Ultra Fast Hormones Research
At Ultrafast Hormones we are passionate about research and science and believe that surgeons who are also scientists should be a driving force in a biomedical research and make broad contributions to medicine. Surgeon-scientists can make fundamental discoveries that will transform medical practice, create new treatments and develop technologies that save lives.
We are leading and participating in several scientific programmes which aim at improving our patients’ health and quality of life. We encourage young surgeons to incorporate scientific research into their career plans because we believe that smart and motivated doctors placed in supportive environment can be asked hard questions and pursue hard problems. There is no limit of human mind in the future of medicine.
Please contact us if you would like to collaborate or participate in any of our Research Programmes
Intraoperative PHT monitoring during parathyroid Surgery
The biological half-life of circulating PTH is only 5 minutes and this allows surgeon to measure its concentration very quickly. Patients with Primary Hyperparathyroidism have high levels of PTH and removal of abnormal parathyroid will cause 50% reduction of PTH blood concentration in 5 minutes indicating biochemical cure.
We have introduced this stunning technology to our practice 15 years ago, and since we have operated on over a thousand patients with Primary Hyperparathyroidism. We have achieved a cure rate of 98% of them on the first operation, a truly “world class result”.
Five years ago we started work developing a new, ultrafast device that will enable to us measure PTH in 3 minutes in whole blood samples. Eliminating lengthy stages of centrifuging, incubation and washout, this will allow the process to become extra efficient and to be performed with smaller equipment.
PLEASE SEE BELOW
For further information about IOPTH monitoring we recommend reading our paper:
“Modern Parathyroid Surgery and Intra-Operative Hormone Monitoring; Present Status, Future Concepts”. J Steroids & Hormonal Science 2018, 9:1 DOI: 10.4172/2157-7536.1000190
DOWNLOAD PDF Review JoS&HS
Shawky M, Abdel Aziz T, Morley S, Beale T, Bomanji J, Soromani C, Lam F, Philips I, Matias M, Honour J, Smart J, Kurzawinski TR.Clin Endocrinol (Oxf). 2019 Feb;90(2):277-284. doi: 10.1111/cen.13882. Epub 2018 Nov 19.PMID: 30346646
Alagaratnam S, Kurzawinski TR.Horm Res Paediatr. 2015 May 1. doi: 10.1159/000381622. Online ahead of print.PMID: 25966652
Alagaratnam S, Brain C, Spoudeas H, Dattani MT, Hindmarsh P, Allgrove J, Van’t Hoff W,Kurzawinski TR.J Pediatr Surg. 2014 Nov;49(11):1539-43. doi: 10.1016/j.jpedsurg.2014.05.032. Epub 2014 Aug 27.PMID: 25475790
Nadarasa K, Theodoraki A, Kurzawinski TR, Carpenter R, Bull J, Chung TT, Drake WM. Eur J Endocrinol. 2014 Sep;171(3):L7-8. doi: 10.1530/EJE-14-0482. Epub 2014 Jun 17.PMID: 24939719
Phillips IJ, Kurzawinski TR, Honour JW. Ann Clin Biochem. 2005 Nov;42(Pt 6):453-8. doi: 10.1258/000456305774538283.PMID: 16259796
Desigan S, Syed R, Conway GS, Kurzawinski TR, Bomanji JB. Clin Nucl Med. 2007 Apr;32(4):306-8. doi: 10.1097/01.rlu.0000257293.00744.3c.PMID: 17413582
Shawky MS, Sakr MF, Nabawi AS, Abdel-Aziz TE, De Jong MC, García VR, Lam F, Soromani C, Smart J, Honour JW, Kurzawinski TR. J Endocrinol Invest. 2020 Mar 2. doi: 10.1007/s40618-020-01201-z. Online ahead of print.PMID: 32124267
Waller S, Kurzawinski T, Spitz L, Thakker R, Cranston T, Pearce S, Cheetham T, van’t Hoff WG. Eur J Pediatr. 2004 Oct;163(10):589-94. doi: 10.1007/s00431-004-1491-0.PMID: 15241688
Genetic Endocrine Syndromes in Children and Adults
Doctors have known for a long time that some diseases can be inherited and many of the risk factors are genetic. Scientist have now identified 3600 genes for rare Mendelian disorders, 4000 genetic loci for common diseases and 700 genes that drive cancer. Completion of Human Genome Project in 2001 was a massive leap forward and started the era of Genomic Medicine. It was quickly followed by technological advances, which now allows us to sequence all the genes in the genome (3 billion nucleotides) at what used to be a cost of a single gene test. Further large cost reductions can be achieved by shrinking the targets of sequencing. The exome constitutes approximately 1% of the genome but codes for roughly 23000 genes in humans and harbours about 90% of all the mutations with large effects. It is increasingly clear that we are approaching the threshold at which DNA sequencing will become a routine part of the diagnostic process.
