Transcription
All right, so today is our 13th session. Um, today we will have again five cases, uh, with a discussion. And to inform you that there will be no session next Sunday because I am on call. So next Sunday, you guys are free.
All right, so the first case, if you guys can let the people in because I cannot see the team screen. Thank you. So this is a 56-year-old patient, or a male person, who went to GP for routine blood test. And the GP noticed that the the white cell count is high. White cell count is 30 in this patient. Patient does not report any symptoms, but the GP wants an opinion about the high white cell count in this patient. So you have made the blood film and the blood film is at the lab. Anyone from the lab, lab, if they can comment on the blood film? This is power 10 and then I will move to power 50. Anything? It just generated. Not any volunteer who wants to comment from the lab.
The peripheral smear of the patient is showing leukocytosis and the prominent population is small to medium-sized lymphocytes. Okay, so this is your opinion from power 10. Let's go to power 50 now. This is 50 earnings. Okay, so the peripheral smear of the patient is showing, uh, medium-sized, small, small to medium-sized lymphocytes, uh, with a moderate amount of cytoplasm. The nucleus is, um, round to oval shape. The cytoplasmic projections are appreciated, that are covering the circumference of the cytoplasm. Red blood cells are normochromic, normocytic, and platelets are adequate.
So what are these cells? The, uh, the differential, uh, uh, diagnosis is for hairy cell leukemia or variant splenic marginal zone lymphoma. Spill. Okay, so there are neutrophils. We have seen how Jolly bodies in this patient. Were there hairy cells? Are these hairy cells typical of hairy cell leukemia or they look a bit different?
How old is the patient? Dr. How old? 56. The leukocyte count is not favoring the typical hairy cell leukemia, but I cannot appreciate any nuclei in the nucleus. So I can't say it's a radiant. This is a monocyte. Okay, so this blood film does contain some monocytes and there is leukocytosis. There are hairy cells in this patient. And if you make it to power 100, so this is a nuclear. This is a nuclear, right sir? Okay, this one. Multiple nuclei, but this one is the bigger one. This one has a nucleus as well.
All right, so now you are acting as a clinical hematologist and you are sitting in FC path exam. They ask you to report this blood film, five marks. So please report the blood film. Are you asking from the clinical hematologist now? If anyone volunteers, it is okay. If no one volunteers, then you can go ahead. Right, any clinical hematologist? I can try. Yes, go ahead with the report.
Reporting this blood film for the FC path exam. The blood film shows leukocytosis with predominant population of atypical lymphoid cells. Some of them show, uh, medium-sized cells with round nucleus with fine nuclear chromatin and some with prominent zero to two nucleoli and some without, with some with inconspicuous nucleoli. They have abundant cytoplasm, which show circumferential hair-like projection there. But there is also monocytes are also present along with some neutrophils. And this neutrophil also show toxic granulation with normal ovulation. The platelet count seems to be normal to me and the RBC morphology is unremarkable except for for few acanthocytes which could be a storage change. The peripheral blood findings are consistent with a lymphoproliferative neoplasm, most likely hairy cell. And I would like to confirm my diagnosis with flow cytometry on the peripheral blood and along with molecular genetics for V for confirmation.
So I was very impressed from your explanation of the blood film, but the GP and the examiner would not be impressed because the detail that you have mentioned, the GP would not understand what is this doctor saying. So you need to see. I have to. I have to report to the GP. Yes, because this was a GP blood. So you have to use a bit of simple language, okay, so that the GP can understand. Can report it? Yes, hopefully your diagnosis, hopefully your diagnosis will also change in re-reporting. Yes.
So the peripheral findings are favoring involvement by some by involvement by atypical lymphoid cells, most likely lymphoma cells or a ly. I don't know whether the GP is familiar with lymphoproliferative disorder term. Or yes, this is a generic term, so everyone knows. Okay, so peripheral findings are consistent with a lymphoproliferative disorder. So refer this patient to hematology for further investigation and confirmation of diagnosis. The blood film shows leukocytosis. The white cells has many hairy projections and there are multiple prominent nuclei in the white cells as well. The red cells show some artifact with few Jolly bodies noticed as well. Platelet count looks normal. Most likely the blood is consistent with lymphoproliferative disorders. This patient needs flow cytometry for confirmation of diagnosis.
