Marys Medicine

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M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 Analysis of causes that led to the development of vitiligo in
Jeanett's case with recommendations for clinical tests and treatments
Mohammed Ali Al-Bayati, Ph.D., DABT, DABVT
Toxicologist & Pathologist Toxi-Health International 150 Bloom Drive, Dixon, CA 95620 Phone: +1 707 678 4484 Fax: +1 707 678 8505 E-mail: maalbayati@toxi-health.com Submitted: February 26, 2007
Abstract

At the age of two years, Jeanett developed vitiligo within days of receiving her first MMR vaccine and the fourth injection of DTaP and IPV vac-
cines. Furthermore, at five years of age, she developed many more unpigmented spots on her body with acrofacial vitiligo, following receipt of the
second injection of MMR and the fifth injection of DTaP and IPV vaccines. Jeanett's susceptibility to developing adverse reactions to vaccine was
notable a few hours after birth following receiving her first injection of the hepatitis B vaccine. Furthermore, the intensity and the frequency of her
adverse reactions to vaccines were significantly increased following receipt of more doses of hepatitis B, DTaP, IPV, Hib, and MMR vaccines.
Jeanett's health condition during her second year of life, when she was not given any vaccine was better than during her first year of life, when she
received several vaccines.
It is likely that the MMR vaccine induced the depigmentation of Jeanett's skin through local and systemic autoimmune reactions. Synergistic ac-
tions between the MMR vaccine and other vaccines given to Jeanett could also be involved in causing the depigmentation of her skin. I believe that
Jeanett should not receive any vaccine in the future. Vaccines probably will aggravate her present illness and trigger more illnesses. Jeanett was
treated with corticosteroids ointment but the steroid did not help in stopping the depigmentation of her skin. Recommendations for clinical tests and
treatment plans are presented in this report that I believe will help Jeanett's pediatrician to better monitor and treat her vitiligo.
Copyright 2007 Pearblossom Private School, Inc., Publishing Division. All rights reserved. Keywords: Amoxicillin; autoimmune reactions; calcipotriol; copper sulfate; corticosteroids; depigmentation; Diphtheria, Tetanus, and Pertussis (DTaP) vaccine; ad-verse reactions to vaccines; Elccon®; Hib; hepatitis; inactivated polio (IPV) vaccine; Measles, mumps, and rubella (MMR) vaccine; melanin; melanin sysnthesis; melanogenesis; tyrosinase assay; Tylenol®; vitiligo; vitix; Zithromax®.
1. Summary of the case and findings

cine was notable following receipt of her first injection of the hepatitis B vaccine, given a few hours after birth. Jeanett was Jeanett is an 8-year-old white female. She developed white born on January 22, 1999 in California and appeared healthy. unpigmented spots (vitiligo) on her skin at the age of 2 years Her birth weight was 5 pounds and 6 ounces (2.4 kg) and her and 4 months that appeared on her fingers, toes, ankles, and length was 19.5 inches (49.5 cm). knees (Figure 1). Vitiligo is pigmentary disorder characterized The medical data described in this report show that vaccines by areas of depigmented skin resulting from the loss of epider- had negative impacted on Jeanett's health. For example, her mal melanocytes or the loss of melanocytes' ability to produce health was significantly better during her second year of life melanin. Her vitiligo started within days of receiving her first without vaccine than during the first year of life, when she re- measles, mumps, and rubella (MMR) vaccine and the fourth ceived vaccines (Table 1). Furthermore, the intensity and the injection of Diphtheria, Tetanus, and Pertussis (DTaP) and inac- frequency of her adverse reactions to vaccines were signifi- tivated polio (IPV) vaccines on May 29, 2001 (Table 2). cantly increased following receipt of more doses of hepatitis B, Furthermore, Jeanett's vitiligo got worse following receipt DTaP, IPV, Hib, and MMR vaccines. Serious systemic adverse of the second injection of MMR vaccine and the fifth injections reactions to vaccine and even death have been reported in chil- of DTaP and IPV vaccines on September 1, 2004. She devel- dren. The severity of adverse reactions to vaccine is expected to oped many more unpigmented spots on her body and acrofacial be found more often in genetically susceptible children and sick vitiligo (Figures 1, 2). In addition, Jeanett's joints became swol- children. Jeanett was administered vaccines on many occasions len and she developed a limp within 10 days following vaccina- while she was sick. tion. Also, Jeanett's skin became hypersensitive to sunlight. Her In addition, local and systemic autoimmune illnesses have skin always burns and never gets tanned when exposed to also been reported in some healthy children and adults who sunlight. Jeanett was treated with corticosteroid ointment and received DTaP, polio, Hib, and MMR vaccines. These include this treatment did not help in stopping the progress of the de- arthritis; rheumatoid arthritis; myelitis; optic neuritis; multiple pigmentation of her skin. sclerosis (MS); Guillain Barre Syndrome (GBS); glomeru- The review of Jeanett's medical record revealed that lonephritis; pancytopenia/thrombocytopenia; chronic fatigue; Jeanett's susceptibility to developing adverse reactions to vac- Systemic Lupus Erythematous (SLE); and diabetis (Section 6). doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 Clinical and experimental studies have demonstrated that 2. Jeanett's adverse reactions to vaccines received during
cellular and humoral autoimmune disorders play important her first year of life
roles in the pathogenesis of vitiligo in genetically susceptible individuals. These disorders cause the loss of melanocytes Jeanett is a white female child. She was born on January 22, and/or target certain enzymes involved in melanin synthesis or 1999 in Ridgecrest Community Hospital, Ridgecrest, Califor- crucial to the survival of melanocytes (Section 7). nia. Her weight was 5 pounds and 6 ounces (2.4 kg) and her MMR vaccine contains attenuated live viruses and others length was 19.5 inches. She appeared healthy at birth. She was immunogenic substances (Table 14). Viral infections have been discharged from the hospital on January 23, 1999 and her dis- known to cause autoimmune illnesses. It is conceivable that charge weight was 5 pounds and 3 ounces (2.36 kg). Jeanett attenuated viral vaccines could induce autoimmunity in a man- was breast-fed and received an Enfamil formula. ner similar to what has been proposed to explain the viral- She was vaccinated five times during her seven months of life and she suffered from adverse reactions to vaccines. Below autoimmunity association (Section 6). are the descriptions of the adverse reactions observed in It is likely that the MMR vaccine induced the depigmenta- Jeanett's case [1]. tion of Jeanett's skin through local and systemic autoimmune reactions. Synergistic actions between the MMR vaccine and 2.1. Jeanett's adverse reactions to hepatitis B vaccine given at other vaccines given to Jeanett would also explain the depig- birth and 3 days of age mentation of her skin. Below are recommendations that I be- Jeanett received the first hepatitis B vaccine injection in the lieve will help Jeanett's pediatrician to better monitor and treat right thigh at two hours after birth and she developed jaundice her vitiligo and autoimmune condition. within a few hours. Her skin color became dark yellow-brown. Furthermore, Jeanett's jaundice got worse after receiving the 1) Blood tests previously performed in Jeanett's case listed in second