Since M1 I've never really understood what LDH supposed to be used for. It shows up all the time in questions about all kinds of body systems which are not related to each other. Most of the time it doesn't really seem to be that relevant for getting the right answer anyway, since other given lab values usually guide you in the right direction. So, what the hell exactly is an elevated LDH supposed to mean?

https://www.nature.com/articles/s41467-018-07857-9

ABSTRACT

Although numerous therapeutic strategies have attempted to target aerobic glycolysis to inhibit tumor progression, these approaches have not resulted in effective clinical outcomes. Murine squamous cell carcinoma (SCC) can be initiated by hair follicle stem cells (HFSCs). HFSCs utilize aerobic glycolysis, and the activity of lactate dehydrogenase (Ldh) is essential for HFSC activation. We sought to determine whether Ldh activity in SCC is critical for tumorigenesis or simply a marker of the cell type of origin. Genetic abrogation or induction of Ldh activity in HFSC-mediated tumorigenesis shows no effect on tumorigenesis as measured by number, time to formation, proliferation, volume, epithelial to mesenchymal transition, gene expression, or immune response. Ldha-null tumors show dramatically reduced levels of glycolytic metabolites by metabolomics, and significantly reduced glucose uptake by FDG-PET live animal imaging. These results suggest that squamous cancer cells of origin do not require increased glycolytic activity to generate cancers.

INTRODUCTION

Most tumors are characterized by increased glucose uptake and lactate production, a phenomenon known as the Warburg effect or aerobic glycolysis. Elevated glucose uptake and glycolysis can power the production of essential metabolites and cell products required for proliferation1,2,3. Aerobic glycolysis culminates in the NADH-dependent reduction of pyruvate to lactate by lactate dehydrogenase (Ldh)3,4,5,6. Although lactate was once considered a waste product of glycolysis, it has been argued that lactate production may be a primary purpose of the Warburg effect, as lactate impacts angiogenesis, immune response, acidification of the microenvironment, motility of cancer cells, and the regeneration of NAD+5,7,[8]

Hi guys,

I´m reading a paper right now in which the authors performed an LDH assay. Now, as far as I know, and as far as they indicated in their methods section, LDH assays are used to assess cell death (since LDH is released in the supernatant from ruptured cells). However, in the paper, they state that high LDH release corresponds to high metabolic activity and indicates promotion of (tumor) cell metabolism in the respective condition. I´m really confused by this since I don´t see how cell death necessarily relates to metabolic activity, unless this is typical for tumor cells? If anyone can explain this, I would be super thankful!

I'm in my college's biochem course right now; just covered glycolysis and during part of a lecture, my professor was talking about lactate fermentation and the energy problem it brings up. There's balance between all the atoms coming in and out (C6 H12 O6 and all NAD/NADH), so apparently the reaction shouldn't happen without an external energy source.

I just have no idea what the source of that is.

Edit: should mention my professor was talking about redox potentials between the oxidation of the aldehyde to carboxylic acid and the reduction of pyruvate to lactate, how the energies don't match up well between those reactions

High serum LDH levels confer poor prognosis of melanoma and normally means that liver metastases are present, there is plenty of literature on pubmed/google scholar etc. that confirms that it is a good prognostic biomarker; however I want to know whether the levels drop after effective treatment (e.g. with vemurafenib/dabrafenib, ipilimumab, chemo etc.), or do they stay the same, or has this not been tested yet?

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

https://doi.org/10.1016/j.jnutbio.2022.108941

https://pubmed.ncbi.nlm.nih.gov/35017000

Abstract

OBJECTIVE

the present study examined the effect of the isocaloric low-carbohydrate ketogenic diet (LCKD) with or without exercise training for 6 weeks on postpartum weight retention (PPWR), body composition, metabolic profile and physical activity performance in postpartum mice.

METHODS

postpartum mice were assigned to 4 groups (n=8/group) as follows: (1) those on a control diet without aerobic exercise (CN), (2) those on a control diet with aerobic exercise (CN EX), (3), those on a LCKD without aerobic exercise (LCKD), (4) those on a LCKD with aerobic exercise (LCKD EX). CN EX and LCKD EX mice performed 6 weeks of exercise training on a treadmill. After the 6-week intervention, physical activity performance was determined.

RESULTS

postpartum mice in all groups experienced progressive reductions in body weight over the study period. The LCKD group had the smallest reduction in PPWR (p<0.05). The LCKD group had significantly higher total cholesterol, low-density lipoprotein cholesterol and lactate dehydrogenase levels, and liver lipid concentrations with a worsened glucose tolerance, compared to the CN group (p<0.05). The LCKD group showed significant reductions in physical activity performance, whilst the LCKD EX group showed significantly improvement in endurance performance, and paralleled the concomitant elevation in blood ketone levels.

CONCLUSIONS

6-week LCKD feeding on its own was less effective for reducing PPWR, and more detrimental to postpartum metabolic outcomes and physical activity performance of the postpartum mice. The feasibility of a LCKD with or without exercise during the postpartum period as a strategy for managing PPWR and improving postpartum metabolic profiles should be carefully considered.

