Symptoms to Diagnosis

A 24-year-old man with severe hemolytic anemia and variable Coombs test results

Sindu Iska, MD, María Herrán, MD, You Li, MD, Maria Teresa Bejarano, MD, Chakra P. Chaulagain, MD and Chieh-Lin Fu, MD
Cleveland Clinic Journal of Medicine March 2026, 93 (3) 159-168; DOI: https://doi.org/10.3949/ccjm.93a.25079

A 24-year-old man, previously healthy, was admitted to a local hospital because of dark urine, jaundice, fatigue, and confusion. He said he had no dysuria, fever, night sweats, abdominal pain, vomiting, diarrhea, or weight changes. He also said he had not traveled recently, had not contracted any infections, had not been exposed to anyone who was sick, did not use alcohol, and had not started any new medications.

On admission, the patient’s temperature was 98.7°F (37.1°C), heart rate 106 beats per minute, blood pressure 121/67 mm Hg, respiratory rate 18 breaths per minute, and oxygen saturation 97% while breathing room air.

The patient seemed lethargic but responded to verbal and physical stimuli and had no focal neurologic deficits. He was visibly jaundiced, with yellow sclera. His lungs were clear to auscultation, without wheezing or crackles. His heart rate and rhythm were regular, with no murmurs or extra heart sounds. He had normal bowel sounds and no abdominal distension, guarding, or rebound tenderness. No lymph nodes were palpable, and his spleen seemed normal on percussion.

Results of initial blood work and urinalysis are shown in Table 1 and Table 2, respectively. A peripheral blood smear showed spherocytosis with teardrop cells, but no schistocytes. A polyspecific direct Coombs test (also called a direct antiglobulin test) was positive, while monospecific antiglobulin testing was negative (more about these tests below).

View this table:
TABLE 1

The patient’s blood test results on presentation

View this table:
TABLE 2

The patient’s urine test results on presentation

DIAGNOSIS

1. Which of the following is the most likely diagnosis?

  • Autoimmune hemolytic anemia

  • Nonimmune-mediated hemolytic anemia

  • Nonhemolytic anemia

The patient had low hemoglobin, low haptoglobin, an elevated reticulocyte count, elevated lactate dehydrogenase, and elevated unconjugated bilirubin, consistent with hemolytic anemia. In addition, his peripheral blood smear showed spherocytes, a hallmark of hemolysis. His white blood cell count was also elevated, predominantly due to elevated neutrophils, and although this finding is uncommon in hemolytic anemia, it could be attributed to a stress response to hemolysis.

In autoimmune hemolytic anemia, the patient’s immune system is destroying their red blood cells. The first step in diagnosing it is a direct Coombs test, using polyspecific antihuman globulin that detects immunoglobulin (Ig) G and the complement fragment C3d bound to red blood cells. If this test is positive, it usually means the patient has either IgG or C3d, or possibly both, on their red blood cells, but it doesn’t tell you which one is present or if both are. Therefore, the next step is monospecific testing for antibodies to either IgG or C3d individually (this testing is done reflexively by the laboratory if the polyspecific test is positive).1,2

However, positive test results do not always indicate clinically significant autoimmune hemolytic anemia. For example, false-positive results can be due to red blood cell alloantibodies from prior transfusions or certain monoclonal antibodies used to treat multiple myeloma.3,4 Similarly, physical signs can also be nonspecific: dark urine may be due to hemoglobinuria from intravascular hemolysis, often with no red blood cells in the urine on microscopy.

In our patient, the diagnosis of autoimmune hemolytic anemia was supported by the laboratory and clinical findings, with a positive result on the polyspecific direct Coombs test, even though the results of monospecific testing were negative.4

TYPES OF AUTOIMMUNE HEMOLYTIC ANEMIA

Some cases of autoimmune hemolytic anemia occur after a patient experiences a triggering event such as viral illness or starting a new medication and are thus termed secondary, while others, such as in our patient, have no identifiable triggering event and are thus called primary.

