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Interstate 77 in North Carolina
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This article is about the section of Interstate 77 in North Carolina. For the entire route, see Interstate 77.
Interstate 77
Route information
Maintained by NCDOT
Length
105.7 mi[1][2] (170.1 km)
Existed
1965 – present
Major junctions
South end
I-77 / US 21 at the SC line near Fort Mill, SC
I‑485 in Charlotte (twice)
I‑85 in Charlotte
I‑40 in Statesville
I‑74 near Mount Airy
North end
I-77 at the VA line near Mount Airy
Location
Counties
Mecklenburg, Iredell, Yadkin, Surry
Highway system
Interstate Highway System
Main
Auxiliary
Suffixed
Business
Future
North Carolina Highway System
Interstate
U.S.
State
Scenic
← US 76 NC 78 →
In the U.S. state of North Carolina, Interstate 77 (I-77) is a 105.7-mile (170.1 km) Interstate Highway, which serves the city of Charlotte and the Western Piedmont. It is part of a highway that goes from Columbia, South Carolina in the south to Cleveland, Ohio in the North, serving as a major link between the Midwest and South Atlantic regions of the U.S.
Contents
[hide]
1 Route description
1.1 HOV lanes
1.2 Dedicated and memorial names
2 History
3 Future
4 Auxiliary routes in North Carolina
5 Exit list
6 See also
7 References
8 External links
Route description[edit]
Virginia-North Carolina state line on I-77
Interstate 77 begins at the South Carolina state line, near Fort Mill, in concurrency with US 21. I-77 goes through the city of Charlotte as a major north–south corridor, connecting the Center City with the suburbs of Pineville, Huntersville, Cornelius, and Davidson. Shortly after entering North Carolina, it expands to six lanes. Between I-485 (exit 2) and I-277 (exit 9), the highway experiences massive traffic congestion during weekday rush hours (7:00-9:30 a.m./4:00-6:30 p.m.) due to commuter traffic. Just north of Center City, I-77 makes a unique interchange configuration with Interstate 85, with north and southbound lanes crisscrossing briefly. Between I-85 (exit 13) and I-485 (exit 19), I-77 features the state's only HOV lanes. After I-485, I-77 reduces to five lanes (three lanes northbound), then to four lanes after Gilead Road (exit 23).
At Lake Norman, I-77 crosses into Iredell County and becomes a more suburban interstate, passing by Mooresville and then Statesville, where it intersects with Interstate 40. It turns more rural outside of Statesville and becomes entirely rural after exiting Iredell County. For the rest of I-77's stretch through North Carolina, the only possible rest stop is the town of Elkin; the speed limit through this area is 70 mph (110 km/h). The final 5 miles (8.0 km) of I-77 is concurrent with Interstate 74 to the Virginia state line (where I-74 ends), all within view of the Blue Ridge Mountains.[1]
HOV lanes[edit]
Interstate 77 has the first and only High occupancy vehicle (HOV) lanes in North Carolina, located in Mecklenburg County.[3] Opened since December 2004, they are enforced 24 hours a day, seven days a week and are closed for general traffic unless otherwise posted. They are identified by a "diamond" symbol and overhead signs and are located on the leftmost lanes. Vehicles with two or more occupants can use the HOV lanes. Emergency vehicles when responding to emergencies, mass transit vehicles, privately owned buses, and motorcycles may also use the lanes. Violators are subject to a fine of up to $100 plus court costs; as well as two points against their driver's licenses for each HOV infraction.[3] In 2015, construction began on converting the existing HOV lanes into variable tolling lanes, to be completed in 2018.
Northbound
The northbound HOV lane begins north of I-85 interchange (exit 13) and ends north of the W.T. Harris Boulevard interchange (exit 18).[3]
Southbound
The southbound HOV lane begins south of the W.T. Harris Boulevard interchange (exit 18) ends south of the exit ramp for I-277 (exit 11) and features a bypass of the I-85 interchange.[3]
Dedicated and memorial names[edit]
I-77 in North Carolina feature a few dedicated or memorialized stretches of freeway.
Blue Star Memorial Highway – unofficial North Carolina honorary name of Interstate 77 throughout the state.[4]
Bill Lee Freeway – official North Carolina name of Interstate 77 from Woodlawn Road to the Mecklenburg-Iredell county line, named for William States Lee III (approved on 5 September 1996).[5]
Charles M. Shelton Highway – official North Carolina name of Interstate 77 in Surry County (approved on 7 April 2000).[5]
General Paul R. Younts Expressway – official North Carolina name of Interstate 77 from the South Carolina state line to Woodlawn Road, in Mecklenburg County (approved on 24 June 1965).[5][6]
History[edit]
I-74 & I-77 near Pine Ridge
Iredell County Rest Area
Interstate 77 was not part of the original plans for 714 miles (1,149 km) of the nation's Interstate Highway System in North Carolina when they were conveyed in 1956 by the then-North Carolina State Highway Commission. I-77 was added in 1957, increasing the state's mileage to 776 miles (1,249 km).[7]
On 4 August 1959, the commission selected the routing of I-77 to run between Interstate 85 in Charlotte and a point on the Virginia border in Elkin. That would change in late 1960, when the commission voted to route the highway just west of Mount Airy, saying the route would serve the most people.
With construction beginning in the 1960s, I-77 would gain additional mileage in October 1964 when a two-mile (3 km) extension was granted by the U.S. Bureau of Public Roads. Instead of ending at I-85, I-77 now ended at Independence Boulevard (U.S. 74) in downtown Charlotte. Another extension was granted in the late 1960s that extended I-77 from Independence Boulevard to the South Carolina border. The latest extension also included a relocation of U.S. 21 from the city's surface streets to the new interstate.
I-77 opened to traffic in the following segments:
1965: Yadkin and Surry counties.
1966: A 23-mile (37 km) stretch in Iredell County.
1967: Stretches in Mecklenburg, Yadkin and Iredell counties.
