Hematomorph Session for Morphology

Yes, yeah. 713. Her here in the pin. Here, see, there is one skin feeling wound. Don't know. Maybe she's sleeping on this side. The the morning already saw any or anything. It's drying, but yeah, we'll see tomorrow. Maybe you're okay.

E. E. Morning, everyone. Can you hear me? Yes. Hi, good. So, we will make a start. If anyone else wants to join, please let them in. So, this is the first case. This is, um, a 50-year-old man who went to GP because of abdominal discomfort. The GP did an examination and he found out that there is splenomegaly in this patient, which is 17 cm, and no other abnormal finding in the patient. The full blood count shows hemoglobin of 98, L count of 181, and white cell count of 23. So, this is the power 10 for this patient. So, I would like any volunteer. [Music] To this power. Anyone? No. I think, think from this power, you can see, um, an increase in the number of some, um, medium to large-sized cells. Um, I can't comment further, but yeah, we can go. Power at Power 10, you have seen medium-sized cells. So, let's go to Power 50 oil slide and and let's see what do you see in the. So, what do you now is present in this in this slide? So, these cells have a very irregular border. I'm not sure if these are like, um, smudge cells or they are like, you're right. These are smudge cells. They burst out during slide preparation. And what about these cells? Yeah, um, these have a more like, um, a dark, um, dense chromatin. They are monomorphic. Uh, I think, and they are more like slightly, maybe medium-sized, we can say. Okay. So, if you, whatever, take this cell and this RBC and this RBC, they are almost the same. They are small-sized mature lymphocytes. Okay. So, you have smudge cells, you have small mature lymphocytes. What else abnormality do you see in the back? What about platelets? Yeah, I can see some platelets. So, I don't think there is, um, any remarkable morphological abnormality with them. Yeah. Okay. Yeah, this is like spherocytes. Okay. Why spherocytes will appear in this platform? Is there any association between spherocytes and this blood? Can there be like an autoimmune hemolysis here? Yeah. Auto. Okay. Right. So, now, um, for example, you are sitting in part two exam and they ask you to report this blood film. How would you report it? Uh, I would say, um, the large, like a large number of, um, smudge cells and, uh, gain and increase, uh, number of, uh, small mature-looking, uh, with a condensed chromatin, monomorphic, um, looking lymphocytes, um, and keeping with maybe a lymphoproliferative disorder, likely CLL. And we have an evidence of, um, some hemolysis, likely associated. What advice would you give to the GP? Because this is a GP referral. GP did the blood test. He don't, he doesn't know what to do with lymphoproliferative disorder. So, um, it can be a two-week waiting, um, referral to hematology. Yes. So, always read in the scenario whether this is a GP referral or this is a hospital blood. Because if, if it is a GP referral, then you have to give advice to the GP and act accordingly. You will say the blood contains lympho. The blood film contains multiple small mature lymphocytes and smudge cells. Platelet counts are normal. There are multiple spherocytes indicating a hemolytic process going on. The impression is that of hemolytic anemia secondary to a likely chronic lymphocytic leukemia. We need to do flow cytometry and hemolytic screen for this. This patient to confirm the diagnosis. You will send peripheral blood sample to HMDs for flow cytometry and you do a hemolytic screen, a DAT test as well, find out if it is a. And then you will advise the GP, please refer this patient the fast track basis or two-week referral to hematology. And if the patient becomes symptomatic, what flow cytometry do you expect here? CD5 and CD23 positive. Mhm. And what about 43? 200? FMC? Yeah. 200 also positive. 200 is positive. 43 is positive. What about FMC? See will be negative. Negative. Yes. What are the treatment indications in the CLL patient? When would you treat a patient for CLL? So, when we have like a duplication of the lymphocytic or have a thrombocytopenia, spleen also, I think large spleen might be an indication. And patient becomes symptomatic due to either hyperviscosity or is it, it is causing cytopenias like anemia, thrombocytopenia due to high count and or recurrent infections. So, when the lymphocyte doubling time is less than 6 months or the count increase more than 50% in two months, and you have massive splenomegaly. Again, this patient has 17 cm and he has abdominal discomfort because of that. Or if there are cytopenias that does not respond to standard therapy, like this patient has hemolytic anemia and if he's not responding to steroids, this is this will be a second indication in him to treat his CLL. First one was massive