What Regular Sickle Cell Follow-Up Checks: Organs, Blood Counts and Iron Levels

The folder is thicker than it was last year. She sits in the waiting room with a stack of printouts, each one a column of abbreviations and reference ranges, and the same thought she has had at every visit since her son turned two: they keep drawing blood, they keep booking scans, and he looks fine. So what, exactly, are they looking for?

That question sits at the heart of sickle cell follow up monitoring. Most of what a specialist clinic does between crises is quiet work: watching numbers drift, catching an organ that is starting to struggle before it announces itself, and checking whether the treatments themselves are leaving a footprint. None of it is dramatic. Nearly all of it matters.

This explainer walks through the three things a follow-up visit is built around, blood counts, organs and iron, and explains why each test is ordered, how often it typically comes around, and what the results can and cannot say.

How sickle cell follow up monitoring works, in plain language

Sickle cell disease is an inherited condition in which an altered form of hemoglobin, the oxygen-carrying protein inside red blood cells, makes those cells stiff and crescent-shaped when oxygen is low. Two things follow. The misshapen cells break apart early, surviving roughly 10 to 20 days instead of the usual 120, which is why anemia is constant (Mayo Clinic). And they snag in small blood vessels, starving tissue of oxygen, which is what causes pain episodes and, over years, slow injury to organs.

Follow-up monitoring exists because most of that organ injury does not hurt while it is happening. Kidneys leak protein silently. Arteries in a child’s brain narrow without a headache. Iron from transfusions settles into the liver for years before anyone feels it. A planned schedule of tests is the only reliable way to notice these changes early enough to act.

A typical visit has a rhythm. The clinician asks about pain, fatigue, sleep, school or work, and any hospital visits since last time. There is a physical examination: growth and puberty in children, blood pressure, oxygen saturation, a feel for the spleen and liver, a look at the eyes and legs. Then blood and urine samples go to the laboratory, and a few times a year, or once a year, imaging is added: an ultrasound of the brain’s arteries in children, an echocardiogram of the heart when indicated, an MRI to estimate iron.

Think of it as three overlapping layers. Blood counts tell the team what the disease is doing right now. Organ tests reveal what it has already done. Iron measurements track a side effect of treatment. The rest of this article takes each layer in turn.

Why every sickle cell annual check up starts with blood counts

The complete blood count, or CBC, is the one test that appears at nearly every visit. It measures hemoglobin, the white cells that fight infection, and the platelets that help blood clot. In sickle cell care it comes with a reticulocyte count: reticulocytes are red cells so newly made that they still carry traces of their factory machinery, and their number shows how hard the bone marrow is working.

Here is the concept that changes how people read their own results: the personal baseline. Because sickle red cells die early, most people with the condition live with a hemoglobin level that would look alarming in someone else. That lower level is their normal. What the team watches is not whether the number sits inside the printed reference range (it usually does not) but whether it has moved away from that person’s own usual value.

The reticulocyte count adds the second half of the story. In steady state it runs high, because the marrow is constantly replacing lost cells. If hemoglobin falls and reticulocytes fall with it, the marrow has stopped keeping up, which can happen when a common childhood virus, parvovirus B19, temporarily shuts down red cell production (NHS). If hemoglobin falls but reticulocytes climb, cells are being destroyed or trapped faster than usual. Same low hemoglobin, two different problems, two different responses.

White cells and platelets matter too. Both often run mildly high in sickle cell disease, so a sharp change from baseline, rather than any single value, is what prompts a closer look for infection or, in someone taking hydroxyurea, for a medicine effect. Every result on that printout is being compared with the last one, not with a stranger’s average.

What hemoglobin, reticulocytes and the other lab markers actually tell the team

Beyond the CBC, a routine blood panel in sickle cell clinics usually includes a handful of markers that each answer a specific question.

Bilirubin is a yellow pigment released when red cells break down. Lactate dehydrogenase, usually shortened to LDH, is an enzyme that spills out of ruptured cells. Together they gauge hemolysis, the rate of red cell destruction. A persistently high pair suggests a more hemolytic pattern of disease, which has been linked with complications such as leg ulcers and high pressure in the lung arteries (Cleveland Clinic). Rising bilirubin also raises the question of gallstones, which form from the excess pigment and are common in sickle cell disease.