1968: A stretch of highway in the Davidson and Cornelius areas in Mecklenburg and Iredell counties.
By 1972, I-77 was open from Exit 28 (NC 73) to Exit 73 north of Elkin. The last two sections of the highway to open to traffic was the stretch from Cornelius to Charlotte in 1975 and from Exit 73 to the Virginia state line in 1977.
In April 2001, I-74 was overlapped with I-77 from the Virginia state line to exit 101.[8]
On December 17, 2004, I-77 was widened to six-lanes with HOV lanes, between I-85 to the proposed location of I-485 (later opened 8 December 2008).[3]
On June 28, 2013, a new interchange was added in Mooresville, exit 35: Brawley School Road. The interchange was built with additional shoulder space and lights that will not need to be moved when I-77 is eventually widened in area.[9]
In 2015, NCDOT signed a contract with I-77 Mobility Partners to begin construction and eventual management of the toll lanes starting in 2018.[10] However, new criticism erupted before the financial agreement was made when local politicians discovered the contract was amended in 2014 giving I-77 Mobility Partners a 50-year non-compete clause. The clause eliminated any future widening of additional free-lanes between Charlotte Center City and Mooresville; or if any additional free-lanes were added, then NCDOT would have to pay the developer compensation.[11][12]
On February 1, 2018, NCDOT opened a new rest area located in the median of I-77, at mile marker 58. Construction of the 5,000 square feet (460 m2), $15 million facility started in the spring of 2015. With the opening of the facility, four older rest areas in Iredell and Yadkin counties, built in 1972-73, were closed.[13]
Future[edit]
Woodlawn Road & Billy Graham Parkway overhead sign
Interstate 77 is planned to have its existing southbound travel lanes widened (not add more lanes), between I-277/NC 16 (Brookshire Freeway) to I-85 in Charlotte. Estimated to cost $16.5 Million, the purpose of the project is to widen the lanes back to proper Interstate standards as agreed with FHWA, when NCDOT were given design exceptions when adding the HOV lanes in 2004. Construction is tentatively scheduled to begin in late 2016.[14]
As of June 2016, HOT lanes are being constructing along Interstate 77. The project is broken into two parts: the first is constructing new travel lanes from I-485 interchange (exit 19) to West Catawba Avenue (exit 28), at an estimated cost of $57 million. The second would be to convert the existing HOV lanes from Brookshire Boulevard (exit 11) to I-485 (exit 19). After completion, drivers and motorcyclists can still use the lane for free if qualified under HOV rules, non-compliant drivers will be charged a toll.[15][16][17][18]
The I-40/I-77 interchange (exit 51) is undergoing a major upgrade in three phases: reconstruction of nearby intersections on both interstates, reconstruction and widening of I-40/I-77 interchange, and construction of new ramps at the interchange. The estimated cost for the entire project is $251 million and construction began in March 2012. It will replace the current interchange, which was built in the late 1960s.[19][20][21]
Auxiliary routes in North Carolina[edit]
Interstate
City
Type
Notes
Interstate 277 Charlotte Beltway A complete loop around Charlotte center city
Exit list[edit]
County
Location
mi[1]
km
Exit
Destinations
Notes
Mecklenburg Charlotte
0.0
0.0 I-77 south / US 21 south – Rock Hill, Columbia Continuation from South Carolina
0.9
1.4 1A Westinghouse Boulevard Formerly exit 1 before August 2010
1.8
2.9 1B I‑485 – Huntersville, Pineville Formerly exit 2 (southbound) before August 2010
2.8
4.5 3 Arrowood Road Formerly exit 2 (northbound) before August 2010
3.7
6.0 4 Nations Ford Road
4.8
7.7 5 Tyvola Road Single-point urban interchange
6.0
9.7 6A Woodlawn Road south – Queens University To Pfeiffer University
6.2
10.0 6B NC 49 (South Tryon Street) / Billy Graham Parkway To Billy Graham Library
7.3
11.7 7 To NC 49 / Clanton Road
8.3
13.4 8 To NC 160 / Remount Road Northbound exit and southbound entrance
9.0
14.5 9A NC 160 (West Boulevard) Southbound exit and northbound entrance
9.4
15.1 9B I‑277 north / US 74 east (John Belk Freeway)
9.5
15.3 9C US 74 west (Wilkinson Boulevard) to US 29 to NC 27
9.9
15.9 10A US 29 / NC 27 (Morehead Street) Southbound exit and northbound entrance
10.4
16.7 10 Trade Street / Fifth Street Signed southbound as exits 10B (east) and 10C (west)
11.0
17.7 11A I‑277 south / NC 16 south (Brookshire Freeway east) – Downtown Charlotte
11.2
18.0 11B NC 16 north (Brookshire Freeway west) Northbound left exit
12.4
20.0 12 Lasalle Street / Atando Avenue
13.3
21.4 13 I‑85 – Greensboro, Spartanburg Signed as exits 13A (north) and 13B (south)
15.8
25.4 16 US 21 north (Sunset Road) to NC 115 North end of US 21 overlap; signed as exits 16A (north/east) and 16B (west)
To Historic Latta Plantation/Carolina Raptor Center; parclo
18.6
29.9 18 NC 24 (W.T. Harris Boulevard) To Northlake Mall; parclo
Huntersville
19.7