hepatitis B vaccine injection three days later on January Section 5 of this report are not specific to identify the autoim- 25, 1999. Her jaundice continued for 11 days (Table 1). Fur- mune mechanisms involved in triggering the depigmentation of thermore, it was reported that Jeanett's urine had a foul smell Jeanett's skin. My review of the medical literature reveled that the following tests can be useful in identifying the specific auto- immune mechanisms involved in Jeanett's vitiligo: (a) Evaluat- 2.2. Jeanett's adverse reactions to vaccines given at two months ing cutaneous melanogenesis using tyramide-based tyrosinase assay (TTA) as described in Section 7. (b) Measuring the serum Jeanett was given inactivated polio vaccine (IPV); Haemo- levels of antibodies against tyrosinase and other components of philus influenzae type B (Hib); and Diphtheria, Tetanus, and melanocytes and performing other immunological tests that are Pertussis (DTaP) vaccines on March 26, 1999 (Table 1). She described in Section 7 of this report. developed fever over a period of three days following vaccina- tion. Her eye's crossed and she had seizures. Jeanett's urine had 2) Jeanett was treated with corticosteroid locally and systemi- a foul odor and her urine culture tested positive for bacterial cally on several occasions and these treatments were not helpful infection. Furthermore, her stool contained white puss and she in stopping the progress of her vitiligo or reducing the severity was treated with antibiotic [1]. of her illness. Clinical studies have shown treatments (applica- tion on skin) of children and adults suffering from vitiligo with 2.3. Jeanett's adverse reactions to vaccines given at about five vitix and 1,25-dihydroxyvitamin D3 (calcipotriol) were helpful months of age in inducing repigmentation of the skin. In addition, clinical Jeanett was vaccinated again with Polio, DTaP, and Hib study also showed that treatment of children suffering from vaccines on June 14, 1999 at Sage Community Clinic (Table 1). vitiligo with Aspirin orally at a daily dose of 300 mg for 12 She developed fever that lasted for a few days and a cough that weeks reduced the severity of their illness. These studies are stayed for more than two weeks. Jeanett also developed fever described in Section 7 of this report. The future use of any of (101oF or 38.3oC) and cough 2 months after receiving the vac- these medications and treatment plans in Jeanett's should be cines. She was seen by a doctor on August 17, 1999 at the done as recommended and supervised by Jeanett's physician(s). Pleasant Valley Pediatric Medical group, Camarillo California 3) My review of Jeanett's medical records revealed that the medical staffs who administered vaccines to Jeanett during her 2.4. Jeanett's adverse reactions to vaccines given at seven first five years of life did not do benefit/risk analyses prior to months of age administering vaccines to Jeanett. Her medical record clearly Jeanett was vaccinated with DTaP and Hib for the third time shows that she suffered from adverse reactions to vaccines fol- on August 23, 1999. She developed a chronic cough that lasted lowing each treatment with single vaccine or multiple vaccines. for few weeks and her cough did not clear up with the treatment In addition, the medical staffs ignored Jeanett's mother warning of the over-the-counter cough medications. She required two that vaccines are causing illness in her daughter's case. I believe emergency trips to the hospital for treatment. She also devel- that Jeanett should not be given any vaccine in the future. Vac- oped common cold on October 20, 1999. Furthermore, Jeanett cines probably will aggravate her present illness and trigger suffered from bacterial infection on December 24, 1999 and was treated with Amoxicillin syrup [1]. doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 Table 1. Vaccines given to Jeanett during the first year of her life and adverse reactions developed following vaccinations
Treatment
Jeanett's
Illness developed and symptoms
B • Jaundice (her skin color became dark yellow brown). B • Her jaundice got worse and continued for 11 days. Hepatitis B; DTaP; Hib; • Developed fever for three days, seizures, and bacterial infec- • Developed fever for a few days and chronic cough. Hib • Developed chronic cough. 1Diphtheria, Tetanus, and Pertussis (DTaP); Haemophilus influenzae type B (Hib); Inactivated polio vaccine (IPV).
3. The status of Jeanett's health during her second year of
noticeable. Her mother sought out doctors that specialized in life without vaccines
this area of treatment. Jeanett was 2 years and 4 months old. Furthermore, Jeanett was given the second injection of Jeanett did not receive any vaccine during her second year of MMR vaccine and the fifth injections of DTaP and IPV vac- life (January 1, 2000 to December 31, 2000). Her eyes regained cines on September 1, 2004 (Table 2). She was five years and 7 normal function (uncrossed) and she began to develop well. Her months old. Jeanett's vitiligo got worse and she developed body weight on December 21, 2000 was 12.5 kg. Her medical many more unpigmented spots on her body (Figure 2). She also record shows that she had only two episodes of illness between developed acrofacial vitiligo (Figure 1). In addition, Jeanett's January 1 and December 31, 2000. Her physician saw her on joints became swollen and she developed a limp within 10 days June 19, 2000 for an earache and on December 12, 2000 for a following vaccination. Furthermore, her skin became hypersen- fever and cough [1]. sitive to sunlight. Her skin always burns and never gets tanned when exposed to sunlight. She was treated with corticosteroid 4. Vaccines given and the development of vitiligo and other
ointment but it did not help in stopping the depigmentation of health problems in Jeanett's case

On May 29, 2001, Jeanett received her first measles, mumps, Furthermore, Jeanett had her first visit with a doctor at the and rubella (MMR) vaccine and the fourth injection of Diphthe- vilitigo and skin pigmentation Institute of Southern California ria, Tetanus, and Pertussis (DTaP) and inactivated polio (IPV) on December 23, 2004 and she was treated with corticosteroid vaccines. She developed vitiligo within days following receipt and vitamins. Her blood analysis of January 14, 2005 showed a of these vaccines. She was 2 years and 4 months old [1]. Fur- high level of anti-nuclear Antibody (ANA). thermore, Jeanett was injected again with MMR, DTaP, IPV 4.2. Jeanett's other health problems associated with the devel- vaccines on September 1, 2004 after which her vitiligo got oped of vitiligo worse. Jeanett developed many unpigmented spots on her body The vaccines cited in Table 2 also caused other systemic (Figures 1, 2). Below are the descriptions of Jeanett's skin le- health problems in Jeanett's case in addition to vitiligo. Table 3 sions and her other illness developed following receipt of these lists the dates that Jeanett was examined by pediatricians and Table 4 lists Jeanett's medications received during a period of
4.1. Depigmentation of Jeanett's skin following vaccinations
30 months following the receiving of her fist MMR vaccine on Jeanett had green mucous discharge from her nose and cold on May 29, 2001 and her mother took her to see her pediatri- Furthermore, Table 5 contains a list of Jeanett's medications cian. Jeanett was given the first MMR vaccine and the fourth received during a period of 20 months following receiving her injection of DTaP and IPV vaccines (Table 2). Within days of second injection of MMR vaccine. The intensity and severity of Jeanett's skin lesion and the incidence of her other systemic receiving vaccines, Jeanett developed white unpigmented spots illness were significantly increased following receipt of the sec- on her skin that appeared on her fingers, toes, ankles, and knees ond MMR vaccine as compared to receipt of her first MMR (Figure 1). The vitiligo continued to spread and became more