Creatinine and the estimated filtration rate derived from it describe kidney function, but with a well-known catch. Sickle kidneys tend to push creatinine into the urine more efficiently than average, so the blood level can look reassuring while filtering is already declining. That is why a urine test for albumin, a protein that should not leak through healthy filters, is a more sensitive early signal and is part of routine screening (NHLBI).

Liver enzymes track the liver, which is exposed to sickling, to gallstone complications and, in transfused people, to iron. A measurement of fetal hemoglobin, the form of hemoglobin babies make and which does not sickle, is often added for anyone taking hydroxyurea, since raising that percentage is how the medicine works.

Depending on age and history, the panel may include vitamin D and folate, since rapid red cell turnover consumes folate, and a check of red cell antibodies in anyone who has ever been transfused. None of these numbers is read alone. The value lies in the pattern, and in the trend across visits.

Sickle cell blood test frequency: how often is often enough?

There is no universal calendar, and clinics adjust the schedule to genotype, age and how eventful the past year has been. Guidance from national health services offers typical ranges: children are usually reviewed roughly every 3 to 6 months, while adults with stable disease are commonly seen once or twice a year, with more frequent contact during pregnancy, after complications, or when a treatment is started or adjusted (NHS). The table below summarizes what is typically checked and why; the actual rhythm is set by the treating team.

Test	What it looks for	Typical rhythm (team decides)
CBC with reticulocytes	Drift from personal baseline; marrow response; medicine effects	Every routine visit; more often around treatment changes
Kidney and liver blood tests	Filtration, liver strain, gallstone-related changes	At least yearly
Urine albumin	Early kidney leak before creatinine changes	Yearly from later childhood onward
Ferritin	Iron stores after transfusion	Yearly; more often when transfused regularly
Liver MRI for iron	Direct estimate of liver iron	When transfusion history or ferritin trend warrants
Transcranial Doppler	Narrowed brain arteries, stroke risk	Yearly, ages 2 to 16, in HbSS and HbS beta-zero thalassemia
Dilated eye exam	Retinopathy	Regularly from childhood
Echocardiogram, lung function	Lung artery pressure, chronic lung change	When symptoms or findings prompt it

Two patterns are worth noticing. Laboratory tests cluster at every visit because they are cheap in effort and quick to change. Imaging is spaced further apart because the changes it detects develop over years. And the whole schedule tightens whenever something is in flux, then relaxes again once results have been stable for a while.

Iron overload in sickle cell: why transfusions create a hidden problem

Transfusion is one of the most useful tools in sickle cell care. It dilutes sickle cells with healthy donor cells, raises oxygen delivery, and, given regularly, is the standard way to lower stroke risk in children whose brain arteries show worrying flow (NHLBI). The trade-off is iron.

Every unit of donor red cells carries iron locked inside its hemoglobin. When those cells reach the end of their life, the iron is released, and the human body has no active mechanism for excreting it. Menstruation and shed skin remove tiny amounts; nothing removes a transfusion’s worth. Someone receiving occasional transfusions during severe illness may never accumulate much. Someone on a monthly program can build a meaningful burden within a couple of years, and the surplus settles in the liver first, then in the heart, the pancreas and the hormone-producing glands (NHS).

The problem is that stored iron is silent for a long time. Fatigue, joint aches, delayed puberty, diabetes or heart rhythm problems appear only once organs have been affected. That is why iron monitoring is scheduled rather than symptom-driven, and why it begins as soon as regular transfusion does.

Two things reduce the load. The first is the transfusion method itself: an exchange transfusion, in which a machine removes the patient’s sickle cells while replacing them with donor cells, adds far less net iron than a simple top-up, and teams often prefer it for long-term programs for exactly that reason. The second is iron chelation therapy, a class of medicines that bind iron so it can leave the body in urine or stool. Whether chelation is needed, which agent suits a given person, and how it is adjusted are decisions for the prescribing clinician, guided by the measurements described next.

How iron is measured: ferritin, MRI and what the numbers can and cannot say

Ferritin is the protein that stores iron inside cells, and a small amount circulates in the blood in proportion to those stores. It is the everyday iron test because it needs only a blood sample. It is also the most misread test in sickle cell care.