31.7 19 I‑485 – Matthews, Pineville Signed as exits 19A (north/inner) and 19B (south/outer)
23.0
37.0 23 Gilead Road – Huntersville
25.5
41.0 25 NC 73 – Concord, Huntersville
Cornelius
28.3
45.5 28 US 21 south – Cornelius, Lake Norman South end of US 21 overlap, to be converted into a diverging diamond interchange in August, 2013[22]
Davidson
29.8
48.0 30 Griffith Street – Davidson To Davidson College
Iredell Mooresville
31.7
51.0 31 Langtree Road – Mooresville
33.3
53.6 33 US 21 north – Lake Norman North end of US 21 overlap
35.0
56.3 35 Brawley School Road Single-point urban interchange
36.2
58.3 36 NC 150 – Lincolnton, Mooresville Planned diverging diamond interchange[22]

41.8
67.3 42 US 21 / NC 115 – Troutman half-clover interchange

45.5
73.2 45 Amity Hill Road – Troutman, Barium Springs
Statesville
48.7
78.4 49A US 70 (Garner Bagnal Boulevard) half-clover interchange
49.0
78.9 49B Salisbury Road – Downtown Statesville half-clover interchange
50.1
80.6 50 East Broad Street – Downtown Statesville
51.3
82.6 51 I‑40 – Winston-Salem, Hickory Signed as exits 51A (east) and 51B (west) southbound; cloverleaf interchange

54.0
86.9 54 US 21 – Turnersburg

59.0
95.0 59 Tomlin Mill Road – Olin

65.5
105.4 65 NC 901 – Harmony, Union Grove
Yadkin Brooks Crossroads
73.7
118.6 73 US 421 – Yadkinville, Winston-Salem, Wilkesboro, Boone Signed as exits 73A (south) and 73B (north); cloverleaf interchange

79.0
127.1 79
US 21 south / US 21 Bus. north – Jonesville South end of US 21 overlap
Jonesville
81.9
131.8 82 NC 67 – Jonesville, Boonville, Elkin
Surry Elkin
83.7
134.7 83 US 21 north – Sparta, Roaring Gap North end of US 21 overlap; southbound exit is via exit 85
84.8
136.5 85
NC 268 Byp. – Elkin

93.2
150.0 93 Zephyr Road – Dobson
Oak Grove
100.0
160.9 100 NC 89 – Mount Airy, Galax
Pine Ridge
100.8
162.2 101 I‑74 east – Mount Airy, Winston-Salem East end of I-74 overlap; semi-directional T interchange
Stewarts Creek Township
105.7
170.1 I-77 north – Wytheville Continuation into Virginia
1.000 mi = 1.609 km; 1.000 km = 0.621 mi
Concurrency terminus
Incomplete access
See also[edit]
Carowinds
Interstate 74
Lake Norman
Lake Norman State Park
Northlake Mall
Uptown Charlotte
References[edit]
^ Jump up to: a b c Google (27 January 2011). "I-77 in NC" (Map). Google Maps. Google. Retrieved 27 January 2011.
Jump up ^ "Route Log - Main Routes of the Eisenhower National System Of Interstate and Defense Highways - Table 1". Federal Highway Administration. Retrieved 4 October 2014.
^ Jump up to: a b c d e "NCDOT: HOV Lanes". Retrieved 1 November 2011.
Jump up ^ "NCDOT: NC Blue Star Memorial Marker Locations". Retrieved 19 June 2011.
^ Jump up to: a b c "North Carolina Memorial Highways and other Named Facilities" (PDF). Retrieved 26 August 2012. [permanent dead link]
Jump up ^ "General Paul R. Younts Expressway". Retrieved 27 January 2011.
Jump up ^ North Carolina Department of Transportation. Facts: Interstate 77, NCDOT Web site. Retrieved 21 April 2007.
Jump up ^ "I-74 Segment 1". Archived from the original on 1 April 2011. Retrieved 2 January 2011.
Jump up ^ Staff (June 28, 2013). "Opening of Exit 35 on Interstate 77 Signals the End of the Brawley School Road Widening Project in Mooresville". North Carolina Department of Transportation. Retrieved June 28, 2013.
Jump up ^ "NCDOT Announces Financial Close on I-77 Express Lanes Project" (Press release). North Carolina Department of Transportation. May 20, 2015. Retrieved May 20, 2015.
Jump up ^ Perlmutt, David (May 19, 2015). "Mecklenburg commissioners side with towns asking for I-77 toll road project delay". The Charlotte Observer. Retrieved May 20, 2015.
Jump up ^ Harrison, Steve (May 20, 2015). "Toll lane opponent: DOT overlooked best free-lane option". The Charlotte Observer. Retrieved May 20, 2015.
Jump up ^ "New Rest Area to Open in Iredell County this Week" (Press release). North Carolina Department of Transportation. January 29, 2018. Retrieved February 1, 2018.
Jump up ^ "NCDOT: I-77 Improvements - Mecklenburg County". Retrieved 27 January 2011.
Jump up ^ "NCDOT: Project I-5405". Retrieved 1 November 2011.
Jump up ^ "HOV lanes will change to toll lanes on I-77". Retrieved 1 November 2011. [permanent dead link]
Jump up ^ "I-77 HOV lanes in NC could add toll". Archived from the original on 7 November 2011. Retrieved 1 November 2011.
Jump up ^ "I-77 Feasibility Study HOV-to-HOT Lanes Conversion" (PDF). Retrieved 1 November 2011. [permanent dead link]
Jump up ^ "NCDOT: Project I-3819". Archived from the original on 29 October 2011. Retrieved 1 November 2011.
Jump up ^ "DOT Report: Interchange At I-40, I-77 To Cost $250M". Archived from the original on 3 July 2011. Retrieved 1 November 2011.
Jump up ^ "The Construction of I-40/I-77 Interchange" (PDF). Retrieved 1 November 2011. [dead link]
^ Jump up to: a b Marusak, Joe (4 February 2012). "New interchange planned for bottlenecked I-77 exit". Charlotte, NC: Charlotte Observer. Archived from the original on 1 June 2012. Retrieved 2 March 2013.
