Hemolysis Puns

Hi. My friend's sister had surgery in the beginning of September. It was ovarian cyst laparoscopy. The surgery was successful. There were no complications.

Suddenly she started to feel weak 12.10.2021. Temperature was 37 °C. Later nausea, vomiting and bruises all over her body. She called an ambulance, but they said that she probably has a cold. They made an electrocardiogram, it was ok. They suggested drinking more warm water and left her. Later, neurological symptoms appeared, sometimes she felt a numbness of the limbs, but it went away within an hour. A few days later she called an ambulance again, but they did the same things as previous time and left her at home.

She was admitted to the hospital 21.10.2021. At this moment she could not even walk normally. There are some results of blood tests (only values that do not get in a reference range) that was made at the moment she got to the hospital.

*Please ask if you need units for analyses and other analysis results. It is just hard to translate everything. I think you noticed that English is not my native language.

At the hospital she had a CT scan of the brain. Doctors said that neurologically she is healthy. So 21.10.2021 she had double pathology: 1) Hemolysis, 2) Thrombocytopenia

Doctors thought that it was idiopathic(corrected, see UPD1) thrombocytopenic purpura. So, 13.10.2021 they started thrombocytopenia treatment. They prescribed plasmapheresis therapy and glucocorticoids. Unfortunately they did not get any positive results.

Also they checked thyroid, tumor markers, indicators for antiphospholipid syndrome, lupus -everything is ok. Autoimmune diseases were excluded as well. The ultrasound of the abdominal organs and brachiocephalic arteries did not help to find a problem.

25.10.2021 neurological symptoms disappeared. But 30-31.10.2021 she got liver failure.

Today we got results for a cuprum test, but it was ok. So Wilson's disease is also excluded. Tomorrow doctors are going to a consultation and decide what to do next. But it seems that they are out of ideas and we would lose this g

We have just made the switch from Roche Cobas 6000 to the 8000 lines, both with an ISE unit, 502, 702, and 801 unit. We are also now working up the serum indices which we didn't have previously. Does anyone have any thoughts or information on how they handle patients on cyanokit while running the indices? Today I quickly played around with it on a sample that was not visiably hemolyzed, icteric, or lipemic. H-4, I-0, L-1. Then added a bit of Cyanokit to mimic a patient receiving it and it threw the hemolysis index up to 204 and lipemic index up to 48. So I'm thinking these patients will still require a real human eye...what is your experience? Don't want the it calling a patient hemolyzed when it is not truly hemolyzed and just the cyanokit. TIA!

Hi guys Could someone Pls summarize the lab findings and distinguishing features BTW intravascular and extravascular hemolysis

Thank u in advance

In hemolytic disease of the newborn:

mother has antibodies against some surface antigen of the fetal RBC -> IgGs cross the placenta -> bind the RBCs in utero -> RBC hemolysis.

Theoretically, the baby doesn't have to be born for this to happen. Do we know then why the term "newborn" is in the name of the disease? Is it because we can first "see" the disease once the baby is born?

Hi,

I got diagnosed with beta Thal Minor recently.

My blood test showed signs of pathological Hemolysis:

• High Bilirubine levels (>79µmol/L on multiple dates, fasted and not)
• Low Haptoglobine (<0.08g/L)
• High reticulocytes (95Giga/l 1.45%)

Currently waiting for G6PD, Pyruvate Kinase and Coombs test.

We also found slight Splenomegaly, and my doctor said he doubts its beta thal related.

What do you think guys, are these results beta Thal Minor related or not?

Since the nature of Distilled Water is hypotonic and lacking minerals, does it still provide hydration and nutritional value to the body? And does its hypotonic nature bring harm to the body by causing hemolysis in red blood cells?

Two water‐soluble large‐sized quaterphen[n]arenes (WQPns, n=3, 4) were designed and synthesized. Macrocycles WQP3 and WQP4 could strongly complex with an antimicrobial peptide, pexiganan (PXG). Host–guest complexation served to not only efficiently decrease the PXG's hemolysis in rabbit red blood cells, but also substantially enhance its metabolic stability in presence of proteinase K, rat plasma and liver or kidney homogenates.