Table 2. List of adverse reactions including vitiligo developed following vaccinations

Treatment
Jeanett's
Reactions type and Symptoms
Developed unpigmented spots on her skin that appeared on her fingers, toes, an- kles, and knees. • Developed more unpigmented spots in her skin of her body and her face. • Her joints became swollen. She developed a limp within 10 days following vaccination. • Her skin became hypersensitive to sunlight. 1Measles, Mumps, and Rubella (MMR); Diphtheria,Tetanus Toxoids, and acellular Pertussis (DTaP); Inactivated polio vaccine (IPV). doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 Table 3. Jeanett's visits to her doctors and her symptoms
5. Clinical tests performed to monitor Jeanett's health fol-
during 30 months following her first MMR injection1
lowing the development of her vitiligo and their significance
Date Illness
developed
• Fever and cough Jeanett's skin depimentation started within days following • Fever and cough receiving her first MMR vaccine and other vaccines on May 29, • Cough and earache 2001 (Table 2). She was two years and four months old. The • Cough, fever, and vomiting following are the results of Jeanett's clinical tests performed following the development of her skin lesions until June of • Cold for 8-10 days 2006 and their significance. 5.1. Hematology tests 1Jeanett received her first MMR vaccine on 5/29/2001. The blood tests performed during the period of December 2004 and November of 2005 show that Jeanett did not suffer Table 4. Jeanett's medications received during a period of
from anemia and her platelet counts were within the normal 30 months following her first MMR vaccine1
range (Table 6). Her total white blood cell count and differential count were within the normal range (Table 7). In addition, her Date Medications CD4T cell and CD8 T cell counts performed on November of
06/04/2001 Tylenol® 2005 were within the normal range (Table 8). These data indi- 08/06/2001 Amoxicillin cate that she did not suffer from infection or have any inflam- Elocon® (0.1% cream) mation in tissues during the time of testing. 10/25/2002 Zithromax® (200 mg/5 mL syrup) Amoxicillin/Clavu (400 mg/5 mL) Table 6. Jeanett's hematology values, Dec. 2004 through
1Jeanett received her first MMR vaccine on 5/29/2001. Nov. 2005
Reference
Table 5. Some of Jeanett's medications prescribed during a
12/23/04
07/25/2005
11/30/2005
period of 20 months following her 2nd MMR vaccine1
date Medications Hemoglobin
Omnicef® (250 mg/5 mL) 12/01/2004 Zithromax® (200 mg/5 mL) Apexicon® E 0.05% cream Protopic 0.1% ointment Zithromax® (200 mg/5 mL) 322 352 406 150-400 Prednisolone (5 mg/5 mL) Augmetin (250 mg/5 mL) Trimethobenzamide (100 mg/Capsule) APAP w/codeine Elixir (120-12/5 mg) Table 7. Jeanett's white blood cell counts, Dec. 2004
through Nov. 2005
Amoxicillin (250 mg/5 mL, suspension) Reference
12/23/04
07/25/05
11/30/05
Sulfamethoxazole/Trimetho (oral suspension) 7,200 11,500 8,900 cell (cells/µL) 11/19/2005 Dexamethasone 3,744 7,418 4,886 Fluticase 50 mg nasal spray Zithromax® (200 mg/5 mL) 2,628 3,151 3,364 Vigamox® (drops) Amoxicillin (250 mg/5 mL, suspension) Amoxicillin (250 mg/5 mL, suspension) MAPAP cold medicine Promethazine (6.25 mg/5 mL) 1Jeanett received her second MMR vaccine on 09/01/2004. doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 Table 8. Jeanett's T-cell subsets counts on Nov. 30, 2005
Table 11. Jeanett's thyroid function tests performed Dec.
Reference
2004 through Jan. 2006
11/30/05
CD4 (cells/µL ) CD8 (cells/µL ) CD3 (cells/µL ) 2,126 1,220-3,000 9.3 8.7 10.2 - 5.3-11.6 5.2. Jeanett's liver, kidney, adrenal, and thyroid functions tests Free T3 (pg/mL) 4.4 Jeanett's serum and urine analyses indicate that her kidney 4.32 2.8 1.87 1.87 0.7-6.4 and liver functions were normal in the period between Decem- ber of 2004 and November of 2005 (Tables 9, 10). Furthermore, her serum cortisol, thyroid hormone, and TSH were also within the normal range (Tables 10 and 11). 5.3. Levels of trace elements and folic acid in Jeanett's blood Jeanett's blood analysis performed on November 30, 2005 Table 9. Jeanett's serum analyses performed Dec. 2004
revealed that her levels of zinc, copper, magnesium and folic through Nov. 2005
acid were within the normal range (Table 12). These elements Reference
are important for the functions of melanocyte, immune system, 12/23/04
11/30/05
and bone marrow. Alk phosphotase (IU/L) Table 12. Levels of trace elements and folic acid in Jeanett's
blood detected on Nov. 30, 2005
Total Bilirubin (mg/dL) 11/30/2005
Total protein (g/dL) Copper (µg/L) Plasma Magnesium (mg/dL) Serum Potassium (mEq/L) Folic acid (µg/L) Serum Chloride (mEq/L) 5.4. Autoimmune panel tests Table 13 contains the list of 21 clinical tests performed in Creatinine (mg/dL) December of 2004 and July and November of 2005 in Jeanett's case to detect autoimmune illness. Her results were within the normal range except for the level of the antinuclear antibody Cortisol (µg/dL) (ANA) in serum that was found slightly elevated on December Table 10. Jeanett's urine analysis performed on Oct. 30,
Table 13. Jeanett's autoimmune panel tests performed Dec.
2004 through Nov. 2005
Reference
10/30/2005
12/23/04
11/30/05
Negative Negative Specific gravity (g/mL) Anti-SCl-70 AB Negative Anti-SM AB Negative Anti-RNP AB Negative Anti-LA AB Negative Bilirubin Negative Urobilinogen (EU/dL) Nitrite Negative Amorphous crystals Ca oxalate crystals doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 Table 13. Jeanett's autoimmune panel tests performed Dec.
myelitis, 4 SLE, 100 optic neuritis, 101 GBS, 29 glomeru- 2004 through Nov. 2005 (Continued)
lonephritis, 283 pancytopenia/thrombocytopenia, and 183 MS events reported in individuals who received HBV. In addition, a 12/23/04 7/25/05 11/30/05
total of 465 positive re-challenge adverse events were observed following adult HBV that occurred sooner and with more sever- ity than initial adverse event reports. A case-report of arthritis Cardiolipin, IGG occurring in identical twins was also identified [6]. Cardiolipin, IGA Ronchi et al. also reported three cases of immune thrombo- Cardiolipin, IGM cytopenic purpura after the first dose of recombinant hepatitis B vaccine occurred in infants under 6 months of age. Antiplatelet antibodies were detected in the blood of these children. Other possible causes thrombocytopenic purpura in these children were excluded. [7]. Jeanett was also given inactivated polio (IPV); Haemophilus influenzae type B (Hib); and Diphtheria, Tetanus, and Pertussis (DTaP) vaccines at the age of two months (Table 1). She devel- oped fever over a period of three days, seizures, and her eye's crossed. Jeanett's urine had a foul odor and her urine culture tested positive for bacterial infection. Furthermore, her stool contained white puss and she was treated with antibiotic. * Circulating complement binding immune complexes In addition, Jeanett felt sick following vaccination with Po-
6. The likely causes of Jeanett's vitiligo and other health
lio, DTaP, and Hib vaccines that she received at the age of five problems