Traditionally the genetic diagnosis of the Mendelian disorder relied on the establishment of the clinical diagnosis followed by sequencing of previously implicated genes. This has been replaced by panels of genes, which in turn is superseded by whole exome and genome sequencing. Next generation sequencing, in comparison with gold standard Sanger technique, is 99.97% accurate and will generate massive amounts of ‘big data’, some of it of unknown significance. It is therefore very important that clinicians engage with genetic revolution early and incorporate this fascinating discipline into their practices.
Germline and somatic RET gene mutations are responsible for a range of rare diseases, including Multiple Endocrine Neoplasia type 2, sporadic medullary thyroid cancer and phaeochromocytomas, Hirschsprung’s disease, intellectual disabilities, congenital kidney and urinary tract abnormalities. Although individually rare, collectively they carry a significant burden to the patients and health care systems because of their complexity and multiple co-morbidities. Their rarity also affects our ability to conduct research into the mechanism of RET associated diseases and recruitment into clinical trials. Optimal care is difficult to deliver because patients with these conditions are looked after by a wide variety of centres across the UK. Awareness and understanding of RET associated diseases can be poor and the majority of patients affected are children.
We propose to establish a RET Research Collaborative Network with the aim of facilitating the exchange of ideas and collaborative initiatives leading to innovative projects and grant applications, and to coordinate research with ongoing clinical care to encourage recruitment into laboratory based projects and clinical trials. We have also initiated creation of the RET and Endocrine Tumours UK Registry for which we are actively seeking funding. We believe that such a network will also enable earlier diagnosis of RET mutations, ensure better treatment options for patients and improve clinical outcomes.
The RET@CRICK meeting, which took place in June 2019, was envisaged as a stepping stone towards this goal. This one-day conference attracted over 100 scientists, clinical leaders as well as junior doctors and young researchers from all over the world. The day consisted of four sessions, each comprised of Scientific, Clinical and New Research talks, followed by an open forum discussion and networking breaks. Presentations covered important aspects of RET related diseases including MEN2, MTC, Hirschsprung’s disease, animal models and RET targeting in oncology, as well as the role of RET in development and physiology. RET@CRICK was an excellent opportunity for both scientists and clinicians to test new ideas, find potential collaborators and get engaged in world class translational research.
Prete FP, Abdel-Aziz T, Morkane C, Brain C, Kurzawinski TR; MEN2 in Children UK Collaborative Group.
Br J Surg. 2018 Sep;105(10):1319-1327. doi: 10.1002/bjs.10856. Epub 2018 Apr 17. PMID:29663329
Castinetti F, Waguespack SG, Machens A, Uchino S, Hasse-Lazar K, Sanso G, Else T, Dvorakova S, Qi XP, Elisei R, Maia AL, Glod J, Lourenço DM Jr, Valdes N, Mathiesen J, Wohllk N, Bandgar TR, Drui D, Korbonits M, Druce MR, Brain C, Kurzawinski T, Patocs A, Bugalho MJ, Lacroix A, Caron P, Fainstein-Day P, Borson Chazot F, Klein M, Links TP, Letizia C, Fugazzola L, Chabre O, Canu L, Cohen R, Tabarin A, Spehar Uroic A, Maiter D, Laboureau S, Mian C, Peczkowska M, Sebag F, Brue T, Mirebeau-Prunier D, Leclerc L, Bausch B, Berdelou A, Sukurai A, Vlcek P, Krajewska J, Barontini M, Vaz Ferreira Vargas C, Valerio L, Ceolin L, Akshintala S, Hoff A, Godballe C, Jarzab B, Jimenez C, Eng C, Imai T, Schlumberger M, Grubbs E, Dralle H, Neumann HP, Baudin E.