splenomegaly. And if the patient has constitutional symptoms, then we would treat this patient with CLL therapy. All right. So, the next patient is also a 50-year-old man with a name and abdominal discomfort. His hemoglobin is also 90 and he has splenomegaly as well. Up for. All right. I need a second volunteer for this. This is power 10. A general overview of the film. Anyone who wants to volunteer from the left side and from the clinical side? Maybe there is a bit of cell aging like. [Music] Let's go to Power 50 then. For example, you are sitting in part two exam and in the scenario they asked you that this patient has anemia and what sort of differential diagnosis comes to your mind? Did you, um, anemia like maybe sidero? I was thinking about sidero. Cytosis. What else? That way. And the age is 50. I would expect. Hemolysis. And a young patient. This is a 50-year-old who was previously normal but now he has only anemia or pancytopenia. I would say anemia and expl. She mentioned Gemia. Sorry. Autoimmune anemia and hemolysis. This patient has low white cell count as well and platelet count is low as well. You can see from the blood. Yes, he has the pancytopenia with splenomegaly. Right. Yeah. So, now, what do you think if he has pancytopenia and splenomegaly, then what will the differential? Which leukemia? Sor. A leukemic leukemia. One, one of the. We don't see any blast here yet. Aplastic. Aplastic leukemia. Uh, I don't see blast, but, uh, still in aplastic, this is one of the differential. I meant, what are the common differential? Aplastic may be very uncommon. Hairy cell? Okay. Hairy cell. Be myelofibrosis. Yes. Is it differential? Marginal? Lymphoma? Which one? Marginal. Marginal zone lymphoma. Marginal zone only in for. Then they would have some, uh, atypical lymphocytosis. N that will or plasma type of cells that will give you a clue that this may be a. Yeah. Coming to this slide, what do you think are the features in this one? So, there are teardrop cells. You can see. Um, I think in the other side I have seen some polychromatic cells. Poly. There is teardrop. This teardrop. This teardrop. This patient has a lot of bit of hemolysis. We haven't seen any platelet clumps in this patient. And the neutrophil is a bit low as well. Although we have seen only two neutrophils up now. Okay. Yeah. Yes, because if splenomegaly is big, spleen will eat everything, both red cells and the. And there are one or two, uh, fragments. I think a bit higher power field now. This is an artifact. You can see this is in in one line. So, this is artifact. These are not fragments, not true fragments. This is also a line on the on the red cell. You can see this. Yes. Yeah. So, these are different. Um, how would you report this patient? Uh, this patient's blood film. This looks like minimal. Some granules here. And this looks like a reactive granulocyte. How would you report this thing for the exam purpose? None of you are going for part two exam this year? I mean, in the spring. I'm still in the bar to stage. Oh, but you people may be reporting blood films in the hospital, right? Yeah. I can participate. Dr. Ra. This WBC shows mild total leukopenia, mild absolute neutropenia, some activated lymphocytes are seen. Regarding RBCs, there is, um, anisocytosis in the form of normocytic, normochromic, some tear drop cells. There are some spherocytes occasionally. I think, regarding platelets, no remarkable morphology except of the low platelet counts. I mean, um, it looks like moderate, uh, hypochromia or even marked. I don't know the number of platelets. It is low. It is 120. Oh, okay. M from opinion. What is this one? Yeah. Poikilocytosis. Poikilocytosis. Patient has and they have hypofunctional hyposplenism. I always comment on the dominant abnormality. This patient has a lot of teardrop cells. Comment first on the teardrop cells. And this patient's blood shows anemia with multiple or numerous red cell drops and target cells. The platelet count looks low. There are no platelet clumps and no blast seen. There are few reactive lymphocytes and granulated neutrophils. The impression is likely, the impression is of likely myelodysplastic, myeloproliferative disorder or myelofibrosis. We need to do, we need to send blood to HMDs or MPN panel to confirm the diagnosis. We need to biopsy. Cell Dr. Sorry. Are these like, how will Jolly bodies in the red cells? They are towards the periphery and they are round. [Music] Round. So, they. Sorry. P. Hammer. P. Hammer. And Hammers are the iron accumulation, ferritin accumulation. They can be anywhere in the, in the red cell, and they are not typical circular like this one. They are having irregular shapes. In the end, we will see one blood film of human bodies. As Dr. Amir, the spherocytes in this film, we should not worry about the mainly teardrop cells are more, but spherocytes are also