The reason is that ferritin doubles as an inflammation marker. Infection, a pain crisis, surgery, even a recent transfusion all push it upward regardless of how much iron is actually stored. A single high value drawn during a hospital admission may mean very little. Clinics therefore look for the trend across several readings taken in steady state, and they treat ferritin as a screen that raises or lowers suspicion rather than as a verdict (NHLBI).

For a direct estimate, the modern standard is MRI. Iron distorts the magnetic signal in a predictable way, and specialized sequences translate that distortion into an estimate of liver iron concentration; the same principle applied to the heart shows whether iron has reached the muscle. The scan is painless, involves no radiation, and has largely replaced liver biopsy, which is now reserved for unusual situations. How often it is repeated depends on the transfusion program and the previous result.

Two limits deserve a plain statement. MRI estimates iron; it does not measure it directly, and different scanners and methods produce slightly different numbers, so teams prefer to follow a person on the same machine over time. And ferritin can also run low: people who are rarely transfused, particularly menstruating women, sometimes develop ordinary iron deficiency alongside sickle cell anemia. Iron supplements are never assumed to be helpful or harmful in this condition; they are a question for the treating team, answered with data.

Which organs sickle cell follow-up checks, and why each one matters

Sickle cells can obstruct vessels anywhere, but certain organs are especially exposed because of how their blood supply works. The follow-up schedule maps onto that vulnerability.

Kidneys come first. The inner part of the kidney is naturally low in oxygen and high in concentration, the exact conditions that promote sickling, so the ability to concentrate urine is often lost early in childhood. Later, filters begin to leak albumin, and function can decline. Yearly urine albumin and blood pressure checks are the front line (NHLBI).

The liver and gallbladder are next. Rapid red cell breakdown produces pigment gallstones, iron accumulates in transfused people, and past transfusions carry a small historical risk of viral hepatitis, so liver enzymes and, where relevant, hepatitis screening and vaccination are routine.

Lungs and heart are checked together. Repeated episodes of acute chest syndrome, a pneumonia-like complication, can leave scarring, and some adults develop pulmonary hypertension, meaning raised pressure in the arteries that carry blood through the lungs. Oxygen saturation is recorded at each visit; an echocardiogram, an ultrasound of the heart, is arranged when breathlessness, low saturation or examination findings prompt it (Cleveland Clinic).

Eyes are examined with dilating drops because blocked retinal vessels can trigger fragile new vessels that bleed, a change called sickle retinopathy. It is more frequent in the HbSC form of the disease and is usually symptom-free until late, which is why examinations begin in childhood.

The list continues: hips and shoulders for avascular necrosis, in which bone loses its blood supply and collapses; the skin of the lower legs for ulcers; hearing in children; growth and puberty; and, increasingly recognized, mood, sleep and cognition. The spleen, which usually stops working in early childhood, is protected rather than tested, through vaccination and, in young children, a preventive antibiotic (CDC).

Transcranial Doppler sickle cell screening: the stroke check that changed childhood care

Of all the tests in the follow-up schedule, the transcranial Doppler is the one with the clearest story behind it. A transcranial Doppler, or TCD, is an ultrasound that measures how fast blood is moving through the large arteries at the base of the brain. Blood speeds up as it squeezes through a narrowing, so unusually fast flow is an indirect sign that an artery has been damaged by sickling and that a stroke is more likely.

The scan is painless. A child lies still while a small probe is held against the temple and the back of the neck; there are no needles and no radiation. Current guidance recommends it once a year from age 2 through age 16 for children with the HbSS and HbS beta-zero thalassemia genotypes, the forms of the disease with the highest stroke risk (NHLBI, CDC).

What happens next depends on the reading. A normal result is repeated the following year. A borderline result is usually repeated sooner. An abnormal result typically leads to a conversation about regular transfusions, because keeping the proportion of sickle hemoglobin low has been shown in guideline-level evidence to reduce the chance of a first stroke in these children; the decision, and any later step-down to other treatment, rests with the pediatric hematology team.

TCD does not detect everything. So-called silent strokes, small injuries that cause no obvious weakness but can affect learning and attention, are picked up on MRI rather than ultrasound, and some clinics add brain MRI or formal cognitive assessment at intervals. Parents who notice a change in school performance, concentration or behavior should raise it, because that observation is part of the monitoring too.

Who is monitored most closely, and who is usually asked to wait

Not everyone with sickle cell disease needs the same schedule, and the differences follow the biology.