Lancet Diabetes Endocrinol. 2019 Mar;7(3):213-220. doi: 10.1016/S2213-8587(18)30336-X. Epub 2019 Jan 16. Erratum in: Lancet Diabetes Endocrinol. 2019 Mar;7(3):e3. PMID: 30660595
Caimari F, Kumar AV, Kurzawinski T, Butler G, Sabbaghian N, Foulkes WD, Korbonits M.
Clin Endocrinol (Oxf). 2018 Jul;89(1):110-112. doi: 10.1111/cen.13613. Epub 2018 May 4. No abstract available. PMID: 29633305
Gundara JS, Jamal K, Kurzawinski T.
Mol Cell Endocrinol. 2018 Jul 5;469:85-91. doi: 10.1016/j.mce.2017.03.032. Epub 2017 Apr 4. Review. PMID: 28385665
Ultrafast, simple and cost effective
Hypoparathyroidism is a metabolic disorder caused by lack of the parathyroid hormone, which leads to hypocalcaemia and hyperphosphatemia. This presents with acute symptoms such as pins and needles sensation, tetany, cramping, tachycardia and altered mental status. Long term symptoms include soft tissue calcification and psychiatric symptoms. The most common cause of hypoparathyroidism is removal or damage to the parathyroid glands during neck operations. This is called post-surgical hypoparathyroidism and occurs in 25- 60% of surgical neck explorations. Around 90% of these resolve within 6 months, while 2-5 % persist after one year. A recent study in Denmark reported a prevalence of 24/100000 inhabitants. Among those, only a minority (2/100000) where due to non-surgical causes. Similar data is shown in a recent study in USA. Hypoparathyroidism affects approximately 256000 people in the European Union.
At least 20% of patients that undergo thyroid and parathyroid surgery develop hypocalcaemia. The effective management of hypocalcaemia, while avoiding hypercalciuria and other complications, is a therapeutic challenge. It is mandatory to control calcium blood levels and adjust treatment to avoid complications during months after thyroid and parathyroid surgery. Currently, routine postoperative calcium measurements require taking 10 ml of venous blood, which is sent to the main laboratory for analysis. It is painful and takes many hours for the results to become available. This leads to prolonged hospital stay and delay in adjusting medications. Once the patients are discharged, they must travel back to the hospital for blood tests and because of this, calcium levels are done infrequently and calcium dose is adjusted irregularly. There is an urgent need to develop and test a new simple point-of-care handhold device able to measure calcium concentrations in patients undergoing thyroid and parathyroid surgery. Measurements should ideally be performed by patients themselves and the results available instantly allowing for immediate decisions to adjust medications. This would prevent complications and improve outcomes in patients with hypoparathyroidism.
We have obtained REC permission to conduct a prospective, single arm study of equivalence between concentrations of ionized and total calcium in venous and capillary blood measured on the main platforms and new device. Primary objective of the study is to establish the equivalence between measurements of total and ionized calcium in blood performed on “gold standard” platforms and new prototype. Secondary objectives is to find a correlation between calcium measurements and symptoms of hypocalcaemia in patients undergoing thyroid and parathyroid surgery at UCLH.
Our study aims to test a new device which will disrupt current paradigm in that
- Calcium would be tested faster: patients and doctors would get results in just a few minutes. This would have an impact on treatment adjustment and early discharge.
- Calcium testing would become easier: there would be no need to get 10 ml on venous blood to measure calcium concentration. A capillary blood would be enough. Patients would be able to measure calcium concentration themselves at home, which would avoid trips to the hospital to get blood tests done.
- Calcium testing would be cheaper: Each device can be used up to 1000 times. This would allow our patients to test calcium and adjust their medication more frequently, improving management of the disease.
Thyroid and Parathyroid Surgery in Children
Thyroid and parathyroid surgery in children is very uncommon and these operations constitute a minute proportion of thyroidectomies and parathyroidectomies performed in adults. In our centre we have operated on almost 200 children with thyroid and parathyroid problems and have developed significant global expertise in this unique field. We feel very privileged by the trust parents and children put in us and over 15 years we have published several papers on this subject (see Further reading). We are also leading on several national projects such as writing CCLG Guidelines for Endocrine Tumours in Children, RET National Research Network and Paediatric Thyroid Cancer Registry.
