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Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Clipping is a handy way to collect and organize the most important slides from a presentation. Keep up to date with the news you're not supposed to know via RINF on Facebook, on Twitter and subscribe to our YouTube Channel for our videos. Many people will discover that questions they had often asked had already been asked by others and answered. Even those Science teachers who know this difference between sickle cell anaemia [2 haemoglobin S genes that is ACHEACHE] and sickle cell trait [1 haemoglobin S gene, that is NORMACHE] teach, wrongly, that the AS phenotype (the NORMACHE) is immune to malaria. Finally, Haemoglobin a€?Aa€™ (Normal Adult Haemoglobin) has nothing to do with Blood Group A. So what makes the difference between the sickle cell trait phenotype on the one hand, and the sickle cell anemia and normal haemoglobin phenotypes, on the other hand as far as malignant malaria is concerned? The nature of the sickle haemoglobin S, together with the behaviour of the malaria parasite is what makes the difference. If the person infected has sickle cell anaemia [SS], then the mere onset of fever, diarrhoea, vomiting, and other complications precipitates serious sickle cell crisis. But, it may be asked, if the AS child (with just 1 Haemoglobin S gene) appears to be thus protected from the lethal effects of Falciparum malaria, why is the SS person (with 2 Haemoglobin S genes) not doubly protected? Sickle cells are red blood cells with the potential to change from round to sickle shape under certain conditions.
The majority of persons who tested Positive on Sickle Testing in the early days were Black, but later White people in the Mediterranean, Arabs in the Middle East, and Indians were also found to be Sickling Positve. Note that when we talk about Normal Haemoglobin being 'A', we are not talking about 'Blood Group A'. Yes, Nature using the sickling mutation to select NORMACHE 'AS' for survival over and above the non-sickling NORMNORM 'AA' and the double sickling genes ACHEACHE 'SS'. Sickle traits (children and adults with AS phenotype) do suffer from malaria, though with less complications, and they need protection as others.
The Haemoglobin 'S' gene is not the only 'abnormal' haemoglobin gene which causes illness when inherited together with another haemoglobin S gene. A simple test that can be done even in a little-equipped laboratory in the African bush, involving placing a drop of blood on a glass slide, is all that is necessary to detect the presence of sickle cells. Sickle cell crisis occurs when a significant number of the red blood cells of a patient with Sickle Cell Disease (no normal-haemoglobin gene inherited, ie SS or SC, or SD, or S beta-Thalassaemia, or. What harms one ACHEACHE person may not harm another, as for example in the case of the Ghanaian ACHEACHE SC man who ached as soon as he ate oranges.
Fever, fatigue, high altitude (as when some SS person embarks a plane at Accra [sea-level] and disembarks the next day at Addis Ababa or Nairobi [7-8,000 ft]), diarrhoea and vomiting causing dehydration, prolonged squatting as mentioned above or curling up in a chair for hours thereby trapping blood cells in the legs without benefit of oxygenation in the lungs [the so-called tourniquet effect - see July Person History on this website], underwater swimming, pregnancy and prolonged labour, smoking, alcohol, opiates like morphine and heroin which suppress breathing, severe exercise, the rainy season especially when caught in the rain, cold weather, some personal idiosyncrasies like 'eating rice and beans', severe asthmatic attack, infections of organs like the lung (pneumonia), urinary tract and gall bladder, heavy periods, pregnancy, surgical operations, long lorry drives or car journeys, hot weather with profuse sweating. Should these circumstances of incompetently administered general anaesthesia be repeated with a Sickle Cell Trait person undergoing surgery, that patient would also die, but at post-mortem 'total sickling' would be reported. SC-phenotype people suffer very badly when fluids are with-held before surgery, and their combined S & C haemoglobins solidify quicker than other haemoglobin combinations when things go wrong. For general anaesthesia therefore, my advice is to treat all sicklers as if they had the disease, and give plenty of Oxygen and fluids intravenously.
One eminent American Pathologist (an expert in post-mortem material) made the following statement: "Of the Hb SS, SC, Sbeta-Thalassaemia and AS states, gross haematuria is most frequently observed in Hb AS". On the other hand, haematuria in sickle cell traits as seen by Clinicians and not deduced from post-mortem material is very rare. Some reports, often quoted, like that of Goodwin and colleagues in Urology 1950, Volume 63, pages 79-96 entitled: 'Haematuria and sickle cell disease' were published before the discovery of haemoglobin C.