External links[edit]
Route map: Google
KML file (edit • help)
Display on Google Maps
Template:Attached KML/Interstate 77 in North Carolina
KML is from Wikidata
Media related to Interstate 77 in North Carolina at Wikimedia Commons
NCDOT: I-77 Express Lanes
NCRoads.com: I-77
North Carolina @ AARoads - Interstate 77

Interstate 77
Previous state:
South Carolina North Carolina Next state:
Virginia
[hide]
v
t
e
Auxiliary routes of Interstate 77
North Carolina
277
Ohio
1771
277
1Cancelled
Retrieved from "https://en.wikipedia.org/w/index.php?title=Interstate_77_in_North_Carolina&oldid=823518667"
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Interstate 77
Interstate Highways in North Carolina
Transportation in Mecklenburg County, North Carolina
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Transportation in Yadkin County, North Carolina
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Transportation in Charlotte, North Carolina
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text:
Dakota language
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Dakota
Dakhótiyapi, Dakȟótiyapi
Pronunciation
[daˈkʰotijapi], [daˈqˣotijapi]
Native to
United States, with some speakers in Canada
Region
Primarily North Dakota and South Dakota, but also northern Nebraska, southern Minnesota; southern Manitoba, southern Saskatchewan
Ethnicity
Dakota
Santee, Sisseton, Yankton, Yanktonai
Native speakers
290 (2016)[1]
Language family
Siouan
Western Siouan
Mississippi Valley Siouan
Dakotan
Sioux
Dakota
Language codes
ISO 639-2
dak
ISO 639-3
dak
Glottolog
dako1258[2]
This article contains IPA phonetic symbols. Without proper rendering support, you may see question marks, boxes, or other symbols instead of Unicode characters. For an introductory guide on IPA symbols, see Help:IPA.
Dakota (Dakhótiyapi, Dakȟótiyapi), also referred to as Dakhota, is a Siouan language spoken by the Dakota people of the Sioux tribes. Dakota is closely related to and mutually intelligible with the Lakota language. It is critically endangered, with only around 290 fluent speakers left out of an ethnic population of almost 20,000.
Contents
[hide]
1 Morphology
1.1 Nouns
1.2 Verbs
1.3 Possessive pronouns and pronominal affixes
2 Syntax
2.1 Nouns and verbs
3 Dialects
4 Writing systems
5 Sound system
5.1 Vowels
5.2 Consonants
6 Comparison of the dialects
6.1 Phonological differences
6.2 Lexical differences
6.3 Grammatical differences
7 Learning Dakota: language revitalization efforts
7.1 Software and mobile apps for learning Dakhóta
7.2 Curriculum, textbooks, and other materials for teaching and learning Dakhóta
8 Notable speakers
9 References
10 Bibliography
11 External links
Morphology[edit]
Nouns[edit]
Dakota, similar to many Native American languages, is a mainly polysynthetic language, meaning that different morphemes in the form of affixes can be combined to form a single word. Nouns in Dakota can be broken down into two classes, primitive and derivative. Primitive nouns are nouns whose origin cannot be deduced from any other word (for example make or earth, peta or fire, and ate or father), while derivative nouns are nouns that are formed in various ways from words of other grammatical categories. Primitive nouns stand on their own and are separate from other words. Derivative nouns, on the other hand, are formed by the addition of affixes to words in other grammatical categories, such as verbs, adjectives, and other nouns.[3]
Verbs[edit]
Verbs in Dakota can appropriate, through agglutination and synthesis, many of the pronominal, prepositional, and adverbial or modal affixes of the language. There are many verbal roots, all of which are only used once certain causative prefixes are added, forming participles. Like in English, Dakota verbs also have three persons, the first, the second, and the third. Person is indicated through the addition (first and second person) or subtraction (third person, the verb is used in its simplest form) of personal pronoun affixes. There are two forms of tense in the language, the aorist (sometimes called the indefinite) and the future. In order to express the future tense, the words kta or kte are placed after the verb, much in contrast to expressing the aorist tense, which requires no marking, but is instead derived from the context of what is being said.[4]
Possessive pronouns and pronominal affixes[edit]
In order to show possession in Dakota, a possessive pronoun must be prefixed onto whichever noun is being possessed. Two forms of possessive nouns occur, the natural class and the artificial or alienable class. Natural class pronouns express possession that cannot be alienated, and when prefixed to a noun, signifies the different parts of one’s self. For example, the possessive natural article pronoun mi-, which means “my,” can be added to nouns such as “eye,” in miista, or “words,” in mioie. Meanwhile, artificial possessive pronouns are used to signify property and possessions that can be transferred or traded. For example, the artificial pronoun ta- or ti-, which is equivalent to the singular her or him, can be prefixed onto nouns such as “bow,” in tinazipe, and “friend,” in takodaku.[5]
Syntax[edit]
Nouns and verbs[edit]
Dakota is mainly a subject-object-verb (SOV) language, where nouns, whether they are the subject or object, always come before the verb. And when two nouns are used in the same clause, where one is the subject and the other is the object, the subject is most usually placed first. Verbs are also usually placed after adjectives that are used to qualify either the subject or the object and adverbs that qualify the verb. When additional words are used within a clause that are not either nouns or verbs, the nouns, both subject and object, are always placed at the beginning of the clause.[6]
Dialects[edit]
Dakota has two major dialects with two sub-dialects each (and minor variants, too):[7]
Eastern Dakota (a.k.a. Santee-Sisseton or Dakhóta)
Santee (Isáŋyáthi: Bdewákhaŋthuŋwaŋ,[8] Waȟpékhute)
Sisseton (Sisíthuŋwaŋ, Waȟpéthuŋwaŋ)
Western Dakota (a.k.a. Yankton-Yanktonai or Dakȟóta/Dakhóta, and erroneously classified, for a very long time, as “Nakota”[9])
Yankton (Iháŋktȟuŋwaŋ)
Yanktonai (Iháŋktȟuŋwaŋna)
Upper Yanktonai (Wičhíyena)
The two dialects differ phonologically, grammatically, and to a large extent, also lexically. They are mutually intelligible to a high extent, although Western Dakota is lexically closer to the Lakota language with which it has higher mutual intelligibility.
Writing systems[edit]
For a comparative table of the various writing systems conceived over time for the Sioux languages, cf. the specific section of the article Sioux language.
Sound system[edit]
Vowels[edit]
Dakota has five oral vowels, /a e i o u/, and three nasal vowels, /ã ĩ ũ/.