Indications for thyroidectomy in children include benign and malignant diseases such as:
- thyrotoxicosis (Graves’ disease, toxic adenoma)
- symptomatic multinodular goitre causing dysphagia, stridor, pain or discomfort and malignant diseases such as
- solitary nodules suspected of being malignant
- thyroid cancer (papillary, follicular, medullary)
- prophylactic thyroidectomy for Multiple Endocrine Neoplasia (MEN2a,2b).
Graves’ disease (GD) can affect patients of all ages and is common in adults with approximately 2% of women and 0.2% of men diagnosed with this condition. It is however rare in children and they represent only 1–5% of all patients with Graves’ disease. Grave’s disease accounts for about 15% of thyroid disorders during childhood and the estimated prevalence varies between countries, from 1/10,000 in the United States to 1/100,000 person-years (for children aged 0–15 years) in the UK and Ireland. GD is more frequent in children with other autoimmune conditions and a familial history of autoimmune thyroid disease and is much more frequent in female than in male subjects.
The management algorithm of children with GD, similarly to adults, include initial treatment with the antithyroid drugs (propylthiouracil, methimazole or carbimazole) followed by either surgery or radioactive iodine in patients not responding to medical therapy. Literature suggests that paediatric thyroidectomies are associated with low operative risk and low rates of disease recurrence. Furthermore, a retrospective database analysis of paediatric cervical endocrine operations performed in the United States between 1999 and 2005 supports that high-volume, endocrine-specialist surgeons performing thyroidectomy have improved operative outcomes when compared with paediatric surgeons, otolaryngologists, and general surgeons.
Hypocalcaemia is the most common complication following thyroidectomy for Grave’s disease and is the main cause of the need for prolonged hospitalisation incurring significant costs for the health system and affecting patient comfort. These features have previously been described in the adult population undergoing thyroidectomy but are less well known for the paediatric population as the incidence of the disease is much lower in this group (see FAQ Thyroid)
Multiple Endocrine Neoplasia type 2 is a genetic disease caused by the mutation of RET gene. It is an autosomal dominant disease, so children have 50% chance of inheriting this mutation from parent with MEN2. This hereditary cancer syndrome is associated with Medullary Thyroid Cancer (MTC), phaeochromocytoma and hyperparathyroidism. Estimated prevalence of MEN2 (1 in 30,000) implies that in the UK there may be about 2000 patients, who will or have already developed MTC.
Early identification of affected children followed by prophylactic thyroidectomy is currently the only effective strategy to prevent development and spread of MTC. In the past, clinical observation with regular measurement of basal and stimulated calcitonin was the only available-if imperfect- strategy aiming at early diagnosis. Establishing causative role of RET in MEN2 allowed for clear and early distinction between affected and non-affected children[5, 6].Correlation between specific RET mutations and the onset and course of MTC enabled risk stratification based on genetic signature and led to recommendations for prophylactic thyroidectomy at the earliest stages of C-cell disease. The modern strategy for prophylactic management of MTC in MEN2 syndrome, based on tailoring surgery to subcategories of patients with distinct risk for disease, has to be complemented by precisely timed, safe and meticulously performed surgery, as thyroidectomy in young children is known to have a higher rate of complications as compared to adults. (see Research, genetic endocrine syndromes in children and adults)
Papillary (PTC) and follicular (FTC) thyroid carcinomas are rare among children and young people (CYP) and comprise about 0.7% of all childhood cancers. More than 90% of CYP presenting with these differentiated thyroid cancers (DTC) have PTC (including follicular variant of papillary cancer) and about 10% of them FTC. In the United Kingdom, there are approximately 145 new cases of DTC in CYP reported annually, but only about eight of them occur in CYP under the age of 16, as that the incidence of DTC gradually rises with age. An increasing incidence of PTC has been mainly responsible for the overall rise in the incidence of paediatric DTC.
