DR. LAZAR | DR. SEIDEMAN | DR. SMITH
Dr. Marius Lazar
Neurology | Psychiatry | Dermatology (Immunodermatology) | GP
Trends come and go, we get older, hopefully also wiser; but two things never change: my glasses have always been round - and I will never put profit before your health.
For Dr. Marius Lazar, medicine is much more than just a job. As a neurologist, psychiatrist, dermatologist (immunodermatology) and, of course, general practitioner, he compassionately helps patients with rare diseases, worldwide. As native of Transylvanian Saxony, who lived for a long time in Africa as a diplomat's son, he practices in English and German.
You can see him in person or via video consultations worldwide. Dr. Lazar offers the entire spectrum of diagnostic procedures of evidence based medicine in cooperation with local colleagues in the countries where his patients live. At the same time, Dr. Lazar is director of the Lazar Medical Consortium Group, which provides evidence-based health care worldwide.
Here, in his private practice Dr. Lazar is specialized in rare neurologic diseases (orphan diseases) as well as difficult cases at the crossroads of dermatology and immunology. He takes a multidisciplinary approach to providing excellent, individualized patient-centered care by bringing together a collaborative care team with different perspectives. His patients have access to a team of specialists, the latest diagnostic methods, personalized treatments and the latest research.
All of this on the basis of providing affordable help for everyone and at a strict distance to the pharmaceutical industry or any other lobby group.
For people with orphan diseases, it can be difficult to understand their condition, the medical problems they may encounter, and the options for treating their symptoms. That's why Dr. Lazar relies on a network of specialists in the diagnosis and treatment of such diseases who share his ethical standards.
Professor Dr. David Seideman
Neurology and Neuroimmunology
Dr. Seideman is a Senior Professor at the Jewish University of Colorado for the scientific study of consciousness. He is also the most experienced senior physician in Dr. Lazar's private practice. In addition, he is the medical director of the Lazar Medical Consortium Group. He was already involved in the treatment of rare diseases when the term was just being introduced. Throughout his career, his focus has been on his work as a clinician, but he has never lost touch with science (intensified as of 2021). Prof. Dr. Seideman works hard to apply the standards of evidence-based medicine to the treatment of rare diseases as much as possible. We apologize that Professor Seideman currently has a waiting list of about six months for consultations. Thoroughness is his standard, and that takes a lot of time.
Languages: English, Hebrew, German, Russian
Dr. Lucas Smith
Internist - Endocrinology
As director of Hellenic Health™ (part of the Lazar Group) Dr. Smith, neurologist and internist (endocrinology) is Dr. Lazar’s senior assistant in his private practice. Dr. Smith is a highly specialized neurologist (orphan/rare/ultra-rare diseases) with a strong focus on the effects of neuropsychiatric syndromes on other organ systems. Appointments with Dr. Smith directly are available through the service center of the Lazar Clinic Group. In Dr. Lazar’s neurological private practice he is his senior assistant and stand-in in his absence.
Languages: English, Greek, German
Dr. Ali Ahmadi
New to the team since June 2022 is Dr. Ali Ahmadi. Born in Iran, he was a senior physician in neurology and psychiatry at various hospitals in his home country. Dr Lazar and Dr Ahmadi met a few years ago at a conference. Now that his two sons are at university, Dr Ahmadi has taken the step of leaving the world of large hospitals behind and opening a new chapter in his career as a specialist in psychiatry, neurology and neuropsychiatry. Dr Ali Ahmadi is an excellent diagnostician and will certainly be of lasting help to the patients of Lazar, Seideman & Smith.
Languages: English, Persian
Dr. Olga Ivanova
GP and Internist
Dr. Jonathan Feldman
GP and Dermatologist
Lazar Medical Consortium Group™
Evidence-based healthcare. Everywhere.
The Lazar Group works with 120 doctors worldwide.
With 3500+ including our partners.
All we do happens under the constant supervision of the non-profit Supervisory Board of Lazar Medical Consortium Group.
Together. Closer to you than you might think.
As an international reference practice for rare diseases, we cannot have every patient come to Athens or even fly around the world ourselves. Therefore, we have excellent partners in countless countries. Look at the world map: in the colored nations, we have partner physicians and infrastructure at our disposal. For our patients this means short distances and the comforting feeling of being in safe hands.