more. How should we interpret that? Yes, this patient may be having some sort of blood loss from some. That's why a few teardrops have appeared. But this patient is still admitted with us. We don't have any source of bleeding, no melena, no abdominal bleed in it, no hemolysis. Even reticulocyte count is low, hemoglobin is high normal, LDH. We could not find the reason of these two spherocytes which are present in his. So, in the exam, we should comment or we should go with. You have to mention in the exam any abnormality that you see in the blood film. You have to mention because it may be present in their key. All right. So, do you know different causes of myelofibrosis? Marrow fibrosis, post polycythemia vera, post essential thrombocythemia progressing to myelofibrosis, and primary myelofibrosis. Yes. What else? There's a table in the BSH guideline. Remember that. It will be a small question in the morphology section of part two. You have infectious causes like HIV, TBs. You have medication causes like TPO agonists, trob. Any metastatic solid organ cancer can lead to bone fibrosis. Some hematological disorders, you mentioned hairy cell leukemia, then Hodgkin lymphoma, myelodysplastic syndromes, they all lead to myelofibrosis. Some of the autoimmune diseases have a potential as well, like Sjogren's syndrome. Then congenital disease like gray platelet syndrome, as myelofibrosis. And next one is iron radiation. Radiation-induced myelofibrosis as well. What prognostic score do you usually use in your practice for myelofibrosis? Although there are a lot of scores for myelofibrosis, but which one do you usually use? DIPSS Plus. Okay. DIPSS Plus score. Okay. So, this patient has a DIPSS Plus score of, let's say, high. He is in high-risk category. What treatment can you offer to him? So, my goal of treatment will be allogeneic stem cell transplant. But I will start him with a JAK inhibitor first to manage his symptoms. But like, it would be the ultimate transplant. You will see whether the patient is transplant eligible or not eligible. If he is transplant eligible, then you will give him a JAK inhibitor, you reduce his spleen size, and then you would take him to allogeneic transplant if a donor is available. And if he is not fit for transplant, then you can give him a JAK inhibitor if he responds to that. Okay, continue. If he does not respond, then look for any other JAK inhibitor. Like, if you have started with Ruxolitinib, then you go, you should go to Fedratinib. You can use Fedratinib as a first line as well or a second line. The Fedratinib has been removed. I think last month there was some news about the Fedratinib that we no more use Fedratinib because of its serious CNS side effects. Yes. So, what is the serious side effect of Ruxolitinib? Cytopenias. Um, one of the side effects. Yes. Cytopenias. And if you stop it without weaning, inflammatory response. SIRS. Yes. SIRS withdrawal symptoms. Yes. All right. So, the next film is an aspirate. This was again a 56-year-old young man. 56 is considered a young man in the UK. He will call the person old when he says that I'm old, otherwise they are young. So, he was completely fine. He was playing golf and suddenly he started complaining of rib pain. And when we examined his rib, there was a fracture over there. It was a non-traumatic fracture in this patient. And the full blood count showed hemoglobin of 90, normal white cell count, and normal platelet count. So, because of his, um, fracture and anemia, we decided to do a marrow for him. So, this is the aspirate and this is power 10. Any volunteer comment on this? So, it's a cellular aspirate and you can see increased, like, I think normal or a little bit increased number in this section of the slide. There are no, but there are some other interesting cells. [Music] There is some [Music] background. Are these cells? Sorry. Are these plasma cells? This is a plasma cell. Plasma cell. Plasma cell. This is a dysplastic plasma cell. Two nuclei. Another dysplastic with three nuclei. And this white area is the halo. Halo. Halo. This aspirate has multiple plasma cells. What do you think is going on with this young? Likely it's a myeloma. Then we just need the percentage to know what state, what exactly. Like, is it? It doesn't look like definitely it's more than being an M-US, but between smoldering and like multiple myeloma, it is definitely not M-US. The bone marrow has quite a lot of plasma cells there, more than 60%. You can see all of these cells are plasma cells. So, what is the diagnostic criteria from myeloma? When should I call it as a myeloma? Then more than 60% plasma cells in bone marrow is enough to say myeloma. Okay. Than 10% and CRAB criteria. And what is the CRAB criteria? Hypercalcemia, renal failure, anemia, and bone lesions. Bone lesions. And bone lesion. What are myeloma-defining events? One of your