------------------------------------------ Info ------------------------------------------

Open Access: False

Authors: Yi-Ju Hsu - Chi-Chang Huang - Ching-I Lin -

Additional links: None found

https://www.mdpi.com/1420-3049/26/19/5914/htm

Some highlights in no particular order:

> "Among the substances investigated, the essential oils of Myristica fragrans (nutmeg), Heracleum transcaucasicum, Heracleum anisactis, Anethum graveolens (dill), Apium nodiflorum, Petroselinum crispum (parsley), Pycnocycla bashagardiana and Piper sarmentosum, all containing high concentrations of myristicin, ranging between 12% and 96% of the composition, are noteworthy. "
>
>" An interesting publication discusses the anticonvulsant and inhibitory effects on glial activation of Myristica fragrans (nutmeg) extract. This material, containing about 11% myristicin, was tested in male NMRI rats that were induced to have seizures. Behavioral studies have shown that pretreatment with nutmeg extract effectively reduced seizure behavior, decreased cell death in the hypothalamus and improved glial activation [71]. "
>
>" A publication on the aqueous extract of the aerial part of parsley (Petroselinum crispum) sought to investigate the antihypertensive activity of the plant. In vivo studies were performed with male albino rats, and an in vitro study used isolated thoracic aorta rings. The results show a potent vasorelaxant activity in aortic vascular rings, while in animals the extract induced a decrease in blood pressure parameters. More detailed studies showed that there was a blockage of calcium channels present in the vascular wall, but also suggest that other pathways may be involved in the antihypertensive effect such as, for example, increased nitric oxide synthesis [67].
>
>The ability of myristicin to protect neurons from hypoxia-induced injuries was investigated. To conduct these assays, rat dorsal root ganglion (DRG) neurons were used. The results showed that myristicin reduced the viability of neurons when exposed to concentrations greater than 50 mM. However, at lower concentrations, it significantly increased cell viability in neurons when exposed to hypoxia, as it protected against hypoxic injury, not causing apoptosis. Complementary trials showed that myristicin decreased cleaved caspase-3 and bcl-2 levels in these hypoxia-induced neurons. Therefore, it was observed that it can reverse hypoxia-induced apopto

https://doi.org/10.1021/acs.analchem.1c03884

https://pubmed.ncbi.nlm.nih.gov/34958203

Abstract

Flexible and wearable sensors have attracted much attention for their applications in health monitoring and the human-machine interaction. The most studied wearable sensors have been demonstrated for sensing a limited range of metabolites such as ions, glucose, uric acid, lactate, etc. Both sweat and urine contain numerous other physiologically relevant metabolites indicative of health and wellness. This work demonstrates the use of the wearable sensor for the detection of β-hydroxybutyrate (HB) in sweat. HB is an important biomarker for diabetic ketoacidosis, a condition caused by the accumulation of ketone bodies in hyperglycemia or metabolic acidosis patients. Herein, we fabricated an integrated sensing system coupling an HB detection chamber with a serpentine electrode for sensing physiological signals such as pulse beat, vocal cord vibration, etc. The real-time HB detection was based on a β-hydroxybutyrate dehydrogenase enzymatic reaction. The stability of the enzyme and the cofactor couple was achieved by cross-linking networks and a redox mediator, thereby achieving high selectivity and low detection limits to HB in urine and sweat. The dual-functional sensor was integrated with a signal processing circuitry for signal transduction, conditioning, processing, wireless transmission, and real-time convenient health monitoring display to a smartphone via home-developed software.

------------------------------------------ Info ------------------------------------------

Open Access: False

Authors: Xieli Zhang - Yong Xia - Yang Liu - Samuel M. Mugo - Qiang Zhang -

Additional links: None found

Hello,

My primary care doctor has officially given up on trying to diagnose me. He thinks it's a good idea for me to seek care out of state but he's never had anyone in my circumstance and doesn't know the specifics of where exactly to send me. I spoke with my neurologist who I see for epilepsy, his input was that he sends people to UCSF but he doesn't think that applies to my situation since he doesn't believe my condition is neurological. I've had a painful undiagnosed illness for the last 11 months and it's RAPIDLY (on a day-by-day basis) getting worse. I don't really expect a diagnosis online, I'm really just looking for advice on how to get going out of state.

Things I've tried so far: calling Johns Hopkins, Mayo, and Cleveland Clinic. I've done this because I know these places by reputation, I really have no idea if they're where I should be going. I do not know what I'm doing. These places told me they want money up front (I don't have enough for what they're asking) and that the wait times are generally 6 months, I feel pretty strongly I'll be dead by then.