So can you show me some Jolly bodies? Okay, so let's move around while we are seeing the Jolly bodies. What do you think is the diagnosis here? Or I should say, what is the expected flow cytometry here in this patient? So this is a hairy cell. I do not do it. This patient has a prominent nucleus. [Music] And there is leukocytosis and yourself mentioned that there is monocytes as well. So do you think this goes against hairy cell leukemia? I don't remember the name. The new name of hairy cell variant. What is it called now? According to new, new WHO, it's splenic. I think it's splenic. Splenic lymphoma. Marginal zone lymphoma with prominent nuclei. Because this patient, if this patient was having PCL, it should have pancytopenia. There should be few white cells in this patient and there should be no monocytes in this patient. So this goes against hairy cell leukemia. It is hairy cell leukemia variant or the new name is splenic lymphoma leukemia with prominent nuclei.
So we do not ask the GP to refer the patient to hematologist. If we directly advise to do the bone marrow and the flow cytometry. Sorry, not bone marrow, the flow cytometry on peripheral blood. Or we say, send sample for flow cytometry and refer the patient to hematology for further investigation including bone marrow and cytogenetics or molecular genetics. So this sample which is present in the lab, it can be sent to HMDs within 24 hours. And if it does show hairy cell leukemia variant, then what we do in practice is to call the patient to see for any symptoms. If he is asymptomatic, then we ask the GP to refer to hematology through a proper channel. If the patient is symptomatic, then we ask the patient to come to our hematology assessment clinic. We will assess you, then we take the patient from there. So it depends on the patient's symptoms. But you are just seeing the blood film, you don't know about the patient yet. To get the information, you have to ask the GP. Yes, so there may be a delay. There may be a delay in the patient referred to you. So the best action is to call the patient yourself and ask him how are you feeling today? We have seen your blood film, it shows abnormal cells. If the patient says that I'm feeling unwell, I ask him to come to hematology assessment area. If the patient says he's okay, then explain the peripheral blood film report and blood test, say that the GP will refer you to hematology, then we will see you in our clinic. This is a good practice, although it is not mentioned anywhere in the books to do like that. The book says ask the GP to refer the patient urgently to hematology.
All right, so you have seen now hairy cell leukemia variant. And what is the expected flow cytometry in this position? Um, it will be same as hairy cell, that include the CD 11c, CD 25, CD 11c, but it will be deficient in, yes, deficient in CD 10, CD 103 and CD 123 may be present or absent. Yes, it is CD 25 negative but CD 11c positive. What is the molecular mutation here? It's the same V600E. Yes. And what is the first line treatment if the patient is symptomatic? Cladribine and rituximab. Yes. Cladribine and rituximab. The response rate is low, but this is the first line therapy for hairy cell leukemia variant or the new name which is very long. Okay, so this was the hairy cell leukemia variant. Anyone who is working in NHS and has access to nickas film, they can see the film number 2203. This is hairy cell leukemia variant 2203.
Right, now the second patient is again a 56-year-old male patient who presented to oncology assessment area because of worsening fatigue and tiredness. He has a background diagnosis of pancreatic cancer and he is on chemotherapy for that. This patient's full blood count shows hemoglobin of 80, platelet count of 100, and white cell count of four. So this is our 10, just an overview. So any volunteer from the lab side? I want a lab person specifically for this.
The peripheral smear of this patient is showing anisocytosis and poikilocytosis of red blood cells. There is microcytic, hypochromic picture as well as microspheres. Okay, yes. There is microcytosis, hypochromia, polychromasia, fragmented RBCs. Okay.
So what are your thoughts after looking at this blood film? This might be a case of hemolytic anemia. Hemolytic anemia is a very broad term, and there is a 560-page book on hemolytic anemia. So which, which hemolytic anemia may the patient? Circulation parameters are normal. Patient is a, he is only having fatigue and he is having therapy for pancreatic cancer. Some sort of cancer associated. So there are a lot of fragments in the blood. So as a lab person, what should you do when you see a film like this? MMTS 13. So as a lab person, you should pick up the phone and call the clinical hematologist that I am seeing a lot of fragments in this patient's blood film. Can you please come and review this blood film because this is a hematological emergency? You think this is a hematological emergency because there is a lot of fragments, patient has anemia, thrombocytopenia, and you think that this can be a TTP?
Okay, so now this film has gone to clinical hematologist and you are the clinical hematologist. Report this blood film please for the exam purpose. Dimorphic picture, fragmentation, some microspherocytes, polychromasia. What else in the report? Report contains three segments: description of the cells, your impression, and suggestion. Suggestive of microangiopathic hemolytic anemia, query TTP for urgent for reticulocytes and LDH, and also urgent plasma exchange.