So what would we do with a known Sickle Cell Trait (Hb A proportion greater than Hb S) passing blood in the urine? Students researching these matters are advised also to look up my comments on this article: Konotey-Ahulu FID.
If this website has been of help to you, feel free to make a donation to enable us investigate enquirers who wish to know whether they are carrying an ACHE gene or not, and thus help them make decisions that will prevent the burden of this hereditary ACHEACHE ailment of Sickle Cell Disease and other Haemoglobinopathy. The standard policies of many providers- including aetna, cigna and humana, to name a few- cover overseas emergencies. We are continuing to take big steps to show the world we"re a leader in sustaining use of our olympic venues.
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I repeat: malaria affects sickle cell anaemia patients more seriously than it does others. Malaria does kill both the AA NORMNORM child and the SS ACHEACHE child before the age of 4 years when general immunity strengthens, unless they are given prophylactic drugs. Always refer to the adult NORM Haemoglobin a€?Aa€™, as a€?Haemoglobin Type Aa€™, not Blood Group A. When the Anopheline mosquito bites a person and injects malarial parasites into the body, red cells are invaded and the parasites multiply in these erythrocytes (red cells) until they burst, releasing more parasites into the body, to produce severe febrile illness with serious consequences.
If the patient with malaria has entirely normal haemoglobin genes [AA] then the malarial parasites, unless quickly eliminated by vigorous treatment, can also prove catastrophic.
The answer is that the fever, diarrhoea, vomiting have already provoked a sickle crisis before any beneficial effect of sickling-against-malarial-parasite can be seen. The term came into use when an American Physician, Dr James Herrick, in Chicago, observed in 1910 some peculiar shaped cells in the blood of a West Indian student.
Adults resident in highly malarious regions develop some kind of immunity against malaria whether they are AA or AS. Haemoglobin C, for instance, with its highest concentration in the world found in Upper Ghana and Burkina Faso, when inherited together with sickle haemoglobin S produces cold season rheumatism (sickle cell crisis) in the person with 'SC' phenotype [S from 1 parent, C from the other]. This simple Sickle Test is based on the fact that red blood cells which contain Haemoglobin S, can be made to alter their shape from round to sickle shape by adding a reducing agent to the blood. A=60%, S=37%) get into Sickle Cell Crisis like those with Sickle Cell Disease (SS, SC, Sbeta-Thal, etc)? If someone with 'Sickle Cell Trait' is found to develop sudden, severe musculo-skeletal pains like happens with Sickle Cell Anaemia, then the 'sickle trait diagnosis' as the cause of the problem is wrong.
The patient would not be awake to report a 'sickle cell crisis', just as the unfortunate AA patients were unable to complain of lack of Oxygen before they died. I myself had once assumed that a healthy, robust man who died under anaesthesia for eye surgery in London was 'Sickle Cell Trait' until I met his AS widow with their SS and SC children. First of all, we must remember that millions of people pass blood in the urine all over the world.
To clinicians working in populations where 1 in 5 healthy persons, including international athletes, have the sickle cell trait (AS, with A greater than S) this statement is grossly incorrect, for that was not their experience. They must always be told the proportion of patients of which sex, which phenotype, etc that get which symptom. For while 1 in 50 of sickle cell disease patients seen by the same Clinician (Dr Konotey-Ahulu) have been known to complain of passing blood in the urine "There is absolutely no doubt that the incidence of renal haematuria from in vivo sickling in sickle cell traits is very rare, being less than 1 in 1000 sickle traits per lifetime (definition of 'lifetime' is taken as the duration of life of the adult who is investigated). When bleeding occurred, it was found (as demonstrated on page 213b, of 'The Sickle Cell Disease Patient') that the urine from the bleeding kidney had a heavy growth of bacteria. Never be content with being told that 'Sickle Cell Trait' is the cause of your serious symptoms like painful spasms, epilepsy, high blood pressure, headaches, renal failure, etc. Do not allow Insurance Companies to load your Premium because of Sickle Cell Trait, for it is not a disease. If you are getting symptoms exactly like those with known sickle cell disease, yet you continue to be called "Sickle Cell Trait" then get a second opinion, because learning that you really have, say, Sickle Cell haemoglobin C Disease (SC) or Sickle Cell beta-Thalassaemia (Sbeta-Thal), and not Sickle Cell Trait (AS) could make you stop playing Rugby football where a tackle could rupture your enlarged spleen. Conflicts had been steadily increasing earlier this decade, including several high-profile instances of bears attacking and killing tourists and hikers.