About me:

Age: 33, Sex: Male, Height: 5'10", Weight: 135lbs, Smoke/Drugs/Drink: Never

Medications: Topamax, 125mg

Existing Conditions: Epilepsy

intrauterine growth retardation, mother induced birth early

Symptoms:

How it started:

11 months ago in December of 2020 I woke up feeling like I had a weight slammed into the center my chest, my limbs were swollen, discolored, veins bulging, aching, in pain. A few days after that the chest pain subsided and the symptoms below have persisted.

Pain:

When sitting feeling of pressure building in thighs

When standing feeling of pressure building in calves

When sitting I feel like there's a tube deep in the back of my right leg that's being squeezed like a hose with a kink in it

Immense unbearable penile pain

Intermittent pain in the pubic area

Intermittent pain in the hands and feet

Specific veins hurt intermittently

Dorsal vein in the penis most frequently hurts, sometimes a specific vein in the hand or foot will bulge and be painful

Numbness:

Intermittent numbness in calves, arms, feet, and nose

Numbness in calves/feet after sitting for 10 minutes

Numbness in feet after exercise

Discoloration:

Knees and feet turn bright red intermittently

Calves and thighs turn blotchy with dark purple net-like patterns of veins while standing

Fingernails intermittently turn dark purple

Every week or so I urinate out some pain

CBC & Differential

Test Name

Leukocytes

Result

12.6 x10e9/L

Above High Normal

Reference Range

4.0-11.0

Test Name

Erythrocytes

Result

5.57 x10e12/L

Reference Range

4.60-6.20

Test Name

Hemoglobin

Result

169.0 g/L

Reference Range

135-180

Test Name

Hematocrit

Result

0.491 L/L

Reference Range

0.370-0.500

Test Name

MCV

Result

88.3 fL

Reference Range

79.0-97.0

Test Name

MCH

Result

30.4 pg

Reference Range

27.0-32.0

Test Name

MCHC

Result

344.0 g/L

Reference Range

310-360

Test Name

Erythrocyte Distribution Width (RDW)

Result

13.4 %

Reference Range

11.5-14.5

Test Name

Platelets

Result

262.0 x10e9/L

Reference Range

150-400

Test Name

MPV

Result

9.4 fL

Reference Range

7.4-10.4

Test Name

Neutrophils

Result

8.0 x10e9/L

Above High Normal

Reference Range

1.5-7.5

Note

Note: Change effective October 19, 2021 Relative(%) Differential values no longer reported

Test Name

Lymphocytes

Result

3.6 x10e9/L

Reference Range

1.1-4.4

Test Name

Monocytes

Result

0.7 x10e9/L

Reference Range

0.2-0.8

Test Name

Eosinophils

Result

0.3 x10e9/L

Reference Range

0.0-0.6

Test Name

Basophils

Result

0.1 x10e9/L

Reference Range

0.0-0.2

Renal Function Panel Test Name Sodium Result 139.0 mmol/L Reference Range 135-145 Test Name Potassium Result 4.2 mmol/L Reference Range 3.5-5.0 Test Name Chloride Result 108.0 mmol/L Reference Range 98-110 Test Name Carbon Dioxide Result 20.0 mmol/L Below Low Normal Reference Range 21-30 Test Name Anion Gap (Na, K, Cl, CO2) Result 15.2 mmol/L Reference Range 9.0-18.0 Test Name Creatinine Result 77.0 umol/L Reference Range 60-130 Test Name Urea Result 4.2 mmol/L Reference Range 3.0-7.1 Test Name Phosphate Result 1.18 mmol/L Reference Range 0.75-1.55 Test Name Urate Result 408.0 umol/L Reference Range 200-500

Glomerular Filtration Rate/1.73 Sq M Predicted (MDRD)

Test Name

Glomerular Filtration Rate/1.73 Sq M Predicted (MDRD)

Result

>=60

Reference Range

See below

Note

Interpretation: Units: mL/min/1.73 sq. metre >=60 : no demonstrable renal damage 30 - 59 : moderate renal damage 15 - 29 : severe renal damage <15 : renal failure If individual is African descent multiply result by

Glucose Test Name Glucose Result 6.2 mmol/L Reference Range 3.6-11.0 Note Fasting: 3.6 - 6.1 Random: 3.6 - 11.0

Lipid Profile

Test Name

Triglyceride

Result

3.38 mmol/L

Above High Normal

Reference Range

0.35-1.70

Test Name

Cholesterol

Result

5.59 mmol/L

Above High N

Hey all. I'm having a weird night.

My person tonight:

A&O x 4 spheres

HR 65

BP 135/70

RR 2-6, gasping (not agonal)

Sats 80-94% R/A consistent with resp pattern, 94-96% on 1L O2

Afeb.

Hx chronic liver injury

Elevated bicarb, LFTS, lactate dehydrogenase

pH 7.34

Patient is mildly obtunded, but can talk, walk, perform basic ADLs, carry a basic conversation, and do simple mathematics (addition, subtraction) when asked.

Doc ordered VBG and chest imaging, and has decided not to worry about it.

This is obvs chronic, because pt is stable and not crashing, and has been doing this for 2 days.

Any ideas?