Hematologic Diseases - Science topic

Ian J Martins It is recommended to choose whether to fast or not according to the type of marker and the purpose of the test. For example, for markers that may be affected by insulin or blood sugar fluctuations, it may be more reliable to measure in a fasting state. For more stable protein markers, there may not be a strict fasting requirement. The fasting state may be helpful for certain specific biomarkers, but whether fasting is necessary should be based on the specific test requirements and marker characteristics.

Dear Morvarid,

There are a number of methods to extract RNA. If you are intending to use an RNA extraction kit, any reliable company offers high quality kits. However, more conventional methods also result in high quality RNA. Depending on your aim (whether you test blood cells in an experiment or not) RNA can be extracted from blood and from isolated PBMC. In order to have high quality RNA, you must have highly viable cell pellet. Either extract RNA right after spinning your cells, OR snap-freeze using liquid nitrogen and store in a reliable -80 freezer until RNA extraction.

One of the oldest locus specific databases for hemoglobin disorders is HbVar available at http://globin.bx.psu.edu/hbvar

You can also check for Hemoglobin variants in the Biorad Library

You can also check hemoglobin variants on Ithanet

There seems to be an inverse relationship between platelet count and Hb level as long as both the counts are within normal range . when there is low platelet count (1.5- 2.5 lakhs/mm3 ) there is higher haemoglobin level and when platelet count is high (>2.5 lakhs/mm3) haemoglobin level is comparatively reduced. Also, when there is low haemoglobin level, (below 11 mg/dL), there is higher platelet count and if haemoglobin level is high (ll-14g/dl),there is compartatively low platelet count.

Polycythemia vera is a type of blood cancer. It causes your bone marrow to make too many red blood cells. These excess cells thicken your blood, slowing its flow, which may cause serious problems, such as blood clots.

I think it is right an avenue of knowledge worth exploring.

Do you know the work by Prof. Gómez Moreno (Ángel Gómez Moreno (Universidad Complutense de Madrid), "Coronavirus, Population Genetics, and Humanities", Mirabilia, 30 (2020, 1): Special Issue: https://www.revistamirabilia.com/sites/default/files/pdfs/01._gomezmoreno.pdf ).

But, I think we need the contributions from a wide shared knowledge from lots of disciplines.

A world wide pandemic needs earn solutions from a world wide knowledge contributions.

Do you know, my colleagues, about any more works in this same or similar approach?

My so many thanks

Hi Dr.

May be

I do the same things, but using CBC tests performed by hematological analyzer. I study and create ML models for classifications blood diseases

10.1371/journal.pntd.0005679

10.1186/s12879-015-1248-6

10.1016/j.vaccine.2015.02.030

These are the DOI of three article concerning your question. All three are free PMC article so you can easily download them.

Dear Monika,

The exact diagnosis of your father is probably smoldering multiple myeloma (SMM), according to the information you gave about his medical data. SMM is defined as following criteria:

Serum monoclonal protein: IgG or IgA ≥3 g/dL, or

Bence Jones protein ≥500 mg/24 h  and/or

Clonal bone marrow plasma cells between 10% and 60% and

Absence of myeloma-defining events or amyloidosis.

The risk of progression to symptomatic multiple myeloma of SMM is about 10% annually.

Experts in hematology consider SMM as an excellent setting to test the efficacy of novel theurepatic drugs such as ixazomib, pomalidomide, elotuzumab, and daratumumab in myeloma treatment.

Despite standard care of SMM is close clinical observation until development of symptoms, International Myeloma Working Group recommends therapy for SMM cases at high risk (about 50% risk for progression to symptomatic multiple myeloma).

For more information please visit:

Dear Professor Kou Hayakawa

It is my honor that you are among my scientific networks members

Studies on the clinical use of CBC have increased in recent years. CBC in psychiatric respect, it is an easy and inexpensive method to utilize hematologic parameters in cases where we cannot get clear information from the patients. RDW is a parameter of complete blood count (CBC) and investigated recently in different situations. We have investigated in our different studies and demonstrated such issues as follow:

1. According to the comparison of CBC values, RDW_CV (%) was significantly higher (p = 0.026*) in the opioid use disorder (OUD) group (n=61) compared to the healthy control group (n=61).