Abstract

Traditional macrocyclic hosts have finite cavity sizes, generally 5–10 Å, which are commonly adaptive to recognize small guests rather than biological macromolecules. Here two water‐soluble large‐sized quaterphen[n]arenes (WQPns, n=3, 4) were designed and synthesized. These two hosts present significantly distinct recognition abilities. Specifically, they could strongly complex an antimicrobial peptide, pexiganan (PXG) with the association constants (Ka) of (4.20±0.23)×104 M−1 for PXG/WQP3 and (2.46±0.44)×105 M−1 for PXG/WQP4. Complexation of PXG by WQP3 and WQP4 served to decrease the hemolysis of PXG in rabbit red blood cells in a statistically significant way. Furthermore, host–guest complexation was shown to substantially enhance metabolic stability of PXG in presence of proteinase K, rat plasma and liver or kidney homogenates.

https://ift.tt/38Btq1I

came a cross few cards in Anking About what type of hemolysis can be found in AIHA? Some of the cards say the cold AIHA is Intravascular and Warm AIHA is Extravascular, other cards say the opposite, soo which one is it?

checked FA doesnt say any, I always assumed both can cause Intravascular hemolysis, as both Ig G and Ig M are complement activatiors, I assume extravascular can be due to oppsonization by C3b, but is really more dominant than MAC

Any ideas !?

Hi all,

Thanks for reading this. Apparently, between hereditary spherocytosis, hereditary elliptocytosis, and pyruvate kinase deficiency, only pyruvate kinase deficiency may classically present with neonatal hemolytic anemia. In my mind, this implies any/or of the following (reasonably, didn't want to go crazy with the assumptions):

• The RBC morphological deviation in PKD is so severe that it's particularly targeted by the spleen.
• The RBC morphological deviation by some unrelated mechanism causes increased filtration and destruction by the spleen.

I can't find anything in the literature specifically not this question. Would appreciate any input.

I know it's true that urobilinogen is increased in hemolysis, because of increased conversion of CBR to urobilinogen. I also know that there's no increase in urine conjugated bilirubin because there's no obstruction that makes CBR leak into blood stream. I just couldn't understand why increased urobilinogen would make the urine dark although it's a colorless chemical?

https://preview.redd.it/aqu8qt6utr661.png?width=1366&format=png&auto=webp&s=7d6f53bbc978eceeb3d2e0c32715f9cb2acb8210

https://preview.redd.it/g8bzg9tstr661.png?width=1366&format=png&auto=webp&s=d90efa743b86af3746a5707508965add29d2e67b

I had my Benlysta yesterday. I was due for labs. I got the results and several of my tests were marked with a caution about hemolysis. I've never seen this on my labs that I recall. I've done some looking into it. I'm curious about any of your experiences if you'd be willing to share.

PMID: 5104458. Cannot find DOI.

Link: https://pediatrics.aappublications.org/content/47/4/723

Edit: Found, only tried the pubmed link in my searches before, thanks.

Hey everyone!

I was wondering what is your place of Employment’s policy when it comes to hemolysis and potassium. Do y’all recollect or do y’all report everything but the potassium?

It’s always a sticky situation with the potassium!

Traditional macrocyclic hosts have finite cavity sizes, generally 5‐10 Å, which are commonly adaptive to recognize small guests rather than biological macromolecules. Here two water‐soluble large‐sized quaterphen[n]arenes (WQPns, n = 3, 4) were designed and synthesized. These two hosts present significantly distinct recognition abilities. Specifically, they could strongly complex an antimicrobial peptide, pexiganan (PXG) with the association constants (K a ) of (4.20 ± 0.23) × 10 4 M ‐1 for PXG/WQP3 and (2.46 ± 0.44) × 10 5 M ‐1 for PXG/WQP4. Complexation of PXG by WQP3 and WQP4 served to decrease the hemolysis of PXG in rabbit red blood cells in a statistically significant way. Furthermore, host‐guest complexation was shown to substantially enhance metabolic stability of PXG in presence of proteinase K, rat plasma and liver or kidney homogenates.

https://ift.tt/38Btq1I