Autoimmune hemolytic anemia can be classified into several serologic types (Table 3).1–11

View this table:
TABLE 3

Types of autoimmune hemolytic anemia

Warm-antibody autoimmune hemolytic anemia

In this type, the culprit is usually IgG antibodies that, in the laboratory, bind to erythrocytes at 37°C, and so the monospecific direct Coombs test is typically positive for IgG. It is the most common type of autoimmune hemolytic anemia, accounting for 60% to 70% of cases.1,3,4

Antibody-dependent cell-mediated cytotoxicity is the primary mechanism of red blood cell destruction, leading to extravascular hemolysis. However, confirmation with an eluate (done reflexively by the laboratory), a solution containing antibodies that have been detached and recovered from the red blood cell surface (Figure 1), is not always positive if the antibodies have low affinity for the reagent, are present in low concentration, or are not IgG (eg, are IgA).2,4

Figure 1
Figure 1

After a positive direct Coombs test, which detects antibodies and complement bound to red blood cells, the antibodies can be washed off the red blood cells and the eluate tested to confirm the result.

Cold-antibody autoimmune hemolytic anemia

In cold-antibody autoimmune hemolytic anemia, IgM autoantibodies known as cold agglutinins lead to intravascular hemolysis by fixing complement to red blood cells at a low temperature and detaching at 37°C, leaving C3d on the cell surface.4 Monospecific direct antiglobulin testing is positive for C3d, as C3d causes agglutination (or clumping) of red blood cells without antiglobulin antisera in microtiter wells at 4°C.5

Cold-antibody autoimmune hemolytic anemia includes cold agglutinin disease, defined as a clonal proliferative disease. In contrast, cold agglutinin syndrome refers to a secondary condition associated with Mycoplasma pneumoniae, Epstein-Barr virus, lymphoma, or other causes.5,6

The cold agglutinin titer can be used to determine whether cold antibodies are present. Another parameter that can be measured is the thermal amplitude, ie, the highest temperature at which the IgM antibodies cause the red blood cells to clump; higher thermal amplitudes (above 30°C) can have more severe hemolysis.5,6

Mixed autoimmune hemolytic anemia

Mixed autoimmune hemolytic anemia results from both a warm IgG antibody and a cold IgM antibody associated with lupus or lymphoma or that is idiopathic. The direct Coombs test is typically positive for IgG and C3d.7 Intravascular and extravascular hemolysis also characterize the syndrome. The disease is usually chronic with intermittent periods of deterioration.

Paroxysmal cold hemoglobinuria

A biphasic IgG antibody (Donath-Landsteiner antibody) causes this rare condition, binding complement at low temperatures and leading to complement-mediated intravascular hemolysis at higher temperatures, after the IgG detaches from the red blood cells.8 Consequently, only complement is detected on the red blood cells.

Paroxysmal cold hemoglobinuria is typically more frequent in children, in whom it is transient, occurring 1 to 2 weeks after an upper respiratory tract infection, while cases in adults have been associated with tertiary syphilis.8

Coombs-negative autoimmune hemolytic anemia

The distribution of IgG antibodies on circulating red blood cells is not uniform, so the direct Coombs test may not detect them even if they are there. Less commonly, other antibodies such as IgA and IgM may be present instead of IgG; however, these can be detected if special antiglobulin test reagents are used.

Drug-induced autoimmune hemolytic anemia

Drug-dependent autoantibodies, molecular mimicry, and nonspecific factors can all induce hemolysis. The drugs most often implicated are antibiotics (particularly penicillin and cephalosporins) and oncology medications such as platinum-based agents and immune checkpoint inhibitors.9

Passenger lymphocyte syndrome

In this subtype, B lymphocytes from the donor graft (which can be either a solid-organ or a hematopoietic stem cell transplant) get into the recipient’s circulation, producing antibodies against recipient red blood cells.10

Nonimmune-mediated hemolytic anemia

Nonimmune-mediated hemolytic anemia is suggested by a negative direct Coombs test with supportive evidence of an alternative etiology. Hereditary causes include disorders of erythrocytic enzymes, membrane defects, and qualitative and quantitative hemoglobin disorders.11 Acquired causes include thrombotic microangiopathies, paroxysmal nocturnal hemoglobinuria, infections (eg, malaria, babesiosis, viruses), drug and metal intoxication, and dysfunction of prosthetic cardiac valves.

Thrombotic microangiopathies such as thrombotic thrombocytopenic purpura are considered when schistocytes are present on the peripheral smear with thrombocytopenia. Testing to differentiate among the thrombotic microangiopathy subtypes includes measuring the level of activity of ADAMTS13 (a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13), a plasma metalloprotease enzyme that plays a crucial role in regulating blood clotting by cleaving von Willebrand factor protein.

