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Hematopoiesis Case Studies

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Case studies are board-style questions with explanations and links to related articles featured in  Hematopoiesis , an e-newsletter that is sent to hematology trainees on a quarterly basis.

• A 73-Year-Old Man With Extensive Bruising
• A 2.5-Year-Old Girl With Fever and Pancytopenia
• 21-Year-Old With Duodenal Adenocarcinoma and a History of T- cell Lymphoma
• 78-Year-Old Woman with Thrombocytopenia and Splenomegaly
• 48-Year-Old Woman With Weight Loss, Hepatomegaly, and Splenomegaly
• Diagnosis of a 64-Year-Old Man With Anemia and Thrombocytopenia
• Prenatal Management of 21-Year-Old Woman to Reduce Risk of Severe Thrombocytopenia and Intracranial Hemorrhage
• Three-year-old Boy With Pancytopenia
• COVID-19 Management in Patients With Hematologic Malignancies
• 25-Year-Old Woman Referred to Clinic for Erythrocytosis
• 60-Year-Old Woman With Headache and Blurred Vision
• Chronic Immune Thrombocytopenia Purpura
• New Therapies for Acute Myeloid Leukemia
• Sickle Cell Disease – A 25-Year-Old in Transition
• Supportive Care in Multiple Myeloma
• Managing Toxicities in CAR T Cell Therapy
• Bicytopenia and Syndromic Features in a Four-Year-Old Child
• Emerging Therapies in Hemophilia
• 47-Year-Old Woman With New-Onset AML and Leukostasis
• The Smart Choice for Prevention of Recurrent Venous Thromboembolism
• 36-Year-Old Man with Severe Low Back Pain and BCP-ALL
• 52 Year-Old Woman with Fatigue and Neuropathy
• 29-Year-Old Woman with Postpartum Hemorrhage
• 30 Year-Old Female with Pancytopenia and Fatigue
• Progressive Fatigue and Cytopenias in a 70-Year-Old Man
• 32-year old man with neurologic changes and cytopenias
• 44-Year-Old Man with Fever, Abdominal Pain, and Pancytopenia
• Unexplained Thrombocytopenia in a Child
• Neutropenia in a Patient with Rheumatoid Arthritis
• 50-Year-Old Woman with Fibrous Capsule after Breast Augmentation
• 32-Year-Old Female with Multiple Ecchymoses
• 32-Year-Old Female with Anemia and Confusion
• GI Bleed in a Patient with Amyloidosis
• 32-Year-Old Man Admitted to Hospital With Diffuse Lymphadenopathy
• Image Challenge: 54-Year-Old Man With Abnormal Circulating Lymphocytes
• Image Challenge: Hematology Consult - Middle-Age Woman With Neutropenia and Splenomegaly
• Image Challenge: Hematology Consult - Middle-Age Man With Neuropathy and Splenomegaly
• Image Challenge: Bone Marrow Aspirate (August 2012)
• 65-Year-Old with History of Waldenström Macroglobulinemia (May 2012)
• Cervical Adenopathy, Weight Loss, and Night Sweats (February 2012)
• 12-Year-Old Boy With Normocytic Anemia and Bone Pain (August 2011)
• Putting Two and Two Together (May 2011)
• Four-Year-Old Male with Red Urine and Fever (February 2011)
• Intermittent Epistaxis in a Young Boy
• Prognostic Factors in Acute Lymphocytic Leukemia
• 55-Year-Old Male With Multiple Myeloma and Prognosis of Undetermined Significance
• 24-Year-Old Woman With Dark-Colored Urine
• Personalizing Anticoagulation: Determination of Warfarin Dosing
• Microcytic Anemia Refractory to Oral Iron Supplementation
• ITP is Also a Platelet Production Problem
• A 26-Year-Old Man With History of Fatigue, Fevers, and Gingival Bleeding
• Finding the Best Prognostic Outcome in a Patient With AML
• Bcl-6 and Its Relationship to Diffuse Large B-Cell Lymphoma
• A 78-Year-Old Man With Elevated Leukocytes and Anemia
• Flow Cytometry Pattern in APL
• Identifying One of the 5q- Syndrome Genes
• Do You Know JAK?

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Explore the latest case studies  and articles  from  Hematopoiesis .

