MUDr. Dana Maňasková


Vyhledávání na medicinman.cz
 

Medikace

Abirateron (acetát)


Amlodipin

  • Výrazný otok dolních končetin po amlodipinu byl odstraněn snížením dávky kalciového blokátoru a zvýšením dávky ACEI perindoprilu při zachování normotenze.
    • Došlo také k odstranění velkých výkyvů systolického TK (rozdíl až 100 mm Hg) ve dne, provázených tachykardií. [7]
  • V uvěřejněné studii zahrnující aktivní sledování se objevily otoky u 25 % pacientů užívajících amlodipin v dávce 10 mg denně [10]
  • Kombinace s léky inhibující renin-angiotenzinový systém (ACEI/CCB nebo ARB/CCB) snižuje podíl tohoto vedlejšího účinku [10]
    • Důvodem je postkapilární dilatace a normalizace hydrostatického tlaku [10]
  • Po snížení dávky CCB amlodipinu na polovinu (5 mg) a zvýšením dávky ACEI perindoprilu na dvojnásobek (10 mg) v průběhu 3 týdnů k výraznému ústupu otoků.
    • Výrazně se zvýšila kvalita života pacienta a jeho schopnost pohybu i sexuální aktivita [10]
  • Po dalším snížení dávky amlodipinu na 2,5 mg nebyly ani známky prosáknutí kolem kotníků [10]
    • Přitom kompenzace hypertenze byla velmi dobrá [10]

Anabolika


Arsenic trioxide

  • Treatment for recurrence of acute promyelocytic leukemia
  • Side effects about CLS were increased [17]

Arteriální dilatace

Přímá arteriální vazodialtancia

Bloktory kalciových kanálů

Alfa adrenergní antagonisté

Thiazolidiny


Betablokátory

  • Pokud zhorší prokrvení ledvin / srdeční selhání

Blokátory vápníkových kanálků



Calcium channel blocking drugs

  • May worsen swelling in the legs

Capecitabinum (Xeloda)


Dieuretika

  • Pokud způsobí hypkalemii
    • Současná hypomagnesemie v pozadí činí hypokalemii rezistentní k doplňování draslíku
  • Když dojde k depleci vitamínu B1 - thiaminu
  • Z nadměrného užívání diuretik


ELZONRIS

  • CD123-directed cytotoxin
  • Treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) [26]

Filgrastim (Neupogen)

  • Episodes varied in severity and frequency of capillary leak syndrome [30]
  • Recombinant granulocyte colony-stimulating factors (G-CSF)
    • To stimulate the proliferation and differentiation of granulocytes, especially polymorphonuclear
      • In various forms of neutropenia induced by chemotherapy
    • To help release blood stem cells from the bone marrow of healthy donors [30]
  • Symptoms of CLS improved or recovered with
    • Supportive or corticosteroid treatment
    • Discontinuation of filgrastim
  • In most cases, CLS symptoms occurred after the first dose of filgrastim
  • In two cases, symptoms occurred after the first dose and then reoccurred during the second
  • Six cases of CLS had a fatal outcome. [30]



Antidiabetika typu glitazonů


Glukokortikoidy


Granulocyte colony-stimulating factor

  • Treatment in hematologic cancer
  • Side effects about CLS were increased [17]

Hormonální antikoncepce

Hormonální substituční terapie



Hormony

  • 2-methoxyestradiol (Panzem)

Hydralazin


IL-1-beta


IL-1

  • Can accelerate the occurrence of CLS [17]

IL-11


IL-12



IL-6


IL-8

  • Can accelerate the occurrence of CLS [17]

Ibalgin

  • Málo časté - vzácné NÚ

IL-2

  • IL-2 could enhance the
    • Cytotoxic T lymphocyte activity
    • Increase fas ligand and perforin
    • Lymphocyte-activated killer cells
    • Endothelial cells in close contact
      • Start the autolysis to endothelial cell damage [17]
  • Při terapii maligného melanomu - NÚ jsou až život ohrožující otoky


Velký příjem tekutin (převodnění infuzemi)


Interferon 1beta

  • In patients with multiple sclerosis
  • Also can cause CLS [17]

Interferon gamma


Interleukin 17


Inzulín

  • Zahájení léčby inzulinem u diabetiků 1. typu spojené se vznikem přechodných otoků