Medical examinations for telemedicine patients
Possible thanks to our international partners.
All state of the art laboratory tests are available in more than 30 countries.
MRI, CT, TCS
Our partner practices and clinics perform examinations with MRI, CT and TCS (sonography of the brain). Scintigraphy is also still possible but less common than in the past. Due a three-step diagnostic procedure you will get an unusually high level of safety.
All standard neurological tests are being provided by carefully selected partners in over 50 countries.
Our social responsibility
Everyone should have access to the best possible care.
Social fee system
The diagnosis and treatment of rare diseases is complex and requires ongoing consultations between all the physicians involved. Therefore, high costs are a consequence of this process. In order to cushion these effects, we have a fee system that is graduated according to the financial strength of the patients. In this solidarity system, wealthy and well-insured patients enable the treatment of less well-off patients in a mixed calculation.
Videos (from inspiring colleagues)
What is neurology?
Why the world needs neurologists.
A key factor for a high quality standard.
Dr. Josep Dalmau
Dr. Sanil Rege
Live to the fullest.
We’ll care for the rest.
Also known as Oslo Syndrome. The “iron brother” of Wilson’s Disease
A silent epidemic of Wilson’s iron brother.
Evidence-based medicine (not eminence-based medicine) has shown for many years that homozygous mutations of the HFE gene H63D are by no means negligible. Latest since 1999 (Nielsen et al.) it has been known that this mutation can cause polymorph alterations in the carrier’s iron metabolism. Not the HFE gene H63D itself is a polymorphism as few, but all the louder "scientists" with good connections to the pharmaceutical lobby and their chelation pharmaceuticals fantasized in the early days of these new diagnostic methods two and a half decades ago. It is the clinical picture of a homozygous H63D mutation that is terribly polymorph. This means it makes quite some of its carriers ill but the type of anomaly in the iron metabolism can be very different among the patients. H63D usually causes a mild hereditary hemochromatosis only after a second hit, however, it can also cause numerous other disorders of iron metabolism, such as hypotransferrinemia, changes in binding capacity, etc. which can lead to clinically relevant and even catastrophic symptoms.
In addition, it may lead - among other symptoms - to damages of the heart and the substantia nigra via a causal relationship that remains to be investigated, most likely via a cascade-like dysfunction in iron metabolism. The clinical facts are compelling. Any physician who dismisses mutations of the HFE gene H63D as clinically irrelevant risks the health of his patients and doesn’t work lege artis (=not according to scientific medical practices). Therefore all main researcher working on Oslo Syndrome (synonyme for the research term “H63D syndrome”) have a moral duty to inform the medical community and the public.
Homozygous mutations of the HFE gene H63D have not been taken seriously enough for many decades, despite the fact that a homozygous mutation of gene H63D is a Pandora's box. It has been linked to liver disease, bone and joint disease, diabetes mellitus, heart disease, hormonal disorders, porphyria cutanea tarda (PCT), infertility, stroke, severe neurodegenerative disease, cancer, venous peripheral artery disease, hereditary hemochromatosis (after a second hit), and Oslo syndrome. In the years since the discovery of HFE and its mutations, researchers have focused their studies primarily on the C282Y mutation because it is particularly common in people with elevated iron levels. About 85% of people with abnormally high iron levels have two copies of C282Y, so this mutation has been studied more intensively. Other mutations, such as S65C or H63D, have not attracted the attention of researchers. The S65C mutation can lead to mild to moderate hepatic (liver) iron overload, especially in combination with other mutations. Increased serum iron indices and iron overload have been observed in C282Y/ S65C compound heterozygotes. In scientific evaluation, H63D stands out as a significant modifier of disease onset, disease progression and even response to therapy. H63D is associated with arterial rigidity, pro-oxidation, higher total and low-density lipoprotein cholesterol, acute lymphoblastic leukemia (ALL), decreased sperm production, and higher risk of type II diabetes mellitus, and hereditary hemochromatosis after a second hit.