• Announcing Hematopoiesis, Our New ASH Trainee Council Newsletter by Trainees and for Trainees
• A Primer on Advocacy for the Hematology Trainee
• Blood Smear: The Fifth Vital Sign in Hematology
• Chimeric Antigen Receptor T-cell Therapy: What Fellows Need to Know
• The Blood Sisters Project
• Case Study: A 73-Year-Old Man With Extensive Bruising
• Case Study: A 2.5-Year-Old Girl With Fever and Pancytopenia

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Case Studies in Hematology and Coagulation

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This compendium of 200 case studies is the result of a unique collaboration of leading hematologists, hematopathologists, and oncologists. It serves as both a case-based guide to the diagnosis and management of patients suffering from hematologic conditions and a valuable teaching tool.

The editors have compiled an invaluable collection of cases covering common and rare entities—from anemias and acute leukemias to plasma cell, platelet and coagulation disorders. Cases are presented in an easy-to-follow format, grouped by related conditions. The final two sections present 27 self-study challenge cases that include answers (with images) provided by the authors of each case.

A broad range of topics in hematology and coagulation are covered in this CaseSet, including:

• Myeloproliferative Disorders
• Myelodysplastic Syndromes
• Lymphoproliferative Disorders
• Lymphomas and Their Mimicks
• Plasma Cell Disorders
• Platelet Disorders
• Hematologic Infectious Diseases
• Other Hematologic Disorders
• Bleeding Disorders
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• v.14(4); 2022 Apr

The Case Report of a 97-Year-Old Patient With Chronic Anemia and Hemoglobin Value of 1.7 g/dl and Review of the Literature

Andreas kyvetos.

1 2nd Department of Internal Medicine, General and Oncology Hospital of Kifissia “Agioi Anargyroi”, Athens, GRC

Stefani Panayiotou

Panagiota voukelatou, ioannis vrettos, georgios boulmetis.

Although hemoglobin levels beneath 6.5 g/dl are considered to be life-threatening and the patients theoretically suffer from a cluster of symptoms, few cases of patients who seek medical assistance when their hemoglobin levels had fallen beneath 3 g/dl have been reported in the literature. Here, we describe the case of a 97-year-old patient who was transferred to the emergency department with dyspnea and the initial screening tests showed a hemoglobin level of 1.7 g/dl, due to iron deficiency. The patient was hemodynamically stable, and no ischemic lesions were seen on the electrocardiogram. His dyspnea was due to a lower respiratory tract infection and bilateral pleural effusion. He was bedridden for two years. His absence of physical activity in combination with the slow onset of anemia and the absence of severe underlying pulmonary and cardiovascular diseases could hide the symptoms until additional stressful events, such as the respiratory tract infection and the deterioration of heart function, occurred. So, we must keep in mind that in elderly patients with reduced physical activity and without severe pulmonary and cardiovascular comorbidities, the symptoms of severe anemia may go unnoticed until hemoglobin reaches life-threatening levels.

Introduction

The symptoms of anemia like dyspnea, tachypnea, palpitations, cold skin, heart failure, cognitive dysfunction, etc. depend, inter alia, on the severity of anemia, the rapidity of its onset, the age, and the physiological status of the patient. Various adaptive mechanisms are mobilized by the human body in order to counterbalance the effects of anemia, although almost every organ system is finally affected [ 1 ]. The most significant adaptive responses involve the cardiovascular system. These adaptive responses include increased cardiac output and redistribution of blood flow toward the heart and central nervous system and away from the splanchnic vascular beds [ 2 ].

In cases of chronic anemia, it has been postulated that the hyperkinetic response in patients at rest, occurs only when hemoglobin level falls beneath 7 g/dl [ 3 ]. Moreover, in hemoglobin levels beneath 7.5 g/dl, 100 ml of arterial blood contains 10 ml of oxygen instead of 20 ml in healthy subjects [ 1 ]. Nevertheless, certain symptoms or complications experienced by a patient cannot be determined with the accuracy of hemoglobin levels alone [ 4 ]. Heart, lung, and cerebrovascular diseases, as well as age, may limit the adaptive responses to anemia [ 2 ]. On the other hand, in young and otherwise healthy persons, chronic anemia may remain unnoticed until hemoglobin level falls beneath a critical level or episodes of exertional stress occur [ 1 ].