Kortikoidy


Kortikoidy

  • Activation of mineralocorticoid receptors to promote fluid retention (Schimmer and Funder, 2017), which per se could disrupt fluid balance and contribute to lymphedema independently of other effects on the blood and lymphatic circulations. Common clinical protocols utilize pre-medication with corticosteroids prior to chemotherapy as a prophylactic strategy to deter infusion reactions (Boulanger et al., 2014). A correlation between corticosteroid use and cancer-related lymphedema has only been anecdotally reported, and no dedicated studies have directly assessed the role of corticosteroids in cancer related lymphedema. Interestingly, other anti-inflammatory and immunosuppressive agents are being investigated as potential treatments for lymphedema (as described in the next section), suggesting that properties unique to the corticosteroids may account for their apparent involvement in the development of lymphedema.
  • www.frontiersin.org/articles/10.3389/fphar.2022.850586/full

Nifedipin


OKT3 monoklonální protilátky


Pegfilgrastim

  • Episodes varied in severity and frequency of capillary leak syndrome [30]
  • Recombinant granulocyte colony-stimulating factors (G-CSF)
    • To stimulate the proliferation and differentiation of granulocytes, especially polymorphonuclear
      • In various forms of neutropenia induced by chemotherapy [30]


Phomaketide A

  • Isolated from the fermented broth of Phoma sp.
  • NTOU4195
  • Exhibit anti-angiogenic and anti-inflammatory effects
  • Anti-lymphangiogenic without an evidence of cytotoxicity inhibited
    • Cell growth
    • Migration
    • Tube formation of lymphatic endothelial cells (LECs)
  • Reduced LECs-induced lymphangiogenesis via
    • Vascular endothelial growth factor receptor-3 (VEGFR-3)
    • protein kinase Cdelta (PKCdelta)
    • Endothelial nitric oxide synthase (eNOS) [37]
  • Enhanced the protein levels of various protease inhibitors, including:
    • Cystatin A,
    • Serpin B6,
    • Tissue factor pathway inhibitor (TFPI)
    • Tissue inhibitor matrix metalloproteinase 1 (TIMP-1)
  • Impeded tumor growth and lymphangiogenesis
    • By decreasing the expression of LYVE-1
      • Specific marker for lymphatic vessels, in tumor xenograft animal model
  • Phomaketide A may impair lymphangiogenesis
    • By suppressing VEGFR-3, PKCdelta, eNOS signaling cascades
    • Simultaneously activating protease inhibitors in human LECs [37]

Pioglitazon

  • Proti metforminu a gliklazidu bývá terapie provázena otoky

Pramipexol

  • Agonista dopaminu použ. u Parkinsonovy nemoc [11] - kasuistika popisující anasarku
  • Náhrada pramiexolu za pergolid v dávce 3krát 1mg/den a po přechodné diuretické terapii (amilorid 5 mg/den a hydrochlorothiazid 50 mg/den)
    • Došlo k ústupu edémů, jejichž velikost se vrátila opět na úroveň před započetím léčby pramipexolem [11]
  • Měnit dobře zavedenou terapii Parkinsonovy nemoci je riskantní, i když se jedná o léky ze stejné lékové skupiny.
    • I drobné odchylky v účinku mohou způsobit rozdílnou klinickou účinnost:
      • Delší poločas pergolidu (15–20 hodin) oproti pramipexolu (8 hodin)
      • Farmakodynamice (větší afinita pergolidu k receptorům D1)
  • T.č. je odklon od ergotových agonistů dopaminu (např. pergolid, kabergolin)
    • Sice vzácné, ale velmi závažné komplikace v podobě fibrózy srdečních chlopní, retroperitonea a pleury
    • Není doporučováno zahajování léčby těmito preparáty u nových pacientů
    • Kteří ergotový přípravek již užívají
      • Pravidelně screeningová vyšetření
      • Zaměnit za přípravek non-ergotový (např. pramipexol, ropinirol) [11]
  • Edémy DK při terapii agonistou dopaminu dosahuje dle rozdílných studií 5–45 %
  • Rizikové faktory byly rozpoznány:
    • ženské pohlaví,
    • Kardiální onemocnění
    • Diabetes mellitus [11]
  • Nebyla prokázána závislost na dávce ani na době podávání agonisty dopaminu [11]
  • V naprosté většině případů je řešením ukončení léčby agonistou dopaminu, což mívá za následek zhoršení příznaků PN
    • Další možnost – tedy záměna agonisty dopaminu za jiný
    • Jednotliví pacienti jsou různě citliví k efektu rozdílných preparátů [11]
  • Podávání diuretik mívá naopak malý efekt u těchto edémů
    • Někdy však může být účinné podávání venofarmak [11]