Being a carrier of the H63D hemochromatosis mutation is also a risk factor for earlier onset and longer duration of kidney disease in type II diabetics. The most striking risk associated with H63D is that for neurodegenerative disease. Connor and colleagues were among the first researchers to examine the role of H63D in brain iron accumulation, oxidative stress, and neurotransmitter performance. Connor reported that the HFE variant H63D contributes to many of the processes associated with various types of dementia. These processes include increased cellular iron, oxidative stress (free radical activity), glutamate dyshomeostasis (abnormal balance), and an increase in tau phosphorylation (abnormal levels of tau proteins can lead to dementias such as Alzheimer's disease). As demonstrated by Jacobs, Papadopoulos Kaufmann, and colleagues (2012, 2015, 2017, 2019, 2020, 2021) using solid patient data, the numerous damages in parenchymal tissues, heart, and brain (substantia nigra and basal ganglia) can be explained by insidious non-transferrin-bound iron (NTBI) intoxication as a consequence of chronic transferrin saturation of >50%. This constellation (Oslo Syndrome) is similar to Wilson's disease, except that NTBI iron, rather than copper, is the culprit here. In addition, the damage caused by Oslo Syndrome is more widespread in the body, affecting not only the liver and brain severely but also the heart, and in men, the testes. Synucleinopathies are a major problem of Oslo Syndrome, but other forms of cognitive decline are also common. Connor states further that HFE H63D cells have been shown to have more oxidative stress, further supporting their role as modifiers of neurodegenerative diseases. He found that patients homozygous for H63D had earlier signs of mild cognitive impairment and earlier onset of dementia disease than patients with normal HFE H63D or H63D heterozygote individuals.
Despite these crystal clear fact, which have been known for over 25 years now, many clinicians still dismiss homozygous HFE-H63D mutations as irrelevant. Even some of the highest authorities in the field of iron metabolism seem to be trapped in the knowledge of the early 1990s. As physicians specialized in rare diseases, we regularly see patients with complex syndromes consistent with those mentioned before. Just as regularly homozygous mutations of HFE gene H63D are found as primum movens (primary cause) of complex metabolic and toxic syndromes. It is also typical for treating colleagues to ignore this finding, as old textbooks (and new ones copy-pasted from old ones) still state that the HFE gene H63D or its homozygous mutation would be clinically irrelevant. This is false, misleading and potentially fatal misinformation. The knowledge about the high clinical relevance is neither new nor a fringe topic. HFE H63D is not a strong hemochromatosis gene, however, with a second hit it can easily cause hereditary hemochromatosis. But even more important than this, a homozygous mutation of the HFE gene H63D is, according to overwhelming evidence, responsible for many cases of complex syndromes associated with heterogeneously altered iron metabolism.
It is evident from all this that Oslo Syndrome is a not so very distant relative of Wilson's disease, only with NTBI iron instead of copper as the causative agent. But why does every GP/primary care provider have at least some basic knowledge of Wilson's disease and not Oslo Syndrome? It was concluded, after professional discussion in the centers of competence, that the term H63D syndrome is difficult to remember and, moreover, does not do justice to the multifaceted nature of the disease. Therefore H63D syndrome was renamed Oslo Syndrome (for clinical settings) as a result of the 4th H63D Syndrome Conference. Why Oslo? In the Norwegian capital, researchers from around the world agreed for the first time on the leading symptoms of H63D syndrome.
Only seemingly independent diseases. It’s a one cause syndrome.
As we shall discuss later, narcolepsy with cataplexy is a hallmark symptom of brain damage in Oslo Syndrome. However, there is an anomaly in Oslo Syndrome patients.As Adams et al. (2021) could prove Oslo Syndrome patients who “succeeded” in inhibiting an incipient seizure and did not fall asleep developed other symptoms that appear to the observer as ”sleep-related partial inhibition or reduction of body functions while being awake”. This is a broad area for future research, as it may even help explain comorbidities in primary narcolepsy. There are more symptoms to be found in this very unique phenomenon after attack inhibition. In order to not overwhelm the reader we focussed here on the most important ones: interestingly, the reduced function of gastric motility in particular could be part of the explanation why narcoleptics tend to be overweight. On the one hand, during inhibited attacks there is still food in their stomach from meals taken hours ago and, at the same time, other biosensors send signals to the brain that it is time to eat again. Thus, even during and shortly after a narcoleptic seizure, we see slightly elevated serum glucose levels, even if full seizures have been inhibited and the patient has remained awake. These values suddenly drop again once gastric motility returns to normal.