According to several grading systems for anemia, hemoglobin levels beneath 6.5 g/dl are considered life-threatening [ 5 ], and the patient theoretically suffers from a cluster of symptoms. However, a few cases of patients have been reported in the literature [ 6 - 12 ] who seek medical assistance when their hemoglobin levels had fallen beneath 3 g/dl and therefore their hematocrit levels were beneath 10%.

In this report, we describe the case of a “too hard to die” 97-year-old patient who was transferred to the emergency department with dyspnea and the initial screening tests showed a hemoglobin level of 1.7 g/dl, and we review and discuss the reported cases of other “too hard to die” patients with hemoglobin concentrations beneath 3.0 g/dl due to chronic anemia. This paper is an extended version of a work presented at the 24ο Panhellenic Congress of Internal Medicine, Athens, Greece, on 3-6 November 2021.

Case presentation

A 97-year-old patient was admitted to the emergency department due to shortness of breath for one week, without other symptoms. According to his medical history, the patient suffered from anemia, treated with 247.25 mg ferrous sulfate, 5 mg folic acid daily, and hypothyroidism treated with levothyroxine sodium 75 mcg. His relatives were aware of his anemia but they preferred to treat it with per-os medication without investigating the cause of the anemia. They reported that the patient’s stools for several days were tarry but they believed it to be due to the iron he was receiving. Six months ago, he was diagnosed with pulmonary embolism which was effectively managed with apixaban 110 mg twice daily and two years ago he had an ischemic stroke that left him bedridden.

At the time of presentation, he appeared pale and lethargic (Glasgow Coma Scale 7/15) with tachypnea (30 breaths/min). Bilateral crepitations and rhonchi were present in lung auscultation. There was a systolic murmur throughout the precordium. A digital rectal examination was performed and it was negative for melena. His blood pressure was 120/60 mmHg with a regular pulse rate of 90 beats/min. Other findings from the physical examination were unremarkable. The laboratory test revealed hypochromic microcytic anemia, with hemoglobin value of 1.7 g/dl (normal range: 12-16 g/dl), hematocrit 6.9% (normal range: 37-48%), red blood cell count of 1.53 Μ/ml (normal range: 4.5-6.3 Μ/ml), mean corpuscular volume of 75 fl (normal range: 80-96 fl), and mean corpuscular hemoglobin of 23.8 pg (normal range: 27-34 pg). The complete blood count was examined twice in order to avoid a laboratory error in measurement. Other laboratory results showed: white blood cells 6.47 K/μl (normal range: 4.0-11.0 Κ/μl), platelets 121 Κ/μl (normal range: 150-400 Κ/μl), C-reactive protein 3.56 mg/dl (normal range: <0.5 mg/dl), creatinine 1.7 mg/dl (normal range: 0.6-1.4 mg/dl), urea 135 mg/dl (normal range: 10-50 mg/dl), total bilirubin 0.7 mg/dl (normal range: 0.2-1 mg/dl), ferritin 20 ng/ml (normal range: 11-204 ng/ml), folicid acid >40 ng/ml (normal range: 3.1-20 ng/ml), cobalamin 700 pg/ml (normal range: 187-883 pg/ml), erythrocyte sedimentation rate 10 mm/h (normal range: 2-20 mm/h), direct Coombs test negative, a normal urinalysis test, high sensitivity troponin I (HS-TnI) 34 pg/ml (normal range: <11.6 pg/ml), and brain natriuretic peptide (BNP) 804.30 pg/ml (normal range: <100 pg/ml). No ischemic lesions were seen on the electrocardiogram (Figure  1 ) and the second sample of HS-TnI was within the normal range. Hematological consultation was requested and the blood smear revealed normal platelets count of 199 Κ/μl and microcytic red blood cells with hypochromia. Erythropoietin levels and total iron-binding capacity were not performed due to the lack of these laboratory tests in our hospital.

Cardiac echocardiography was performed that showed signs of heart failure with preserved ejection fraction and grade I diastolic dysfunction. A chest CT scan revealed a lower respiratory tract infection and a bilateral pleural effusion (Figure  2 ) compatible with his heart failure. An abdominal CT scan was performed that did not reveal any pathology.

It revealed a lower respiratory tract infection (blue arrows) and bilateral pleural effusion (red arrows).