Front
Central
Back
high
oral
i u
nasal
ĩ ũ
mid
e o
low
oral
a
nasal
ã
Consonants[edit]
Labial
(-ized)
Dental/
Alveolar
Palatal
(-ized)
Velar/
Uvular
Glottal
Nasal
m [m] n [n]
Stop
aspirated
ph [pʰ]
pȟ [pˣ] th [tʰ]
tȟ [tˣ] čh [tʃʰ]
kh [kʰ]
kȟ [kˣ]
voiceless
p [p] t [t] č [tʃ] k [k] ’ [ʔ]
ejective
p’ [pʼ] t’ [tʼ] č’ [tʃʼ] k’ [kʼ]
voiced
b [b] d [d] g [ɡ]
Fricative
voiceless
s [s] š [ʃ] ȟ [χ]
ejective
s’ [sʼ] š’ [ʃʼ] ȟ’ [χʼ]
voiced
z [z] ž [ʒ] ǧ [ʁ]
Approximant
w [w] y [j] h [h]
Comparison of the dialects[edit]
Phonological differences[edit]
In respect to phonology Eastern and Western Dakota differ particularly in consonant clusters. The table below gives the possible consonant clusters and shows the differences between the dialects:[7]
Dakota consonant clusters
Santee
Sisseton
Yankton
Yanktonai
b
ȟ
k
m
p
s
š
t
h
k[10]
g
bd ȟč kč mn pč sč šk tk hm km gm
ȟd kp ps sk šd hn kn gn
ȟm ks pš sd šb hd kd gd
ȟn kš pt sm šn hb kb gb
ȟp kt sn šp
ȟt sp št
ȟb st šb
sb
The two dialects also differ in the diminutive suffix (-daŋ in Santee, and -na in Yankton-Yanktonai and in Sisseton) and in a number of other phonetic issues that are harder to categorize. The following table gives examples of words that differ in their phonology.[7]
Eastern Dakota
Western Dakota
gloss
Santee
Sisseton
Yankton
Yanktonai
hokšídaŋ hokšína hokšína boy
nína nína nína / dína[11] very
hdá kdá gdá to go back[12]
hbéza kbéza gbéza ridged
hnayáŋ knayáŋ gnayáŋ to deceive
hmúŋka kmúŋka gmúŋka to trap
ahdéškadaŋ ahdéškana akdéškana agdéškana lizard
Lexical differences[edit]
There are also numerous lexical differences between the two Dakota dialects as well as between the sub-dialects. Yankton-Yanktonai is in fact lexically closer to the Lakota language than it is to Santee-Sisseton. The following table gives some examples:[7]
English gloss
Santee-Sisseton
Yankton-Yanktonai
Lakota
Northern Lakota
Southern Lakota
child šičéča wakȟáŋyeža wakȟáŋyeža
knee hupháhu čhaŋkpé čhaŋkpé
knife isáŋ / mína mína míla
kidneys phakšíŋ ažúŋtka ažúŋtka
hat wapháha wapȟóštaŋ wapȟóštaŋ
still hináȟ naháŋȟčiŋ naháŋȟčiŋ
man wičhášta wičháša wičháša
hungry wótehda dočhíŋ ločhíŋ
morning haŋȟ’áŋna híŋhaŋna híŋhaŋna híŋhaŋni
to shave kasáŋ kasáŋ kasáŋ glak’óǧa
Grammatical differences[edit]
Yankton-Yanktonai has the same three ablaut grades as Lakota (a, e, iŋ),[13] while in Santee-Sisseton there are only two (a, e). This significantly impacts word forms, especially in fast speech and it is another reason why Yankton-Yanktonai has better mutual intelligibility with Lakota than with Santee-Sisseton.
Some examples:
English gloss
to go [12] I shall go to go back [12] he/she/it will go back
santee-sisseton
yá bdé kte hdá hdé kte
yankton-yanktonai
yá mníŋ kte kdá/gdá kníŋ/gníŋ kte
lakota
yá mníŋ kte glá gníŋ kte
There are other grammatical differences between the dialects.
Learning Dakota: language revitalization efforts[edit]
Software and mobile apps for learning Dakhóta[edit]
A Dakota 1 app was previously available for iPhone, iPad, and other iOS devices.[14] The Association on American Indian Affairs website offers an extensive selection of Dakotah learning resources, including CDs, DVDs, flashcards, and software.[15]
Curriculum, textbooks, and other materials for teaching and learning Dakhóta[edit]
A Level 1 Speak Dakota! textbook is available from the Dakhóta Iápi Okhódakičhiye. Developed by Dakota language speakers, teachers, and linguists, the textbook is the first fully illustrated Dakota language textbook that is linguistically and pedagogically consistent. Dakota language learning materials are also available on their website.[16]
Notable speakers[edit]
Dallas Goldtooth, Dakota member of the 1491s, language teacher and environmental activist
Gwen Westerman, Dakota educator, writer and artist
References[edit]
Jump up ^ Dakota at Ethnologue (19th ed., 2016)
Jump up ^ Hammarström, Harald; Forkel, Robert; Haspelmath, Martin, eds. (2017). "Dakota". Glottolog 3.0. Jena, Germany: Max Planck Institute for the Science of Human History.
Jump up ^ Riggs, Stephen Return; Dorsey, James Owen (1983). Dakota Grammar: With Texts and Ethnography (reprint ed.). Minnesota Historical Society Press. ISBN 0873514726.
Jump up ^ Riggs, Stephen Return; Dorsey, James Owen (1983). Dakota Grammar: With Texts and Ethnography (reprint ed.). Minnesota Historical Society Press. ISBN 0873514726.
Jump up ^ Riggs, Stephen Return; Dorsey, James Owen (1983). Dakota Grammar: With Texts and Ethnography (reprint ed.). Minnesota Historical Society Press. ISBN 0873514726.