months (Table 1). She developed a fever that lasted for a few days and a cough that continued for more than two weeks. Jeanett's susceptibility to developing adverse reactions to Jeanett also developed fever (101oF or 38.3oC) and cough at vaccine appeared early in life. She suffered from adverse reac- two months after receiving these vaccines and she was seen by tions to her first injection of the hepatitis B vaccine that was a doctor on August 17, 1999. Furthermore, Jeanett was vacci- given a few hours after birth. She developed jaundice and the nated with DTaP and Hib for the third time on August 23, 1999 severity and the duration of her jaundice was significantly in- (Table 1). She developed a chronic cough that lasted for a few creased after receiving her second injection of the hepatitis B weeks and her cough did not clear up with the over-the-counter vaccine given three days later (Table 1). cough medications. She required two emergency trips to the Systemic illnesses and autoimmune disorders have been re- hospital for treatment. ported in some children who received hepatitis B vaccine. For Local and systemic reactions and autoimmune illnesses have example, the database from the 1994 National Health Interview also been reported in some children who received DTaP, Polio, Survey (NHIS) in the USA was analyzed to evaluate the vac- and Hib vaccines. For example, in the USA, reports to the Vac- cine related adverse reactions. It included 6,515 children less cine Adverse Event Reporting System (VAERS), concerning than six years of age who received the hepatitis B vaccine. infant immunization against pertussis between January 1, 1995 Hepatitis B vaccine was found to be associated with prevalent and June 30, 1998 were analyzed. During the study period, arthritis, incident of acute ear infections, and incident of there were 285 reports involving death, 971 non-fatal serious pharyngitis/nasopharangitis [2]. reports (defined as events involving initial hospitalization, pro- Furthermore, hepatitis B vaccine induced autoimmune dis- longation of hospitalization, life-threatening illness, or perma- orders at 2 to 4 weeks after vaccinations in some individuals. nent disability), and 4,514 less serious reports after immuniza- These include erythema nodosum; thrombocytopenia; myasthe- tion with any pertussis-containing vaccine [8]. nia gravis; uveitis; Reiter's syndrome; arthritis; systemic lupus Furthermore, Rennels reported that extensive local reactions erthematosus; and central nervous system demyelination [3-6]. were recognized to occur after administration of the fourth and For example, Geier and Geier examined the adverse events fifth booster doses of diphtheria-tetanus-acellular pertussis and positive re-challenge of symptoms reported in the scientific (DTaP) vaccines in children. Retrospective evaluations suggest literature and to the Vaccine Adverse Event Reporting System that entire proximal limb swelling occurs in 2 to 6% of children (VAERS) following hepatitis B vaccination (HBV) [6]. The given booster doses of DTaP vaccines. The pathogenesis of VAERS and PubMed (1966-2003) were searched for autoim- these reactions probably is multifactorial. Evidence suggests mune conditions in individuals who received HBV. These con- that both antigen content and prevaccination immunity have ditions included arthritis, rheumatoid arthritis, myelitis, optic roles [9]. Jeanett received five injections of DTaP during the neuritis, multiple sclerosis (MS), Guillain Barre syndrome first four years of her life (Tables 1, 2). (GBS), glomerulonephritis, pancytopenia/thrombocytopenia, It has been reported that children who react to the first injec- fatigue, and chronic fatigue, and Systemic Lupus Erythematous tion of a vaccine also react to the repeated injections of the (SLE). They found that HBV was associated with serious ill- same vaccine. For example, Deloria et al. examined the occur-
nesses. There were 415 arthritis, 166 rheumatoid arthritis, 130 rence of common reactions in 2127 infants within 48 hours after doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 immunization at 2, 4, and 6 months with one of 13 acellular The following is a summary of reports on the adverse events DTP (DTaP) or whole-cell DTP. Data on at least two consecu- of vaccines reported to the USA Vaccine Adverse Event Re- tive immunizations were available for 357 DTP recipients and porting System (VAERS) from Jan. 1, 1991, through Dec. 31, 1770 DTaP recipients [10]. 2001. VAERS received 128,717 reports. A total of 14.2% of all For these analyses, reactions evaluated included fever of reports described serious adverse events, which by regulatory 100.4oF (38oC) or greater, redness of 21 mm or larger, swelling definition include death, life-threatening illness, hospitalization of 21 mm or larger, moderate or severe pain, moderate or severe or prolongation of hospitalization, or permanent disability. The fussiness, loss of appetite, drowsiness, and vomiting. They most commonly reported adverse event was fever (25.8%) fol- found that reactions after a second or third immunization with lowed by injection-site hypersensitivity (15.8%), rash (11.0%), either DTP or DTaP vaccine are more likely to occur in infants injection-site edema (10.8%), and vasodilatation (10.8%) [15]. who had the same reaction after the preceding immunization Medical records indicate that Jeanett is very susceptible to developing adverse reactions to vaccine. In addition, she was In another study, 211 two-month-old infants were vaccinated administered vaccines on many occasions when she was sick with IPV and DTaP and some of them developed systemic ad- which also increased her susceptibility to vaccine injury. It has verse reactions at 24 hours post-inoculation. These included: been reported that ill children have failed to respond adequately Fever > 102.2oF (0.5%); irritability (24.6%); tiredness (31.8%); to vaccine as compared to healthy children. For example,
anorexia (8.1%); and vomiting (2.8%) [11]. Sakaguchi et al. Krober et al. examined 47 infants with colds and 51 well infants also reported eight children who had systemic urticaria within at the age of 15 to 18 months, who received the standard mea- 30 minutes after administration of acellular diphtheria-tetanus- sles-mumps-rubella (MMR) vaccine, for their response to de- pertussis (DTaP) vaccine which contain gelatin as a stabilizer velop the measles antibody. Pre-vaccination serum samples were obtained prior to vaccine administration and post- Haemophilus influenzae type B (Hib) vaccine has also been vaccination serum samples were obtained 6 to 8 weeks later. known to cause acute and chronic health problems in some chil- Measles antibody was measured in these serum samples by an dren. For example, 365 infants were inoculated with Hib, and indirect fluorescein-tagged antibody test. Ten (21%) of 47 in- some of them developed systemic adverse reactions. The fol- fants with colds failed to develop the measles antibody, while lowing adverse reactions and their percentages occurred in two- only one (2%) of 51 well infants failed to develop an antibody month-old infants during the 48 hours following inoculation: Fever > 100.8oF (0.6%); irritability (12.6%); drowsiness Jeanett developed vitiligo within days following receipt of (4.9%); diarrhea (5.2%); and vomiting (2.7%) [11]. her fist injection of the MMR vaccine and the fourth injection Also, Classen and Classen analyzed data from a Hib vaccine of DTaP and IPV vaccines on May 29, 2001 (Table 1). She was trial and identified clusters of extra cases of insulin dependent two years and four months of age. She developed white unpig- diabetes (IDDM) caused by the vaccine. IDDM occurred be- mented spots on her skin that appeared on her fingers, toes, tween 36 and 48 months post-immunization. In this study, ap- ankles, and knees (Figure 1). proximately 116,000 children in Finland were randomized to Furthermore, Jeanett was given the second injection of receive 4 doses of the Hib vaccine beginning at 3 months of age MMR and the fifth injections of DTaP and IPV vaccines on or one dose