The blood film contains features of microangiopathic hemolytic anemia due to presence of multiple schistocytes, spherocytes, polychromatic macrocytes, and anisocytosis. The platelet count looks okay, although no platelet plugs seen in this patient. White cell count looks okay as well. You have commented on all the three lines. So the blood film is consistent with MAHA. This patient needs urgent review and discussion with TTP consultant to confirm the diagnosis of TTP. So you have commented on the blood film, you have mentioned your, uh, suggest, impression, and suggestion. In TTP diagnosis, the first thing is always to to discuss with TTP consultant according to the BSH algorithm to agree on the diagnosis of TTP. And then the patient would be for transfer to a TTP hospital where plasma exchange will be done. Okay, so I agree this is a MAHA. You cannot call it as TTP because you don't have the MMTS 13 levels for the patient to confirm it as a MAHA.
What is the intervention required in this patient now? Sir, I want to ask a question about type of TTP, whether it is inherited or acquired. Can we think about the antibodies against Von Willebrand Factor? Yes, sir. No, this is not inherited. This is acquired. So antibody should be considered. This is my question from you guys. The patient is on chemotherapeutic drugs. There must be some drug he's taking which is resulting in MAHA. We need to rule out the drugs he is using. Capecitabine does not cause hemolytic anemia, it causes only thrombocytopenia. Pancreatic cancer per se can be associated with MAHA. Okay, this is pancreatic cancer associated MAHA. What urgent intervention is required in this?
So for every patient with TTP and the differential diagnosis, I think starting urgent plasma transfusion, preparing for the first plasma exchange session after with sending the ADAMTS13 level. And then once you obtain the result, if it's above 20, I think you can exclude the TTP and look for alternatives. Okay, but this is a wrong answer. Underline the call. Why this is three? The underlying cause. So TTP is of two types: immune TTP or acquired TTP. If you have an underlying cause for a TTP, then you do not plasma exchange any patient. Even if you plasma exchange the patient, the underlying cause is still present. The patient will go into hemolysis again, and there will be hemolytic anemia, there will be thrombocytopenia. This patient has pancreatic cancer. Pancreatic cancer is the cause of his MAHA. So this is a secondary TTP or acquired TTP. In secondary or acquired TTP, you do not plasma exchange any patient. You will talk to the oncology team that your patient is anemic and thrombocytopenic because of the underlying pancreatic cancer. Please optimize the chemotherapy as per your MDT. This patient does not need plasma exchange for hemolytic anemia. If the TTP is immune or congenital, then only you will do plasma exchange for the patient to replenish the ADAMTS13 levels in the patient. So always think about the scenario. What the scenario is saying? If the scenario says acquired or inherited. So this is the learning point from this case that this patient has pancreatic cancer and this patient has a lot of fragments, suspicion of MAHA, but the cause is pancreatic cancer. You do not need plasma exchange.
So I just have a question. So even if the Adam 13 came back low, something like below 10, then exchange doesn't have a role? Or if we are waiting for the Adam 13 and we are considering this patient as cancer-associated MAHA? I haven't seen any patient up till now who has acquired cause and his ADAMTS13 level is low. Okay, we have so many secondary TTPs here, none of them has low ADAMTS13 less than 10%. All of the secondary TTP, ADAMTS13 is about 30%. Okay, yeah, that's helpful. Thank you. And if the BSH algorithm for TTP, you see it has mentioned clearly, discuss with TTP consultant to agree on diagnosis. The TTP consultant would also ask you this question. If he finds out that there is a secondary cause, he would say, not for plasma exchange. Great, thank you.
Amir, would you expect the patient to have a lower platelet count with the immune-related TTP? Because I think this scenario, the platelet was 100, wasn't it? Yes, but it was from the analyzer. But when you look at the blood film, the platelet count looks towards normal. And this patient is on capecitabine for pancreatic cancer, whose main side effect is thrombocytopenia. So in TTP, in immune TTP, you will have thrombocytopenia because it is a component of the TTP triad: anemia, thrombocytopenia, and renal injury.
