("EEG"). Id.
Dr. Zimmerman referred CHILD to the Krieger Institute's Occupational Therapy Clinic and the Center for Autism and Related Disorders ("CARDS"). Pet. Ex. 25 at 40. She was evaluated at the Occupational Therapy Clinic by Stacey Merenstein, OTR/L, on February 23, 2001. Id. The evaluation report summarized that CHILD had deficits in "many areas of sensory processing which decrease[d] her ability to interpret sensory input and influence[d] her motor performance as a result." Id. at 45. CHILD was evaluated by Alice Kau and Kelley Duff, on May 16, 2001, at CARDS. Pet. Ex. 25 at 17. The clinicians concluded that CHILD was developmentally delayed and demonstrated features of autistic disorder. Id. at 22.
CHILD returned to Dr. Zimmerman, on May 17, 2001, for a follow-up consultation. Pet. Ex. 25 at 4. An overnight EEG, performed on April 6, 2001, showed no seizure discharges. Id. at 16. An MRI, performed on March 14, 2001, was normal. Pet. Ex. 24 at 16. A G-band test revealed a normal karyotype. Pet. Ex. 25 at 16. Laboratory studies, however, strongly indicated an underlying mitochondrial disorder. Id. at 4.
Dr. Zimmerman referred CHILD for a neurogenetics consultation to evaluate her abnormal metabolic test results. Pet. Ex. 25 at 8. CHILD met with Dr. Richard Kelley, a specialist in neurogenetics, on May 22, 2001, at the Krieger Institute. Id. In his assessment, Dr. Kelley affirmed that CHILD's history and lab results were consistent with "an etiologically unexplained metabolic disorder that appear[ed] to be a common cause of developmental regression." Id. at 7. He continued to note that children with biochemical profiles similar to CHILD's develop normally until sometime between the first and second year of life when their metabolic pattern becomes apparent, at which time they developmentally regress. Id. Dr. Kelley described this condition as "mitochondrial PPD." Id.
On October 4, 2001, Dr. John Schoffner, at Horizon Molecular Medicine in Norcross, Georgia, examined CHILD to assess whether her clinical manifestations were related to a defect in cellular energetics. Pet. Ex. 16 at 26. After reviewing her history, Dr. Schoffner agreed that the previous metabolic testing was "suggestive of a defect in cellular energetics." Id. Dr. Schoffner recommended a muscle biopsy, genetic testing, metabolic testing, and cell culture based testing. Id. at 36. A CSF organic acids test, on January 8, 2002, displayed an increased lactate to pyruvate ratio of 28,1 which can be seen in disorders of mitochondrial oxidative phosphorylation. Id. at 22. A muscle biopsy test for oxidative phosphorylation disease revealed abnormal results for Type One and Three. Id. at 3. The most prominent findings were scattered atrophic myofibers that were mostly type one oxidative phosphorylation dependent myofibers, mild increase in lipid in selected myofibers, and occasional myofiber with reduced cytochrome c oxidase activity. Id. at 7. After reviewing these laboratory results, Dr. Schoffner diagnosed CHILD with oxidative phosphorylation disease. Id. at 3. In February 2004, a mitochondrial DNA ("mtDNA") point mutation analysis revealed a single nucleotide change in the 16S ribosomal RNA gene (T2387C). Id. at 11.
CHILD returned to the Krieger Institute, on July 7, 2004, for a follow-up evaluation with Dr. Zimmerman. Pet. Ex. 57 at 9. He reported CHILD "had done very well" with treatment for a mitochondrial dysfunction. Dr. Zimmerman concluded that CHILD would continue to require services in speech, occupational, physical, and behavioral therapy. Id.
On April 14, 2006, CHILD was brought by ambulance to Athens Regional Hospital and developed a tonic seizure en route. Pet. Ex. 10 at 38. An EEG showed diffuse slowing. Id. At 40. She was diagnosed with having experienced a prolonged complex partial seizure and transferred to Scottish Rite Hospital. Id. at 39, 44. She experienced no more seizures while at Scottish Rite Hospital and was discharged on the medications Trileptal and Diastal. Id. at 44. A follow-up MRI of the brain, on June 16, 2006, was normal with evidence of a left mastoiditis manifested by distortion of the air cells. Id. at 36. An EEG, performed on August 15, 2006,
showed "rhythmic epileptiform discharges in the right temporal region and then focal slowing during a witnessed clinical seizure." Id. At 37. CHILD continues to suffer from a seizure disorder.
Medical personnel at the Division of Vaccine Injury Compensation, Department of Health and Human Services (DVIC) have reviewed the facts of this case, as presented by the petition, medical records, and affidavits. After a thorough review, DVIC has concluded that compensation is appropriate in this case.
In sum, DVIC has concluded that the facts of this case meet the statutory criteria for demonstrating that the vaccinations CHILD received on July 19, 2000, significantly aggravated an underlying mitochondrial disorder, which predisposed her to deficits in cellular energy metabolism, and manifested as a regressive encephalopathy with features of autism spectrum disorder. Therefore, respondent recommends that compensation be awarded to petitioners in accordance with 42 U.S.C. § 300aa-11(c)(1)(C)(ii).
DVIC has concluded that CHILD's complex partial seizure disorder, with an onset of almost six years after her July 19, 2000 vaccinations, is not related to a vaccine-injury.
PETER D. KEISLER
Assistant Attorney General
TIMOTHY P. GARREN
Torts Branch, Civil Division
MARK W. ROGERS
Torts Branch, Civil Division
VINCENT J. MATANOSKI
Torts Branch, Civil Division
s/ Linda S. Renzi by s/ Lynn E. Ricciardella
LINDA S. RENZI
Senior Trial Counsel
Torts Branch, Civil Division
U.S. Department of Justice
P.O. Box 146
Benjamin Franklin Station
Washington, D.C. 20044
DATE: November 9, 2007
Hannah Poling's seizures did not begin until six years after the date of vaccination, yet the US government acknowledges they were, indeed, linked to the immunizations of July, 2000.
(*) the true estimate is higher - 1 in 86. The 1 in 116 figure is from Baird 2006. This was not recalculated for this commentary to ensure people would recognise the figure and not have to wonder where 1 in 86 came from. The Baird 2006 figure is 116.1 in 10,000 (ie 116.1:10,000 (90.4-141.8) for cases on the autistic spectrum..
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E-mail Clifford Miller