starting after 24 months of age. A control-cohort September 1, 2004 (Table 2) and her vitiligo got worse. She included all 128,500 children born in Finland in the 24 months developed many more unpigmented spots on her body (Figure prior to the Hib vaccine study. The difference in cumulative 2). She also developed acrofacial vitiligo. She was 5 years and incidence between those receiving 4 doses and those receiving 0 doses is 54 cases of IDDM/100,000 (P = 0.026) at 7- year It has been reported that MMR vaccine caused acute and (relative risk = 1.26). chronic illnesses in some children when given alone or concur- Most of the extra cases of IDDM appeared in statistically rently with other vaccines. These include malaise, sore throat, significant clusters that occurred in periods starting at approxi- cough, rhinitis, headache, dizziness, fever (101-102.9 oF), rash, mately 38 months after immunization and lasting approximately nausea, vomiting, diarrhea, fever, regional lymphadenopathy, 6 to 8 months [13]. Jeanett received three injections of Hib vac- parotitis, orchitis, nerve deafness, vasculitis, otitis media, hear- cine during her seven months of life (Table 1). ing loss, conjunctivitis, aseptic meningitis, measles, thrombocy- In a second study, distinct rises in the incidence of IDDM in topenia, allergy, and anaphylaxis [11, 18-23]. children occurred 2 to 4 years following the introduction of the MMR contains attenuated lives viruses and others immuno- MMR and pertussis vaccines [14]. Jeanett also received several genic substances (Table 14) and viral infections have known to injections of these vaccines (Tables 1 and 2). cause autoimmune illnesses. It is conceivable that attenuated Jeanett's health was significantly better during her second viral vaccines can induce autoimmunity in a manner similar to year of life without vaccine than in her first year of life, when the mechanisms proposed to explain the viral-autoimmunity she received vaccines (Table 1). Serious systemic adverse reac- association [3]. tions to vaccines and even death have been reported in children Koga et al. described a case of a child who developed bilat- who received vaccines and the severity of the adverse reactions eral acute profound deafness and aseptic meningitis within 14 is expected to be more in genetically susceptible children and days after receiving MMR vaccine. The cause of this deafness sick children [11, 15-17]. was presumed to be the mumps vaccination. The basis for the doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 presumption was as follows: The meningitis after MMR vacci- MMR vaccine has also caused allergic reactions in some nation was elicited by the Polymerase Chain Reaction (PCR) individuals because it contains gelatin and other antigens. For method to be caused by the mumps vaccine. The complication example, Nakayama et al. evaluated 366 reports of individuals of the central nervous system (CNS) after measles vaccination suffered from adverse reactions after immunization with mono- occured within 14 days after injection and the onset of vomiting valent measles, mumps, and rubella vaccines containing 0.2% and gait disturbance of the case occurred at 24 days after vacci- gelatin as stabilizer. These reports were categorized as follows: 34 with anaphylaxis, 76 with urticaria, 215 with nonurticarial Furthermore, a 7-year old girl developed unilateral total loss generalized eruption, and 41 with local reactions only. In 206 of hearing at 13 days following MMR vaccination and the live individuals from whom serum was available, IgE antibodies to attenuated mumps-virus vaccine was suspected to be the cause gelatin were detected in 25 of 27 (93%) with anaphylaxis, 27 of of the injury [19]. Stewart and Prabhum also reported six indi- 48 (56%) with urticaria, and 8 of 90 (9%) with a generalized viduals who developed hearing loss after the MMR immuniza- eruption. None of a group of 41 patients with only local reac- tion and MMR remained a possible etiology. They stated that tions at the injected site and none of a control group of 29 sub- any risk associated with attenuated viruses must be weighed jects with no adverse reaction had such antibodies [23]. against the risks of the natural diseases [20]. In addition to systemic illnesses, vaccines also induced the Cases of aseptic meningitis associated with measles, mumps, proliferation of B and T cells in the site of vaccine injection. and rubella vaccine were sought in thirteen UK health districts For example, Maubec et al. reported 9 individuals who devel- following a reported cluster in Nottingham, which suggested a oped cutaneous and subcutaneous pseudolymphoma at the site risk of 1 in 4,000 doses. Cases were ascertained by obtaining of hepatitis B (8 cases) and hepatitis A (1 case) vaccination. vaccination records of children with aseptic meningitis diag- Histopathologic studies showed dermal and hypodermal lym- nosed from cerebrospinal fluid samples submitted to Public phocytic follicular infiltrates with germinal center formation. Health Laboratories or discharged from hospital with a diagno- The center of follicles was mostly composed of B cells without sis of viral meningitis. Both methods identified vaccination 15 atypia, whereas CD4+ T cells were predominant at the periph- to 35 days before onset as a significant risk factor and therefore indicative of a causal association. With both, half the aseptic Molecular analysis of clonality revealed a polyclonal pattern meningitis cases identified in children aged 12 to 24 months of B-cell and T-cell subsets. Aluminium deposits were evi- were vaccine-associated with onset 15 to 35 days after vaccine. denced in all cases by using histochemical staining in all cases, This study confirmed that the true risk was substantially higher and by microanalysis and ultrastructural studies in one case. than suggested by case reports from pediatricians, probably Associated manifestations were vitiligo (1 case) and chronic about 1 in 11,000 doses [21]. fatigue with myalgia (2 cases) [24]. Furthermore, in Japan, at least 311 meningitis cases sus- It is likely that the MMR vaccines induced the depigmenta- pected to be vaccine-related were identified among 630,157 tion of Jeanett's skin through local and systemic autoimmune recipients of the measles-mumps-rubella trivalent (MMR) vac- reactions. Synergistic actions between the DTaP, IPV, and the cine. These cases were identified based on the notification of MMR vaccines in causing the depigmentation of Jeanett's skin cases and the testing of mumps viruses isolated from cerebro- are also possible. The roles of autoimmune disorders in the spinal fluid for their relatedness to the vaccine by nucleotide pathogenesis of vitiligo are described in section 7 of this report. sequence analysis [22].
Table 14. Some of the immunogenic ingredients, preservatives, and additives reported in vaccines administered to Jeanett [11]

Vaccine type
Composition
Each 0.5 mL dose contains 0.25 mg aluminum; 10 μg of hepatitis B antigen; 4.5 mg sodium chloride; 0.49
mg disodium phosphate dihydrate; and 0.35 mg sodium dihydrogen phosphate dihydrate.
Each dose (0.5 mL) contains 0.625 mg aluminum; 25 Lf Diphtheria toxoid; 10 Lf tetanus toxoid; 25μg Diphtheria,Tetanus pertussis toxin; 25 μg filamentous hemagglutinin; 8 μg pertacin; 2.5 mg 2-phenoxyethanol; 4.5 mg sodium Toxoids, and acellu- chloride; and 0.1 mg formaldehyde. lar Pertussis (DTaP) Each 0.5 mL dose contains 40 D antigen units of type 1, 8 D antigen units of type 2, and 32 D antigen units Inactivated polio vac- of type 3 poliovirus. Also present are 0.5% of 2-phenoxyethanol and 0.02% of formaldehyde (preserva- tives), 5 ng neomycin, 200 ng streptomycin, and 25 ng polymyxin.