The patient was treated with furosemide, ceftriaxone 2 g once daily and clindamycin 600 mg three times daily. A total of 5 units of packed RBCs were transfused resulting in a hemoglobin value of 8.7 g/dl. The renal function at the admission was impaired but gradually it was improved and the discharge creatinine was 0.8 mg/dl. Gastroscopy and colonoscopy were scheduled but his relatives refused any further investigation to identify the cause of anemia. Although the investigation for the cause of anemia was inadequate, the history of tarry stools in a patient receiving anticoagulant, in combination with a ferritin value of 20 ng/ml made us assume that the main cause of his anemia was chronic bleeding from the gastrointestinal tract. So, he received 1 g of intravenous iron. The patient had a remarkable recovery to his preadmission state and he was discharged home 11 days after.

Our patient had one of the lowest hemoglobin levels that have ever been reported. To our knowledge, the lowest hemoglobin concentration that has ever been reported in a non-trauma patient is 1.2 g/dl (hematocrit of 3.0%) due to paroxysmal nocturnal hemoglobinuria. The 21-year-old male patient was presented with profound weakness and abdominal pain, although hemodynamically stable [ 6 ]. The second-lowest reported hemoglobin was 1.3 g/dl (hematocrit of 4.7%) and it was due to iron deficiency, because of chronic uterine bleeding [ 7 ]. The patient was a 44-year-old woman with weakness and dyspnea at rest. She had regular pulses, normal arterial pressure, and 25 breaths per minute. She had severe lactic acidosis and inverted T waves in leads III, aVF in her ECG.

Likewise, an extremely low hemoglobin level, in a patient with chronic anemia, has been reported by Jost et al. They presented a 29-year-old woman with celiac disease, bulimia nervosa, and iron-deficiency anemia. She had a hemoglobin level of 1.7 g/dl. She was malnourished and she reported exhaustion, fatigue, and abdominal pain but no critical symptoms [ 8 ]. On the other hand, a 76-year-old woman had critical symptoms with hemoglobin 2.4 g/dl due to gastric adenocarcinoma. She was hemodynamically unstable and reported increased fatigue, reduced activity, intermittent nausea or vomiting, and melena. Clarke and Weston-Smith reported a case of folate deficiency in a 50-year-old woman with hemoglobin of 2.6 g/dl. They reported that the patient was stable, alert, and keen to avoid admission. She had a soft ejection systolic murmur and her ECG was in normal sinus rhythm of 90 beats per minute with ST-segment depression in lateral leads [ 10 ].

Another case that was presented by Reibke et al. was a 32-year-old male with hemoglobin 2.9 g/dl due to B12 deficiency and minor beta-thalassemia [ 11 ]. Finally, extremely low hemoglobin levels have been reported by Bhatia et al., who performed coronary hemodynamic studies on 14 patients with chronic anemia. They reported three patients with hemoglobin levels ≤3.0 mg/dl; they had hemoglobin levels of 1.6 mg/dl, 2.4 mg/dl, and 3.0 mg/dl, and all of them were between 23 to 25 years old. Two of them had iron-deficiency anemia due to ankylostomiasis and the third had B12 deficiency [ 12 ].

All of these patients had no underlying pulmonary and cardiovascular diseases and they developed gradually severe anemia. This gradual onset allowed the compensatory mechanisms to take place and so, the patients arrived at the emergency departments with hemoglobin levels much lower than that considered to be life-threatening. The difference with our patients is that almost all, with one exception [ 9 ], were less than 50 years old and so, theoretically, they had satisfactory adaptive responses to anemia. The exception [ 9 ] was referred to as a 76-year-old woman with gastric adenocarcinoma that arrived at the emergency department with hypotension and tachycardia. This woman had symptoms compatible with anemia for several weeks.

In contrast, our patient was hemodynamically stable, and he had no profound symptoms until the time dyspnea was developed due to both the lower respiratory tract infection and also the deterioration of cardiac function which was triggered probably both by anemia and the respiratory tract infection. What hid the patient’s symptoms from his relatives, according to our opinion, was the non-existent, even the minimal, physical activity of this elderly. His absence of physical activity in combination with the slow onset of anemia and the absence of severe underlying pulmonary and cardiovascular diseases could hide the symptoms until the time of additional stressful events, such as the respiratory tract infection and the deterioration of heart function, occurred.