Reverse call lookup is also very enticing when we suspect that someone is checking up on us. White people in Greece, Sicily, Turkey, and their offspring around the world suffer from sickle cell anaemia (sca). A sickle cell anaemia child is one who has inherited sickle cell genes from both parents [S from father, and S from mother] producing the phenotype SS, which I have come to call ACHEACHE, that is one ACHE gene from father, and the other ACHE gene from mother. In the sickle cell trait [AS], however, as soon as the parasite begins to multiply in the red cell, using up the cell's oxygen supply, the AS cell changes from round to sickle shape and does not reach bursting point before the spleen mops it up, preventing further progress of the disease. To be a sickle cell trait [AS] in a malarious environment appears to be better than not having sickle genes at all [AA], or having 2 sickle genes [(SS) - References , 10 to 18, 21 & 22]. Those who inherit this ability from both parents were those who fell sick, and were found to have anaemia.
The spleen which helps in producing immunity is usually shrunken in adult SS people, so they should always be doubly protected in malarious regions with prophylactic drugs and mosquito nets, as should other sickle cell disease phenotypes. The haemoglobin S and C genes in West Africa are so common that 1 in 3 of the inhabitants has one trait or the other. A common educing agent is a 2% solution of sodium meta-bisulphite], or by depriving the blood of oxygen through covering it on the slide using a cover-slip sealed round with Vaseline. People often thought that all the red cells flowing in the blood vessels of someone with sickle cell disease were distorted and sickled. One child died off the Tema beach in Ghana when he had been strictly told that swimming could trigger his sickle cell crisis. Sore throat, ear ache, tooth ache, leg ulcers are other infections that can spark off a sickle cell crisis.
In the Sickle Cell Trait, the amount of sickle haemoglobin S is always less than that of normal Haemoglobin A. Competently-administered general anaesthesia never threatened a Sickle Cell Trait as Consultant Anaesthetists Professor Kofi Oduro and Dr John Searle amply demonstrated. The mother had given her S gene to both daughters while the father's S and C genes were distributed between them.
I researched that article, and wrote to the British Medical Journal January 15 1972 (Volume 1, pages 177 -178, 1972): "Actually, in their paper entitled 'sudden death in sickle-cell trait' the authors relied on the 'SA' electrophoretic pattern without quantification of A2, A, or S in three of their cases, and in the fourth who did not even have haemoglobin electrophoresis they were content to call it sickle-cell trait because 'a sickle cell preparation at autopsy was positive'". If sickle cell traits did not ever pass blood in the urine from the same conditions that caused other people to pass blood in the urine (a symptom known as haematuria) they would be super human.
When that particular Pathologist (whom I knew personally) began his medical practice 'Haemoglobin C' had not been discovered. Although true renal infarction is rare (and remember it happens to those without sickle cells as well), when it occurs even in one sickle cell trait, the incidence is 100% in that one person in whom it occurs. Even Sickle Cell Disease Patients are increasingly getting health insurance, now that each person is considered on an individual health performance basis.
I read in a reputable medical journal on 13th September 1997 the following statement made by a professor of haematology: "Avascular necrosis of femoral head in a patient with heterozygous (haemoglobin SC) sickle cell anaemia". True, sickle cell anemia is also sickle cell disease, but always add the phenotype SS when you mention "sickle cell anaemia"so that it is not confused with the SC phenotype as the professor did. There are too many companies that say they are the best when it comes to reverse cell phone lookup. In fact, the highest incidences of the sickle cell gene (S, for short) are not found in Africa at all; they are in India and Saudi Arabia [References 1 to 10]. Doctors who have been wrongly taught have been known to advise their sickle cell anaemia patients travelling from Europe to the Tropics not to bother taking anti-malarial tablets because the sickle cells make them immune to the parasite.
In childhood, this makes the difference between survival ofthe AS NORMACHE child, and death of AA NORMNORM and SS ACHEACHHE children. Without testing the blood, it is not possible to identify a person who has inherited sickling from just one parent, because such a person is not sick, and looks exactly like those without sickle cells. If someone with Blood Group A, also has Haemoglobin AA Phenotype ['A' gene from father and 'A' from mother] it is sheer coincidnece, and the two things have nothing to do with each other. As mentioned above Health workers in Europe and USA have been known to tell Africans with sickle cell anaemia [SS] travelling back to their malarious countries that they do not need anti-malarial cover because they are already protected by sickling.