Haemophilus Influ- Each 0.5 mL dose contains (0.4% sodium chloride) contains 10 μg of purified Haemophilus capsular poly- Each 0.5 mL contains no less than the equivalent of 1,000 TCID Measles, Mumps, and 50 (tissue culture infectious doses) of the U.S. Reference Measles live virus; 20,000 TCID 50 Mumps live virus; and 1,000 TCID50 of the U.S. Refer- ence Rubella live virus. The 3 live viruses are mixed before being lyophilized. It also contains additives. doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 7. Causes and pathogeneses of vitiligo reported in some
Machado et al. conducted a study to evaluate the trosinase cases published in the literature
mRNA presence in normal skin and vitiligo areas. Tyrosinase mRNA was negative in 93.75% of vitiligo areas [28]. Kitamura Vitiligo is pigmentary disorder characterized by areas of et al. have compared the expression of endothelin (ET)-1, the depigmented skin resulting from the loss of epidermal melano- ET-1 receptor (ET(B)R), granulocyte macrophage colony cytes or the loss of melanocyte's ability to produce melanin. stimulating factor (GM-CSF), stem cell factor (SCF), the SCF Recent studies have indicated that vitiligo areas contain inactive receptor (KIT protein), tyrosinase, and S100 alpha between or dormant melanocytes [25-28]. lesional and non-lesional vitiligo epidermis [34]. They reported In human skin, melanin is produced by melanocytes and the following changes in vitiligo epidermis that may be associ- transferred to epithelial cells. Melanin formation requires the ated with the dysfunction and/or loss of melanocytes: enzyme tyrosinase, which catalyzes multiple reactions in the melanin biosynthetic pathway. Han et al. reassess cutaneous 1) Analysis by reverse transcription-polymerase chain reaction melanogenesis using tyramide-based tyrosinase assay (TTA). In (RT-PCR) and by western blotting for ET-1 and SCF demon- the TTA procedure, tyrosinase reacts with biotinyl tyramide, strated up-regulated expression of these cytokines in lesional causing the substrate to deposit near the enzyme. These bioti- vitiligo epidermis. nylated deposits are then visualized with streptavidin conju- 2) Immunohistochemistry with antibodies to melanocyte mark- gated to a fluorescent dye [29]. ers revealed that at the edge of the lesional epidermis, melano- In the skin and eye, TTA was highly specific for tyrosinase cytes remain and express tyrosinase, S100 alpha and ET(B)R, and served as a sensitive indicator of pigment cell distribution but not KIT protein or melanocyte-specific microphthalmia- and status. In clinical skin samples, the assay detected pigment associated transcription factor (MITF-M). Quantitation of the cell defects, such as melanocytic nevi and vitiligo, providing staining revealed a slight or moderate decrease in the number of confirmation of medical diagnoses [29]. Below are descriptions S100 alpha, tyrosinase, and ET(B)R-positive cells at the edge of of some of the causes and mechanisms reported in the literature the lesional epidermis. In contrast, the number of cells express- in people suffering from vitiligo. ing KIT protein was markedly decreased at the edge of the le- sional epidermis compared with the non-lesional epidermis. At 7.1. Evidence of autoimmune disorders causing vitiligo the center of the lesional epidermis, there was complete loss of Clinical and experimental studies have demonstrated that melanocytes expressing KIT protein, S100 alpha, ET(B)R, cellular and humoral autoimmune disorders play important and/or tyrosinase. roles in the pathogenesis of vitiligo in genetically susceptible individuals. These disorders cause the loss of melanocytes 3) Western blotting revealed down-regulated expression of c-kit and/or target certain enzymes involved in melanin synthesis or and MITF-M proteins at the edge of the lesional epidermis in crucial to the survival of melanocytes. For example, Lucchese et al. provided evidence for the pres- ence of humoral immune responses against tyrosinase in the Zailaie found that low-dose oral aspirin treatment of active sera of individuals suffering from vitiligo. They analyzed the vitiligo patients caused significant reduction in the acute serum sera from individuals with vitiligo for reactivity toward tyrosi- immunologic markers of T cell activation, V-IgG activity and nase peptide sequences and detected five autoantigen peptides sIL-2R concentration with concomitant arrest of disease activity that have anti-tyrosinase response [30]. Okamoto et al. also demonstrated that individuals with In this study, 18 female and 14 male individuals with a re- vitiligo had significant anti- tyrosinase-related protein-2 (TRP- cent onset of non-segmental vitiligo were divided into 2 equal 2) IgG titers in their serum. TRP-2 is highly expressed in groups. One group received a daily single dose of oral aspirin melanocytes [31]. In addition, the serum levels of certain im- (300 mg) and the second group received only placebo for a pe- munologic markers including immunoglobulin G (IgG) anti- riod of 12 weeks. melanocyte, vitiligo antibodies (V-IgG), and soluble inter- Serum V-IgG activity and sIL-2R concentration were deter- leukin-2 receptors (sIL-2R) were increased in individual suffer- mined before and at the end of treatment period. The V-IgG ing from vitiligo. These changes are associated with augmented activity was measured using cellular enzyme-linked immu- humoral and cellular immunity involved in melanocyte cytotox- nosorbent assay (ELISA) following incubation of IgG antibod- icity during the active phase of non-segmental vitiligo [32]. ies with an adult cultured melanocytes. Serum sIL-2R concen- Furthermore, Mandelcorn-Monson et al. evaluated T cell tration was measured using the highly sensitive quantitative reactivity to MelanA/MART-1, tyrosinase, and gp100, in HLA- sandwich ELISA utilizing a commercially available kit. A2-positive individuals with vitiligo. Antigen-specific T lym- The serum V-IgG activity and sIL-2R concentration of the phocyte reactivity to gp100 peptides was seen in 15 of 17 active vitiligo patients (0.81 +/- 0.23 optical density (O.D.), (88%) individuals. These findings implicate T cell reactivity to 1428 +/- 510 pg/ml) were significantly increased compared gp100 in individuals with active disease. They support the con- with that of controls (0.27 +/- 0.1 O.D., 846 +/- 312 pg/ml; cept of an immunopathologic mechanism in vitiligo, in which p<0.05, p<0.01). Aspirin-treated vitiligo patients showed sig- cell-mediated responses to normal melanocyte antigens play a nificant decrease in serum V-IgG activity and sIL-2R concen- crucial part [33]. Palermo et al. also reported the presence of
tration (0.32 +/- 0.08 O.D., 756 +/- 216 pg/ml) compared with cytotoxic T lymphocytes directed to melanocyte antigens in that of placebo-treated patients (0.83 +/- 0.19 O.D., 1327 +/- vitiligo patients [26]. 