Letter:

Attached is a column I sent to Professor Peter Hindmarsh, who is the insulin expert for the prosecution, citing the views of Dr Svilena Dimitrova , Professor Alan Wayne Jones and Dr Adel Ismail

I wrote;

Please find attached statements from expert witnesses instructed by Letby’s barrister,  casting doubt on the safety of the Baby F conviction. In addition, one expert states you made three errors in your analysis. 

Do you wish to comment on these? More broadly, have you considered the possibility that you might have been wrong in your analysis? 

Please let me know either way if you wish to respond, and may I have your response tomorrow by 4 PM?

Many thanks

Dr Phil Hammond

He replied:

Thank you

This case is subject to a potential appeal as well as further charges that the CPS are considering

As such it would not be right to comment at this stage.

Regards

Peter Hindmarsh

Are there any paediatric endocrinologists or insulin experts out there prepared to argue that the blood results were indeed definitive proof of exogenous insulin? I have not been able to find a single one, but I have found experts prepared to argue the opposite in detail.

Attachment:

ASK THE EXPERTS

Given the weaknesses in the non-medical evidence, Letby’s fate will likely come down to which experts the CCRC and CoA believe. In terms of the insulin cases (aka “the strongest evidence”), only one of the four prosecution experts who believe the blood tests prove insulin was given to the babies has gone public. Dr Evans told the court there was "only one explanation" for the "astonishing" blood readings. "These were very, very striking results. There's only one explanation for this. [Child F] had received insulin from some outside source.” However, Evans is not an insulin expert and may not have been aware of the non-specificity of the tests used. He told MD; “I didn’t even know that there was more than one way of measuring insulin until I read the comments from Wayne Jones.” Professor Wayne Jones is a recognised international authority in forensic toxicology who has published extensively in over 100 peer-reviewed journals. Dr Adel Ismail is a retired Consultant in Clinical Biochemistry & Chemical Endocrinology, and a recognised expert in immunoassays and mass spectrometry. Both believe there were serious errors in the insulin evidence.

I asked them why the immunoassay test for insulin could not be relied upon.

“Immunoassays are not reliable enough for unequivocal identification of exogenous insulin administration, particularly in forensic cases. A positive immunoassay test result should be considered as a “presumptive positive” until verified by follow up tests available in all routine biochemistry laboratories, including referral for analysis by the gold standard liquid-chromatography-mass spectrometry testing method available in specialised laboratories. There is clear undisputable evidence that the particular type of immunoassay is prone to produce falsely high insulin results, making its reliability questionable in a legal context.
Using a positive insulin immunoassay test result without confirmation for use in evidence in a murder trial is reckless, and further testing should have been done before drawing the conclusions that exogenous insulin had been administered to the babies.
There are several possible explanations apart from exogenous insulin. It could be the precursor to insulin (proinsulin), or any one of the intermediate products of proinsulin, which are called “split proinsulins”. It could also be protein molecules (such as antibodies) related to bacterial/viral infection, or even maternal insulin antibodies which cross the placenta and are thus passed on the newborn baby. Recent studies and FDA submissions have clearly shown that the Roche Elecsys immunoassay - the same as the one used in this case - can and have produced multiple falsely elevated insulin readings.”

I asked them if the “undetectable” C peptide in Baby F was evidence of exogenous insulin

“The analytical reporting of the C-peptide immunoassay result as <169 pmol/L caused considerable confusion, because it was interpreted as undetectable by the prosecution witnesses. In actual fact, the Roche Elecsys immunoassay used in this case can quantitate accurately levels ≥5.0 pmol/L, thus making the reporting of <169 pmol/L difficult to comprehend.
In this case, the laboratory failed to recognise that the insulin and C-peptide levels should not have been processed (or in this case – sent away for processing), in the absence of a confirmed hypoglycaemia result that is based on a contemporaneous serum glucose measurement. The triad of confirmed to be accurate results of a high insulin, low C-peptide and low blood sugar is mandatory for making a correct interpretation of these results with regards to potential exogenous insulin administration.
Additionally, even in the absence of a proven hypoglycaemia in this case, if these insulin/C-peptide results were obtained, the laboratory should have advised that should exogenous insulin administration be suspected, these samples should be submitted for verification by further appropriate tests before suggesting exogenous insulin administration and thereafter performed further verification tests locally and forwarded to a laboratory who can carry out these tests (Guildford).”

I also asked Dr Svilena Dimitrova, a consultant neonatologist and instructed expert witness who has produced a detailed report on Baby F if there were more plausible explanations for Baby F’s prolonged hypoglycaemia (low blood sugar) than insulin poisoning?

Baby F became unable to absorb enteral feeds due to early signs of infection, as evidenced by increased nasogastric aspirates and vomiting. His reliance on intravenous glucose was compromised by an incorrectly positioned long line, with its tip in the groin, leading to extravasation (fluid leaking into the surrounding tissues rather than being delivered in the vein) and subsequently ineffective sugar infusion delivery.
There was also a significant delay in the recognition and management of hypoglycaemia. Clear signs of long line failure, including increasing pump pressures, alarms and documented observations of a "positional" line, were overlooked. Despite persistent hypoglycaemia, no examination was performed overnight. The issue was only recognised on the morning ward round, delaying corrective interventions.
Additionally, the medical management of the persistently noted hypoglycaemia was inadequate. Despite clear evidence of infection and increased sugar requirements, continuous sugar rates (measured in GIR = glucose infusion rates) were not adjusted appropriately. Instead, multiple sugar boluses were administered, exacerbating hypoglycaemia due to endogenous insulin surges.
Appropriate incrementation of the background sugar infusion amount was only made at 19:00, nearly 17 hours after the initial hypoglycaemic event.
Flaws in expert analysis and misinterpretation of laboratory results further complicated the case. Professor Hindmarsh’s calculations of glucose infusion rates (GIR) were factually incorrect. His conclusion that Baby F had “hyperinsulinaemic hypoglycaemia” were erroneous and was based on making incorrect presumptions of a confirmed hypoglycaemia, a reliable elevated insulin result and a C-peptide level that was undetectable. Neither of these three assertions are factually correct. In summary, there were very clear reasons why Baby F was hypoglycaemic, very clear reasons as to why the hypoglycaemia resolved when it did and there is no evidence that exogenous insulin administration ever occurred. In turn, there is plentiful evidence of poor medical and nursing care and of misinterpretation of the medical and scientific evidence available by the expert witnesses.”

Ultimately, it will all come down to a battle of the expert witnesses…

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