Conclusions

Symptomatic anemia is a common finding in elderly patients. Whereas, in elderly patients with reduced physical activity and without severe pulmonary and cardiovascular comorbidities, the symptoms of severe anemia may go unnoticed until hemoglobin reaches life-threatening levels. Careful surveillance of these patients is mandatory with regular clinical examination and laboratory blood tests, especially for those who are receiving anticoagulant therapy.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

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Consent was obtained or waived by all participants in this study

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Hematology Case Study: 75 Year Old Man with Leukopenia

A 75 year old male first presented earlier this year with abnormal CBC results. The patient has a history of Type 2 diabetes, high blood pressure and atrial fibrillation. He was diagnosed with non-small-cell lung cancer (NSCLC) 6 years ago. His stage II NSCLC was completely removed with surgery. Surgery was followed up with adjuvant cisplatin-based chemotherapy to reduce the chance that the cancer would return. In June, he was referred to the hematology oncology department following consecutive CBCs that revealed leukopenia and thrombocytopenia. The CBC results from these specimens are shown below in Table 1.

The peripheral blood sample from June was sent for flow cytometry. A leukemia/lymphoma phenotype was performed. Result comments noted proportionately decreased granulocytes with a left shift and 4% blasts. The blasts were CD34+, CD117+, HLA-DR+, CD13+ and CD33+ and were identified as myeloblasts. There were proportionately increased atypical monocytes with CD23 expression. Lymphocytes were also proportionately increased and included an increased population of CD57+, CD3+ T cells consistent with T-cell large granular (LGL) expansion. Immunophenotypic findings raised a concern for a myelodysplastic process. The hematologist discussed the findings with the patient and the patient was scheduled for a bone marrow biopsy. The procedure was performed 3 weeks later. CBC results on the day of the procedure are shown below in Table 2.

Bone marrow aspirate showed markedly increased myeloblasts (55%), consistent with acute myeloid leukemia (AML), nonacute promyelocytic leukemia (APL) type. The phenotype of the blasts was CD13+, CD33+, CD117+ and HLA-DR+. Blasts were negative for CD34. Several genomic variations were found in the specimen. These included variations in IDH2, SRSF2, STAG2 and ASXL1. Diagnosis: Increase in myeloblasts consistent with AML, nonAPL type.

In July, 20 days after the bone marrow procedure and AML diagnosis, the patient was scheduled to begin his first cycle of Azacitidine (Vidaza). Based on his critical hemoglobin, the patient received 1 unit of packed RBCs followed by his first Vidaza injections. This Cycle 1, Day 1 chemotherapy was well tolerated, and he returned home. The following day he returned for his second treatment. His CBC showed good response to the previous day’s transfusion and his Cycle 1, Day 2 Vidaza was administered without incident. However, that evening the patient presented to the ER with nausea, vomiting and nose bleeds. The patient was admitted to the hospital and received another RBC transfusion. For the next several days the patient continued to do poorly, requiring additional RBC transfusions, and the Vidaza treatments were deferred, then discontinued. The patient had several ER visits and hospital admissions with transfusions over the next 2 weeks. During this time, we saw his blast% on his differential peak at over 60%. The patient was transferred to the palliative care team with care and comfort measures. CBC results from Cycle 1, Day 1 and subsequent CBC results are shown below. Note the sharp increase in blasts over a 2-week period.

AML is the most common acute leukemia in adults. In AML with minimal differentiation, evidence of bone marrow failure is characterized by anemia, neutropenia, and thrombocytopenia. The median age for patients with AML in the US is 66-67, and those who are older than 55-65 at diagnosis often have challenges and lower odds for long term survival. These older patients tend to have poor tolerance to traditional aggressive chemotherapy because of other health issues. This patient was likely not a good candidate for strong chemotherapy because of his age and health history. In these more fragile patients, Vidaza may be used. Vidaza is a class of drug called a hypomethylating agent that works by switching off DNA methyltransferase. This switches on genes that stop the cancer cells growing and dividing. The goal is to reduce the number of abnormal blood cells and to control cell growth.

As you can see from the CBC results, the onset of this patient’s AML was very abrupt, and the disease progressed rapidly. He has several risk factors that made him more likely to be diagnosed with AML. Older age is a risk factor for AML, and AML is more common in males than females. He has a history of smoking which is a behavioral risk factor associated with AML. Additionally, patients with cancer who are treated with certain chemotherapy drugs are more likely to develop AML in the years following treatment. This patient was treated with cisplatin following lung cancer surgery. Cisplatin is an alkylating agent which has been linked to an increased risk of AML.