Hereditary spherocytosis is screened for with the eosin-5-maleimide binding test and osmotic fragility test.

Enzymatic and membrane defects in red blood cells can be tested for with molecular genetic testing. A glucose-6-phosphate dehydrogenase (G6PD) level can identify G6PD deficiency, an X-linked hereditary disorder triggered by fava beans, sulfa drugs, primaquine, nitrofurantoin, and many others.12

Hemoglobinopathies can be detected by hemoglobin electrophoresis.

Paroxysmal nocturnal hemoglobinuria. Flow cytometry with FLAER (fluorescently labeled aerolysin) analysis is the gold standard for identifying the lack of glycosylphosphatidylinositol anchors on cell surface proteins, such as CD55 and CD59, crucial for diagnosing paroxysmal nocturnal hemoglobinuria.

Lymphoproliferative disorders can also cause nonimmune-mediated hemolytic anemia via hypersplenism or marrow infiltration; therefore, computed tomography and bone marrow biopsy may be indicated if these are suspected.

CASE CONTINUED: HE IS TREATED, DISCHARGED, READMITTED

In view of the patient’s altered mental status and profound anemia, he was admitted to the intensive care unit. A noncontrast computed tomographic scan of the head excluded overt bleeding, infarction, and intracranial masses. He received 4 units of packed red blood cells and was started on oral dexamethasone 40 mg daily, planned for 4 days. His cognitive status improved. After the transfusion of red blood cells, his hemoglobin level increased to 8 g/dL.

To look for other treatable causes of profound anemia, he underwent an extensive evaluation that included iron and folate studies. Paroxysmal nocturnal hemoglobinuria, hereditary red blood cell disorders, and G6PD deficiency were not detected. His ADAMTS13 levels were normal. Tests for Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, hepatitis A, hepatitis B, hepatitis C, and COVID-19 were negative. The cold agglutinin titer was within the normal range. Bone marrow biopsy was performed to evaluate for a lymphoproliferative disorder and demonstrated erythroid hyperplasia with a normal karyotype without additional findings. A transthoracic echocardiogram revealed no valvular abnormalities for shear hemolysis. A magnetic resonance imaging scan of the abdomen showed periportal edema and gallbladder wall thickening, with no biliary dilatation. There was no evidence of splenomegaly or lymphadenopathy.

The patient was discharged after 3 days in the hospital. However, 2 days later his symptoms had returned and he was readmitted, this time to our hospital.

At this time his hemoglobin level was 5.7 g/dL, haptoglobin less than 10 mg/dL, total bilirubin 3.3 mg/dL, reticulocyte count 44%, and lactate dehydrogenase unquantifiable. This time, the polyspecific and monospecific IgG direct antiglobulin tests were positive but the eluate confirmation for IgG antibodies was negative. Prednisone 1 mg/kg daily was started.

ADDITIONAL TESTING NEEDED

2. What additional tests can be performed for a patient with clinically evident autoimmune hemolytic anemia if the direct antiglobulin test is positive but the eluate is antibody negative?

  • Super Coombs test (extended direct antiglobulin test panel)

  • Repeat direct Coombs test with an alternative method

  • No further testing

If results of the direct antiglobulin test vary and eluate testing is negative, there are several possible explanations.13,14 For example, older red blood cells typically have higher IgG levels than younger ones, especially during active hemolysis. Therefore, the surviving cells would tend to be younger, with lower IgG levels, and not close enough together for the direct Coombs test to cause cross-linking, producing false-negative results. Also, the nature of IgG on the red blood cell surface varies among individuals, and low-affinity IgG may only be detectable in the eluate after red blood cells are washed with large volumes of saline, which removes residual plasma that could neutralize the anti-IgG reagent used in the direct Coombs test. Furthermore, less common immunoglobulins such as IgA and IgM may be present on the surface of red blood cells.13,14

An extended direct antiglobulin test panel, also known as a super Coombs test, can be ordered at specialized laboratories to detect antibodies not detected by standard methods, namely IgG bound at low levels, low-affinity IgG, and IgA.15 IgA warm-antibody autoimmune hemolytic anemia has a presentation similar to that of the IgG variety, while IgM warm-antibody autoimmune hemolytic anemia tends to be more aggressive due to complement activation and is often misdiagnosed as cold agglutinin disease or paroxysmal cold hemoglobinuria.