Sir, I have to clear one point, please. Sir, I have read and read in postgraduate that for the immune cause, you have to replenish the ADAMTS13. So you give the patient the plasma. Plasma infusion is the treatment. And in case of acquired, where there are autoantibodies against Von Willebrand Factor, then you have to plasma exchange to neutralize the antibodies. So what about this case? So immune is the one which contains antibodies. Inherited is the one which has no antibodies and no ADAMTS13. And acquired TTP is the one which has some secondary cause. Right, sir? Got it. Now, so you immune, immune because there is antibody present in the patient. Inherited is the one which has no antibodies, but there is no ADAMTS13 as well in the patient. There is genetic deficiency in the patient. And acquired is the one which has some secondary cause. The acquired is the term which we use generally in all hematological diseases who has like AIHA or secondary IM. But Amir, is it still, if it is secondary, still it is immunemediated? Am I right? But there is a cause for this one. Yeah, there is a cause. But in practice, we are sending for ADAMTS13 and we start exchange till we know. If there is a cause present, like patient has malignancy, patient has malignant hypertension, or patient has infection or any autoimmune disease, you do not plasma exchange because you will plasma exchange now, but after two days later, this patient will come back with anemia, thrombocytopenia again because you haven't addressed the main cause, which is either the cancer or DIC or infection or autoimmune disease. Yeah, thank you.
This is another 50-year-old patient who was referred to emergency because of worsening fatigue. The full blood count shows leukocytosis, white cell count is 40, patient has anemia, hemoglobin is 98, and platelet count is 140. This is the power 10. So power 10 confirms the lymphocytosis. Yes, there is lymphocytosis in this patient. Now we will move to power 50. You can make it more clear.
To comment on the three lines. The red blood cell showed anisocytosis with some spherocytes as well. The platelet, there is no clump, but few numbers. I did not see any giant platelets. White blood cells, there is multiple blood look because of high nucleus cytoplasmic ratio and here there is bi-loop as well. Where was bi-loop? Um, in the top of the neutrophil is that there is pile of nucleus. This one. And this is lymphocyte. This is lymphocyte. Okay, but there is, um, vacuole. There is one vacuole. So consistent with multiple blasts, most probably of lymphocytic origin. So the film showed thrombocytopenia with lymphocytosis and blasts present. This is suggestive of acute lymphoblastic leukemia. So you think that this is neoplastic leukemia? Yeah, but there are neutrophils present. Band forms are present. Yeah, so the granulocytes are present, but the lymphocytes are predominant. Okay, these are lymphocytes again, but even the large ones are not immature. Haven't immature. I didn't think. And most of them have indentation and the nucleus, the nucleus is slightly, the nucleus is slightly mature. But this is a condition with open chromatin. Am I right? Slightly, not completely, because it is more bluish than reddish, and there is polychromasia as well in the red blood cells. So can I comment on it? Yes.
So the peripheral smear of the patient is showing lymphocytosis with prominent population of small to medium-sized lymphocytes with many of them have hardly a rim of pale cytoplasm. The nucleus, nuclear chromatin is smooth and many of them have indentation or cleaved nucleus. The red blood cells are normocytic, normochromic and the platelets are adequate on peripheral smear. And my impression for this is lymphoproliferative disorder. Immunophenotyping is suggested to reach the final diagnosis. This is most probably follicular lymphoma. Maybe. So you think this is likely follicular? But the cells of follicular lymphoma are small in size. Yes. Less likely. So what is the diagnosis here? Because I, those who say this is ALL is wrong. This is CLL. Those who say this is CLL is wrong. No, those who say follicular is wrong. Man, those who say mantle is wrong. I think maybe TCL. Those who say this is lymphoproliferative is correct. So you always say a lymphoproliferative disorder. Likely lymphoproliferative disorder. You need some further test to confirm your diagnosis. So on blood film, you do not give diagnosis unless and until it is very, very clear. So this is a lymphoproliferative disorder. But when you do flow for this patient, it can come out as CLL. It can come out as follicular lymphoma. It can come out as CL. It can come out as blast form of mantle cell lymphoma as well. So you need flow cytometry to confirm your diagnosis. I say lymphoproliferative because the cells have a nucleus which is a bit mature compared to blasts and yes, they some of them have indentation as well, so which makes the lymphoproliferative diagnosis more favorable.
So now, what is meant by indentation? Indentation will find a cell for you. If you were present in a previous session and you had seen the follicular lymphoma cells, they were having very clear indentation through and through. Can you see indentation here? Okay, I did not attempt. But this indentation is the indentation, kidney-shaped nucleus, you mean? Yes, but sometimes it is through and through. You think that this is B, but it is not B. Yeah, because of that I commented it is B. Okay, thank you. Thank you. So if you see this cell, if it is clear to you or not. This cell has indentation starting from here. This line. This whole part is indented from this one. It is very clear to me in the microscope, but you mean like folded chromatin. Folded. Yes. Okay, like this one has indentation now. And any other clear cell that I can find for you. But when we will be doing the follicular lymphoma next time, you will see a lot of indentation. But this one is very clear. If it appears, you can see this indentation. Yeah, it is clear. Yeah, thank you.