2. We have found that RDW_CV (%) value was 12.09 ± 2.00 in violent suicide attempt group (VSA); 12.44 ± 1.50 in non-violent suicide attempt group (NVSA); 12.27 ± 1.99 (0.747) in healthy control group. Our study suggests that there is a relationship between hematological parameters and OUD, especially the immune cells. There was no change in parameters associated with RBCs except RDW_CV. This result, which is not significant, is similar to some statements in the literature, but incompatible with some. Rasheed and Iqtidar (1) investigated the hematologic parameters of 100 heroin dependents and suggested a statistically significant decrease in HGB, HTC, RBC count, and platelets count in heroin addicts as compared to control subjects. Verde Méndez (2) demonstrated that for both sexes, the levels of HTC and HGB were similar in the control groups and opiate addicts.

References:

1. Rasheed, A.; Iqtidar, A. Hematological Profile, Serum Electrolytes and Iron Level Investigations in Heroin Addicts. Acta. Pharmaceutica. Turcica. 1997, XXXIX(2), 59–63.

23. Verde Méndez, C. M.; Díaz-Flores, J. F.; Sañudo, R. I.; Rodríguez Rodríguez, E. M.; Díaz Romero, C. Haematologic Parameters in Opiate Addicts. Nutr. Hosp. 2003, 18(6), 358–365.

Group O is a universal donor ? No antigen

Scientists may have found a reliable way to use a bacterial enzyme to convert any type of blood into type O, which is compatible with nearly everyone.

At National Meeting & Exposition of the American Chemical Society, a team of researchers from the University of British Columbia described how they were able to use enzymes derived from bacteria in the human gut to remove markers called antigens from AB, A and B blood, effectively turning the blood into type O.

First part of Jason's answer is correct, but the offspring carrying both traits would not suffer from severe anaemia and would be perfectly fine! He would have 1 functional beta gene and 3 functional aplha genes a situation that is prefectly compensated.

Dear dr. Mostafa,

For diagnosis, a detailed history of the lesion and its systemic association is needed. The lesions could be a type of small vessel vasculitis, rash of hypercoagubility state, embolic rashes (given the history of AF) or circulatory insufficiency. These can be differentiated by taking biopsy. But it could be a dermatological dyspigmentation problem, so it is worth to take dermatological consultation as well.

Hi, Ondrej.

My apology for that I missed your point. How about to use any antibiotics in the culture of zebrafish embryos? Puromycin is one of them that has been used in protein synthesis for biochemical and cell biological purposes. There is no specific inhibitors that block only the hemoglobin synthesis as you know well. The developing zebrafish embryos have so fast cell cycles. Because this kind of treatments including other heavy metals or hypoxia or something else would cause delayed or impaired embryonic development, leading to defects or teratogenic effects in overall development or disorganized embryonic tissues where temporal developmental signals are so crucial. It is not a straight-forward way using a drug inhibitor, rather complicating interpretation from deformed fry.

Although puromycin is a small molecule, you probably have to remove the chorion. Need tests. Good luck.

Good news

Hope the patient will improve quickly

Thanks for all colleagues

Very difficult. How is HCV-RNA? 

HemaApp measures hemoglobin levels and screens for anemia non-invasively by illuminating the patient’s finger with a smartphone’s camera flash.

                                                                          OR

ToucHb is a completely non-invasive (no blood!), portable, instant and cost-effective (affordable!) hemoglobin screening device to diagnose and monitor anemia in rural areas in developing countries.

Dear David Rotter,

Thank you for your kind answer and for the very interesting paper. 

from a pratical point of vue, yes we've to actively look for  iron surcharge in HbSS people : many have aditional alpha talassemia deletions, causing microcytosis  - micro and anemia byitself may increase the iron absortion; even if they aren't transfusion dependent, they are transfusioned sometimes; at least in western countries diets trend to have high iron content; some still have poor muscle mass (and muscle can "harbour" a lot of iron); some of them will have heterozigoty for haemochromatosis; and the role of free iron from intravascular hemolysys as described

all that together make iron surcharge a serious issue, not so much for pediatrics, but for the adult group, which longevity is improving

According to the EPAR of Blincyto:

"Other effects [observed after each infusion] included transient increase in body temperature, CRP, liver enzymes, and bilirubin. This is consistent with the potential effects of cytokine released, notably IL-6".