colleagues mentioned all plasma cells more than 60%. What are the other two events? Percentage of involved to uninvolved light chain more than 100. Involved to uninvolved free light chain more than 100 ratio. And the last one, two, two bone lesions more than 5 mm in MRI. Yes. You will be asked what are the, what is the criteria of myeloma diagnosis? You have to write all these three bone-forming features and the CRAB. But for diagnosis, you should have only one myeloma-defining event, either plasma cells more than 60% or involved to uninvolved light chain more than 100 ratio or two or more than two focal lesions on the imaging which is more than 5 mm. Right. So, you received a result of cytogenetics. This patient and your colleague asked whether he is a standard risk cytogenetic patient or high-risk cytogenetic patient. Do you remember any standard risk or any high-risk? Cytogenetics. I think 14;17 is high risk. Translocation 14;17. Yeah. 14;16. There is no 14. Oh, sorry. 14;16 is a high risk. Translocation 14;20 also high risk. 14;20 is a high risk. 11;14 standard risk. 11;14 is a standard risk. Yes. Hyperdiploidy. Good risk. Yes. So, remember hyperdiploidy is standard risk everywhere. And hypodiploidy is bad risk everywhere. Except AL. In AL, hyperdiploidy is a standard risk. Is it hyperdiploidy? Yes. In hyperdiploidy is a standard risk. And hypodiploidy like trisomy 7 or deletion 17p, they are poor risk. All right. So, your patient is 14;16 and he is standard risk. Sorry, he is a high-risk patient. And you are now staging him. Whether he is stage one, stage two, stage three. Or RS. What are the other components of the staging system for myeloma? One, you have done cytogenetics. And the other LDH. LDH. Beta-2 microglobulin. And albumin. Yes. All right. So, this patient was well enough before all this happened. He has no comorbidities. What treatment option can you provide to him? Is a first-line. Dara-VD. Can it is the recommended now? Dara-VRD or Dara-VTD. We use VTD. Maybe different trusts, different individualized protocol. If the patient is fit and if the MDT is as well, then we can give them Dara-VTD. And what is the maintenance of the Dara-VTD and transplant? After transplant, any th Thom. Autologous. Autologous. So, you have given him four cycles of Dara-VTD and you have autografted him and then you have given further two cycles. Then you do maintenance for this patient. Which you use. Do you know any new therapy that is going on in your hospital for myeloma patients? Later in those patients who are refractory to multiple lines of therapy, do you use any new therapy in your hospital? Bi-specifics. Which one do you use in your hospital? Amivantamab. Yeah. And Teclistamab. Okay. What is the common side effect of these bi-specifics that you are worried for? CRS and ICANS. ICANS. And CRS. I think ICANS incidence is less. And bi-specific and CRS is common. But we have seen less incidences of CRS up. But yes, they are the common side effects. And I have no experience with. All right. So, this is another 50-year-old patient which has low hemoglobin and he is very tired and fatigue with the. So, this is the general overview of the slide. These are artifacts. So, these are not WMS. This is then overview. Let's move to power 50 to see what's going on. All right. Any volunteer who wants to comment on this? Anyone? Yeah, I can go for that. Yes. So, what do you see in the blood? Yeah. So, um, there is a low number of red cells and, um, and call this picture with, um, few few target cells or I'd say more than few occasionally target cells. Um, few elliptocytes. Right. Um, yeah, and also like, um, couple of target, um, couple of teardrop cells. I think the platelet count is, um, there is a need for analysis in the platelet. I think the number might be adequate. Does this all right? Yeah. Um, looks like spherocytes. One, it's not quite clear, but I think might be a bit polychromasia. This one. This one. This one is, um, fragmented red cells. Yeah. It's not simple, but like, yeah, fragmented red cells. Yeah. Side. Yeah. But not these ones. This one and this, because this is an artifact. You can see a line here, right? Yeah. So, yeah, um, spherocytes again. No, this big is a reticulocyte. Spherocyte cannot be this. Yeah. Polychromatic cell then. Yeah. I think the platelets are reduced to be. All right. So, what do you think is going on in in this patient? Yeah. So, um, there are, um, mainly red cell, mainly like there is red cell changes in terms of, um, anemia and, um, fragmented cells and, um, hemolysis features in terms of polychromasia and, um, cell and polychromasia. Sorry. I, I think, uh, I would like to exclude TTP. Mhm. What? Yeah. Um, in the exam, every slide will not be a diagnostic slide. They may give you some slide for for the differential diagnosis as well, or they may ask you just write six points, six