Any West African visiting this web site has a 1 in 3 chance of being NORMACHE AS (one parent donating 'S' gene, and the other 'A') or NORMACHE AC (one parent passing on 'C' and the other 'A', making them AS or AC phenotypes and (if they have not had their blood tested) they do not know they are Traits. No, the red cells are usually round and malleable like those of a person without Haemoglobin S. He disobeyed, and paid the ultimate price.A  Great pity that, because Sickle Cell Disease ACHEACHE patients are often very brilliant, having inherited from the same parents some excellent genes that their non-aching brothers and sisters do not possess. Poorly administered general anaesthetic, and depriving the patient of fluids for hours before surgery can be dangerous. I have seen people referred to as 'Sickle Cell Trait' merely because the father is Sickle Test Positive, but the mother is not. This flawed publication is typical of many articles which have maligned sickle cell traits, some of whom competed at the Mexico Olympic Games at more than 7,000 ft above sea level and beat the whole world. The SC phenotype would be known to him as 'Sickle Cell Trait', and he might unconsciously be carrying his previous terminology into the era of haemoglobin electrophoresis. Continuing to come back to my own family, to say Dr Konotey-Ahulu's AS mother never passed blood in the urine during her entire life of 89 years adds little to the argument, but it is just mentioned for the record. One e-mail received from Mrs Helen Sachs in the USA asked whether 'Sickle Cell Trait' could change overnight into 'Sickle Cell Disease': "A 32-year old friend of mine died yesterday suddenly in hospital. Yet many, many, doctors and other health professionals do not know the difference between the two phenotypes. These will be looked at later in the Academic FAQ's, but we must now add the exclusion of Haemoglobin Quebec-Chori as the 11th relevant criterion. When hiring a caregiver for a senior, it is important to make sure the background check includes a criminal check for each county the person has lived in and goes beyond just a computer search as some counties do not maintain daily updates of their computer records.
Yes you must have physical possession of the smartphone that the spy phone software will be installed on. Moreover, disputes regarding the terms of the settlement itself may be adjudicated on a section 6 motion on the basis of declarations or evidence. The number is going to be of invaluable help in requesting information to your service provider. The tusk rzr rear bumper, cargo rack, and spare tire carrier is perfect for your polaris ranger rzr side by side utv.
Dangerous advice, as malaria is the commonest cause of sickle cell crisis in Africa [ See also Question 8. To suffer from cold season rheumatism, there must be contributions of ACHE from both parents. Blood sample was taken from a person, a drop placed on a glass slide, and examined under the microscope.
Nobel Prize winner Linus Pauling proved in 1949 that sickle haemoglobin was a different protein from normal haemoglobin, known as Haemoglobin A. This is highly dangerous advice based on ignorance, because such patients have been known to return to the temperate zone, suffer devastating sickle crisis, and hardly anyone has thought of excluding malarial parasitaemia as the precipitating cause of the crisis. Take Dr Konotey-Ahulu, for instance; his mother was NORMACHE Sickle Cell Trait [AS] and she did not know it, and his father Haemoglobin NORMACHE Haemoglobin C Trait [AC], and he did not know it. A quick method used to detect sicklers before a general anaesthetic is through a Solubility Test, using molarity phosphate buffer.
It is when CIRCUMSTANCES make the body's internal environment lack oxygen, or get too hot, or too 'acidic', or too sluggish, that red blood cells with Haemoglobin S change shape into sickle-shape (or mini-cigar shape), clogging up the tiny vessels and causing severe pains wherever the clogging up occurs - around joints, in the abdomen, in the head, in the male organ (priapism), in the ribs, in the bones of the back, and limbs, etc. Learning to keep out of trouble, by avoiding known harmful circumstances makes them able to use their brilliant genes to achieve great things in life.