In recent years, a growing interest in the subject of DTC in CYP resulted in two publishing phenomena. Firstly, a number of original publications and reviews concluded that DTC in CYP and adults is not the same disease. CYP, compared to adults, present with more advanced stages of disease and have higher recurrence rates, but at the same time, their overall survival rates are excellent and better than for adults A more favourable tumour biology is thought to be an important factor attributing to the reported 40-year survival rate of about 98%. Moreover, adjuvant radioactive iodine (131I, RAI) has been shown to improve disease-free survival in CYP but not in adults. Even in CYP where metastatic spread has occurred – mostly lung metastasis, very rarely bones – survival rates are good, with CYP being either in remission or having stable disease. A general consensus emerged that CYP, therefore, should not necessarily be treated by the pathway proposed by adult patients. Secondly, as a response to these unique features of paediatric DTC, new American Thyroid Association (ATA) Paediatrics Guidelines were written and published in 2015. Their aim was to steer away from the one-size fits all protocols and introduce a more tailor-made approach, which by taking into account different features of CYP with DTC, will avoid under- or over-treatment. (see FAQ Thyroid)
Indications for parathyroid surgery in children include sporadic and familial hyperparathyroidism and in neonates Neonatal Severe Hyperparathyroidism.
Primary Hyperparathyroidism (PHPT) affects patients of all ages. In adults it is a very common condition, and much is known about its epidemiology, clinical course, accuracy of imaging and outcomes of surgical treatment. In contrast, PHPT in children is very rare and such information is sparse, as only about 200 cases have been described in the world literature.
Surgical management of PHPT in adults has seen a sea of change in the last two decades. The main drivers for this change were faster and more sensitive biochemical assays, increased ability to detect genetic mutations and more accurate imaging of abnormal parathyroid glands. Clarity of biochemical and genetic diagnosis and better imaging allowed for the introduction of ‘key hole’ parathyroid surgery. Majority of adult patients could be now selected for Minimally Invasive Parathyroidectomy and benefit from the surgery performed through smaller incisions, better scars, less pain and reduced hospital stay.
The influence of these new developments on surgical management of children with hyperparathyroidism has not thus far been well documented.
Primary hyperparathyroidism(PHPT) in children is a rare disease with a prevalence of 2-5 in 100.000]. Many publications from 1970s and 1980s misquoted this figure as incidence, further adding to the confusion how common this condition in children really is. In comparison with prevalence of PHPT in adults, quoted as 1-4 in 1000, PHPT in children is 100 times less frequent. The only attempt to establish incidence of PHPT in children comes from the French study by Mallet et al who estimated it as 1 case per 300,000 live births. Comparison with the incidence in adults, generally quoted at 30 per 100,000 confirms the rarity of this condition.
Primary hyperparathyroidism in children has a bimodal age distribution, which reflects its different aetiology in very young and older children.
In neonates and infants it is caused exclusively by inactivating mutations of the calcium sensing receptor (CaSR) gene located on chromosome 3q which is inherited in an autosomal dominant way. The CaSR is present on many cells but it is functionally important on the cells of parathyroids and kidneys. Neonates, who are homozygous for these functionally inactivating mutations develop Neonatal Severe Hyperparathyroidism (NSHPT). They present with very high parathyroid hormone levels causing increased osteoclastic activity, hypercalcaemia and a severe bone disease. Reduced calcium excretion at the distal nephron results in hypocalciuria despite high serum calcium. NSHPT is therefore known as ‘bones but not stones’ hyperparathyroidism. Heterozygous children have typically a more benign form of a disease known as Familial Hypocalcuric Hypercalcaemia (FHH). FHH is characterised by a mild asymptomatic hypercalcaemia with a paradoxically low urinary calcium, and does not normally require treatment.
In older children and adolescents, primary HPT is caused by development of either adenoma or hyperplasia of the parathyroid glands and can be sporadic (65 – 70%) or familial (27 – 31%). Parathyroid carcinoma in children is very rare, with only few cases reported in the literature.