The most intensive monitoring goes to people with HbSS, in which both inherited hemoglobin genes carry the sickle change, and HbS beta-zero thalassemia, which behaves almost identically. Within those groups, certain periods draw extra attention: the first years of life, when the spleen is failing and infection risk peaks; the stroke-screening years of childhood; the months after starting or adjusting hydroxyurea; any regular transfusion program; pregnancy; and the aftermath of a serious complication such as acute chest syndrome.

People with HbSC and HbS beta-plus thalassemia generally have milder anemia and fewer crises, so laboratory visits can often be spaced further apart. Two checks are not relaxed for them, though: eye examinations, because retinopathy is more common in HbSC, and attention to hip pain, because avascular necrosis occurs across genotypes.

Some tests are deliberately deferred. Transcranial Doppler screening was validated in HbSS and HbS beta-zero thalassemia, so children with other genotypes are usually not scanned routinely. Liver MRI for iron is reserved for those with a meaningful transfusion history or a rising ferritin trend, because an untransfused person has little reason to be overloaded. And several measurements, ferritin chief among them, are held back during or just after an acute illness, since inflammation distorts the result and a reading taken in steady state a few weeks later is more useful.

People with sickle cell trait, who carry one altered gene and one normal one, do not have the disease and do not need this monitoring. What they are usually offered instead is genetic counseling, so that they understand the implications for future children (MedlinePlus).

How monitoring changes when you take hydroxyurea or receive regular transfusions

Treatment adds its own layer to the schedule, because the medicines that quiet the disease also need watching.

Hydroxyurea is the longest-established disease-modifying medicine for sickle cell disease. It works mainly by coaxing the bone marrow to make more fetal hemoglobin, which does not sickle and dilutes the effect of the sickle form; it also lowers the white cell count and makes red cells slightly larger and more flexible. The benefit builds gradually, typically over several months rather than weeks (NHLBI). Its main laboratory concern is that it can suppress the marrow too far, dropping white cells, platelets or reticulocytes. For that reason blood counts are checked more frequently when the medicine is started and after any adjustment, then spaced out once results are steady. The fetal hemoglobin percentage is followed as a marker of response. How the dose is set, when it is changed, and what count thresholds prompt a pause are entirely matters for the prescribing clinician; the monitoring exists precisely so those decisions rest on data rather than guesswork.

Regular transfusion brings a different checklist. Before each session the team measures hemoglobin and the percentage of sickle hemoglobin, since the aim is to keep that percentage low. Donor blood is matched more extensively than for the general population to reduce alloimmunization, the process of forming antibodies against donor red cells that makes future transfusions harder to match. Antibody screens, ferritin, liver tests and periodic MRI for iron round out the program, alongside hepatitis B vaccination.

Newer disease-modifying medicines and gene-based therapies each come with a monitoring plan specific to how they work. Whatever the treatment, the same principle applies: no one should start, stop or change it on the basis of a single result or a magazine article. Bring the question to the team.

What the weeks between visits usually look like

A follow-up visit does not end when the blood is drawn. Most routine laboratory results return within a few days, and clinics generally contact people only when something needs action; silence usually means the numbers sat where they were expected to. Imaging reports take longer, and a result such as a borderline Doppler reading typically triggers a phone call and an earlier repeat rather than a wait for the next annual slot.

Between visits, the monitoring quietly continues at home. Many teams give families a written care plan that lists the person’s baseline hemoglobin, usual medicines, allergies and the local emergency contact, so that an unfamiliar emergency department can compare a new blood count against the right reference. A thermometer at home matters because fever is treated as a potential emergency in anyone without a working spleen (NHS). Some people keep a simple pain and hydration diary, which turns a vague sense of a rough month into information the clinician can use.

Once a year, or thereabouts, the schedule bunches into a larger review. Vaccinations are brought up to date, the eye appointment and any scans are coordinated, school or workplace letters are refreshed, and there is time for the longer conversations: growth and development in a child, contraception and pregnancy planning in adults, mood and sleep at any age.

Life events reset the rhythm. Pregnancy moves care into a joint obstetric and hematology clinic with much more frequent contact. Surgery, even minor surgery, prompts a pre-operative review because anesthesia and dehydration raise the risk of sickling. A hospital admission is usually followed by an earlier clinic visit to re-establish baseline. The timeline flexes; the underlying logic, comparing today with the person’s own yesterday, stays the same.