Right, so the immunophenotype for this patient is CD19 positive, CD5 positive, CD20 positive, CD10 negative, and CD23 negative. This is, this is going with the B marker except of the CD, CD5, which is a T marker. So CD5 positive, CD1 negative. What are the two conditions in lymphoproliferative disorder, B-type, where CD5 and mantle? This patient. Yeah, this patient has CD23 negative, so it goes with mantle. Right. This patient is asymptomatic at the moment and his white cell count is 30. Would you treat this patient or not? I think so. Has anemia and thrombocytopenia. Yeah, because he came with progressive fatigue. The blood picture shows anemia. There is thrombocytopenia. It means the bone marrow has been involved. You will investigate further with PET scan. Now, PET scan is recommended for mantle cell lymphoma. You will do bone marrow biopsy in this patient to see bone marrow involvement and then you will discuss the case in MDT for different options.
All right, so I have noticed that the mantle cell lymphoma cells are a bit larger than CLL and they are a bit more square-shaped. This is my finding after seeing multiple mantle cell lymphoma patients. That the lymphocytes are a bit large and they have square-shaped lymphocytes. Square-shaped? Yes. Square-shaped. This is my personal experience finding in the mantle cell lymphoma. It is not mentioned anywhere. But whenever I see a patient who has lymphocytosis, a bit larger than the red cell, and they are like square shape, then I think that this patient's flow cytometry will be like, [Music] mantle.
So this patient is again 56 years old. All my patients will be 56 years old because 56 was my roll number in a medical college for 5 years. And he is admitted because of severe anemia and chest infection. The biomedical scientist has seen the blood film and says there are multiple rouleaux formation in this. The patient has a background of chronic liver disease secondary to alcohol. So this is power 10.
So the peripheral smear of the patient is showing prominent agglutination of the red blood cells, decreased WBC count, and low platelet count. Okay, so there is thrombocytopenia, rouleaux formation. Acanthocytes are also appreciated. There are again the same neutrophils are showing toxic granulation and vacuolation. So my impression is that the patient is having some autoimmune pathology that is causing this picture of the red blood cells, and infection for WBCs.
Okay, so you say that this patient has toxic neutrophils. There is thrombocytopenia. There is anemia. Does this acanthocytes signify anything or not? Liver disease, beta-lipoproteinemia, or maybe because of alcoholism. Right. Have you heard the name of spur cell anemia? Yes. Yeah. So spur cell anemia is a feature of alcoholic liver disease where there is a lot of acanthocytes in a patient. These patients will have thrombocytopenia because liver is affected. So once liver is affected, then you do not make thrombopoietin, and you will have thrombocytopenia. This patient has anemia because of the spur cells. Spur cell lifespan is very, very small. As soon as they go to spleen, they are destroyed. These people are usually transfusion dependent because of the spur cells. Why this patient has this rouleaux or agglutination? Because this patient has lung infection. So this is infection-induced red cell agglutination or rouleaux formation.
So spur cell anemia can appear both in part one and in part two as a slide as well. They have appeared before. Spur cell anemia was a case in my part one exam as a MCQ. And if you go through the list of the questions in the past paper for part two, you will find many spur cell anemia cases. If you see new, if you see acanthocytes in the blood film, some of the blood cells are normal, some of them are acanthocytes. So you need to remember few conditions in your mind where they can appear. One is this spur cell anemia because of chronic liver disease. Second is abetalipoproteinemia where there is enzyme deficiency. I have forgotten the name of the enzyme, but it starts with MTP enzyme. You can check in the theory. MTP enzyme deficiency. And these patients have red cell lipid defect, and they turn into acanthocytes and are destroyed. And the third cause is myeloid syndrome. Those patients will have some hint in the history. Either they will have some neuro problem, they will be coming with seizures to you, or they will tell you that there is no crossmatch available for crossmatch blood available for this patient. The patient's blood reacts with everything because they have absence or very weak K antigens. This K small X phenotype, etc. So these three cases, they can appear in both part one as MCQs and in part two as short cases as well. And they have appeared previously. Abetalipoproteinemia and chronic liver disease were the short cases in Autumn 2023 exams.
