Huidziekte pigment verdwijnt - Oorzaken, Behandelingen en Hoop voor de Toekomst

Quiz

1. Scientist from NASA are trying to grow vegetables in space. They have lights to grow the vegetables that come in different wave lengths. Which wavelengths of light should be used to grow vegetables?
A. 400-500 nm
B. 500-600 nm
C. 700-800 nm

A is correct. To answer this question, refer to the first picture in the article. The absorbance, or amount of light that each wavelength absorbs is shown by the different colored lines. A high absorbance means the pigment can transfer energy from that wavelength. The 500-600 nm area has a very low absorbance, and the 700-800 nm wavelength is above the range chlorophyll reacts to. Therefore, the 400-500 nm range has the highest absorbance. The vegetables, in this range, would be able to use the energy supplied by the lights.

2. Clouds in the atmosphere can filter certain wavelengths of light. On sunny days, more red light makes it to the surface of Earth. On cloudy days, more blue light. Why is it important for plants to have both chlorophyll a and chlorophyll b?
A. Both are needed to work together to produce sugar.
B. On certain days, different wavelengths can provide energy.
C. Plants contain both by accident.

B is correct. The variable amount of light present on the surface of the Earth requires that plants have pigments that can work with different qualities of light. If plants only had one or the other versions of chlorophyll, they would not be able to function on certain days, and would die. Both versions of chlorophyll allow them to exploit a variety of environments and conditions.

3. Plants contain other pigments besides chlorophyll, two of which are xanthophyll and carotene. These pigments do not reflect green, but red and yellow. In plants that lose their leaves in the fall, the leaves turn from green to red, yellow and brown in the fall. If xanthophyll and carotene are present the whole time, why are the leaves only red and yellow in the fall?
A. Chlorophyll is dissolved in the fall, leaving only the red and yellow pigments.
B. Cold temperatures allow the red and yellow pigments to reflect light.
C. The sunlight changes in the fall, revealing the red and yellow colors.

Introduction

Normally, NF-kB protects against cell death, it is maintained within cells in an inactive state and becomes activated to induce an inflammatory response secondary to bacterial, viral, or stress. Derangement of IKBKG results in its inability to protect cells against apoptosis, hence more cell death occurs in response to stimuli.[6]

Due to X-linked dominant inheritance, IP is usually lethal in males during embryogenesis.[7] However, cases in males have been reported in the literature. This can be explained by somatic mosaicism, hypomorphic mutations, or the presence of an extra X chromosome, as in Klinefelter syndrome. Females inherit one X chromosome from each parent, and one X chromosome becomes inactivated through lyonization. Inactivation of a single X chromosome is not seen in all cells. Therefore, females are functionally mosaic, meaning they have two cell lines. Skin lesions develop along the Blaschko's lines.[8] These lines reflect embryonic stem cells' migration path during development and are invisible unless a pigmentary skin disorder is present.[9]

Pathophysiology

NF-kB is a transcription factor involved in expressing multiple genes, including cytokines, chemokines, growth factors, adhesion molecules, and regulators of apoptosis.[16][17] NF-kB activation prevents apoptosis induced by the tumor necrosis factor (TNF) family of cytokines. NF-kB is mainly inactive in most cells, and various stimuli trigger activation of NF-kB. These stimuli include interleukin-1 (IL-1), TNF alpha, antigen receptors (T-cell receptor and B-cell receptor), genotoxic stress (ultraviolet radiation, gamma radiation, reactive oxygen intermediates), lipopolysaccharide (bacterial endotoxin), and double-stranded RNA (viral infection).[18]

The 'canonical' NF-kB is a heterodimer consisting of p50 and p65 (RelA).[19] NF-kB is kept inactivated in the cytosol when it is complexed with inhibitory protein IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha). Various stimuli activate the IκB kinase (IKK) after attaching to and activating the receptors. IKK phosphorylates IkB, which leads to the degradation of IkB and thereby activation of NF-kB. Activated NF-kB enters the nucleus to bind with response elements (RE) of DNA (deoxyribonucleic acid) and brings out the various changes in cellular functions.[20] The mutation of IKK results in complete disruption of the signaling pathway and virtually no NF-kB activity after stimulation of NEMO/IKK-deficient cells.

Peripheral eosinophilia is noted in patients with IP. The increased production of eosinophils in the bone marrow and increased migration of eosinophils into the circulation causes this eosinophilia. An activated eosinophil secretes granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine that induces eosinophil differentiation and maturation in the bone marrow. Activated IKK cells have been found to induce elevated expression of GM-CSF in peripheral eosinophils via the NF-kB pathway.[21]

GM-CSF works as an autocrine factor to promote eosinophil survival, further elevating peripheral counts. IL-5, a cytokine released by Th2 (T-helper type 2) cells, stimulates the production of eosinophils in the bone marrow and their release into the peripheral blood. NF-kB pathway activation indirectly stimulates the transcription of IL-5. Currently, the mechanisms of NF-kB pathway activation and T helper cell participation in IP are not precisely known. Eotaxin is thought to contribute to tissue eosinophilia in recent studies of the pathophysiology of IP. Several eotaxin promoters possess NF-kB binding sites, including one encoding an eotaxin chemokine previously isolated from blister fluid and crusted scales of patients with IP.[22]

Wat merk ik bij zomergist?

U krijgt vlekjes, vooral op uw hals, uw borst en uw rug. Vaak zitten ze ook in uw gezicht, of op uw armen en benen.

De grootte van de vlekjes is verschillend. Soms zijn ze klein (zo groot als een rijstkorrel), soms groter (zo groot als een euro). De vlekjes liggen vaak tegen elkaar aan, hierdoor kan een vlek groter worden dan een euro.

De vlekjes zijn wit als uw huid donker is of bruin door de zon. Op een lichte huid zijn de vlekjes meestal rood of bruin.

Op de vlekjes zitten vaak kleine schilfers (velletjes). De vlekjes kunnen jeuken.

Onderzoek & diagnose van vitiligo

De huidverandering is bij vitiligo zo duidelijk en kenmerkend, dat uw arts over het algemeen alleen aan de huiduitslag al kan zien dat u vitiligo heeft. Vanuit de diagnose kan wel gestart worden met een behandelplan bij Bergman Clinics | Huid & Vaten kunt u terecht voor UVB lichttherapie.

Vitiligo is een ziekte waarvan het verloop lastig te voorspellen is. Het kan langzaam uitbreiden of hetzelfde blijven. Er zijn ook voorbeelden van mensen bekend waarbij de vitiligo spontane verbetering liet zien.

Doormiddel van UVB lichttherapie bij Bergman Clinics | Huid & Vaten kunt u de huid stimuleren om pigment aan te maken. Deze therapie dient in een aaneengesloten periode te worden gegeven. In het begin zal zullen de vitiligovlekken reageren met kleine bruine puntjes. Na maanden van behandeling vormen de vele puntjes een soort ingekleurde vlek.

Wat kan ik zelf doen ?

Wanneer u vitiligo heeft is uw huid zeer gevoelig voor zonlicht. De vitiligoplekken kunnen zeer gemakkelijk verbranden in de zon. Daarom is het belangrijk om uw huid te bedekken wanneer u in de zon gaat. U kunt ook zonnebrandcrème gebruiken, maar dan is het belangrijk te realiseren dat dit maar een korte tijd bescherming biedt

Wilt u meer weten over de behandelmogelijkheden van vitiligo bij Bergman Clinics? U kunt gerust even bellen op 088 9000 500. Onze medewerkers beantwoorden uw vragen graag. Tevens is het mogelijk om direct een afspraak in te plannen.