What people often get wrong about sickle cell follow-up monitoring

Some misunderstandings surface so regularly in clinic that they deserve direct correction.

“I feel fine, so I can skip this year.” Feeling well is good news about crises, not about organs. Kidney protein leak, retinopathy, narrowed brain arteries and liver iron are all symptom-free in their early, most treatable stages. The visit is designed for exactly the years when nothing seems wrong.

“Anemia means I should take iron.” The anemia of sickle cell disease comes from red cells breaking early, not from a shortage of iron. Most people with the condition have normal or high iron stores, and anyone who has been transfused may already have too much. Iron supplements are appropriate only when a test confirms true deficiency, and that judgment belongs to the care team.

“My creatinine is normal, so my kidneys are fine.” Sickle kidneys clear creatinine unusually well, which flatters the blood test. A normal creatinine alongside albumin in the urine is a familiar early picture, and it is the urine result that counts.

“A high ferritin means I am overloaded.” Ferritin rises with any inflammation. One high reading during an admission is not a diagnosis; a steady upward trend in calm periods, or an MRI estimate, is what the team acts on.

“The stroke scan is only for children who have had symptoms.” Transcranial Doppler screening is offered to children who feel entirely well. Its purpose is to find risk before the first event, which is why it is scheduled by age rather than by symptoms (CDC).

“Adults grow out of the need for follow-up.” The reverse is closer to the truth. Organ complications accumulate with age, so adult care shifts from stroke prevention toward kidneys, lungs, heart, bones and eyes, and the visits remain just as necessary.

Questions to ask your care team

A follow-up visit works best as a two-way exchange. Bringing a short list turns a review of numbers into a conversation about what they mean for one particular life. These are the questions that people most often wish they had asked.

• What is my (or my child’s) baseline hemoglobin, and how far would it have to fall before you would want to know the same day?
• Which results from today changed compared with last time, and does any trend concern you even if each value looks acceptable?
• Is there albumin in the urine, and if so, what does the plan for kidney protection look like?
• How much transfused blood has been given over the years, and what do the ferritin trend and any MRI say about iron?
• For a child: when is the next transcranial Doppler due, what did the last one show, and what would an abnormal result lead to?
• When was the last dilated eye examination, and how often should it be repeated for this genotype?
• Are vaccinations complete, including pneumococcal, meningococcal, influenza and hepatitis B?
• For anyone taking hydroxyurea: how often are counts being checked at the moment, and what is the current fetal hemoglobin percentage?
• Which symptoms should prompt an emergency visit rather than a wait for clinic, and is there a written plan I can carry?
• Who do I contact between visits with a question, and how quickly can I expect a reply?
• Is there anything about work, school, exercise, travel or pregnancy planning that should be discussed before it becomes urgent?

Answers will differ from person to person, and some will change year to year. Writing them down alongside the result printouts makes the folder in the waiting room considerably less mysterious.

When to call your doctor

Scheduled monitoring catches slow problems. Fast ones need a different response, and the care plan should say who to call and where to go. Seek urgent medical care, without waiting for the next appointment, for any of the following (NHS, CDC):

• A temperature of 38°C (100.4°F) or higher, at any age. Without a working spleen, a fever can signal a bloodstream infection that progresses within hours.
• Chest pain, new breathlessness, a persistent cough or a sudden drop in oxygen saturation, which may indicate acute chest syndrome.
• Sudden weakness or numbness on one side, a drooping face, slurred speech, confusion, a severe headache or a seizure, all possible signs of stroke.
• In a child, a rapidly swelling or painful abdomen with unusual paleness, sleepiness or a racing heartbeat, which can mean blood is pooling in the spleen.
• Marked new pallor, exhaustion or fainting, suggesting a fall in hemoglobin well below baseline.
• A painful erection that will not subside, which can cause lasting damage if untreated.
• Sudden change or loss of vision, or new floaters or flashes.
• Pain that is not controlled by the agreed home plan, or vomiting that prevents fluids from staying down.
• Worsening yellowing of the eyes or skin, dark urine or right-sided upper abdominal pain.

Between those extremes sits a middle category: a new ache in a hip or shoulder, a leg wound that is slow to heal, unexplained tiredness that lasts weeks, a child whose schoolwork has slipped, or a persistent change in mood or sleep. These do not require an ambulance, but they do deserve a phone call rather than a note for next year. Every decision about what to do with a symptom or a result belongs to the treating team; the role of monitoring, scheduled or not, is to get the right information in front of them in time.