Moreover, a treatment-emergent adverse events of "Blood bilirubin increased" was observed in 7.9% of patients (4.2% grade 3 or higher).

All these data were from adults, however the assessors concluded that "treatment with blinatumomab is also associated with transient elevations in liver enzymes. The majority of the events were observed within the first week of blinatumomab initiation and did not require interruption or discontinuation of blinatumomab (see SmPC sections 4.4 and 4.8). A review of 27 subjects who met the criteria of AST/ALT ≥ 3 x ULN and total blood bilirubin ≥ 2 x ULN revealed that the rapid onset of elevations in liver enzymes coincided with the onset of clinical signs and symptoms of CRS with or without infection and concomitant hepatotoxic medications (data not shown). This finding suggested that these plausible alternative aetiologies were also present. [...] Management of these events may require either temporary interruption or discontinuation of blinatumomab (see SmPC sections 4.2 and 4.4).

Hope this could be useful!

Odoardo

By using semiquantitative Syphilis RPR test from Biolife Italia - Mascia Brunelli the dilutions of positive sera are made using saline only (not human serum diluted in saline)

Dear colleague,

I personally have seen changes in bone marrow morphology in lymphoma patients prior to any chemo. Mostly, I saw changes in eritroblasts such as binuclear cell morphology, or mitotic figures. Sometimes I saw micromegakaryocytes or pseudo-Gaucher cells. This is rare events. The origin of this changes is unknown to me. My own speculations may be that malignant cells and their microenvironment may produce some cytokines, or substances that disturb regular hematopoiesis. Of course, this need to be evaluated through serious investigations. 

Dear Peter Kubisz, we do evaluate the patients for thrombophilia which also includes ruling out other causes of thromboses( factor 5 maiden, thrombomodulin gene mutation, Anticardiolipin ab, factor deficiencies etc)We do follow the protocol usually. 

However , in arterial thromboses ( after opening of the artery either surgically or thrombolysis) we use continuous infusion of heparin initially, followed by oral anticoagulants. If a patient does not respond to warfarin I shift to dabigatran / or other recent congeners. If I am not able to find the cause for arterial thromboses ,the patient has to be on life long anticoagulants and only on anti platelets for venous thromboses. However if there is recurrence of thromboses on anti platelets in the latter , we shift the pt to  oral anticoagulatants.

In our Hospital,  the first therapy, for ineligible tranplanted patient is MPT.,exept renal  insufficienty.  If  patient have the renal insuffitiety, the  base therapy is  VD.

Best wishes

Dear Peter, 

Perhaps these papers are of interest for you although all are not considered with hemophiliacs: 

bacterial glutaminases are depleting glutamine from the blood, leaving it unavailable for the tumor cells.  glutaminase inhibitors are blocking the cancer cells from utilizing the glutamine once it is inside the cells.

In the case of secondary polycythemia due to COPD or smoking, the increase in red blood cell production is supposed to counterbalance the decrease in SpO2, so that Oxygen Delivery(and thus, consumption) remains stable. In cases like these, when polycythemia constitutes a physiological response, I believe an example can be drawn from other physiological responses, such as sinus tachycardia, a condition that may alarm the patient, yet seldom does it have a serious impact or consequences itself. Therefore, although I think such cases merit consideration and follow-up, no additional burden on thrombotic risk is usually carried with them. Of course, every patient is unique and given a heavy-burden history of thrombotic risk, measures might be necessary.  Secondary polycythemia due to other causes(erratic EPO production, for example) is a different story. 

Mazin, I do fully agree with you concerning hydroxycarbamide action in SCD. However, every aspects of SCD pathophysiology are overlapping and intertwined. You are perfectly right to outline the role of stress reticulocytes and neutrophils in targeting vasoocclusion. But with no haemolysis and the resulting anaemia, no stress reticulocytes! Also, haemolysis releases free heme, a major component of inflammation and neutrophil activation.