In children with sporadic PHPT, similarly to adults, the commonest pathology reported in the current literature is a solitary parathyroid adenoma (67 – 100%). Children with familial PHPT have either multiple adenomas or hyperplasia involving all glands. Familial causes include Multiple Endocrine Neoplasia type 1 and 2a (MEN1, 2a), Hyperparathyroidism-Jaw Tumour Syndrome (HPT-JT) and Familial Isolated HPT (FIHPT). In MEN 1, hyperparathyroidism is the commonest manifestation and affects up to 90% of patients who develop mulitgland hyperplasia The incidence of PHPT in MEN 2a is lower (20%) and is often caused by a single adenoma, though multigland hyperplasia can occur. HPT-JT syndrome, caused by the HRPT2 mutation, is most commonly associated with single gland disease and carries a 10 – 15% risk of parathyroid carcinoma Familial isolated PHPT is diagnosed when hyperparathyroidism is present in a patient with a history of at least one first degree relative affected, in the absence of other endocrine disorders or a family history of MEN. Mutations in families with FIPHPT have been detected in the MEN, HRPT2 and CaSR genes and the disease can involve single or multiple parathyroids. (see FAQ Parathyroids)
Neonates with NSHPT are all symptomatic and present with variety of symptoms including hypotonia, gastrointestinal and neurological symptoms frequently associated with severe bone demineralisation and skeletal abnormalities. Characteristic feature of PHPT in older children is late presentation with at least 80% of children having symptoms and features of end organ damage prior to the diagnosis [2-6;8;9]. This is in sharp contrast to adults, where a majority of patients (80%) are diagnosed on routine blood tests and are asymptomatic. Symptoms in children could be vague and non-specific, frequently affecting gastrointestinal, renal, musculoskeletal and neurological systems. Delayed diagnosis could be a consequence of calcium levels not being part of the routine blood tests in children, thereby resulting in later and more symptomatic presentations. This interestingly draws parallels with PHPT diagnosis in adults in previous decades, when routine calcium measurement was not the norm and most patients had symptoms at diagnosis . More frequent measurement of calcium and PTH in children with otherwise unexplained symptoms could lead to earlier diagnosis and less complications.
de Jong M, Nounou H, Rozalén García V, Christakis I, Brain C, Abdel-Aziz TE, Hewitt RJ, Kurzawinski TR.
J Pediatr Surg. 2019 Jul 19. pii: S0022-3468(19)30463-4. doi: 10.1016/j.jpedsurg.2019.06.027. [Epub ahead of print]
Prete FP, Abdel-Aziz T, Morkane C, Brain C, Kurzawinski TR; MEN2 in Children UK Collaborative Group.
Br J Surg. 2018 Sep;105(10):1319-1327. doi: 10.1002/bjs.10856. Epub 2018 Apr 17.
Alagaratnam S, Kurzawinski TR.
Horm Res Paediatr. 2015 May 1. [Epub ahead of print]
Alagaratnam S, Brain C, Spoudeas H, Dattani MT, Hindmarsh P, Allgrove J, Van’t Hoff W, KurzawinskiTR.
J Pediatr Surg. 2014 Nov;49(11):1539-43. doi: 10.1016/j.jpedsurg.2014.05.032. Epub 2014 Aug 27.
Chng CL, Kocjan G, Kurzawinski TR, Beale T.
Endocr Pract. 2014 Dec;20(12):e241-5. doi: 10.4158/EP14236.CR.
Sinha CK, Decoppi P, Pierro A, Brain C, Hindmarsh P, Butler G, Dattani M, Spoudeas H, KurzawinskiTR.
Eur J Pediatr Surg. 2015 Oct;25(5):425-9. doi: 10.1055/s-0034-1384649. Epub 2014 Aug 21.
Waller S, Kurzawinski T, Spitz L, Thakker R, Cranston T, Pearce S, Cheetham T, van’t Hoff WG.
Eur J Pediatr. 2004 Oct;163(10):589-94.
Diseases of the adrenal glands which require surgery are uncommon and Ultrafast Hormones is very proud that over many years we have developed a substantial expertise and skills in performing this difficult and demanding operations. In the last 20 years there were many advances in managing adrenal diseases and not only we were very quick to adopt them into our practice but also participated in many efforts to improve the outcomes and quality of life after adrenalectomies.
One of the biggest developments in this field was introduction of laparoscopic adrenal surgery and we were one of the first centres in the UK successfully incorporating it into our practice. Over the last 20 years we have performed about 300 of these procedures with excellent outcomes presented at scientific meetings. Last few decades also have seen major advances in managing phaeochromocytomas and paragangliomas and we have published our experience in managing these benign and malignant tumours (see below).
