27 Temmuz 2019 Cumartesi

Vitiligo sufferer, 25, whose face and entire body was covered by light patches claims turning VEGAN has reversed her condition



A woman whose skin was left covered in lighter patches from vitiligo claims going vegan has reversed her condition. 
Jamila Davis, 25, from Florida, was diagnosed with the skin condition, caused by a lack of melanin a pigment of the skin - when she was eight. 
The patches slowly spread across her whole body, meaning strangers would often stare at her because of her unique appearance. 
Miss Davis decided to go vegan after her father died from a stroke in 2017, after the pair had plans to go plant-based together.  

A year into her meat-free diet, the college student was stunned to see her colour returning on parts of her body. Now, her original colour has fully returned on most of her face.
Scientists have yet to prove any diet will treat vitiligo, while experts also say there are none which will make the condition worse either.  
Miss Davis claims she does not use any other standard treatments for her condition and hasn't seen a dermatologist since she went vegan.
Miss Davis said: 'Growing up with it, it never really bothered me. I actually loved the fact I was unique from everyone. 
'But there would be times where kids would stare and point their fingers at me, and others laughing or even saying small hurtful things would get to me.
'Now that I'm reversing it and going through the same process when I lost my pigmentation, I get the stares, points, and even the little ones saying, "mummy what's on her face?" kind of questions. 
'My friends and family say things like it's amazing to watch me change back into my original colour and how I'm so strong and beautiful while embracing myself.'

23 Temmuz 2019 Salı

Vitiligo in horses: What we know so far


The skin condition vitiligo can be unsightly in horses, but it is essentially a cosmetic issue, a just-published scientific review says.
“Therefore, any treatment for this disease should always be discussed with the owners to avoid interventions of dubious efficacy and those with possible adverse effects,” Thierry Olivry and his colleagues wrote in the journal, BMC Veterinary Research.
“However, vitiligo could have a significant and negative impact for the owners of show animals,” the researchers acknowledged.
Vitiligo is an autoimmune disease in which melanocytes in the skin are targeted.
A substantial part of their review into autoimmune diseases affecting skin melanocytes in horses, dogs and cats covered this condition. It has many features that mirror the condition in humans, they said.
In vitiligo, melanocytes are destroyed, resulting in depigmentation.
It is the most common depigmenting condition in humans, affecting 0.5 to 2% of the population. Rates as high as 8.8% have been reported in India.
Signs associated with this destruction are primarily seen in the skin, lips and/or oral cavity.
Vitiligo in humans was first described more than 3500 years ago. In ancient times, vitiligo was confused with leprosy and other depigmenting disorders, and it resulted in discrimination and social stigma that, unfortunately, still persists today.
It was only in the last century that vitiligo has gained more interest among medical researchers.
The first case series of vitiligo in dogs was described in scientific literature in 1971. Scientific reports on vitiligo in horses, cat and dogs are limited.
In the horse, it was first mentioned in the literature in 1931, but it was not until the 1960s that a Dutch veterinarian reported equine vitiligo in three separate papers.