Recombinant human interleukin 2

  • In overdose will occur CLS [17]

Statiny

  • Rosucard
  • Málo časté - vzácné NÚ

Steroidní hormony

  • Glukokortikoidy
  • Anabolické steroidy
  • estrogeny
  • Progesterony

Tagraxofusp


Tamoxifen


Tie2 inhibice


Thyreostatika

  • Dlouhodobé užívání [8]

Vazodilatátory


Vorikonazol


Blokátory vápníkových kanálků

  • Spontaneous depolarization of lymph muscle cells opens voltage-sensitive L-type calcium channels in the plasma membrane to cause Ca2+ influx, activation of contractile proteins, and ultimately the rhythmic contractions of lymph vessels
  • (Azuma et al., 1977; Schmid-Schonbein, 1990; Van Helden, 1993; Gashev, 2002; Zawieja, 2009; Nipper and Dixon, 2011; Choi et al., 2012).
  • Antagonists of the L-type calcium channel that include clinically-used “calcium channel blockers” effectively inhibit lymphatic contractions
    • (Imtiaz et al., 2007; Von Der Weid et al., 2008; Telinius et al., 2014c; Lee et al., 2014).
  • www.frontiersin.org/articles/10.3389/fphar.2022.850586/full

Dextran or serotonin

Doxorubicin

In a more recent larger cohort study that assessed risk factors for lymphedema in 1794 breast cancer patients followed for a median of 10 years, treatment with anthracyclines was associated with a 13.5% incidence of lymphedema by 5 years (Nguyen et al., 2017). Moreover addition of anthracyclines like doxorubicin to the treatment regimen increased the 5 years incidence of lymphedema by more than 2-fold in patients who underwent axillary lymph node dissection and increased lymphedema by more than 3-fold in patients who additionally received radiotherapy (Nguyen et al., 2017).
Doxorubicin’s therapeutic and cytotoxic action is mediated by DNA intercalation and generation of oxidative stress at the tumor site. The planar anthracycline structure of doxorubicin permits specific binding to base pairs of the DNA double helix causing steric hindrance and preventing DNA cleavage by topoisomerase-II. Doxorubicin also chelates iron to yield hydroxyl free radicals that mediate damage to DNA and other cellular structures (Young et al., 1981; Minotti et al., 2004; Thorn et al., 2011). It was assumed until recently that the cytotoxic actions of doxorubicin also damaged the lymphatic circulation and accounted for the higher incidence of lymphedema in patients administered this chemotherapeutic drug. However, our group recently reported that doxorubicin directly impairs the rhythmic contractions of isolated lymph vessels and compromises in vivo lymph flow as an off-target effect (Stolarz et al., 2019; Van et al., 2021). Notably, earlier studies provided evidence that doxorubicin directly alters calcium signaling in skeletal muscle cells and cardiac myocytes by tonically activating ryanodine receptors to mediate release of intracellular calcium stores (Zorzato et al., 1985, 1986; Abramson et al., 1988; Pessah et al., 1990; Saeki et al., 2002). Building on these findings, we demonstrated that clinically achievable concentrations of doxorubicin acutely inhibit rhythmic contractions in isolated rat mesenteric collecting lymph vessels and reduce flow in the in situ mesenteric lymphatic circulation (Stolarz et al., 2019). Additional studies revealed that doxorubicin tonically increased cytosolic free calcium in lymph muscle cells as a mechanism to disrupt the cyclic rises in intracellular calcium required for rhythmic contractions and normal lymph flow. Importantly, the tonic rise in cytosolic free calcium was prevented by pharmacological antagonists of ryanodine receptors but not by blocking other calcium-mobilizing channels (Stolarz et al., 2019). Interestingly, this ability to disrupt Ca2+ signaling also is a feature of other anthracycline medications (Olson et al., 2000; Shadle et al., 2000; Hanna et al., 2011), raising the possibility of a shared effect of anthracyclines on lymphatic contractile function that may to contribute the development of secondary lymphedema. Earlier studies suggest that the disruption of lymphatic contractions and the resulting lymphostasis damages the lymphatic endothelium and fragile lymphatic valve leaflets, setting the stage for long-term compromise of lymph vessel contractile function (Zawieja et al., 1991; Ji and Kato, 2001; Gashev, 2002; Nipper and Dixon, 2011; Choi et al., 2012).