Also interesting is the note on the peripheral blood phenotype interpretation that a T-cell large granular lymphocyte (LGL) expansion was present. These are an increased population of CD57+, CD3+ T cells. LGL clones have been described in AML and a hallmark of this association is cytopenia, as is observed in this patient. The patient’s poor prognosis can partly be attributed to the p.Gly646TrfsTer12 alteration in the ASXL1 gene, identified in the bone marrow interpretation. This alteration is associated with decreased overall survival and poor prognosis which was observed in this patient.

I work in a hospital with a large hematology/oncology practice, and we see a lot of adult leukemia patients. Many of the patients we see regularly have Chronic Lymphocytic Leukemia (CLL). We feel like we get to know these patients, because even though we never see them, we see their CBCs every week, sometimes for many years. This was an interesting case because it reminded me of the sudden onset and rapid progression of AML. It was amazing to see the differentials change so dramatically in a matter of weeks. This patient is currently receiving care and comfort end of life measures.

Fattizzo, B, Bellani, V, et al. Large Granular Lymphocyte Expansion in Myeloid Diseases and Bone Marrow Failure Syndromes: Whoever Seeks Finds. Front. Oncol., Sec. Cancer Immunity and Immunotherapy. 01 October 2021.

Pratcorona M, Abbas S, Sanders MA, Koenders JE, et al.Acquired mutations in ASXL1 in acute myeloid leukemia: prevalence and prognostic value. Haematologica. 2012 Mar;97(3):388-92. doi: 10.3324/haematol.2011.051532. Epub 2011 Nov 4. PMID: 22058207; PMCID: PMC3291593.

https://www.cancer.net/cancer-types/lung-cancer-non-small-cell/types-treatment

Thomas XG, Dmoszynska A, Wierzbowska, et al. Results from a randomized phase III trial of decitabine versus supportive care or low-dose cytarabine for the treatment of older patients with newly diagnosed AML.  Journal of Clinical Oncology  29:2011

Turgeon, Mary Louis. Clinical Hematology Theory and Procedures, 6 th ed, Jones and Bartlett Learning, 2017.

-Becky Socha, MS, MLS(ASCP) CM BB CM  graduated from Merrimack College in N. Andover, Massachusetts with a BS in Medical Technology and completed her MS in Clinical Laboratory Sciences at the University of Massachusetts, Lowell. She has worked as a Medical Technologist for over 40 years and has taught as an adjunct faculty member at Merrimack College, UMass Lowell and Stevenson University for over 20 years.  She has worked in all areas of the clinical laboratory, but has a special interest in Hematology and Blood Banking. She currently works at Mercy Medical Center in Baltimore, Md. When she’s not busy being a mad scientist, she can be found outside riding her bicycle.

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clinical data of fever, recent illness, history of drug intake, differential leucocytic count and white blood cells morpholog is needed

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Case Report: A 19-Years Old Patient with Haemophilia a with High Response Inhibitor Screening and Quantitation and the Bethesda Method

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Marianela Trejos Herrera , Alicia Lopez Campos; Case Report: A 19-Years Old Patient with Haemophilia a with High Response Inhibitor Screening and Quantitation and the Bethesda Method. Blood 2016; 128 (22): 4956. doi: https://doi.org/10.1182/blood.V128.22.4956.4956

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A severe haemophiliac patient, high response inhibitors, 19 years, who was diagnosed at 8 months old and since then he begins to administer factor VIII concentrates. However, a year later after the start of treatment, they were detected inhibitors that behave as high response inhibitors from the start.

He discontinues treatment with Factor VIII concentrate and instead he begins to administer Factor IX concentrate and prothrombin complex as an alternative treatment.

Through his illness, the patient has made significant bleeding at the level of joint and other muscles such as the psoas. It is a bleeding patient at rest up for what is currently administered prophylactically Prothrombin Concentrate 3 times a week.

This case, the comment will be directed towards laboratory diagnosis and its evolution since he was diagnosed in 1994 to date.

From 2013, screening protocols and quantification of both factors and inhibitors were modified in the Specialized Hematology laboratory of Hospital México, due to problems in the sensitivity and specificity of the method and reagents we were using. The results from these patient specific inhibitors are described in the following paragraphs.