392 pg/ml; p<0.01) [32]. doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 7.2. Exposure of individuals to certain chemicals and oxidative improvement on the calcipotriol side compared to 30 percent on stress caused vitiligo the PUVA-only side (p = 0.13), with more intense repigmenta- Boissy and Manga reported that the exposure of individuals tion on calcipotriol-treated areas. Treatment was well tolerated, to phenolic/catecholic derivatives at workplace has caused and no adverse effect was noted [36]. vitiligo in some individuals. Phenolic/catecholic derivatives are Furthermore, Watabe et al. studied the effects of 1,25- structurally similar to the melanin precursor tyrosine and are dihydroxyvitamin D3 on the differentiation of immature preferentially cytotoxic to melanocytes, with high-dose expo- melanocyte precursors using the NCC-/melb4 cell line which is sure resulting in the initiation of apoptosis [27]. an immature melanocyte cell line established from mouse neu- They suggested that tyrosinase-related protein-1 facilitates ral crest cells. They found that 1,25-Dihydroxyvitamin D3 in- toxicity possibly by catalytic conversion of the compounds, hibited the growth of NCC-/melb4 cells and the growth inhibi- which results in the generation of radical oxygen species. The tion was accompanied by the induction of tyrosinase and a ensuing oxidative stress then triggers activation of cellular free change in L-3,4-dihydroxyphenylalanine reactivity from nega- radical scavenging pathways to prevent cell death. Genetic in- tive to positive. In primary cultures of murine neural crest cells, ability of melanocytes to tolerate and/or respond to the oxida- L-3,4-dihydroxyphenylalanine-positive cells were increased tive stress may underlie the etiology of contact/occupational after 1,25-dihydroxyvitamin D3 treatment. These findings indi- cate that 1,25-dihydroxyvitamin D3 stimulates the differentia- Furthermore, a number of experiments showed that kerati- tion of immature melanocyte precursors [37]. nocytes derived from vitiligo lesions produce increased number In this study, electron microscopy also demonstrated that of superoxide anions (hyperactive oxygen and nitric oxide). melanosomes were in more advanced stages after 1,25- Tsiskarishvili studied the effectiveness of complex treatment dihydroxyvitamin D3 treatment. Moreover, immunostaining with cuprum sulfate and vitix in children with vitiligo. Melanin and reverse transcription-polymerase chain reaction analysis is formed from tyrosine by enzyme tyrosinase and cuprum is a revealed that endothelin B receptor expression was induced in cofactor of this photochemical process. A total of 27 children 7- NCC-/melb4 cells following treatment with 1,25- 17 years old with vitiligo (15 boys and 12 girls) were included dihydroxyvitamin D3. The induction of endothelin B receptor in this study and the duration of illness varied from 1 month to by 1,25-dihydroxyvitamin D3 was also demonstrated in neural crest cell primary cultures, but not in mature melanocytes. Preparation vitix was applied directly to the lesions and sur- These findings suggest a regulatory role for vitamin D3 in rounded affected area. Duration of the treatment was 6 months. melanocyte development and melanogenesis, and may also ex- Restoration of pigmentation was observed by the following plain the working mechanism of vitamin D3 in the treatment of patterns: diffuse in 9, follicular in 5 and peripheral in 3 cases. Improvement of clinical condition was observed in 56% of pa- tients. Erythema with mild itching and erythema with peeling 7.4. Zinc deficiency can cause vitiligo were observed as the side effects. Due to the ability to re- Bruske and Salfeld reported significant low blood-levels of establish the free radicals physiological equilibrium in epider- zinc in individuals suffering from vitiligo as compared to mal cells (melanocytes and keratinocytes) vitix shows princi- healthy individuals and individuals suffered from other skin pally new impact on skin with depigmentation. The effect of problems. Their study included data on serum zinc levels of 380 this preparation is based on melon's extract rich in antioxidants individuals with alopecia areata, alopecia androgenetica, psoria- sis vulgaris, vitiligo, rosacea, venous ulcer and atopic eczema. In addition, data on zinc levels from 31 healthy people were 7.3. Treatment with vitamin D3 helped in repigmentation of also included [38]. skin in vitiligo cases It has been reported that 1,25-dihydroxyvitamin D3 and the 8. Conclusions and recommendations
vitamin D3 analog calcipotriol play important role in the matu- ration of the immature melanocytes and treatment with vitamin The medical evidence described in this report clearly indi- D helped individuals with vitiligo to regain pigmentation of cates that vaccines are the likely cause of vitiligo in Jeanett's their skin. Cherif et al. performed a prospective study including case and her illness probably resulted from autoimmune disor- twenty-three individuals with essentially bilateral symmetrical der. Jeanett's susceptibility to developing adverse reaction to lesions of vitiligo to evaluate efficacy of the combination of vaccine was notable following receiving her first injection of calcipotriol and psoralen plus ultraviolet A (PUVA) in the hepatitis B vaccine given after birth. Furthermore, the intensity treatment of vitiligo. Calcipotriol (0.005 %) ointment was ap- of her adverse reactions to the hepatitis B, DTaP, Polio, and Hib plied twice daily over the right side of the body, and the other vaccines increased following receiving more doses of these side was not treated. PUVA was performed three times per vaccines. In addition, the intensity and severity of Jeanett's skin week and all individuals received at least forty-five sessions of lesions and the incidence of her other systemic illness were sig- nificantly increased following receiving the second injection of Individuals were evaluated clinically and photographed all MMR vaccine as compared to receiving her first MMR injec- fifteen weeks. At the fifteenth session, 69 percent of the indi- viduals had minimal to moderate improvement on the cal- My review of Jeanett's medical records revealed that the cipotriol side compared to 52 percent on the PUVA-only side (p medical professionals who administered vaccines to Jeanett = 0.015). At the forty-fifth session, 52 percent showed marked during her first five years of life did not do benefit/risk analyses doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 prior to administering vaccines to Jeanett. Her medical records reactions after consecutive acellular or whole-cell pertussis vaccine im- clearly show that she suffered from adverse reactions to vac- munizations. Pediatrics 1995;96(3 Pt. 2):592–4. [11] Physicians' Desk Reference, 53rd ed., 1999. Medical Economics Com- cines following each treatment with single vaccine or multiple pany, Inc, Montavale, NJ, USA. vaccines. In addition, the medical staffs ignored Jeanett's [12] Sakaguchi M, Nakayama T, Inouye S. Cases of systemic immediate-type mother warning that vaccines are causing illness in her daugh- urticaria associated with acellular diphtheria-tetanus-pertussis vaccination. ter's case. In my opinion, Jeanett should not be given any vac- Vaccine. 1998 Jul.;16(11-12):1138–40. [13] Classen JB, Classen DC. Clustering of cases of insulin dependent diabetes cine in future. Vaccine(s) probably will aggravate her present (IDDM) occurring three years after haemophilus influenza B (HiB) im- illness and trigger more illnesses. munization support causal relationship between immunization and IDDM. It seems that the blood tests previously performed in Autoimmunity 2002;35(4):247–53. Jeanett's case (Section 5) are not specific to identify the auto- [14] Classen JB, Classen DC. Clustering of cases of type 1 diabetes mellitus occurring 2-4 years after vaccination is consistent with clustering after in- immune mechanisms involved in triggering the depigmentation fections and progression to type 1 diabetes mellitus in autoantibody posi- of Jeanett's skin. My review of the medical literature reveled tive individuals. J Pediatr Endocrinol Metab. 2003;16(4):495–508. that the following tests may be useful in identifying the specific [15] Zhou W, Pool V, Iskander JK, English-Bullard R, Ball R, Wise RP, Haber autoimmune mechanisms involved in Jeanett's vitiligo: (1) P, Pless RP, Mootrey G, Ellenberg SS, Braun MM, and Chen RT. Surveil-lance for safety after immunization: Vaccine Adverse Event Reporting Evaluating cutaneous melanogenesis using tyramide-based ty- System (VAERS)--United States, 1991-2001. MMWR Surveill Summ. rosinase assay (TTA) as described by Han et al. 2002 (Section 2003;52(1):1–24. 