Jump up ^ Riggs, Stephen Return; Dorsey, James Owen (1983). Dakota Grammar: With Texts and Ethnography (reprint ed.). Minnesota Historical Society Press. ISBN 0873514726.
^ Jump up to: a b c d Ullrich, Jan (2008). New Lakota Dictionary (Incorporating the Dakota Dialects of Yankton-Yanktonai and Santee-Sisseton). Lakota Language Consortium. ISBN 0-9761082-9-1.
Jump up ^ Formerly Mdewákhaŋthuŋwaŋ
Jump up ^ for a report on the long-established blunder of misnaming “Nakota” the Yankton and the Yanktonai, see the article Nakota
Jump up ^ many Yankton speakers pronounce the following clusters in the same way as the Yanktonai (Ullrich, p. 5).
Jump up ^ in Upper Yanktonay
^ Jump up to: a b c more precisely: ‘he/she/it is going (back)’ (hence elsewhere).
Jump up ^ which means that, in many words ending in -a (which are conventionally cited, in Ullrich’s dictionary (cf. pp. 699/700), with a capitalized final –A/Aŋ), the same -a turns into -e or into -iŋ when some circumstances occur (the word is the last in a sentence, or is modified by suffixes that trigger the ablaut, or, still, is followed by a word that triggers the ablaut, as well).
Jump up ^ "App Shopper: Dakota 1 (Education)". Retrieved 2012-09-12.
Jump up ^ "AAIA Native Language Program". Archived from the original on 2012-12-01. Retrieved 2013-01-19.
Jump up ^ "Dakhóta Iápi Okhódakičhiye/Dakota Language Society". Retrieved 2014-08-29.
Bibliography[edit]
DeMallie, Raymond J. (2001). Sioux until 1850. In R. J. DeMallie (Ed.), Handbook of North American Indians: Plains (Vol. 13, Part 2, pp. 718–760). W. C. Sturtevant (Gen. Ed.). Washington, D.C.: Smithsonian Institution. ISBN 0-16-050400-7.
Parks, Douglas R.; & Rankin, Robert L. (2001). The Siouan languages. In Handbook of North American Indians: Plains (Vol. 13, Part 1, pp. 94–114). Washington, D.C.: Smithsonian Institution.
de Reuse, Willem J. (1987). One hundred years of Lakota linguistics (1887–1987). Kansas Working Papers in Linguistics, 12, 13-42.
de Reuse, Willem J. (1990). A supplementary bibliography of Lakota languages and linguistics (1887–1990). Kansas Working Papers in Linguistics, 15 (2), 146-165. (Studies in Native American languages 6).
Rood, David S.; & Taylor, Allan R. (1996). Sketch of Lakhota, a Siouan language. In Handbook of North American Indians: Languages (Vol. 17, pp. 440–482). Washington DC: Smithsonian Institution.
Parks, D.R.; DeMallie, R.J. (1992). "Sioux, Assiniboine, and Stoney Dialects: A Classification". Anthropological Linguistics. 34 (1–4): 233–255. JSTOR 30028376.
Riggs, S.R., & Dorsey, J.O. (Ed.). (1973). Dakota grammar, texts, and ethnography. Minneapolis: Ross & Haines, Inc.
Shaw, P.A. (1980). Theoretical issues in Dakota phonology and morphology. New York: Garland Publishing, Inc.
Ullrich, Jan. (2008). New Lakota Dictionary & Incorporating the Dakota Dialects of Santee-Sisseton and Yankton-Yanktonai (Lakota Language Consortium). ISBN 0-9761082-9-1.
External links[edit]
Dakota Language Texts, from the Boston Athenæum: Schoolcraft Collection of Books in Native American Languages. Digital Collection.
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Stevens–Johnson syndrome
From Wikipedia, the free encyclopedia
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Stevens–Johnson syndrome
Synonyms
Erythema multiforme major[1]
Man with Stevens–Johnson syndrome
Specialty
Dermatology
Symptoms
Fever, skin blisters, skin peeling, painful skin, red eyes[2]
Complications
Dehydration, sepsis, pneumonia, multiple organ failure.[2]
Usual onset
Age < 30[1]
Causes
Certain medications, certain infections, unknown[1][2]
Risk factors
HIV/AIDS, systemic lupus erythematosus, genetics[2]
Diagnostic method
<10% of the skin involved, skin biopsy[1]
Differential diagnosis
Chickenpox, staphylococcal epidermolysis, staphylococcal scalded skin syndrome, autoimmune bullous disease[3]
Treatment
Hospitalization, stopping the cause[1]
Medication
Pain medication, antihistamines, antibiotics, corticosteroids, intravenous immunoglobulins[1]
Prognosis
Mortality ~7.5%[2][4]
Frequency
1–2 per million per year (together with TEN)[2]
Stevens–Johnson syndrome (SJS) is a type of severe skin reaction.[2] Together with toxic epidermal necrolysis (TEN) and Stevens-Johnson/toxic epidermal necrolysis (SJS/TEN), it forms a spectrum of disease, with SJS being less severe.[2][3] Early symptoms of SJS include fever and flu-like symptoms.[2] A few days later the skin begins to blister and peel forming painful raw areas.[2] Mucous membranes, such as the mouth, are also typically involved.[2] Complications include dehydration, sepsis, pneumonia, and multiple organ failure.[2]
The most common cause is certain medications such as lamotrigine, carbamazepine, allopurinol, sulfonamide antibiotics, and nevirapine.[2] Other causes can include infections such as Mycoplasma pneumoniae and cytomegalovirus or the cause may remain unknown.[1][2] Risk factors include HIV/AIDS and systemic lupus erythematosus.[2]
The diagnosis is based on involvement of less than 10% of the skin.[1] It is known as TEN when more than 30% of the skin is involved and an intermediate form with 10 to 30% involvement.[3] SJS/TEN reactions are believed to follow a type IV hypersensitivity mechanism.[5] It is also included with drug reaction with eosinophilia and systemic symptoms (DRESS syndrome), acute generalized exanthematous pustulosis (AGEP), and toxic epidermal necrolysis in a group of conditions known severe cutaneous adverse reactions (SCARs).[6] Erythema multiforme (EM) is generally considered a separate condition.[7]
Treatment typically takes place in hospital such as in a burn unit or intensive care unit.[1] Efforts may include stopping the cause, pain medication, antihistamines, antibiotics, intravenous immunoglobulins, or corticosteroids.[1] Together with TEN it affects 1 to 2 people per million per year.[2] It is twice as common in males as females.[1] Typical onset is under the age of 30.[1] Skin usually regrows over two to three weeks; however, complete recovery can take months.[1] Overall, the risk of death with SJS is 5 to 10%.[2][4]