Repeating the direct Coombs test using the standard or an alternative method would not detect the IgA antibody.

CASE CONTINUED: SUPER COOMBS TEST AND TREATMENT, BUT HIS ANEMIA PERSISTS

In our patient, although the positive direct Coombs test could be attributed to IgG or passive alloantibodies, we suspected he had another antibody, given his ongoing active hemolysis with a negative eluate and variable direct Coombs test results. Therefore, we ordered a super Coombs test at a reference laboratory (Figure 2). It found IgA and a small amount of IgG, the latter attributed to cross-reactivity in testing,2 which could explain the variable direct Coombs test results. However, because IgA is rare, we performed a confirmation direct Coombs test, which was strongly positive for IgA by gel technique, confirming IgA warm-antibody autoimmune hemolytic anemia, even though the eluate was negative.

Figure 2
Figure 2

Workup of autoimmune hemolytic anemia.

Based on information from reference 1.

He received prednisone for more than 2 weeks, but his anemia persisted, with hemoglobin levels lower than 6 g/dL, necessitating near-daily transfusions.

AUTOIMMUNE HEMOLYTIC ANEMIA REFRACTORY TO GLUCOCORTICOIDS

3. What is the next step in managing autoimmune hemolytic anemia that is refractory to glucocorticoids such as prednisone?

  • Rituximab

  • Intravenous immunoglobulin

  • Immunosuppressants (azathioprine or mycophenolate mofetil)

  • Splenectomy

Severe anemia (with hemoglobin < 6 g/dL) and hemodynamic instability are medical emergencies requiring urgent blood transfusion. Glucocorticoids are started, eg, oral prednisone 1 to 2 mg/kg/day or intravenous methylprednisolone in an equivalent dose.4,16 This dose is continued until the hemoglobin level is above 10 g/dL, which approximately 80% of patients achieve within 2 to 3 weeks. If effective, prednisone should be tapered over 2 to 3 months. But if the anemia persists, all the treatments listed above could be options.

Rituximab, a CD20 monoclonal antibody directed to B cells, is usually added if there is no response to prednisone within 2 to 3 weeks after initiation. However, in severe cases, rituximab is often started along with a glucocorticoid.17

For refractory warm-antibody autoimmune hemolytic anemia, other immunosuppressive agents such as mycophenolate mofetil are used, along with erythropoiesis-stimulating agents.16,18 For patients who are improving but still need transfusions after starting prednisone and rituximab, intravenous immunoglobulin can reduce the frequency of transfusions.19 Splenectomy may be considered for refractory cases and can offer long-term remission.16,20,21

CASE CONTINUED: WE REMOVE HIS SPLEEN

We continued to give our patient prednisone and started folic acid supplements to aid erythropoiesis and rituximab once a week for 4 weeks. Additionally, a 4-day course of intravenous immunoglobulin 0.5 g/kg was administered in an attempt to taper the prednisone. We also started an erythropoiesis-stimulating agent to treat possible inadequate bone marrow compensation from low erythropoietin, but discontinued it due to minimal benefit.18,20

Because his autoimmune hemolytic anemia was refractory to all conventional therapy at week 5, we decided to remove his spleen laparoscopically. Pathologic study revealed a widened red pulp with red blood cells immunostaining for CD68, suggesting an increased macrophage population,22 while the white pulp was preserved. His hemoglobin level markedly improved and stayed between 8 and 10 g/dL within the first few weeks after splenectomy, eventually normalizing at 14 g/dL by 4 weeks after splenectomy.

SUPPORTIVE CARE AFTER SPLENECTOMY

4. What supportive treatment do patients need if they have autoimmune hemolytic anemia, have received multiple transfusions, and have undergone splenectomy?

  • No supportive care is needed

  • Vaccinations for encapsulated organisms

  • Antibiotic prophylaxis

  • Iron overload assessment

These patients definitely need supportive care.