There is no available information that allows an estimate to be made of the global or regional incidence and prevalence of vitiligo in horses, dogs and cats.
However, at Cornell University, it was reported that vitiligo accounted for 0.7% of equine dermatoses examined at the veterinary teaching hospital.
“The prevalence of vitiligo in animals may be much higher than that reported,” the review team said.
“However, because this disease is a primarily cosmetic issue in animals, and it might not motivate owners to seek any veterinary care.”
The breeds of horses affected with vitiligo can be inferred from five reports identified by the authors that included 32 horses.
Among these cases, there were 12 Gelderlands, nine Spanish thoroughbreds, four Arabians, four Belgians, one Oldenburg, one Mecklenburg and a quarter horse.
Other studies did not identify breeds.
The sex of affected horses was available from three reports involving 28 horses, with a female-to-male ratio of two to one.
“Vitiligo is reported to be common in Arabian horses (the so-called “Arabian fading syndrome” and “pinky Arab”) and there are numerous references listing this breed in review papers, equine textbooks and the lay literature,” they said.
However, the published information is limited and may not completely represent how common the condition is among horse breeds.
The age of onset was reported in only seven horses, with a median of 48 months, and a range of 1 to 18 years.
Information on the appearance of the first skin lesions was available for just six horses, all of whom initially developed depigmentation on the head/face region.
The lesion distribution was reported in 11 horses, of which eight (73%) involved the head/face region.
Due to the cosmetic nature of the disease, diagnosis is often made clinically without any need for skin biopsies, they noted.
Turning to treatment, the researchers noted that it can have a devastating psychological impact on the quality of life of affected humans, which is is why treatment of widespread, facial or recalcitrant vitiligo in people can be aggressive.
In horses, treatment and outcome information was available for only 11 horses, across three reports.
It took between one to 12 months for significant repigmentation to occur.
Complete repigmentation occurred in one horse treated with oral nutritional supplements containing, among others, vitamin A, D, B12 and E.
In another report, partial repigmentation occurred after supplementation with high levels of chelated copper. A relapse of depigmentation occurred about five months after the copper supplementation was reduced and then a noticeable clinical improvement occurred when the daily intake of copper was re-increased.
“It is plausible,” they said, “that the depigmentation in this horse was associated with a copper deficiency and not vitiligo.”
Nine horses from one case report had complete repigmentation after 1 year of dietary supplementation with carrots (4–5 kg per animal per day).
The author suspected that the administration of high levels of a thyroprotein-based product might have caused a relative vitamin A deficiency and depigmentation. However, to the authors’ knowledge, there is no evidence that vitamin A deficiency leads to depigmentation in horses but, in humans, several studies have shown that deficiencies of D and B12 vitamins are associated with vitiligo.
“Therefore, the outcome of these nine horses of this report should be interpreted cautiously. A plausible cause could have been an idiosyncratic reaction to high levels of a thyroprotein-based product, or any of its ingredients, as the cessation of this diet led to spontaneous resolution.”
The review team said information on the long-term treatment and outcome of vitiligo in animals was rather sparse, with few published case reports to date.
Given its cosmetic nature in animals, interventions of questionable effectiveness and with possible adverse effects should be avoided.
In show animals, where the condition could have a negative impact on owners, highly potent glucocorticoids could be applied topically (i.e., 0.1% bethamethasone or 0.05% clobetasol). However, it would be practical only for areas with sparse or no hair. It should be used sparingly.
“This recommendation is based on the assumption that the pathogenesis of vitiligo in humans and animals is similar and involves an autoimmune mechanism.”
Giving glucocorticoids orally or by any other internal means is not normally recommended for treatment of vitiligo because the adverse effects outweigh the clinical benefits in animals, they said.
“If topical therapy were to fail, oral supplementation with L-phenylalanine could be attempted for six months, although the clinical remission could be only partial. This supplementation might be tried in addition to the use of topical glucocorticoids.
“It is important to emphasize to the owners that these treatments, if effective, may prevent the progression of depigmentation but they do not guarantee the partial or full repigmentation.”
The authors said there was a need for research to determine, among other things, whether the same genes linked to vitiligo in humans have a role in the disease in cats, dogs and horses.
Phototherapy is a safe and effective treatment in humans. “Therefore, phototherapy treatment, either alone or in combination with other drugs, warrants further clinical trials in animals.”
Olivry was joined in the review by his North Carolina State University colleague Keith Linder; and Heng Tham, from the Virginia-Maryland College of Veterinary Medicine.
Autoimmune diseases affecting skin melanocytes in dogs, cats and horses: vitiligo and the uveodermatological syndrome: a comprehensive review
Heng L. Tham, Keith E. Linder, and Thierry Olivry
BMC Veterinary Research 2019 15:251 https://doi.org/10.1186/s12917-019-2003-9