The biggest breakthrough in this field however is the development of new nuclear tracer, which will revolutionize diagnosis and treatment of patients with Conns syndrome. Hyperaldosteronism is by far the commonest adrenal disease and might affect as much as 1% of any population. Through the combination high blood pressure, low potassium and elevated levels of aldosterone it can cause heart attacks, strokes and kidney failure. One of the most difficult steps in the diagnosis of this condition and stratification for surgery is adrenal venous sampling. It is a difficult, invasive procedure well known for low success rate. Replacing it with non-invasive, cost effective and accurate nuclear scan will a major improvement. Such a research is currently undertaken at UCL/UCLH and TRK is a Co-Investigator on this project. “Image Derived Enzymatic Adrenal Lateralisation of Primary Hyperaldosteronism (IDEAL) has been given 1.4 million funding from Biomedical Catalyst, DPFS/MRC and will include initial studies of autoradiography of surgically removed adrenal glands from PHA patients and kidney donors as well as first in man clinical trial of new nuclear tracer.
Patel N, Egan RJ, Carter BR, Scott-Coombes DM, Kurzawinski TR, Stechman MJ; British Association of Endocrine and Thyroid Surgeons.
Br J Surg. 2019 Oct;106(11):1495-1503. doi: 10.1002/bjs.11297. Epub 2019 Aug 19.PMID: 31424578
Ezzat Abdel-Aziz T, Prete F, Conway G, Gaze M, Bomanji J, Bouloux P, Khoo B, Caplin M, Mushtaq I, Smart J, Kurzawinski TR.J Surg Oncol. 2015 Oct;112(5):486-91. doi: 10.1002/jso.24030. Epub 2015 Sep 4.PMID: 26337393
Menon RK, Ferrau F, Kurzawinski TR, Rumsby G, Freeman A, Amin Z, Korbonits M, Chung TT.Endocrinol Diabetes Metab Case Rep. 2014;2014:140074. doi: 10.1530/EDM-14-0074. Epub 2014 Nov
Ogilvie CM, Rumsby G, Kurzawinski T, Conway GS.Eur J Endocrinol. 2006 Mar;154(3):405-8. doi: 10.1530/eje.1.02096.PMID: 16498053
Riaz S, Syed R, Aziz TA, Alnaim A, Chung TT, Wan S, Kurzawinski TR, Bomanji J.Nucl Med Commun. 2020 Mar;41(3):189-195. doi: 10.1097/MNM.0000000000001142.PMID: 31895761
Over the years we have been involved in many aspects of research which included surgical sepsis, liver transplantation, surgical emergencies and pancreatic cancer. We are still interested in research in these fields and below we include list of our publications from the past.
Johnston TD, Gates R, Reddy KS, Nickl NJ, Ranjan D.Clin Transplant. 2000 Aug;14(4 Pt 2):365-9. doi: 10.1034/j.1399-0012.2000.14040102.x.PMID: 10946772
Transplantation 1998: 65 : 193; DAVIDSON BR, RAI R, KURZAWINSKI TR. Br J Surg 1999: 86 : 447). Biliary complications after liver transplantation reportedly occur at an incidence of 20-30%, 10-15% as bile leaks. …The early leaks, occurring within 1 month of transplant, were successfully managed by observation (DAVIDSON BR, RAI R, KURZAWINSKI TR. …
Kurzawinski T, Deery A, Davidson BR.Br J Surg. 1993 Apr;80(4):414-21. doi: 10.1002/bjs.1800800404.PMID: 8495300 Review.
Swain S, Krause T, Laramee P, Stewart S; Guideline Development Group.BMJ. 2010 Jun 16;340:c2942. doi: 10.1136/bmj.c2942.PMID: 20554661 No abstract available.
Gillams AR, Kurzawinski T, Lees WR.AJR Am J Roentgenol. 2006 Feb;186(2):499-506. doi: 10.2214/AJR.04.1775.PMID: 16423959
Wild D, Christ E, Caplin ME, Kurzawinski TR, Forrer F, Brändle M, Seufert J, Weber WA, Bomanji J, Perren A, Ell PJ, Reubi JC.J Nucl Med. 2011 Jul;52(7):1073-8. doi: 10.2967/jnumed.110.085142. Epub 2011 Jun 16.PMID: 21680696 Free article. Clinical Trial.