Dantrolene

  • To prevent the detrimental effects of doxorubicin on the lymphatic circulation (Van et al., 2021). Dantrolene is a ryanodine receptor type 1 (RYR1) antagonist used clinically to mitigate malignant hyperthermia (Rosenberg et al., 2015; Ratto and Joyner, 2021). However, we considered that this drug could be repurposed as a prophylactic to prevent anthracycline-associated lymphedema. Initial studies confirmed that the molecular target of dantrolene, the RYR1 protein, was expressed by single lymph muscle cells freshly isolated from rat mesenteric lymph vessels. Subsequently dantrolene was observed to prevent the pathogenic rise in intracellular calcium elicited by doxorubicin in isolated lymph vessels. Finally, topical superfusion of the intact mesenteric lymphatic circulation with dantrolene prevented the interruption of lymph flow caused by systemic infusion of doxorubicin (Van et al., 2021). Future longitudinal studies are necessary to evaluate dantrolene as an anti-lymphedema medication, but these initial findings raise the possibility that dantrolene co-administered during chemotherapy may mitigate the detrimental effects of doxorubicin on the lymphatic circulation to preserve lymph flow.
  • www.frontiersin.org/articles/10.3389/fphar.2022.850586/full

Estrogeny kontaminující životní prostředí

    • Metabolity léků které ani nemají estrogenu podobné struktury, ale mají estrogenní aktivitu
      • Biodegradací v půdě třeba i antiepileptika
  • Plísňové toxiny
  • Změkčovadla z plastů
  • estrogeny z HAK v pitné vodě
  • živočišné estrogeny
    • Mléčné výrobky
    • Vejce
  • Vliv střevního mikrobiomu
  • Vlastní tuková tkáň
  • Estrogenní dominance a nadměrná estrogenní stimulace žene tělo ženy směrem k lipedemu
  • Nadbytek estrogenů znamená i vyšší riziko recidivy nádorů estrogen senzitivních tkání
    • Prso, děloha, vaječníky
  • Rostliné estrogeny zadaleka nepovažuji za takovou hrozbu například proti těm, co pochází z vlastní tukové tkáně, mléka a vajec
    • Naopak tyto rostlinné estrogeny mají mnohem slabší účinek na naše receptory a spíše je tedy blokují před těmi živočišnými takže je lze považovat spíše za protektivní než rizikové
    • Kromě toho se fytoestrogeny spíše váží na receptory v kostech než v prsu a děloze a spíše chrání před osteoporózou
    • Ve studiích na ženách po Ca prsu vychází soja spíše jako protektivní než riziková - narozdíl od mléka, které je jednozančně spojeno s vyšší incidencí nádorů a nejen hormonálně senzitivních tkání - je to prorůstová potravina
      • Mimo jiné mléko zhoršuje u mnoha lidí i otoky jako takové


Glibenclamide

  • KATP channel blockers may be useful to restore lymphatic function in diabetes and other conditions characterized by the excessive opening of KATP channels (Zawieja et al., 2016; Davis et al., 2020). One specific antagonist of KATP channels is glibenclamide, which is a common antidiabetic agent. In a study using rats with metabolic syndrome, glibenclamide partially restored the frequency of lymphatic contractions and fractional pump flow in isolated mesenteric lymph vessels (Zawieja et al., 2016). Similarly, glibenclamide exerts an anti-lymphedema action in Cantu syndrome, which is a disease in which KATP channels exhibit gain-of-function (i.e., high open-state probability) associated with a high incidence of lymphedema (Nichols et al., 2013). In a genetic mouse model with this gain-of-function mutation in the KATP channel, glibenclamide partially restored normal resting membrane potential in lymph muscle cells and improved rhythmic contractions in isolated popliteal lymph vessels (Davis et al., 2020). In contrast, glibenclamide does not appear to affect contractions in lymph vessels isolated from control rats and humans (Mizuno et al., 1999; Mathias and von der Weid, 2013; Telinius et al., 2014b). More studies are needed to characterize the therapeutic potential of glibenclamide and other KATP channel blockers to preserve lymphatic function in patients with metabolic diseases, Cantu syndrome and other diseases in which KATP channel activity may be abnormally high.
  • www.frontiersin.org/articles/10.3389/fphar.2022.850586/full