7). (2) Measuring the serum levels of antibodies against tyrosi- [16] Al-Bayati MA. Analysis of causes that led to Toddler Alexa Shearer's nase and other components of melanocytes and performing cardiac arrest and death in November 1999. Medical Veritas 2004 Apr.; 1(1): 86–117. other immunological tests that are described in Section 7 of this [17] Krober MS, Stracener CE, Bass JW. Decreased measles antibody response after measles-mumps-rubella vaccine in infants with colds. JAMA 1991; Jeanett was treated with corticosteroids locally and systemi- 265(16):2095–6. cally on several occasions and these treatments were not helpful [18] Koga K, Kawashiro N, Araki A, Watanabe M. Bilateral acute profound deafness after MMR vaccination--report of a case. Nippon Jibiinkoka in reducing the severity of her vitiligo. Clinical studies have Gakkai Kaiho 1991; 94(8):1142–5. shown treatment of children and adults suffering from vitiligo [19] Nabe-Nielsen J, Walter B. Unilateral total deafness as a complication of with vitix or 1,25-dihydroxyvitamin D3 (calcipotriol) were the measles- mumps-rubella vaccination. Scand Audiol Suppl 1988; helpful in inducing repigmentation of the skin. Clinical study [20] Stewart BJ, Prabhu PU. Reports of sensorineural deafness after measles, also showed that treating children suffering from vitiligo with mumps, and rubella immunisation. Arch Dis Child 1993;69(1):153–4. Aspirin orally at a daily dose of 300 mg for 12 weeks reduced [21] Miller E, Goldacre M, Pugh S, Colville A, Farrington P, Flower A, et al. the severity of their illness. These studies are described in Sec- Risk of aseptic meningitis after measles, mumps, and rubella vaccine in tion 7 of this report. In my opinion implementing these treat- UK children. Lancet 1993;341(8851):979–82. [22] Sugiura A, Yamada A. Aseptic meningitis as a complication of mumps ments or some of them under medical supervision could be vaccination. Pediatr Infect Dis J. 1991;10(3):209–13. helpful to inducing skin repigmentation in Jeanett case and re- [23] Nakayama T, Aizawa C, Kuno-Sakai H. A clinical analysis of gelatin ducing the severity of her illness. allergy and determination of its causal relationship to the previous admini- stration of gelatin-containing acellular pertussis vaccine combined with diphtheria and tetanus toxoids. J Allergy Clin Immunol. 1999;103(2 Pt. References
[24] Maubec E, Pinquier L, Viguier M, Caux F, Amsler E, Aractingi S, Chafi [1] Jeanett's medical records from January of 1999 to January of 2006. H, Janin A, Cayuela JM, Dubertret L, Authier FJ, Bachelez H. Vaccina- [2] Fisher MA, Eklund SA, James SA, and Lin X. Adverse Events Associated tion-induced cutaneous pseudolymphoma. J Am Acad Dermatol. 2005 with Hepatitis B Vaccine in U.S. Children less than six years of age, 1993 Apr.;52(4):623–9. and 1994. AEP 2001;11(1):13–21. [25] Zhang XJ, Chen JJ, Liu JB. The genetic concept of vitiligo. J Dermatol [3] Cohen AD, Shoenfeld Y. Vaccine-induced autoimmunity. J Autoimmun. Sci. 2005 Sep.;39(3):137–46. 1996 Dec.;9(6):699–703. [26] Palermo B, Garbelli S, Mantovani S, Scoccia E, Da Prada GA, Bernabei [4] Meyboom RHB, Fucik H, Edwards IR. Thrombocytopenia reported in P, et al. Qualitative difference between the cytotoxic T lymphocyte re- association with hepatitis B and A vaccines. The Lancet 1995 Jun. 24; sponses to melanocyte antigens in melanoma and vitiligo. Eur J Immunol. 2005 Nov.;35(11):3153–62. [5] Herroelen L, DeKeyser J, Ebinger G. Central-nervous-system demyelina- [27] Boissy RE, Manga P. On the etiology of contact/occupational vitiligo. tion after immunization with recombinant hepatitis B vaccine. The Lancet Pigment Cell Res. 2004 Jun.;17(3):208–14. 1991 Nov. 9;338:1174–5. [28] Machado Filho CD, Almeida FA, Proto RS, Landman G. Vitiligo: analy- [6] Geier MR, Geier DA. A case-series of adverse events, positive re- sis of grafting versus curettage alone, using melanocyte morphology and challenge of symptoms, and events in identical twins following hepatitis B reverse transcriptase polymerase chain reaction for tyrosinase mRNA. Sao vaccination: analysis of the Vaccine Adverse Event Reporting System Paulo Med J. 2005 Jul. 7;123(4):187–91. (VAERS) database and literature review. Clin Exp Rheumatol. [29] Han R, Baden HP, Brissette JL, Weiner L. Redefining the skin's pigmen- 2004;22(6):749–55. tary system with a novel tyrosinase assay. Pigment Cell Res. 2002 [7] Ronchi F, Cecchi P, Falcioni F, Marsciani A, Minak G, Muratori G, Taz- Aug.;15(4):290–7. zari PL, Beverini S. Thrombocytopenic purpura as adverse reaction to re- [30] Lucchese A, Willers J, Mittelman A, Kanduc D, Dummer R. Proteomic combinant hepatitis B vaccine. Arch Dis Child. 1998 Mar.;78(3):273–4. scan for tyrosinase peptide antigenic pattern in vitiligo and melanoma: [8] Braun MM, Mootrey GT, Salive ME, Chen RT, Ellenberg SS. Infant role of sequence similarity and HLA-DR1 affinity. J Immunol. 2005 Nov. immunization with acellular pertussis vaccines in the United States: as- 15;175(10):7009–20. sessment of the first two years' data from the Vaccine Adverse Event Re- [31] Okamoto T, Irie RF, Fujii S, Huang SK, Nizze AJ, Morton DL, Hoon DS. porting System (VAERS). Pediatrics 2000;106(4):E51. Anti-tyrosinase-related protein-2 immune response in vitiligo patients and [9] Rennels MB. Extensive swelling reactions occurring after booster doses of melanoma patients receiving active-specific immunotherapy. J Invest Der-
diphtheria-tetanus-acellular pertussis vaccines. Semin Pediatr Infect Dis. matol. 1998 Dec.;111(6):1034–9. 2003;14(3):196–8. [32] Zailaie MZ. Aspirin reduces serum anti-melanocyte antibodies and soluble [10] Deloria MA, Blackwelder WC, Decker MD, Englund JA, Steinhoff MC, interleukin-2 receptors in vitiligo patients. Saudi Med J. 2005 Jul.; Pichichero ME, Rennels MB, Anderson EL, Edwards KM. Association of 26(7):1085–91. doi: 10.1588/medver.2007.04.00142 M.A. Al-Bayati/Medical Veritas 4 (2007) 1251–1262 [33] Mandelcorn-Monson RL, Shear NH, Yau E, Sambhara S, Barber BH, [36] Cherif F, Azaiz MI, Ben Hamida A , Ben Osman Dhari A. Calcipotriol Spaner D, DeBenedette MA. Cytotoxic T lymphocyte reactivity to gp100, and PUVA as treatment for vitiligo Dermatology Online Journal MelanA/MART-1, and tyrosinase, in HLA-A2-positive vitiligo patients. J Invest Dermatol. 2003 Sep.;121(3):550–6. [37] Watabe H, Soma Y, Kawa Y, Ito M, Ooka S, Ohsumi K, Baba T, Kawa- [34] Kitamura R, Tsukamoto K, Harada K, Shimizu A, Shimada S, Kobayashi kami T, Hosaka E, Kimura S, Mizoguchi M. Differentiation of murine T, Imokawa G. Mechanisms underlying the dysfunction of melanocytes in melanocyte precursors induced by 1,25-dihydroxyvitamin D3 is associ- vitiligo epidermis: role of SCF/KIT protein interactions and the down- ated with the stimulation of endothelin B receptor expression. J Invest stream effector, MITF- M. J Pathol. 2004 Apr.;202(4):463–75. Dermatol. 2002 Sep.;119(3):583–9. [35] Tsiskarishvili N. Cuprum sulfate and vitix in the treatment of vitiligo in [38] Bruske K, Salfeld K. Zinc and its status in some dermatologic diseases--a children. Georgian Med News. 2005 Apr.;(121):48-51. statistical assessment. Hautklinik Klinikum Minden. Z Hautkr. 1987; 62(Suppl 1):125–31. Figure 2. Back view of vitiligo on legs
Figure 1. Front view of vitiligo on legs and hands
doi: 10.1588/medver.2007.04.00142

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Thursday 25 June 2009 Experts urge caution over Tamiflu Debate rages over possible side-effects in teens as health authorities dole out drug as a precaution against pandemic flu Experts meeting in Geneva this week are set to issue World Health Organization (WHO) advisory guidelines for the use ofantiviral drugs in the 2009 flu pandemic. The discussions coincide with the publication of new information about the safety ofthe antiviral drug Tamiflu in teenage children. The fresh analysis1 of an old dataset from Japan, published online this monthby Takashi Yorifuji and colleagues, reignites the dispute over whether the medication can lead some children to behaveabnormally.Japan is the largest consumer of Tamiflu in the world. Prior to the 2009 pandemic, the country consumed 75% of the drug'sglobal supply.

Marine ecology progress series 530:119

Vol. 530: 119–134, 2015 MARINE ECOLOGY PROGRESS SERIES Published June 18 doi: 10.3354/meps11266 Mar Ecol Prog Ser Habitat and trophic ecology of Southern Ocean cephalopods from stable isotope analyses Miguel Guerreiro1,*, Richard A. Phillips2, Yves Cherel3, Filipe R. Ceia1, Pedro Alvito1, Rui Rosa4, José C. Xavier1,2