Wild D, Theodoraki A, Kurzawinski TR, Bomanji J, Reubi JC, Khan R, Bouloux P, Khoo B.Eur J Nucl Med Mol Imaging. 2010 Jul;37(7):1439-40. doi: 10.1007/s00259-010-1455-8. Epub 2010 Apr 24.PMID: 20419372 No abstract available.
Markar SR, Karthikesalingam A, Cunningham J, Burd C, Bond-Smith G, Kurzawinski TR.Ann R Coll Surg Engl. 2011 Nov;93(8):620-3. doi: 10.1308/003588411X13165261994076.PMID: 22041239 Free PMC article.
Kurzawiński T, Ciesielski L.Pol Tyg Lek. 1991 Nov 11-25;46(45-47):901-5.PMID: 1669466 Review. Polish. No abstract available.
Chau I, Cunningham D, Russell C, Norman AR, Kurzawinski T, Harper P, Harrison P, Middleton G, Daniels F, Hickish T, Prendeville J, Ross PJ, Theis B, Hull R, Walker M, Shankley N, Kalindjian B, Murray G, Gillbanks A, Black J.Br J Cancer. 2006 Apr 24;94(8):1107-15. doi: 10.1038/sj.bjc.6603058.PMID: 16622436 Free PMC article. Clinical Trial.
Distante V, Farouk M, Kurzawinski TR, Ahmed SW, Burroughs AK, Davidson BR, Rolles K.Transpl Int. 1996;9(2):126-30. doi: 10.1007/BF00336389.PMID: 8639253
Brett BT, Smith SC, Bouvier CV, Michaeli D, Hochhauser D, Davidson BR, Kurzawinski TR, Watkinson AF, Van Someren N, Pounder RE, Caplin ME.J Clin Oncol. 2002 Oct 15;20(20):4225-31. doi: 10.1200/JCO.2002.11.151.PMID: 12377966 Clinical Trial.
Kurzawinski TR, Deery A, Dooley JS, Dick R, Hobbs KE, Davidson BR.Hepatology. 1993 Dec;18(6):1399-403.PMID: 8244264
Kurzawinski T, Deery A, Dooley J, Dick R, Hobbs K, Davidson B.Gut. 1992 Dec;33(12):1675-7. doi: 10.1136/gut.33.12.1675.PMID: 1487170 Free PMC article.
Raptis DA, Fessas C, Belasyse-Smith P, Kurzawinski TR.Surgeon. 2010 Oct;8(5):239-46. doi: 10.1016/j.surge.2010.03.001. Epub 2010 Apr 2.PMID: 20709279
Mielicki W, Serwa J, Kurzawinski T, Wierzbicki R.Oncology. 1990;47(4):299-302. doi: 10.1159/000226837.PMID: 2367056
Ayaru L, Kurzawinski TR, Shankar A, Webster GJ, Hatfield AR, Pereira SP.J Gastroenterol Hepatol. 2008 Feb;23(2):315-20. doi: 10.1111/j.1440-1746.2006.04562.x.PMID: 18289360
Kurzawiński T, Ciesielski L, Cieślewicz G.Pol Tyg Lek. 1991 Nov 11-25;46(45-47):862-4.PMID: 1669454 Polish.
Kurzawinski TR, Selves L, Farouk M, Dooley J, Hilson A, Buscombe JR, Burroughs A, Rolles K, Davidson BR.Br J Surg. 1997 May;84(5):620-3.PMID: 9171746
Davidson B, Varsamidakis N, Dooley J, Deery A, Dick R, Kurzawinski T, Hobbs K.Gut. 1992 Oct;33(10):1408-11. doi: 10.1136/gut.33.10.1408.PMID: 1446870 Free PMC article.
Davidson BR, Rai R, Kurzawinski TR, Selves L, Farouk M, Dooley JS, Burroughs AK, Rolles K.Br J Surg. 1999 Apr;86(4):447-52. doi: 10.1046/j.1365-2168.1999.01073.x.PMID: 10215812 Clinical Trial.
Kurzawinski TR, Appleby JA, Hardy SC, Fuller B, Cheetham K, Haswell D, Davidson B, Rolles K.Transpl Int. 1994;7 Suppl 1:S489-92. doi: 10.1111/j.1432-2277.1994.tb01426.x.PMID: 11271288 Clinical Trial.