Contents
1 Signs and symptoms
2 Causes
2.1 Medications
2.2 Infections
3 Pathophysiology
3.1 T cell receptors
3.2 ADME
4 Diagnosis
4.1 Pathology
4.2 Classification
5 Prevention
6 Treatment
7 Prognosis
8 Epidemiology
9 History
10 Notable cases
11 Research
12 References
13 External links
Signs and symptoms[edit]
Mucosal desquamation in a person with Stevens–Johnson syndrome
Conjunctivitis (inflammation of eye and eyelid) in SJS
SJS usually begins with fever, sore throat, and fatigue, which is commonly misdiagnosed and therefore treated with antibiotics. SJS, SJS/TEN, and TEN are often heralded by fever, sore throat, cough, and burning eyes for 1 to 3 days.[8] Patients with these disorders frequently experience burning pain of their skin at the start of disease.[8] Ulcers and other lesions begin to appear in the mucous membranes, almost always in the mouth and lips, but also in the genital and anal regions. Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis occurs in about 30% of children who develop SJS.[9] A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and soles of the feet, but usually not the scalp.[10]
Causes[edit]
SJS is thought to arise from a disorder of the immune system.[10] The immune reaction can be triggered by drugs or infections.[11] Genetic factors are associated with a predisposition to SJS.[12] The cause of SJS is unknown in one-quarter to one-half of cases.[12] SJS, SJS/TEN, and TEN are considered a single disease with common causes and mechanisms.[8]
Individuals expressing certain human leukocyte antigen (i.e. HLA) serotypes (i.e. genetic alleles), genetical-based T cell receptors, or variations in their efficiency to absorb, distribute to tissues, metabolize, or excrete (this combination is termed ADME) a drug are predisposed to develop SJS.
Medications[edit]
See also: List of SJS-inducing substances
Although SJS can be caused by viral infections and malignancies, the main cause is medications.[13] A leading cause appears to be the use of antibiotics, particularly sulfa drugs.[12][14] Between 100 and 200 different drugs may be associated with SJS.[15] No reliable test exists to establish a link between a particular drug and SJS for an individual case.[13] Determining what drug is the cause is based on the time interval between first use of the drug and the beginning of the skin reaction. Drugs discontinued more than 1 month prior to onset of mucocutaneous physical findings are highly unlikely to cause SJS and TEN.[8] SJS and TEN most often begin between 4 and 28 days after culprit drug administration.[8] A published algorithm (ALDEN) to assess drug causality gives structured assistance in identifying the responsible medication.[13][16]
SJS may be caused by adverse effects of the drugs vancomycin, allopurinol, valproate, levofloxacin, diclofenac, etravirine, isotretinoin, fluconazole,[17] valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil,[18] lamotrigine, nevirapine,[8] pyrimethamine, ibuprofen,[19] ethosuximide, carbamazepine, bupropion, telaprevir,[20][21] and nystatin.[22][23]
Medications that have traditionally been known to lead to SJS, erythema multiforme, and toxic epidermal necrolysis include sulfonamide antibiotics,[8] penicillin antibiotics, cefixime (antibiotic), barbiturates (sedatives), lamotrigine, phenytoin (e.g., Dilantin) (anticonvulsants) and trimethoprim. Combining lamotrigine with sodium valproate increases the risk of SJS.[24]
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a rare cause of SJS in adults; the risk is higher for older patients, women, and those initiating treatment.[25] Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. Similar to NSAIDs, paracetamol (acetaminophen) has also caused rare cases[26][27] of SJS. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.[10]
Infections[edit]
The second most common cause of SJS and TEN is infection, particularly in children. This includes upper respiratory infections, otitis media, pharyngitis, and Epstein-Barr virus, Mycoplasma pneumoniae and cytomegalovirus infections. The routine use of medicines such as antibiotics, antipyretics and analgesics to manage infections can make it difficult to identify if cases were caused by the infection or medicines taken.[28]
Viral diseases reported to cause SJS include: herpes simplex virus (possibly; is debated), AIDS, coxsackievirus, influenza, hepatitis, and mumps.[12]
In pediatric cases, Epstein-Barr virus and enteroviruses have been associated with SJS.[12]
Recent upper respiratory tract infections have been reported by more than half of patients with SJS.[12]
Bacterial infections linked to SJS include group A beta-hemolytic streptococci, diphtheria, brucellosis, lymphogranuloma venereum, mycobacteria, Mycoplasma pneumoniae, rickettsial infections, tularemia, and typhoid.[12]
Fungal infections with coccidioidomycosis, dermatophytosis, and histoplasmosis are also considered possible causes.[12] Malaria and trichomoniasis, protozoal infections, have also been reported as causes.[12]
Pathophysiology[edit]
SJS is a type IV hypersensitivity reaction in which a drug or its metabolite stimulates cytotoxic T cells (i.e. CD8+ T cells) and T helper cells (i.e. CD4+ T cells) to initiate autoimmune reactions that attack self tissues. In particular, it is a type IV, subtype IVc, delayed hypersensitivity reaction dependent in part on the tissue-injuring actions of natural killer cells.[29] This contrasts with the other types of SCARs disorders, i.e. The DRESS syndrome which is a Type IV, Subtype IVb, hypersensitivity drug reaction dependent in part on the tissue-injuring actions of eosinophils[29][30] and acute generalized exanthematous pustulosis which is a Type IV, subtype IVd, hypersensitivity reaction dependent in part on the tissue-injuring actions of neutrophils.[29][31]