IQ decline in H63D syndrome
A significant number of patients with H63D syndrome develops dementia, most likely due to synucleinopathy. Independent of this issue, a significant drop in IQ can be observed in more than 72% of patients compared to corresponding control groups (Fig. 3). Also executive functions might deteriorate to a remarkable extent. To date, we do not have a satisfactory explanation for this aspect, which is probably still substantially underestimated because the effects are less noticeable in everyday life when compared to dementia. Nevertheless, a linear 50% decrease in professionally measured IQ, as shown in the table below, is not only highly significant but also concerning. Considering that most patients have a profession with certain responsibilities, a significant decline in IQ is a matter of public safety. In this case, physicians must not look away simply because IQ loss is a difficult matter to communicate. As the signs are more subtle than those of dementia, families and caregivers must also learn to recognize the signs and symptoms of IQ loss. One very common early sign is a rise in accidental writing errors, may they be misspelling or using associated words like “wood” instead of “tree”. In most cases, the diagnosis is still made too late, which leads to dangerous work errors, failures in the household, problems keeping up intellectually with peers and the danger of overestimating one's own abilities. Since science and medicine have yet to answer the question of which of the brain damages due to NTBI causes this brain symptom in Oslo Syndrome, let alone how to treat this IQ loss, counseling is usually helpful in learning to live with this progressive limitation. Interestingly, the issue of memory impairment does not seem to match in any way with this loss of brain power we see in patients with Oslo Syndrome. Our patients can remember but not use their knowledge as they could in the past. It’s like they know exactly what a puzzle is and how it should work, but they are not able anymore to use this knowledge in a practical way. So, a businessman with an IQ of 65 at age 47 is not as mentally capable as he was with an IQ of 119 when he graduated from college, even without losing his memory. Because he has no memory loss and since he can still remember things quite well, most people around him will not notice his sharp cognitive decline and distorted executive functions until he makes a big mistake. Therefore, depending on the profession, it should not be a taboo to make these patients leave their jobs (retire) even against their will if their IQ has dropped by 25% within 10 years or if their IQ falls below a cut-off range of 75-85, depending on their job.
Heart conditions due to Oslo Syndrome
Cardiac problems are common in Oslo Syndrome, however, they can be of diverse etiology. Chronically elevated eosinophils, palpitation, calcium channel dysfunction, fibrosis, conduction disturbances (heart blocks) - all of these can occur at high NTBI levels (the basis of the pathomechanism) and cause transient to permanent damage Despite transient symptoms may occur, the prevalence, severity and permanence correlates positively with age. With Oslo Syndrom being sort of a chronic NTBI poisoning this correlation makes sense as well has the fact that younger Oslo Syndrome patients often report palpitations. This leads to the hypotheses that NTBI in lower doses might cause “harmless” functional issues while an accumulation of more NTBI during many years might lead to more severe structural damage. Heart-failure is not common is Oslo Syndrome but it can happen.
Testicular damage in Oslo Syndrome patients
Since NTBI has a strong affinity for parenchymal tissue, the male gonads are a preferred target for this form of free iron. There, it penetrates the cells, causing oxidative damage and, as a consequence, non-dramatic but significant regressive damage to the testes. On sonography (including Doppler), the tissue appears homogeneous, but a mild form of microlithiasis can be seen with more modern sonography equipment, usually models built after 2015. Older sonography devices may miss microlithiasis because the calcifications are often too small for their resolving power. Patients with microlithiasis should be followed up closely for quite a period of time, especially if under 45 years of age, as microlithiasis can occasionally be a sign of testicular cancer or an early warning sign of this undesirable condition. Usually the damage is bilateral, we have not had a case where only one testicle was affected. The spermiogram usually shows somewhat decreased fertility, but this has not become uncommon in the general male population anyway. So far, we are not aware of any treatment that could stop the regressive process in Oslo Syndrome. However, since the effect is usually rather mild, few patients (or their partners) are likely to consider this a relevant problem. Therefore, this aspect of Oslo Syndrome is still largely unknown to urologists and andrologists.