Gestageny

  • HAK u lymfedemu může zhoršit stav

Minoxidil


Mykofenolát mofetil


Nesteroidní antirevmatika


Nitráty


Non-steroidal anti-inflammatory drugs

  • May worsen swelling in the legs [3]

Otoky jako NÚ léků

  • Blokátory vápníkových kanálků
    • amlodipin ( Norvasc)
    • Nifedipin ( Procardia)
    • Felodipin
  • betablokátory
    • Pokud zhorší prokrvení ledvin / srdeční selhání
  • Dieuretika
  • Alkoholismus
  • PPRgamma agonisté
  • Ranpirnáza (Ranpirnase - ter. maligního mezoteliomu)
  • Hormony
    • 2-methoxyestradiol (Panzem)
  • Abirateron (acetát)
  • Vorikonazol
  • Capecitabinum (Xeloda)
  • Mykofenolát mofetil
  • Sirolimus (Rapamycin)

Málo časté - vzácné NÚ

  • Ibalgin
  • Statiny
    • Rosucard

PPRgamma agonisté



Prednison

  • Pacientka s primární amenorhoeou (v.s. Turnerův syndrom) a nulovou aktivitou vlastních vaječníků vysadila svoji dlouholetou hormonální substituci, následně měla pocit, že otéká a zadržuje vodu, tloustne
  • V děloze gynekolog zachytil polyp
  • Injekce prednisonu měla vyvolat menstruaci
    • Menstruace nenastala
    • Klientka udává 3-5 dní častého močení a úlevu od otoků
    • Poté došlo opět k zadržování vody a v ambulanci si stěžuje, že
      • Má naběhlé prsy a zmnoženou tukovou tkáň na zádech, pažích, břichu a že má pocit, že zase zadržuje vodu a na tokonto přichází do lymfologické ambulance.
Napadlo mne, že hormon působil prorůstově a tím snížil na chvíli inzulínovou rezistenci a hladiny inzulínu - tím došlo k uvolnění vody a k močení - avšak za cenu toho, že se klientce zmnožila tuková tkáň. Ptala jsem se, co jí. Dušovala se, že defacto low carb a že toto je nemožné. Když sem se zeptala, co snídá, řekla: Banán a toast. Vida, sacharidy se sacharidy a žádné low carb. Domnívám se, že podobně jako ženy s polycystickými ovárii, že i ženy s Turnerovým syndromem mají tendenci k inzulínové rezistenci. Kromě toho některé ženy s Turnerovým syndromem nemají plně vyvinuté všechny lymatické cévy a mohou mít tendenci k lymfatickým otokům.


Nadužívaní projímadel


Psoraleny


Ranpirnáza (Ranpirnase - ter. maligního mezoteliomu)


Růstový hormon


Sirolimus (Rapamycin)