If you, the reader of this web site, have been having severe sickle cell crisis periodically, and you have been called 'sickle cell trait' merely because one of your parents was 'Sickle Cell Test Negative', then go back to your Doctor and ask for Haemoglobin Electrophoresis. One of the reasons Anaesthetists are advised to give plenty of Oxygen preoperatively and post-operatively to any 'sickler' is that the correct diagnosis of 'Sickle Cell Trait' preoperatively is very poor. He had Haemoglobin SC disease, and the colour sickle test had not distinguished between the Trait state (AS), and the Disease state (SC). The fact is that, in a place like southern Ghana where 1 in 5 perfectly healthy people have the sickle cell trait, we should expect to find that 1 in 5 of all doctors, 1 in 5 of all thieves, 1 in 5 of all soldiers, 1 in 5 of all lawyers, 1 in 5 of hill climbers at 4,000 feet, 1 in 5 of all sudden deaths, 1 in 5 of people vomiting blood, 1 in 5 of all athletes, 1 in 5 of all prostitutes, 1 in 5 of the 'Black Star' Football Team, 1 in 5 of the many past Heads of State, 1 in 5 of all diabetics, 1 in 5 of all fools, 1 in 5 of all heart failure patients, 1 in 5 of those with cerebral palsy, 1 in 5 of all stammerers or stutterers, 1 in 5 of all rogues, 1 in 5 of all Left-handed people, and 1 in 5 of those southern Ghanaians reading this website will be expected to have the Sickle Cell Trait (AS). Other causes of blood in the urine were quickly excluded, like bacterial infection (Eschericia coli, or Proteus, or Tuberculosis, etc), or stones in the kidney, or tumour in the urinary tract, or (in the male) prostate problems. For example, Professor Yeboah and Colleagues at The Korle Bu Teaching Hospital found, between November 1972 and June 1975, that of 202 patients referred to them at the Urology Department with haematuria, only 9 (2%) were sickle-related, and these were all of the SC phenotype.
Her mother asked the Doctor what happened, and he said my friend's Sickle Cell Trait suddenly changed into Sickle Cell Disease and she died". One woman, seeking advice from another website in the USA, said she had "the sickle cell anaemia trait" with some hip problems.
Dr Addae's 10th criterion is worth mentioning here because we are dealing with blood in the urine: "Was there G-6PD Deficiency of the erythrocytes?" Now, this enzyme deficiency found commonly in Mediterranean Europeans and their descendants world-wide, is also found in about 1 in 6 West African males.
The term "sickle cell anaemia" always, without exception, denotes the HOMOZYGOUS STATE (SS).
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You can easily do this using the internet, as this marvelous tool will provide you with all the information you will ever need on all reverse cell phone lookup service providers. When out on the trail, it is always nice to have extra storage space and the tusk rzr rear bumper, cargo rack, and spare tire carrier provides plenty of it. Sickle haemoglobin was first called haemoglobin B, but it made more sense to call it haemoglobin S whose property to gel up and crystallise, causing the cell membrane to alter shape in the absence of oxygen, differentiated it from normal Haemoglobin which remained fluid and non-rigid even in the absnece of oxygen. The colour change that is used to detect Haemoglobin S, and which is useful in unmasking Sickle Cell Anaemia (SS) does not distinguish another Sickle Cell Disease like the SC phenotype (S abnormal, C abnormal) from the Sickle Cell Trait (AS a€“ a€?Aa€™ normal, a€?Sa€™ abnormal) which is not a disease. AEROBIC OXYGEN, The Canadian product from Calgary has been of tremendous help to many of my patients.
Sometimes even certain doctors insist that because Haemoglobin Electrophoresis shows 2 major bands - a Normal A band, together with the mutant S band, that makes it certain that they are dealing with a Sickle Cell Trait Phenotype.
In fact, I have already told readers of this website that my own father had Haemoglobin C Trait (AC) and my mother Sickle Trait (AS, see Genealogy Tree).
None due to sickling occurred below 5 years of age, "and the greatest number (37.9% of all haematuria cases) occurred in the 20-24 age group. Even in patients who did not have sickle cells, there would always be some for whom no cause for blood in the urine could be found.
Her error was not corrected in the reply given to her on that website, suggesting that the "expert" replying to queries also was in the dark as to the difference between "sickle cell anaemia" and "sickle cell trait". This is often a harmless condition, until the person with the Glucose-6 Phosphate Dehydrogenase Deficiency takes medicines like Sulphonamides or certain antibiotics and pain killers, causing red blood cells to be dissolved and passed in the urine and turning it dark like coca-cola. Moreover, the term "heterozygous" denotes dissimilar genes from one's parents, like SC, Sbeta Thalassaemia, SKorle Bu, etc. Also, make sure that you are informed of all the features and expenses your chosen provider offers you – you might even get free lookups with some! A thin cover slip placed on the sample is sealed round with vaseline so that no air got to the blood. One does not need gadgets for doing 3 monthly transcranial Doppler scans to detect which child is going to develop a stroke.A  The nil-by-mouth instruction given to patients due for an operation can be extremely dangerous if doctors and nurses for gret to put fluiods into the patients veins while the operation is delayed.