No direct marker for vaso occlusive crises

You need only hematocrit centrifugees,htc scalas and capillary tubes. Take the capillary blood specimen and centrifuge it. Compare the scalacs. Generally hb=3*htc in humans. İf the fish species different you can detect hb level by ciyanomethemoglobin method with drabkin solutions.

Imatinib is soluable in water, ethanol and DMSO. Just prepare a stock and store @ -20°C. Create dilutions while storing @4°C.

In the haemophilia community, HCV was transmitted through clotting factor concentrates.

haemophilia patients who were treated with coagulation factor concentrates before the

mid-1980s, have been infected with HCV. In the majority of this has led to liver disease i.e. chronic hepatits C followed by cirrhosis and HCC.

Other reports indicate association of  malignant lymphoma and hepatitis in hemophilia patients  www.journalagent.com/tjh/pdfs/TJH_28_3_237_238.pdf

You really need to confirm JMML. If the patient is positive for bcr- abl then its not JMML and using Imatinib/ Dasatinib is justified. They don't have any role in JMML. Allo- SCT is the only curative option. We often use a combination of oral cytotoxic "metronomic" chemotherapy to cytoreduce the counts and keep splenomegaly in check as a bridge to transplant as arranging finances and support for SCT, along with a long waiting period is often an issue with our patients due to resource constraints. This approach doesn't compromise our transplant success when it does take place

Megackariocyte can be stained with anti actine ( Monocloanl anti actine from Amersham and also with anti glicoproteine IIb-IIIa ( anti factor VIII or anti von Willebard factor) that is a membarne glicoprotein from Dakopatts and using biotinilated secondary antobody

 

The homocysteine metabolism is complex and the causes for their plasmatic elevation not ever are known. If the hyperhomocysteinemia is due to dietary causes or a some deficits in concrete enzymes, is posible to have some benefits with vitamin therapy. However, there are some other mechanisms for hyperhomocysteinemia not responding to those supplements. By other hand, the innegable relation of some homocysteine elevations with atherosclerosis and their possible control, deserve more research.

Patient DNA should be tested for deletion/duplication by MLPA for example. Most importantly what is the status of her partner?

Iron deficiency interferes with hemoglobin synthesis that will cause microcytic and hypochromic corpuscles. While B12 or folate defeciency interfere with DNA synthesis that delays the maturation of the corpuscles (macrocytic).

Please report centrifuge speed/gravity in g instead of rpm, this makes it universal for all types of centrifuges and independently of the used rotor diameter

For dead cell exclusion I would suggest 5 min 200g when purification is more important than cell recovery (mosty ~50%).

There could be two mechanisms. One mechanism for the ischemic stroke and one mechanism for the hemorrhagic stroke. Uncontrolled diabetes or for that matter chronic diabetes can lead to atherosclerosis of blood vessels. This causes atherosclerotic plaque development. Dislodgement of the plaque or its fragments can lead to thrombotic or ischemic stroke. Increased thickening of the vessels causes hypertension and increased peripheral vascular resistance. The elasticity of the arteries especially that of cerebral vessels is lost. If vasodilators are given in such conditions the vessels dilate and as a consequence, there could be impaired cerebral perfusion leading to ischemic stroke.

Diabetes causes neovascularization and microvascular aneurysms. Ophthalmoscopic examination may show flame-shaped microhemorrhages, microvascular aneurysms and cotton wool spots etc. Similarly there could be microvascular aneurysms in the cerebral capillary microvasculature. These aneurysms are vulnerable to rupture and may lead to hemorrhagic stroke.

First, you cannot diagnose multiple myeloma through flow cytometry. Only you can decsribe the phenotype of plasma cells in MM. Many papers were published about this topic - mainly Salamanca, Spain authors - Bruno Paiva, Jesus San Miguel, and others. Principally, CD38 and CD138 have to be used as gating markers and than you need minimally CD19 and CD56 to define normal x abnormal phenotype of plasma cells. In confused cases, cykappa/lambda can be used to define clonality and other markers like CD27, CD81, CD20, CD117....to define aberant phenotype of PCs.