Frequently asked questions

How often should sickle cell blood tests be done?

Typically at every routine visit, which for children usually means roughly every 3 to 6 months and for stable adults once or twice a year, according to national health service guidance. Counts are checked more often when hydroxyurea is started or adjusted, during a regular transfusion program, in pregnancy and after complications. The exact rhythm is set by the treating team based on genotype, age and recent history.

What is iron overload in sickle cell, and can it be reduced?

Iron overload is the buildup of iron from transfused red cells, which the body cannot actively excrete, in the liver, heart and hormone glands. It develops mainly in people receiving regular transfusions and is silent until organs are affected. Stored iron can be lowered over time with iron chelation medicines, which bind iron so it leaves in urine or stool, and by using exchange rather than simple transfusion; the plan is decided by the care team.

What does a transcranial Doppler sickle cell scan involve?

It is a painless ultrasound in which a small probe held against the temple and the back of the neck measures how fast blood flows through the brain’s main arteries. Fast flow suggests narrowing and higher stroke risk. Guidance recommends the scan yearly from age 2 to 16 for children with HbSS and HbS beta-zero thalassemia. There are no needles or radiation, and the result guides whether closer follow-up or preventive transfusion is discussed.

What happens at a sickle cell annual check up for an adult?

The visit reviews the year’s pain episodes and admissions, then examines blood pressure, oxygen saturation, heart, lungs, abdomen, skin and joints. Blood tests cover counts, kidney and liver function and hemolysis markers, with urine albumin and ferritin as needed. Depending on findings, an echocardiogram, eye examination or MRI may be arranged. Vaccinations, medicines, mood, sleep and life plans such as pregnancy are also discussed.

Why is my hemoglobin always low, and should I take iron?

It is low because sickle red cells break down after roughly 10 to 20 days rather than 120, and the marrow cannot fully keep up. That is a shortage of cell survival, not of iron, so supplements usually do not help and can add to iron stores that are already high in transfused people. Iron is appropriate only if a blood test confirms genuine deficiency, a judgment for the treating team.

Does everyone with sickle cell need a liver MRI for iron?

No. MRI iron estimation is generally reserved for people with a meaningful transfusion history or a rising ferritin trend, because those who are rarely transfused have little reason to be overloaded. For people on regular transfusion programs it is repeated at intervals the team sets, ideally on the same scanner so results are comparable. The scan is painless and uses no radiation.

Do people with sickle cell trait need this monitoring?

Generally not. Sickle cell trait means carrying one altered hemoglobin gene and one normal one; carriers do not have the disease and do not need scheduled organ, blood count or iron checks. What is usually offered is genetic counseling, so that carriers understand the chance of passing the gene to children. Anyone with the trait who has unexplained symptoms should still discuss them with a clinician.

Why does my child need regular eye tests when they can see fine?

Sickle cells can block small vessels in the retina, prompting fragile new vessels that may bleed or scar, a change called sickle retinopathy. It causes no symptoms until late, when vision can be threatened, so examinations with dilating drops begin in childhood and are repeated regularly. The risk is higher in the HbSC form of the disease, which is why eye checks continue even when other tests are spaced out.

Can I skip follow-up visits if I have had no crises for a year?

It is not advisable. A crisis-free year says little about kidneys, eyes, brain arteries or iron stores, all of which change silently and are most treatable when caught early. Stable people may reasonably have visits spaced further apart, but that decision should be made with the care team rather than by default. If attending is difficult, ask whether some tests can be coordinated into fewer appointments.

What is a baseline hemoglobin, and why does the team keep mentioning it?

Baseline hemoglobin is a person’s usual value when well, which in sickle cell disease is typically far below the general-population range. Clinicians compare each new result against that baseline rather than the printed reference range, because a drop from personal normal is what signals trouble such as marrow shutdown or splenic pooling. Knowing the figure, and carrying it in a written care plan, helps unfamiliar emergency teams interpret a new count correctly.

References

• NHS: Sickle cell disease, living with
• NIH National Heart, Lung, and Blood Institute: Sickle cell disease treatment
• CDC: About sickle cell disease
• Cleveland Clinic: Sickle cell disease

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.