findings in this blood film. It is not necessary that you will have a diagnosis, a confirmed diagnosis in this blood film. And then you have to. No, they can ask you just a differential diagnosis. Okay. So, this patient has, yeah, hemolytic anemia features. You have seen. You have seen spherocytes, you have seen target cells, spherocytes. Yeah. Histocytes. Reticulocyte count is low. Some hemolysis is going on. You can ask you what are the differential diagnosis. Yeah. You mentioned one TTP. One TTP. Yeah. Um, could be also like, um, sepsis and DIC. Um, although not expected like the hemolysis feature. Okay. DIC. Yeah. She. So, you have to write the differential diagnosis of hemolysis. If pregnant, help will be in the differential diagnosis. Syndrome. Yeah. Pregnancy-related as well. Yeah. Yeah. Other differential for MAHA also could be HUS. Can HUS as well? Yeah. Yeah. Could be a secondary TTP secondary to medications, maybe drug-induced. Drug-induced as well. Like, uh, cin. Urine. [Music] Inhibitors. Viruses. Virus. Viruses can induce TTP and hemolysis both. Yeah. You mentioned hemolytic syndrome, pregnancy, drugs, viruses. Could be even sometimes, but like, yeah, yeah. Solid organ malignancy as well. Yeah. Okay. Mediated as well. Evans syndrome. Yeah. Anemia. Yeah. Okay. All right. So, what investigation would you like to do to reach a diagnosis? Yeah. I would like to ask for, uh, the hemolysis screening, including lactate dehydrogenase, hemoglobin, and that. You would like to check the clotting screen. [Music] Um, other, um, to exclude like secondary causes, could be virology, hepatitis B and C, and HIV, and autoimmune screening as well. Protein electrophoresis and, yeah, immunoglobulin as well. Okay. Yeah. And of course, can you send? Would you send ADAMTS13 in this one? Yeah. So, I was going to say like, um, I will see accordingly for. Yeah, fragments are not that much here and coagulation functions are okay. I would not worry for TTP screening. Yeah. What, what's the platelet count? Am, because I don't think it was like, um, severely reduced. Yeah, reduced, but not very reduced. Yeah. 140. 40. Right. How many loops here? 1, 2, 3, 4. 1, 2, 3, 4, 5, 6. Hemolytic is also one of the cause of. Yeah. B12 deficiency also, especially. Yeah. This one has one, two, three, four. Yes. Yeah. Never forget hemolytic test in the hemolysis picture. They can also lead to fragmentations as well. Severe deficiency. Definitely. Yes. So, let's say this patient DAT is positive and his hemoglobin is dropping. Next day, his hemoglobin went to 80. Mhm. What treatment will you start for this patient? Right. If I suspect autoimmune hemolytic anemia, I will start with steroid, prednisone at 1 milligram per kg. How much milligram? 1 milligram per kg. Patient is 90 kg. Yeah. So, like, yeah, if, um, 90 mg, then. And just to consider like, had got no morbidities like diabetes. Yes. The maximum you can give is 80 mg. 80 mg to patient. Okay. Higher doses like 90, 100 are only given with chemotherapy regimen if you are giving someone R-EPO etc. Their weight is high, then you go above 80. Otherwise, in immune TTP and autoimmune anemia, our cap is 80. Right. Okay. So, you have given him 80 mg of prednisone. Yeah. And PPI. Yes. Yeah. And what else? Bone protection. Yeah. And vitamin D, of course. Yes. Folic acid. I would say folic acid. Yeah. What else? VTE prophylaxis is important. Which, which factor is important? VTE prophylaxis. Yes. VTE prophylaxis is important. Yes. And where would you see the response? Yeah. So, I suspect like the first couple of days, should be some increment. I will monitor him with daily full blood count and hemolysis markers. Yeah. If you start patient on steroid, prednisone, you will see the response in two to three weeks' time. You mean the optimum? Yes. Yes. Steroid response takes two to three weeks. The algorithm is given in the BSH guideline. Then if the patient does not show any response in two to three weeks, you will do quick peppering. And then if, for example, we are dealing with primary autoimmune hemolytic anemia, then you would do a biopsy and decide regarding treatment therapy. The second line is rituximab. If you have, yeah, if you have secondary autoimmune anemia, then obviously you have to treat the cause first along with the steroid. Then we don't do bone marrow. If they are steroid failure, they usually respond when we treat the secondary cause. Secondary cause can be infection, can be autoimmune disease, can be a hematological and non-hematological malignancy. As in the first case, we saw a patient of CLL with hemolytic anemia. Do not forget group and save in your investigation. Yes. Because this patient may need blood transfusion. And if the DAT is positive, sometimes group and save is very tricky. You have to send a blood sample to your NHSBT nearest center. We have BN here. And they