All right, so if you are preparing for part two exam, just copy the list of the cases that appeared in the previous exam. Keep it with you. Whenever you collect blood film from the lab, just go to your list and see if any of the disease blood is present or not present. Steal it. Keep it.
This is another lost patient who is admitted because of per rectal bleed. But the full blood count shows anemia, hemoglobin of 90, thrombocytopenia, platelet count of 110, and white cell count of three. So this is the last case. Any volunteer? Can you show it on power of 50? Power 50 for.
So the peripheral smear of the patient is showing acanthocytes, anisocytosis with spherocytes. White blood cell is decreased and there is also very low platelet count. Let's see a few more cells because the cells are very few here. What are these? Myelodysplastic cells. They are hypogranular and hyposegmented. Any blasts? Sorry. And the repeat bite and blisters? No, there are no bites and blisters. This hyp, this is hypolobated neutrophil. B neutrophil. Pure normal. [Music] Monocyte is there. Two more promonocytes with. That's why I don't like peripheral blood films because you have to search for the cells. These monocytes are not normal. You can see there is no nuclear indentation and the vacuolation is towards one side. And this is NRBC. No, this is NRBC. You have seen multiple monocytes, myelodysplastic neutrophils. We have seen one NRBC. Thrombocytopenia is there. Anemia is there. Spherocytes are there as well. What do you think is the likely cause? CMML. Yes. Patient has dysplastic picture and there is monocytosis, abnormal monocytes as well. It does fit with CMML. What type of CMML? Myelodysplastic. What is the criteria for saying it as a myelodysplastic? Why not say less than 13? Less than 13. If it is less than 13, you call it as monomorphic. Myelodysplastic. The peripheral blood blast is just 2%. So again, what is the subgroup of CMML? It's same, ML1. Yes, because the blast percentage in peripheral blood is less than 5%, you will call it as CMML1.
Right, what is the prognostic score used for CMML patients? Anyone knows this? The prognostic score for CMML. So it is CPSSMOL is the prognostic score that we use for CMML. And anyone knows which type of cytogenetics is considered as a poor risk in CMML? Monosomy 7. Yes. Any monosomies or TP53 is there is considered as a bad prognosis. Even if TP53 is present, you do not consider transplant for those patients as well because those patients' transplant outcome is also very bad. And wherever you see TP53, it is a bad prognostic factor, even in leukemia or in lymphoma. In lymphoma, we see TP53 mutation in mantle cell lymphoma, they carry very bad prognosis. Patient outcomes are very bad.
All right, and what is the treatment in this case? Watch and wait, given the white cell count is low. Yes. It is a symptomatic. Treat this patient. Came with bleeding episode because of thrombocytopenia and MDS related anemia. So there is no treatment mentioned in the guidelines for MDS type of CMML. But sometimes the MDT decides to treat it on the line of MDS, but it is individual MDT decision. There is no guideline about that. And if the patient is young and fit, then tissue typing and look for allogeneic stem cell. The only recommended therapy in CMML is azacitidine. But it is for CMML2, which means the blast count is high. You can give azacitidine. Or if it is a myeloproliferative type of CMML, then you can do cytoreduction with hydroxycarbamide. Or if it is a young female, then you can use interferon if she's planning pregnancy.
CMML was my essay question in the exam. They asked us about the criteria for CMML, subgroups of CMML, subtypes of CMML, and what is the treatment recommendations, and would you transplant this patient? So there are five sub-questions in the CMML. So myeloproliferative type of CMML is easy to pick, but myelodysplastic CMML is sometimes a headache. The patient usually comes with frequent symptoms like bleeding or bruising, and these patients end up with a lot of bone marrow biopsy. So every time they come with bleeding secondary to thrombocytopenia, you think that whether this patient has converted to AML or not. But we have such patients currently. She has admitted multiple times with bleeding, and after every three months, we do a bone marrow biopsy for her to see if she has converted to AML because there is no recommended treatment for such patients. And you cannot issue a treatment from NHS to same MDS type of CMML because there's no treatment. Once it is converted to AML, then you decide to give him treatment of AML. And finding a donor for allogeneic stem cell transplant in UK is very difficult as well. So if anyone gets a stem cell donor, he is lucky. If not, then the patient has to wait.
This was the last case. And thank you very much. There will be no session next week because I'm on call, and we will meet the week after. Thank you very much. Have a nice sunny Sunday. Thank you. Thank you. Thank you.