Observations

With the experience and current knowledge of the following it is concluded, according to a literature review that was performed (see Table 1):

1) This time period has persisted inhibitor high title, which is evidenced of the study of mixtures which do not clearly show a potentiation by incubating 2 hours at 37 ° C, since the values of the Control Mix and patient give very similar high values.

2) We were shown only on the date of 14.02.2013, there was a real interference Lupic Anticoagulant (LA), which is confirmed by the method of Russel viper venom.

3) The dates high titer inhibitors were reported against factor VIII (from 6 November 2013 to date), both screening and for the Bethesda, aPTT reagent was used with Kaolin activator which is low sensitivity to LA.

4) On November 20, 2015 there was an error in the interpretation and anti factor VIII inhibitors as negative were reported as potentiation at 37 ° C is not evidenced, but rather was interpreted as interference of an LA, which was communicated to the medical and preventive measures cited in paragraph corrections were made.

5) The last date that the sample was processed, on February 1, 2016, the inhibitor against factor VIII did not affect dilution of silica APTT, so the index ROSNER was not affected (<12) and it was not necessary to mount the LA test, according to the request in identifying protocols inhibitors.

6) Factor VIII deficient plasma is currently being used, which contains von Willebrand factor, as recommended by international guidelines quantization factors.

Conclusions

According to an experience as support center Reference Center in our country, we conclude and recommend the following:

1) Registration of haemophiliac patients with high antibody titer is essential as the description of the protocol to be followed in these patients.

2) The behavior of this inhibitor in the screening test of time and temperature dependence, it was decided to directly mount the Bethesda assay, following the recommendations of the literature on when the use of a reagent with low sensitivity to lupus inhibitor.

3) Within the protocol and as far as we can, we will process the purchase for quantification of factor VIII chromogenic by ELISA methodology, as a confirmatory method.

No relevant conflicts of interest to declare.

Author notes

Asterisk with author names denotes non-ASH members.

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Case report

Journal of Hematology & Oncology welcomes well-described reports of cases that include the following:

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Article within a journal

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Article within a journal (no page numbers)

Rohrmann S, Overvad K, Bueno-de-Mesquita HB, Jakobsen MU, Egeberg R, Tjønneland A, et al. Meat consumption and mortality - results from the European Prospective Investigation into Cancer and Nutrition. BMC Medicine. 2013;11:63.

Article within a journal by DOI

Slifka MK, Whitton JL. Clinical implications of dysregulated cytokine production. Dig J Mol Med. 2000; doi:10.1007/s801090000086.

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Book chapter, or an article within a book

Wyllie AH, Kerr JFR, Currie AR. Cell death: the significance of apoptosis. In: Bourne GH, Danielli JF, Jeon KW, editors. International review of cytology. London: Academic; 1980. p. 251-306.

OnlineFirst chapter in a series (without a volume designation but with a DOI)

Saito Y, Hyuga H. Rate equation approaches to amplification of enantiomeric excess and chiral symmetry breaking. Top Curr Chem. 2007. doi:10.1007/128_2006_108.

Complete book, authored

Blenkinsopp A, Paxton P. Symptoms in the pharmacy: a guide to the management of common illness. 3rd ed. Oxford: Blackwell Science; 1998.

Online document

Doe J. Title of subordinate document. In: The dictionary of substances and their effects. Royal Society of Chemistry. 1999. http://www.rsc.org/dose/title of subordinate document. Accessed 15 Jan 1999.

Online database

Healthwise Knowledgebase. US Pharmacopeia, Rockville. 1998. http://www.healthwise.org. Accessed 21 Sept 1998.

Supplementary material/private homepage

Doe J. Title of supplementary material. 2000. http://www.privatehomepage.com. Accessed 22 Feb 2000.

University site

Doe, J: Title of preprint. http://www.uni-heidelberg.de/mydata.html (1999). Accessed 25 Dec 1999.

Doe, J: Trivial HTTP, RFC2169. ftp://ftp.isi.edu/in-notes/rfc2169.txt (1999). Accessed 12 Nov 1999.

Organization site

ISSN International Centre: The ISSN register. http://www.issn.org (2006). Accessed 20 Feb 2007.

Dataset with persistent identifier

Zheng L-Y, Guo X-S, He B, Sun L-J, Peng Y, Dong S-S, et al. Genome data from sweet and grain sorghum (Sorghum bicolor). GigaScience Database. 2011. http://dx.doi.org/10.5524/100012 .

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