Taxanes

  • Common class of chemotherapy drugs that are well known to cause fluid retention (Béhar et al., 1997; Ho and Mackey, 2014). This drug class, including paclitaxel and docetaxel, is widely used to treat many cancers including breast, lung, head and neck, and prostate cancer (Ojima et al., 2016). Several epidemiological studies have linked taxane chemotherapy to an increased incidence of breast cancer related lymphedema (Lee MJ. et al., 2014; Nguyen et al., 2017; Zhang et al., 2019). For example, in a longitudinal study of 63 breast cancer patients who received axillary surgery and a chemotherapy regimen containing anthracyclines and taxanes, 25–30% of patients developed lymphedema within the first 6 months after completing taxane therapy (Lee MJ. et al., 2014). In a larger cohort study that assessed risk factors for lymphedema in 1794 breast cancer patients, the overall 5-year incidence of lymphedema in patients treated with taxane chemotherapy was approximately 30% (Nguyen et al., 2017). Moreover, addition of taxanes to any treatment regimen resulted in a 33–40% incidence of lymphedema at 5 years (Nguyen et al., 2017).
Taxanes, exert their cytotoxic actions by stabilizing microtubule formation thereby inhibiting mitosis and resulting in apoptosis (Ojima et al., 2016). Taxanes also inhibit tumor angiogenesis, an action that may be partially attributed to their ability to inhibit endothelial cell migration and proliferation (Bocci et al., 2013). These inhibitory actions on endothelial cells may also partially explain the association of taxane drugs with lymphedema, although the literature fails to clarify the mechanism by which this class of drugs may injure the lymphatic circulation. In this regard, a recent study indicates that the common taxane medication, paclitaxel, induces autophagy in human dermal lymphatic endothelial cells (HDLECs) and disrupts gap junctions correlating to loss of the gap junction protein, VE-cadherin. Based on these findings, the authors suggest that paclitaxel disrupts the endothelial barrier dysfunction to increase the permeability of lymph vessels (Zamora et al., 2019). The same authors also reported that paclitaxel modestly attenuates tumor lymph-angiogenesis in a tumor-bearing mouse model, apparently confirming significant drug effects on the lymphatic endothelium albeit in a specific pathological setting (Zamora et al., 2019). Finally, a subsequent report that docetaxel, another commonly used taxane medication, attenuates proliferation and inhibits migration and tubule formation of HDLECs in primary culture provides additional evidence that taxanes may impair endothelial function and limit lymph-angiogenesis (Wong et al., 2020). Indeed, the authors also noted a decreased expression of the endothelium-specific marker LYVE-1 in cultured HDLECs exposed to docetaxel, although expression of Prox-1, another lymphatic endothelium-specific marker was unchanged (Wong et al., 2020). These initial in vitro findings linking taxanes to injury of the lymphatic endothelium have set the stage for proof-of-principle studies to examine the impact of systemic taxane administration on endothelial integrity, lymphatic function and in vivo lymph flow.https://www.frontiersin.org/articles/10.3389/fphar.2022.850586/full

Thiazidolinediones (TZDs)

  • Activate peroxisome proliferator activated receptor gamma (PPAR?), which is a transcriptional factor that upregulates genes responsible for glucose uptake (Vieira et al., 2019). TZDs are widely used for the treatment of type II diabetes, but one of their side effects is fluid retention and edema that occurs in a dose- dependent manner (DeFronzo, 1981; Yamanouchi, 2010; Yau et al., 2013). The incidence of edema is 5–10% in patients taking TZDs as a solo medication. However, administration of TZDs in combination with daily insulin increases edema incidence to 15–20% by an unknown interaction (Scheen, 2004). The mechanisms responsible for this drug-related edema are unclear, but a limited number of studies indicate that TZDs may directly affect lymphatic function. For example, the TZD rosiglitazone is reported to inhibit lymph-angiogenesis in a murine model of human gastric cancer (Chen et al., 2013). In this study, rosiglitazone dose-dependently reduced the lymph vessel density of implanted gastric tumors and decreased expression of VEGF-C and VEGFR-3, common lymphangiogenic markers (Chen et al., 2013). Another study evaluated the impact of rosiglitazone on lymphatic function by using technetium-labelled albumin to measure albumin retention and uptake of interstitial albumin by lymphatics in hindquarters of Zucker Diabetic Fatty (ZDF) rats (Cosson et al., 2009). In previous studies the ratio of low and high frequency peaks (LF/HF ratio) correlated with the half-life of the technetium-labelled albumin disappearance during lymphoscintigraphy (Cohen-Boulakia et al., 2000; Pecking et al., 2008); therefore, LF/HF ratio was used as a surrogate index of lymphatic uptake of albumin. The hind limbs of these diabetic animals exhibited albumin retention and a high LF/HF ratio (which inversely correlates with lymph uptake) as evidence of compromised drainage of lymph fluid. Treatment with rosiglitazone resolved the albumin retention but did not restore lymph uptake to control levels. One interpretation of these data is that rosiglitazone lowers albumin retention by decreasing capillary filtration but does not modify lymphatic uptake. Collectively, these initial studies provide little firm insight into mechanism(s) by which rosiglitazone causes edema in clinical practice, but they serve to emphasize that medications associated with the development of edema may act at multiple sites to disrupt local fluid dynamics including lymph vessel density, capillary filtration, lymph uptake and other processes that maintain the delicate fluid balance in the interstitial space.
  • www.frontiersin.org/articles/10.3389/fphar.2022.850586/full
O úroveň výše

Poslední aktualizace: 6. 10. 2024 23:25:35