Vaccinations. In addition to age-appropriate and COVID-19 vaccinations, patients who undergo splenectomy should be vaccinated against encapsulated bacteria, including Streptococcus pneumoniae (with the 20-valent pneumococcal conjugate vaccine alone or the 15-valent pneumococcal conjugate vaccine followed by 23-valent pneumococcal polysaccharide vaccine after 8 weeks), Haemophilus influenzae type b (Hib vaccine), Neisseria meningitidis (meningococcal ACWY and meningococcal B vaccines), and seasonal influenza, preferably more than 2 weeks before splenectomy.23–25 However, vaccinations may need to be delayed after treatment with B cell–depleting therapy such as rituximab, which decreases antibody formation and immunogenicity.26

Daily antibiotic prophylaxis for at least 1 year after splenectomy is recommended in patients with prolonged immunocompromised states. Penicillin and amoxicillin are the preferred options, while macrolides, cephalosporins, and fluoroquinolones may be alternatives.24

Iron overload assessment. Patients who receive multiple red blood cell transfusions (> 15–20 units) are at increased risk of iron overload, which can lead to organ damage; patients should be monitored for overload by measuring ferritin and transferrin saturation.27 Although these tests are sensitive, they are not specific, and other causes should be evaluated.28 Magnetic resonance imaging of the heart and liver can help assess iron deposition; a liver iron concentration greater than 3 mg/g liver dry weight or a cardiac T2 value less than 20 milliseconds suggests iron overload.29,30

CASE CONTINUED: HE DEVELOPS IRON OVERLOAD

Because prophylactic vaccination is less effective after high-dose glucocorticoid and rituximab therapy, vaccination was postponed until more than 90 days after his rituximab treatment ended.25,26 We gave him amoxicillin daily as prophylaxis against infection.

However, 1 week after splenectomy his aminotransferase levels abruptly began to rise: his aspartate aminotransferase level reached 601 U/L (reference range 10–40), and his alanine aminotransferase level reached 664 U/L (9–46). In addition, his ferritin level reached 5,375 ng/mL (38–380), and his transferrin saturation was greater than 90.7% (20%–55%).

Hereditary hemochromatosis was excluded by testing for variants in the HFE gene. Serologic workup for infectious diseases was unremarkable, and imaging showed no evidence of vascular abnormalities.

Given the degree of elevation in aminotransferases, a magnetic resonance imaging scan of the liver was performed, which showed moderate iron overload (iron concentration > 15 mg/g liver dry weight). A liver biopsy revealed extensive iron overload in both hepatocytes and Kupffer cells, without findings suggestive of an autoimmune etiology or drug-induced liver disease. The aminotransferase elevations were attributed to his many transfusions (33 units of packed red blood cells).

The patient underwent 8 phlebotomies over the next 4 months, until his ferritin had fallen to less than 417 ng/mL. His hemoglobin level has remained stable.

NOT EASILY DIAGNOSED

IgA warm-antibody autoimmune hemolytic anemia is not easily diagnosed. When an immune-mediated hemolysis is highly suspected with variable Coombs test results, IgA warm-antibody autoimmune hemolytic anemia should be considered. Once this is suspected, an extended direct antiglobulin test (a super Coombs test) should be considered to look for IgA antibodies to red blood cells. However, an eluate may be negative for antibodies.

Treatment for refractory autoimmune hemolytic anemia may involve splenectomy. Supportive care includes vaccinations with splenectomy and management of transfusional iron overload.

TAKE-HOME POINTS

  • Suspect immune hemolytic anemia if patients have strong clinical signs of it, even if results on the direct antiglobulin test are variable with negative eluate.

  • Warm IgA autoimmune hemolytic anemia is extremely rare but should be considered in cases of non-IgG autoimmune hemolytic anemia; early super Coombs testing is recommended.

  • Testing for antibodies eluted from the red blood cells may be negative in cases of IgA autoimmune hemolytic anemia and rare subtypes.

  • Splenectomy should be considered for refractory cases of autoimmune hemolytic anemia that do not respond to glucocorticoids, intravenous immunoglobulin, rituximab, or immunosuppressants, especially in IgA autoimmune hemolytic anemia.

  • After splenectomy, vaccinations may be delayed until after rituximab therapy is completed to optimize immunogenicity.

  • Consider appropriate management for iron overload from transfusions.

DISCLOSURES

Dr. Chaulagain has disclosed teaching and speaking for Genzyme/Sanofi and Janssen Pharmaceuticals, Inc, and serving as a research principal investigator for Janssen Pharmaceuticals, Inc. The other authors report no relevant financial relationships which, in the context of their contributions, could be perceived as a potential conflict of interest.

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