Fifteen to twenty drops in a glass of water twice or thrice a day help to keep the red cells in good shape.
The common belief that when you have sickle cell disease you must also have anaemia, ie low haemoglobin level, is dangerously wrong. In these, as in the case of those who are Sickling 'Positive', I went on to find out whether someone kicked them in the back, or they had a car accident, or they were taking blood thinning drugs like Aspirin, or Anticoagulants, or platelet reducing agents, all of which could cause bleeding. Now, take it from me, there is no such thing as "sickle cell anaemia trait", and if the reader of this website fails to spot that mistake then I need to repeat myself more often than I have done already. If this common hereditary condition (passed on from mother to son, and from father to daughter) was not recognised in a Sickle Cell Trait person with a urinary tract infection, and the Doctor gave the person Sulphonamides, what could happen? The term could then be seen to stand for the phenotypes: AS, SS, SC, SbetaThalassaemia, Sickle cell Hereditary Persistence of Fetal Haemoglobin (SFhereditary), or even SKorle Bu. The reason I do not like the use of the term "heterozygous" is that the "AS" phenotype, which is not a disease (it is trait") is also "heterozygous" because dissimilar genes are present.
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If after several hours the cells remained round shape, then the person did not have sickle cells. This si far cheaper than the Hydroxyurea which Haematologists on both sdes opf the Atlantic prescribe for ACHEACHE patients.
Sickle Cell Traits do not escape the consequences of incompetently-administered general anaesthesia, any more than those without sickle cells do. If a Ghanaian dropped down dead in the USA, there was a 1 in 5 chance that he would be Sickle Cell Trait, and if at autopsy the Pathologist found a Positive Sickling Test, would he be entitled to publish the phenomenon as a case of "sudden death in a sickle cell trait"? When, however, haemoglobin electrophoresis was performed these "trait" people were most often found to have Sickle Cell Disease (SC), or if the haemoglobin level was less, they were SS or Sbeta-Thalassaemia. If an examination of the inside of the bladder (cystoscopy) showed blood oozing from the Left ureter, (for the Left kidney almost always bled first in sickle cell states), and kidney scans, with an intravenous urogram (pyelography) revealed that part of the kidney was 'infarcted' then, and only then, should it be assumed that this was 'sickle cell haematuria'. The 'coca-cola urine' would wrongly, very wrongly, be attributed to the 'Sickle Cell Trait'. Surely this is not right, so I advise people to add the phenotype always if they must use the term. To confuse the trait "AS" with the disease for example,"SC" disease, must never be allowed to happen. The "S" & "C" in the phenotype "SC" do not stand for "Sickle" and "Cell", they stand for "Sickle-cell Haemoglobin-C".
The tusk rzr rear bumper, cargo rack, and spare tire carrier also has a place to mount extra fuel packs to allow you to extend the range of your side-by-side. Those whose blood cells turned sickle shape in a reasonably short time, were found to have sickle cell anaemia, while those whose blood cells took a long time to show sickle cells were termed sickle cell trait, especially when they were perfectly healthy and were not anaemic.
People with no abnormal haemoglobin whatever ie those with AA haemoglobin phenotype have been known to die under poorly administered general anaesthesia, such as when the doctor forgets to switch on the OXYGEN supply.
Apart from infection, conditions like dehydration, haemo-concentration, enlarged spleens, and pregnancy were the circumstances that I have known to cause sickle cell infarction, which led to bleeding. It is my established practice to include laboratory tests for these common red cell hereditary characteristics [Abnormal Haemoglobins and G-6PD Deficiency] in the investigation of any African, Mediterranean European, Middle East person, or Indian, referred to me for any reason. To make sure such confusion does not happen some wise doctors refer to the SC phenotype as a double heterozygous state. Thus, on the occasions when haematuria was found in Accra over 6 consecutive years in the Sickle Cell Clinic, young adults and child-bearing women would seem to be most affected, and then only the sickle cell disease patients (SS & SC phenotypes) were involved - The Sickle Cell Disease Patient, Chapter 17.