15 Temmuz 2019 Pazartesi

Breakthrough vitiligo treatment offers longer-lasting results





Longer-lasting treatment for vitiligo could be available within the next few years.
According to John Harris, M.D., Ph.D., director of the Vitiligo Clinic and Research Center at the University of Massachusetts Medical School, a new treatment targets and removes the cells responsible for developing the condition.
He discussed this research at the American Academy of Dermatology Annual Meeting in Washington, D.C.
“Compared to treating psoriasis, we’re in the Dark Ages when it comes to treating vitiligo,” he said. “We hope to be able to give vitiligo patients the treatment they deserve.”
CURRENT TREATMENT
JAK inhibitors, such as tofacitinib, are among the standard vitiligo treatments, targeting the cytokine interferon gamma. The treatment is available both orally or topically, and it blocks interferon gamma signaling. The problem, Harris said, is that the effect is temporary.
“JAK inhibitors and other more conventional treatments work, but when you stop them, the disease comes right back,” he said. “And, it doesn’t just relapse. It returns in the exact same places as before.”
WHAT’S HAPPENING
Harris and other researchers have determined autoimmune memory cells, specifically resident memory T cells, are responsible for vitiligo relapses. These cells attack viral infections on the skin, and several cells linger to ward off future outbreaks. Current treatments turn these cells off, but they re-activate when medication use stops.
“These cells wake back up, and they’re right there waiting,” he said. “And, the white spots return.”
NEW THERAPY
To offer longer-lasting therapy, the new treatment-in-testing targets the cytokine interleukin (IL)-15. It’s an antibody blockade that blocks IL-15 signaling. Results of a mouse study reveal that not only did the antibody turn off the signaling, but it also removed the resident memory T cells from the skin, eliminating the possibility of future relapse.
“This is a drug that you’re, hopefully, going to see in the clinic within the next 5 years. It’s different from psoriasis and TNF inhibitors that were discovered to work by accident. We’re actually going to be able to tell you exactly how it’s working,” he said. “We’re hoping the IL-15 biologic will provide long-lasting results typically not seen in dermatology.”
Ultimately, Harris said, this drug could fundamentally alter how dermatologists treat vitiligo patients. It could give them a tool designed to combat this specific condition.
“The future is bright for vitiligo,” he said. “I like comparing it to other disease like atopic dermatitis and psoriasis because both of those diseases have targeted therapies that really have changed what it means to manage difficult patients. Vitiligo is next in line.”
Reference:
S011 - Inflammatory Skin Diseases: The Translational Revolution. “New Developments in Vitiligo.” John Harris, M.D. 2:15 PM, March 1, American Academy of Dermatology annual meeting.

JAK inhibitors offer hope for vitiligo patients





With several Janus kinase (JAK) inhibitors undergoing clinical trials for vitiligo, their potential approvals will deliver new hope and an entirely new treatment strategy, said an expert at the American Academy of Dermatology annual meeting in Washington, D.C.

"JAK inhibitors are exciting. They're probably going to be the first FDA-approved treatment for vitiligo. We don't have any FDA-approved drugs right now that reverse disease," said John Harris, M.D., Ph.D. He is an associate professor of dermatology at the University of Massachusetts Medical School.
Although JAK inhibitors likely will be the first generation of FDA-approved drugs for vitiligo, he added, researchers are hoping that over time, they will be able to refine this approach to produce even more targeted treatments that are safe and beneficial.
Over the past 10 to 15 years, said Dr. Harris, vitiligo has undergone a surge in research that has outlined the central pathways that drive the disease. "One of those pathways is the interferon gamma (IFN-ƴ) signaling pathway. It seems to be very important for the progression of vitiligo." IFN-ƴ signals through the IFN-ƴ receptor and JAK1 and JAK2, then through STAT1. The discovery that IFN-ƴ drives vitiligo in part came from a mouse model developed by Dr. Harris and colleagues. "We found that the spots appearing in the skin of mice and in people expressed the same IFN-ƴ gene signature."2
More specifically, he said, the researchers used IFN-ƴ knockout mice and IFN-ƴ receptor knockout mice. "And we were able to target IFN-ƴ with an antibody. All these approaches have shown us that the mouse disease is prevented and reversed by blocking the pathway. This finding laid out the rationale for testing drugs that target IFN-ƴ signaling."
Dr. Harris and others hypothesized that blocking JAK1/2 signaling with JAK inhibitors could be an effective treatment for vitiligo. The first case report, published by Brett King, M.D., Ph.D., of Yale University School of Medicine, featured a patient treated with the JAK1/3 inhibitor tofacitinib.3Subsequently, Dr. Harris and colleagues published a case report of a patient treated with the JAK1/2 inhibitor ruxolitinib.4
Additional research with the mouse model showed that when IFN-ƴ is produced in the skin, it activates the chemokines CXCL9 and CXCL10 within the epidermis. These proteins use a positive feedback loop (through the signaling of the CXCL10 receptor, CXCR3) to recruit T cells to the skin. "Essentially, T cells go to the skin, and make IFN-ƴ when they see their target melanocytes. The keratinocytes sense IFN-ƴ and make CXCL9 and CXCL10, and that recruits more T cells. We believe that's what's being inhibited by the JAK inhibitors."
He likens the positive feedback loop to the way ants would find a drop of melted ice cream on a sidewalk. "An ant eventually will stumble across one of those drops and very quickly will lay a trail back to the nest. Soon you'll have 1,000 ants on that spot, devouring it. That's what's happening here — the first T cell is the scout ant, but then it lays a trail for all the other ones to follow. That's where disease occurs." Blocking IFN-ƴ signaling and CXCL10 production inhibits the entire cycle, preventing or possibly even reversing disease, he said.
Because Dr. Harris and colleagues were able to show the key role played by keratinocytes in responding to IFN-ƴ, they hypothesized that topical JAK inhibitors could also be effective because topical agents can target keratinocytes. An 11-patient study showed that topical ruxolitinib was effective for vitiligo.5
Taken together, said Dr. Harris, the above findings all provide rationale for three ongoing clinical trials of JAK inhibitors in vitiligo. Aclaris and Incyte Pharmaceuticals are testing topical ATI-502 and INCB018424, respectively, in phase 2. Pfizer is testing two oral JAK inhibitors, he said. "The Incyte study is the furthest along. It's a two-year study with a six-month primary endpoint. There should be interim data soon." The entire study is scheduled for completion in July 2020.
Other researchers led by Dr. King have also observed that patients whose vitiligo improved with tofacitinib did so on areas of exposed skin.6 "So he hypothesized that this was due to exposure to light. Whether it's sunlight or visible light, it's hard to know. But exposed skin seems to do better with JAK inhibitors, suggesting that light was also beneficial in promoting the reversal of disease."
As part of the same analysis, Drs. Harris and King sampled the skin of a tofacitinib-treated patient. "We found that treatment with a JAK inhibitor actually removed the autoimmune cells from all of her skin, including the (light-exposed) skin that got better and the skin that did not. That suggested to us that the JAK inhibitor is sufficient to remove autoimmunity, the autoimmune cells driving the disease. The possible reason why light is helpful is because it stimulates the melanocytes to regrow."