Patients with advanced Oslo Syndrome often have elevated triglyceride levels with quite high postpradnial peaks. In how far this contributes to the development to Steatosis hepatis is still unclear. However, there is a logical connection between both phenomena. A causality still has to be proven.
More about Transcranial Sonography (TCS) in Oslo Syndrome
Trancranial sonography (TCS) is of paramount importance in patients suffering from advanced stages of Oslo-Syndrome. Caused by a homozygous mutation of the HFE gene H63D, H63D/Oslo Syndrome is known for its diverse symptomatology. However, you will hardly find an Oslo Syndrome patient without tics, REM sleep disorders and/or narcolepsy with cataplexy, distorted executive functions, cardiac damage, liver dysfunction and, not infrequently, damage to the male gonads. Transcranial sonography often shows a Parkinson's-like pattern from the 5th decade of life. As was presented in previous studies (Papadopoulos et al. 2021) narcolepsy with cataplexy is a cardinal symptom of advanced Oslo Syndrome that correlates with findings consistent with brain damage on transcranial sonography (hyper-echogenicity in the substantia nigra and abnormal findings in parts of the basal ganglia), as shown in Fig. 1 at the end of this chapter. TCS is the only method with which one can make NTBI visible. MRI, CT, PET and even biopsies will provide a false-negative result. In biopsies it is due to the fact that NTBI cannot be stained with Prussian blue, a fact that even some histopathologists are not aware of.
In another study (Seideman et al. 2021) 200 patients with relevant cataplexy seizures, defined as more than 2 seizures with falls and/or injuries and/or property damage, aged 24 to 49 years, mean age 32 (169 male, 31 female, no significant sex difference in results) were interviewed using structured questionnaires about their symptoms, course of disease, other aspects of their condition; and each of them had at least one transcranial sonography wit modern equipment and physicians very highly trained for this very specific type of ultrasound procedure. The researchers asked the sonography experts to provide, in addition to their normal reports, a severity scale ranging from zero (normal substantia nigra) to ten (very hyper-echogenic substantia nigra). They found found a striking patterns consistent with the anecdotal description of disease progression as reported by the patients themselves (Fig. 2). As can be seen well in this pooled graph, there seems to be a strong inverse correlation between certain motor symptoms (e.g., tics, hyperkinesia) and narcolepsy with cataplexy. The differences between male and female patients are not significant. The results of transcranial sonography are even more striking. Damage to the substantia nigra appears to correlate with a sharp increase in symptom severity of narcolepsy plus cataplexy in Oslo Syndrome patients, with tics decreasing the more substantia nigra damage becomes visible in TCS. To date, no satisfactory explanation exists for this finding.
The fact that the Oslo Syndrome does not fit into any pre-existing box has been obvious since the beginning of research on the subject. However, the finding that narcolepsy (with cataplexy) is a marker for brain damage progression has important consequences for diagnosis and treatment. For some time, there were discussions and attempts to control the motor symptoms of Oslo Syndrome patients with levodopa. One of the side effects of levodopa is actually narcolepsy. However, the levodopa treatment path has been abandoned which is good news for the patients. Thus, levodopa cannot explain the inverse correlation of symptom development. The strikingly similar course of damage to the substantia nigra and parts of the basal ganglia seen on transcranial sonography is a strong indication that the destruction and scarring in this brain region must underlie the answer to this highly interesting and significant phenomenon.
At the same time, it should caution clinicians to be careful about administering levodopa to patients with Oslo Syndrome. If it cannot be avoided, additional precautions and close follow-up should be mandatory. To an outside observer, tics and symptoms of hyperkinesia may appear drastic, but the heavier burden on the patients is severe narcolepsy with cataplexy.