use warm, warm warming technique or CPD to do the blood grouping and antigen testing in this patient. Because if the DAT test is strongly positive, 4 plus, it is very difficult to find out your blood group. Yeah. So, the blood transfusion may take you hours. The blood transfusion bag may take few hours if the patient needs blood transfusion. So, this is the last slide. This is just regarding some interesting feature that we saw in a patient admitted with severe sepsis in the RC. You need your comment on it as well. What do you guys think? We have Rulu. Rulu. Yes. Because the patient has infection, so we expect here some inclusions in the red blood cells. And you have a left shift. We want to know what are these inclusions. I wish I can more magnify that. Not. Is it parasitic? It's only the that appear in the in the red. I haven't seen any inclusions in the red blood cell. Yes. Malaria is the second one, but this does not seem to be a malaria. Sorry. The mic. So, what are these? I'm trying to magnify it more, but it becomes blur. Tropo. Tropo. Spherocytes are not like this. What are these then? Are the Pappenheimer bodies? You got it. Some another one. But they are so small to bring to focus. Like this is the maximum clearance I can get with this camera. Is it like a bacteria? Um, or like, but bacteria does not come in the red cell. Not in the red cell. Yeah. Inclusions in red cells. Microorganism inclusions are only, I think, two which I remember is one is malaria and second one is Babesia. I think there is no inclusions in the red cell from sepsis, other stuff like that. Let me find. Yeah, it is clear now. Dots. Lot of dots. So, if you Google Pappenheimer bodies, they are just like that. This is my first time I'm seeing Pappenheimer bodies so close in a real patient because we asked from microbiology and they said this is not any organism. Don't. Because the patient has sepsis, we may thought this. They said Babesia does not go into the. So, up till now, we say that this is Pappenheimer bodies. If the something changes in the future, then I will let you know. But because of sepsis, we get high ferritin, especially in a patient which goes towards HUS and then they get Pappenheimer bodies. In these are a bit clear. They are in the form of dot shapes. This is the maximum clearance I can get. Upon. What's the morphological feature between them and, um, and how, um, and how Jolly bodies? How about Jolly bodies? As far as I, I remember, I think it's in H. Jolly bodies will be like one single, like, um, spot and big one. And Pappenheimer bodies like is three multiple small dots. Okay. Let me show you our Jolly bodies. But these are Pappenheimer bodies. Do not forget it. It will appear sometime in the exam. And then the last thing I would show you is the power body. And then I will go to the dinosaur. And then you should enjoy. See, make it 50. So, let's find our Jolly bodies and make it 100. So, this blood film is from a patient who is hyposplenic because he had a road traffic accident and his spleen was removed. And you can see this is how Jolly bodies. This is very round in shape and near the. This thing is different from the one that we saw in the previous blood. There may be more. Let's find out. This one. This is a round dot near the blood cell. Why, uh, why can't we say them as like H bodies? They are also single and attached near to the edge of the cell. See, can we see H bodies on the peripheral blood film? It needs a special stain. We need a specialist stain. Yeah. Prussian blue stain. And they are projection-like red cell membrane projections from the from the red cells. And if they are eaten by macrophages, they will appear as bite cells. For the H bodies, we need a stain. But these ones, you can see they are nice round, big dots. They are the Howell-Jolly bodies. Remnant of nuclear material. Dr. Can you go again for the Pappenheimer granules slide? This one. We will maximize this one. Yeah. So, these are multiple dots, multiple dots like structures. I think this is the the clearest one which now up to now I have seen. The first one I saw at the first look was include, include the halo. Uh, that for that reason I saw Babesia. But at my real life, I didn't see Babesia. I saw it in books. All I have seen one or two cases of Babesia. They make special structures in in the red cell, which we sometimes call as multiple cross. But they, these are not making multiple cross. And the serology for that patient is negative. And he has no travel to Malta ever. And my first impression was that maybe this is Babesia. But this is no, this is not. For the serology is negative. And the ferritin is very high in this patient. So, it is around 8,000 ferritin. So, we think that these are Pappenheimer bodies. All right. I think we should stop here. Much appreciated. Great session. Sorry. Thank you. Thank you. Okay. Welcome.