HSP70i Heat Protein Vitiligo Treatment




‘Temprian’ is an old English word that means ‘to restrain within due limits, to moderate’. At Temprian Therapeutics, we are passionate about finding an efficient treatment for Vitiligo. The company focuses on getting the mutant HSP70i-based drug subject to clinical trials. We will do this by partnering with patients, clinicians, investors, and the pharmaceutical industry. Here is how we look at the challenge: What is Vitiligo? Vitiligo is typically induced by a variety of stress factors ranging from exposure to harmful chemicals, intense sunlight, scrapes and bruises or emotionally draining conditions. The stress results in an immune response, where the body’s own T cells erroneously attack pigment cells (also called ‘melanocytes’) in the skin. Melanocytes are in charge of producing melanin, the pigment that gives the skin its color. Vitiligo tends to be progressive and evolves in stress induced bursts. The rate of pigment loss varies widely between individuals and may in due time result in complete depigmentation.

Why does vitiligo occur? When subject to stress, cells in the skin start producing the heat shock protein HSP70i. This protein acts as a messenger that is crucial for maintaining the viability of the cell during stressful conditions, by shielding cellular molecules. Some heat shock proteins are transported out of the cell, from where they get taken up by so called dendritic cells and transported to local lymph nodes. Here the dendritic cells signal that something is wrong in the skin. This triggers the activation and recruitment of a variety of T cells, reactive with proteins transported by HSP70i. Such target proteins include melanocyte proteins. That leads to vitiligo in patients with pre-existing T cells that carry receptors aimed at recognizing and killing pigment cells. 

Why do T cells attack the body’s own cells?   Activation of melanocyte reactive T cells is based on the T cells responding to a very specific protein transported to dendritic cells by the heat shock protein. The heat shock protein sounds the alarm, and the protein it carries is digested into peptides to form a “key”, that fits into a “lock” on the T cell. The chaperone function of HSP70 is thought to be very important, as it is very well preserved throughout evolution, and can be found in stressed cells from organisms ranging from bacteria to plants and mammals.  

How would the therapy work? The heat shock protein-based vitiligo treatment is based on introducing a slightly modified version of HSP70i into the skin, where the alarm region has been re-engineered. The resulting heat shock protein scientifically named HSP70iQ435A now has the opposite effect on dendritic cells as compared to its natural counter-part.  The modified heat shock protein actually acts as an immuno-suppressant, stalling the release of T cells. The lack of killer T cells in the skin now allows new pigment cells to occupy the skin, reversing the progression of vitiligo. The non-pigmented lesions start filling in with pigmentation. 


How will the drug be induced? The modified protein will be introduced into the skin by a series of DNA injections. Laboratory research with vitiligo disease models show that mice and swine respond well to four weekly treatments, to initiate the path to recovery.