Frontline clinicians should be aware of this symptom shift from often very severe tics in H63D syndrome to narcolepsy with cataplexy while all other symptoms of this very serious illness remain progressive:
Treatment of H63D/Oslo Syndrome
Unlike hemochromatosis the Oslo Syndrome is not curable or profoundly treatable. This is because other than ferritin, NTBI iron cannot be permanently removed from the body. In emergencies, plasma infusions or chelation therapies can remove an acute overload of NTBI iron from the human organism. However, all these methods are risky, only helpful for a short time and thus neither reasonable nor sustainable in the chronically ill. At best, one can try to reduce the transferrin saturation (TFsat) to below 50%, or better below 45%, by means of a low-iron diet. However, since many patients with H63D/Oslo syndrome have low to very low ferritin levels, such a diet should only be undertaken under close medical supervision.
Poor. Especially if organ damage has already manifested. However, we treat in a symptom-relieving manner and improve quality of life quite effectively with a Oslo Syndrome specific medication and diet plan.
Common, but still detected too late in too many patients.
Facts and Figures
Hereditary hemochromatosis (HH) is an autosomal recessive storage disorder that can lead to marked iron deposition in various organs, particularly the liver. Almost all primary (hereditary) hemochromatoses are caused by a mutation in the HFE gene. More than 20 mutations of the HFE gene have been described. Particularly clinically relevant is the HFE gene mutation C282Y.
Prevalence: 5/1,000 for the homozygous form, but penetrance is low. Sex-specific manifestation (phenotype) of HH: Males : Females = 5-10 : 1. About 38-50% of patients with C282Y mutation develop iron overload, about 9-35% develop HH-associated disease. However, the data are not very reliable. Advanced age at diagnosis of hemochromatosis is the main factor for the development of hepatocellular carcinoma in the long-term. Alcohol consumption is the main risk factor for the development of hepatopathy in hemochromatosis patients. Other important risk factors include hepatitis B and C.
The cause of HH is the defective expression of HFE protein on hepatocytes. The HFE protein normally binds to the transferrin receptor and results in transferrin and iron being taken up into the liver. In HFE hemochromatosis, this binding is inadequate and results in premature degradation of the HFE-transferrin complex. Accordingly, the liver receives insufficient information about the iron load in the blood and thus cannot activate hepatic iron hormone production (hepcidin), which would lead to a decrease in iron uptake in the intestine and iron release from the reticuloendothelial system. Intestinal iron absorption increased up to 2-4-fold (corresponding to accumulation by up to 1 g/year), depending on its expression, may lead to progressive toxic iron overload in the parenchymal cells of various organs - especially in the liver and joints, less frequently in the pancreas, heart and pituitary gland.
In most patients, the first symptoms are noticed between the ages of 40-60 years. In women, symptoms are uncommon before menopause because there is some protection via iron loss during menstruation and pregnancies. The symptoms are:Fatigue, upper abdominal pain, arthralgia and osteoarthritis (especially of the metacarpophalangeal joints II and III, OSG, and wrist). Secondary chondrocalcinosis is also possible. Hyperpigmentation especially in sun-exposed areas, hepatomegaly, diabetes mellitus, erectile dysfunction with and without hypogonadism, cardiopathy with cardiac arrhythmias and other heart issues.
Laboratory screening for HH should be performed in the following patients: in case of a “collection” of inexplicable diseases or laboratory abnormalities, elevated liver enzymes (transaminase elevation in HH usually < 2 x the norm, elevated ALT and concomitant MCP arthropathy are particularly sensitive and specific HH signs that can guide to the correct diagnosis in the early stages of HH), type 2 diabetes mellitus with concomitant hepatomegaly and/or NAFLD (“non-alcoholic fatty liver disease”) and/or abnormal transaminase levels, atypical arthropathy, especially in young patients, unexplained cardiopathies (especially young patients with heart failure), sexual dysfunction in younger patients. In case of positive family history:
all first-degree relatives of a patient with HH (homozygous C282Y) between the ages of 18 and 30 yr.