I have known flying long distances (over 8 hours) to precipitate renal bleeding in a Sickle Cell Haemnogliopbin C Disease patient (SC phenotype) but I have never known flying to cause this in the AS phenotype.
Treatment of established renal infarction is bed rest, and plenty of fluids (up to 12 Litres intravenously of Normal Saline has been given before, in 24 hours), with sterilisation of the urine with the appropriate antibiotic. If they do not know their phenotype, they should not say "I am a sickler" and leave it like that, because the doctor, or whoever they are talking to, may be tempted to assume that whatever they are suffering from is caused by sickle cell disease. I prefer to avoid the term altogether when the actual phenotypes can be spelt out - "SC", "SS", "SFhereditary", "AS Trait".
Integrated solidly mounted rear bumper to protect your valuable investment adds an upper rack for more storage rugged spare tire holder for those on-the-trail flats secure frame and cage mounted design adds a sporty full cage look room to add spare fuel container to extend your range. The reason it is called sickle cell anaemia is because anaemia (low haemoglobin level) is the most obvious feature of the SS phenotype.
This approach, with blood transfusion, in the very severe cases, has always been successful in stopping the bleeding in most patients.
Other haemoglobin genes can combine with sickle haemoglobin to cause sickle cell disease of varying degrees of severity, namely Haemoglbins D, E, G, K, O, Korle-Bu, Osu-Christiansborg, etc.
Even deaths of Blacks due to violence at the hands of unscrupulous Prison Officers have been known before to have been attributed to the 'Sickle Cell Trait'. Beta-Thalassaemia is not an abnormal haemoglobin gene (it is a gene for producing an insufficient amount of Normal haemoglobin), nor is Foetal Haemoglobin (which is Normal Haemoglobin for the baby in the womb, but which should disappear in adulthood). The spate of journal articles linking all kinds of symptoms with the 'Sickle Cell Trait' had become so alarming that Professor James Bowman and his colleague Dr S Bernstein in Chicago (University of Illinois) were forced to exclaim that "persons with sickle cell trait will no longer be able to become ill or even die lest they find themselves subject of case report" (Bowman JE, Bernstein S. It requires to be pointed out that people have had one or both their kidneys removed rather unnecessarily.
If Foetal Haemoglobin persists into adulthood it is known as Hereditary Persistence of Fetal Haemoglobin (HPFH) which can combine with sickle haemoglobin gene to cause disease. Having said that, 1 in 5 of all malignant kidney tumour patients in southern Ghana should be found to have the Sickle Cell Trait.
So the sickle cell diseases (all of them ACHEACHE because there is no NORM gene) can include the phenotypes SS (sickle cell anaemia), SC, SD, SE, SG, SK, SO, S Korle-Bu, SOsu-Christiansborg, SBeta-Thalassaemia, SFhereditary, etc. As I write this FAQ, a young lady from the north of England contacted me to ask for advice regarding her frequent painful spasms due, she said, to 'Sickle Cell Trait'. If the Surgeon decided to remove the kidney, it was because of the carcinoma, and not because of the sickle state. The various clinical presentations of the common phenotypes have been compared and contrasted in Konotey-Ahulu's book 'The Sickle Cell Disease Patient' [Reference 9]. She then added (in passing) that she was born with cerebral palsy, and was wheel chair bound. In the most severe cases of sickle cell haematuria in Ghanaian SC patients epsilon-amino-caproic acid (EACA) was tried by Bernard Ribeiro, Professor JMK Quartey, and myself with dramatic results [Ribeiro B, Quartey JMK, Konotey-Ahulu FID, 1979. The message obviously had not got through to her that cerebral palsy (not sickle cell trait) was the cause of her severe painful spasms. In a population where 1 in 5 of all consecutive hospital admissions would be expected to be Sickle Cell Trait (AS), "the results showed conclusively that there was not one sickle cell trait phenotype where at least four were expected" (Konotey-Ahulu in 'The Sickle Cell Disease Patient', page 95).
That did not mean Sickle Cell Traits were not infected by the malarial parasite; what it meant was that they were not being admitted to hospital dying from cerebral malaria because not enough parasitized red cells matured to release huge numbers of malarial parasites to invade the brain. From this point of view the Sickle Cell Trait had protected the children from cerebral malaria.



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