Twice-Daily 2% Tofacitinib Cream Plus UVB Improves Facial Vitiligo Symptoms


A twice-daily 2% tofacitinib cream in addition to narrow-band ultraviolet B (NBUVB) administration has shown promise for improving the symptoms of facial vitiligo, according to the results of a small pilot study published in the Journal of the American Academy of Dermatology.



Patients with vitiligo of the face were recruited from the Pigmentary Disorders Clinic at The University of Texas Southwestern Medical Center (n=11, mean age, 44 years). Only patients who had not received benefit with topical corticosteroids or calcineurin-inhibitors in addition to thrice weekly NBUVB phototherapy or sunlight exposure were enrolled in the study. Treatment consisted of twice-daily 2% tofacitinib cream in addition to thrice-weekly NBUVB over a period of approximately 3 months. At 3-month follow-up, the researchers measured the amount of depigmentation in each participant with the facial Vitiligo Area Severity Index.

The mean time to follow-up was 112 (range, 84 to 154) days. There was a 70% (range, 50% to 87%) mean improvement in the facial Vitiligo Area Severity Index from baseline to 3-month follow-up (0.8 [range, 0.1 to 2.25] vs 0.23 [range, 0.03 to 0.75], respectively). The 30-g tube of tofacitinib costs $320, but because of its small application area, the medication lasted each patient an average of 90 days. No adverse effects were reported.

Study limitations included its small sample size, its use on only the face, and the lack of control groups.
“Future controlled studies with larger sample sizes and long-term follow up should be performed,” the researchers wrote. “If they are confirmatory, topical tofacitinib may become a useful addition to our therapeutic armamentarium for vitiligo.”

10 Temmuz 2019 Çarşamba

Çernobil felaketi: Küba nükleer kazadan etkilenen binlerce çocuğu nasıl tedavi etti?



"Hastanedeymişiz gibi gelmiyordu. Benden daha hasta olan çocuklar bile burada olmaktan memnundu."
Ukraynalı Roman Gerus, bir felaketle başlayan çocukluk anılarını çok iyi hatırlıyor: 26 Nisan 1986'da Çernobil nükleer santralinde bir reaktörün patlaması ile yaşanan ve popüler dizi 'Çernobil'de anlatılan felaket sonrası Gerus'un da aralarında olduğu 23 binden fazla çocuk, Küba'ya tedavi görmeye gitti.
Küba Sağlık Bakanlığı'nın sponsor olduğu tedavi programı, 1990-2011 yılları arasında devam etti.
Mayıs ayında Kübalı ve Ukraynalı yetkililer, o yıllardaki ortaklığı daha küçük çaplı da olsa devam ettirmek istediklerini duyurdu.
Küba'da tedavi gören 'Çernobil çocukları' yaşadıklarını BBC'ye anlattı:
BBC'ye konuşan Roman Gerus, Küba'ya 3 kez gittiğini söylüyor. Tedavi için ilk kez 12 yaşında gittiği ve 6 ay kaldığı Küba'ya, 14 yaşında geri dönüp 3 ay kaldığını, son olarak da 15 yaşındayken gidip 45 günü burada geçirdiğini belirtiyor.
Gerus, "Her gidişim, diğerlerinden farklıydı ama her seferinde çok keyif almıştım. O günleri sevgi ile hatırlıyorum ve aileme gösterebilmek için Küba'ya geri dönmeyi istiyorum" diyor.

Beyaz lekeler



Şimdi 27 yaşında olan Gerus, Çernobil'deki kaza olduğunda henüz doğmamıştı bile. Ancak ailesi nükleer santrale çok yakın yaşadığı için, 10 yaşlarındayken Vitiligo (akderi) hastalığı baş gösterdi.

Vücudunda beyaz noktalar çıkmaya başlayan Gerus'un ailesi onu Ukrayna'da tedavi etmeye çalıştı ama doktorlar ilaçların çok pahalı olduğunu, yardımcı olacaklarına söz veremeyeceklerini söyledi.
Annesi Küba'daki tedavi programından haberdar olduğunda, yaşamı değişti:
"Biri anneme programdan bahsetmiş. Bedava olduğunu söylediklerinde annem inanamamış. 6 aya yakın bekledikten sonra aniden bir telefon almıştık. Karşıdaki ses iki hafta için yola çıkacağımızı söylüyordu. Annem ve babam, Küba çok uzak, ben de çok genç olduğunu için kaygılıydı ama bunu yapmaya karar verdik."