The most important differential diagnoses are: ethyltoxic hepatopathy (liver disease due to alcohol addiction), drug-induced hepatopathy, Steatosis hepatis (NAFLD) due to other reasons, viral liver inflammations, abnormal serum ferritin (+ CRP, ALT/GPT), elevated fasting transferrin (Tf) saturation, abnormal iver function tests (transaminases, bilirubin, alkaline phosphatase). Screening of individuals with a positive family history includes initial HFE genotyping. Interpretation: Tf saturation > 45 % and ferritin in men > 200 ng/ml, in women > 150 ng/ml confirm the suspicion of HH. Tf saturation > 60 % in men or > 50 % in women is reliably diagnostic. Note: In younger patients, Tf saturation may already be elevated but ferritin still normal. Tf saturation is food-dependent and subject to a strong circadian rhythm. However, iron is usually above normal (> 28 μmol/l) and transferrin below normal (< 25 μmol/l) in patients with hereditary hemochromatosis. Transferrin saturation is calculated from iron and transferrin = iron x 0.5 / transferrin, because 2 iron molecules bind to 1 transferrin molecule. The level of serum ferritin reflects the severity of iron overload. However, ferritin is also an acute phase protein, it can be elevated in inflammation, hepatopathies, hemolysis or rarely in neoplasia (different cancers).
If laboratory screening confirms the suspicion of HH, HFE genotyping by PCR should be performed. Informed consent from the patient should be obtained for this. “Iron MRI” should be considered in case of ferritin levels > 1,000 μg/l and elevated transaminases to determine the degree of fibrosis, as marked fibrosis and cirrhosis significantly increase the risk of HCC, and close-meshed ultrasound examinations and alpha1-fetoprotein (AFP) determination are recommended. If liver biopsy is too risky or not desirable, fibroscan can be performed, and liver biopsy may be more predictive of the extent of fibrosis than fibroscan.
Determination of liver iron concentration by MRI is quite reliable for ferritin but completely useless when the task is to detect NTBI iron overload.
Phlebotomy is the treatment of choice. In genetically confirmed hemochromatosis, therapy should be initiated when ferritin levels are elevated (men > 300 μg/l, women > 200 μg (10). The garget is a ferritin at 50-100 μg/l. Deviating from this, target ferriitin values up to 150 μg/l are also accepted in some cases. The initial phlebotomy therapy is scheduled 1 x/week with withdrawal of 450-500 ml whole blood (removing about 250 mg iron), in case of very high ferritin levels every 5 days. Maintenance therapy is normally 3 to 6 phlebotomies per year. Ferritin should be checked after every phlebotomies, also hemoglobin. Increase interval in case of anemia. Phlebotomy therapy relieves symptoms such as fatigue and upper abdominal pain and normalizes laboratory parameters (e.g., transaminases or glucose). Manifest organ damage is only partially reversible; joint pain usually does not respond to phlebotomy therapy.
Depends largely on the severity of organ damage, especially to the liver. Life expectancy is shortened in cases of marked liver fibrosis or cirrhosis, but otherwise normal. A specific low-iron diet is not necessary. Veinlet therapy and balanced diet provides the best starting point for health status Red meat, vitamin C supplements and white wine elevate the iron absorption from the intestine and should be used/consumed carefully. Multivitamin supplements containing iron should not be taken.
Unser “Senior” Team
International, engagiert und dem Menschen zugewandt.
Dr. Marius Lazar
Neurologe & Psychiater
Dr. David Seideman
Dr. Lucas Smith
Dr. Carolina Diamandis
Leiterin der LCG Research
Selbstverständlich kann eine weltweit vernetzte Praxis nicht mit nur drei oder vier Chefärzten alle Patienten versorgen. Wir als Lazar, Seideman & Smith haben daher neben unseren weltweiten Partnerpraxen auch direkt von uns beauftragte Assistenzärzte, die ein unverzichtbarer Teil von Lazar, Seideman & Smith sind. Als pars pro toto seien genannt:
Dr. Sofia Makri
Dr. Olga Ivanova
Dr. Evi Papadopoulou
Ms. Natalia Nikolaidi
Dr. Jonathan Feldman
Dr. Martin Kramer
Dr. Benjamin Steinberg
Bill Watson, M.D.
…und viele mehr
Wir tun alles in uns Mögliche dafür, dass dieses Team möglichst stabil ist und bleibt. Denn wir arbeiten nur mit Kollegen, denen wir voll und ganz vertrauen - fachlich wie auch menschlich. Unsere Patienten haben daher idealerweise stets ein vertrautes Behandlungsteam.
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