25 binden fazla hasta

Gerus başkent Havana'nın 30 km doğusunda bulunan sahil kasabası Tarara'ya geldi.
Eskiden varlıklı Kübalıların rağbet ettiği Tarara'da 1959 Küba devriminden sonra çocuk ve gençler için kamplar yapılmıştı.
Mart 1990 ve Kasım 2011 tarihleri arasında ise kasaba 'Çernobil çocukları' olarak bilinen program kapsamında, felaketten etkilenen çocukların evi oldu.
Küba resmi istatistiklerine göre bu dönemde programa katılan 26 bin 114 kişiden yüzde 84'ü çocuklardı ve önemli bir bölümü Ukrayna, Rusya ve Beyaz Rusya'dan geliyordu.
Tedavi programı, Küba'nın 1990'larda baş müttefiği Sovyetler Birliği'nin dağılması ile yaşadığı zorluklar da dahil, pek çok engele rağmen ayakta kaldı.

Farklı hastalıklar


Tarara'daki bu tesiste hem çocuklar hem de refakatçilerine ayrılan evlerin yanında, iki hastane, bir klinik, okullar, parklar ve bir tiyatro salonu da vardı. Tesis, sahile de yalnızca 15 km uzaklıktaydı.



Kanserden beyin felcine, sindirim bozukluklarından psikolojik rahatsızlıklara pek çok farklı şikayetle gelen hastalar burada tedavi görüyordu.
Doktorlar Julio Medina ve Omar Garcia, programda çocukların dört gruba ayrıldığını söylüyor:
  • Hastaneye yatırılması gereken ve iyileşene kadar adada kalması gerekenler
  • Ciddi sayılmayan ama doktorların gözetimi altında olması gereken sağlık sorunları olup, 60 ve daha fazla gün kalanlar
  • Ayakta tedavi edilen ve 45 ila 60 gün kalanlar
  • Sağlığı görece daha iyi olan ve 45 ila 60 gün kalanlar



1991 ve 1992 yıllarında, 12-13 yaşlarındayken tesiste tedavi gören Ukraynalı Khrystyna Kostenetska, dördüncü gruptandı.
"İki gidişimde de 40'ar gün kaldım. Bu, alçak dozda radyasyon olan insan vücudunun iyileşmesi için gereken süreçti" diyen Kostenetska, çok ciddi sağlık sorunları olanlar ile daha iyi durumda olanlar için iki ayrı alan bulunduğunu söylüyor:
"Her birinde 15 çocuğun kaldığı küçük evlerdeydik. Bizim bulunduğumuz yerde özel bir tedavi yoktu ama göz ve diş muayeneleri oluyordu. Muhteşem denizi, gün batımını ve dondurmalarını hatırlıyorum.
"Ancak ciddi sağlık sorunları olan çocuklar da vardı. Bazılarının vitiligo deri hastalığı olduğu için güneşin altında uzun kollu giyiyorlardı. Küba'nın havası bazılarını tedavi ederken, bazılarının iyileşme sürecini hızlandırmıştı."

Güneşin altında

Roman Gerus, burada iyileşen çocuklardandı.
Küba'ya ikinci gidişinde derisindeki beyaz plakların tamamının kaybolduğunu söyleyen Gerus, "Bazı ilaçlar aldım ama güneş, en iyi ilaçtı. Çok yüzüyorduk. Sahilde olmak tedavinin bir parçasıydı. Hep gitmek istiyorduk" diyor.

Çocukların nasıl seçildiği tartışması



Bazı gazeteciler ise, Ukrayna'nın derin krizde olduğu bir dönemde yaşanan felaketten etkilenen çoğu ailenin çocuklarını tedavi için başka ülkelere gönderecek maddi durumu olmadığına dikkat çekiyor.
BBC Ukrayna Servisi'nden Diana Kuryshko da, çocukların seçilmesi sürecinin tartışmalı yanları olduğunu söylüyor:
"Küba hükümetinin programı duyurulduğunda insanlar çocuklarını oraya gönderebileceklerini düşündüler. Ancak çocuğunuzu gönderebiliyorsanız, çok şanslıydınız. Programa katılan çocukların nasıl seçildiği konusu belirsizdi. Çocukların çoğunun en mütevazi ailelerden seçildiğini söyleyemeyiz."
Buna rağmen Ukrayna'da ve diğer Sovyetler Birliği cumhuriyetlerinde programa bakış olumluydu.
Gerus, "O dönem Küba halkının durumunun ne kadar kötü olduğunu anlayabilmiştim. Yoksulluk yaygındı ama bize karşı, mutfakta çalışanlardan doktorlara kadar herkes çok nazikti" diyor.