Like other SCARs-inducing drugs, SJS-inducing drugs or their metabolites stimulate CD8+ T cells or CD4+ T cells to initiate autoimmune responses. Studies indicate that the mechanism by which a drug or its metabolites accomplishes this involves subverting the antigen presentation pathways of the innate immune system. The drug or metabolite covalently binds with a host protein to form a non-self, drug-related epitope. An antigen presenting cell (APC) takes up these alter proteins; digests them into small peptides; places the peptides in a groove on the human leukocyte antigen (i.e. HLA) component of their major histocompatibility complex (i.e. MHC); and presents the MHC-associated peptides to T-cell receptors on CD8+ T cells or CD4+ T cells. Those peptides expressing a drug-related, non-self epitope on one of their various HLA protein forms (HLA-A, HLA-B, HLA-C, HLA-DM, HLA-DO, HLA-DP, HLA-DQ, or HLA-DR) can bind to a T-cell receptor and thereby stimulate the receptor-bearing parent T cell to initiate attacks on self tissues. Alternatively, a drug or its metabolite may stimulate these T cells by inserting into the groove on a HLA protein to serve as a non-self epitope or bind outside of this groove to alter a HLA protein so that it forms a non-self epitope. In all these cases, however, a non-self epitope must bind to a specific HLA serotype (i.e. variation) in order to stimulate T cells. Since the human population expresses some 13,000 different HLA serotypes while an individual expresses only a fraction of them and since a SJS-inducing drug or metabolite interacts with only one or a few HLA serotypes, a drug's ability to induce SCARs is limited to those individuals who express HLA serotypes targeted by the drug or its metabolite.[32][33] Accordingly, only rare individuals are predisposed to develop a SCARs in response to a particular drug on the bases of their expression of HLA serotypes:[34] Studies have identified several HLA serotypes associated with development of SJS, SJS/TEN, or TEN in response to certain drugs.[29][35] In general, these associations are restricted to the cited populations.[36]
In some East Asian populations studied (Han Chinese and Thai), carbamazepine- and phenytoin-induced SJS is strongly associated with HLA-B*1502 (HLA-B75), an HLA-B serotype of the broader serotype HLA-B15.[37][38][39] A study in Europe suggested the gene marker is only relevant for East Asians.[40][41] This has clinical relevance as it is agreed upon that prior to starting a medication such as allopurinol in a patient of Chinese descent, HLA-B*58:01 testing should be considered.[8]
Based on the Asian findings, similar studies in Europe showed 61% of allopurinol-induced SJS/TEN patients carried the HLA-B58 (phenotype frequency of the B*5801 allele in Europeans is typically 3%). One study concluded: "Even when HLA-B alleles behave as strong risk factors, as for allopurinol, they are neither sufficient nor necessary to explain the disease."[42]
Other HLA associations with the development of SJS, SJS/TEN, or TEN and the intake of specific drugs as determined in certain populations are given in HLA associations with SCARs.
T cell receptors[edit]
In addition to acting through HLA proteins to bind with a T cell receptor, a drug or its metabolite may bypass HLA proteins to bind directly to a T cell receptor and thereby stimulate CD8+ T or CD4+ T cells to initiate autoimmune responses. In either case, this binding appears to develop only on certain T cell receptors. Since the genes for these receptors are highly edited, i.e. altered to encode proteins with different amino acid sequences, and since the human population may express more than 100 trillion different (i.e. different amino acid sequences) T cell receptors while an individual express only a fraction of these, a drug's or its metabolite's ability to induce the DRESS syndrome by interacting with a T cell receptor is limited to those individuals whose T cells express a T cell receptor(s) that can interact with the drug or its metabolite.[32][43] Thus, only rare individuals are predisposed to develop SJS in response to a particular drug on the bases of their expression of specific T cell receptor types.[34] While the evidence supporting this T cell receptor selectivity is limited, one study identified the preferential presence of the TCR-V-b and complementarity determining region 3 in T cell receptors found on the T cells in the blisters of patients with allopurinol-induced DRESS syndrome. This finding is compatible with the notion that specific types of T cell receptors are involved in the development of specific drug-induced SCARs.[35]
ADME[edit]
Variations in ADME, i.e. an individual's efficiency in absorbing, tissue-distributing, metabolizing, or excreting a drug, have been found to occur in various severe cutaneous adverse reactions (SCARS) as well as other types of adverse drug reactions.[44] These variations influence the levels and duration of a drug or its metabolite in tissues and thereby impact the drug's or metabolite's ability to evoke these reactions.[6] For example, CYP2C9 is an important drug-metabolizing cytochrome P450; it metabolizes and thereby inactivates phenytoin. Taiwanese, Japanese, and Malaysian individuals expressing the CYP2C9*3[45] variant of CYP2C9, which has reduced metabolic activity compared to the wild type (i.e. CYP2c9*1) cytochrome, have increased blood levels of phenytoin and an high incidence of SJS (as well as SJS/TEN and TEN) when taking the drug.[6][46] In addition to abnormalities in drug-metabolizing enzymes, dysfunctions of the kidney, liver, or GI tract which increase a SCARs-inducing drug or metabolite levels are suggested to promote SCARs responses.[6][4] These ADME abnormalities, it is also suggested, may interact with particular HLA proteins and T cell receptors to promote a SCARs disorder.[6][47]
Diagnosis[edit]
The diagnosis is based on involvement of less than 10% of the skin.[1] It is known as TEN when more than 30% of the skin is involved and an intermediate form with 10 to 30% involvement.[3] A positive Nikolsky's sign is helpful in the diagnosis of SJS and TEN.[8] A skin biopsy is helpful, but not required, to establish a diagnosis of SJS and TEN.[8]
Pathology[edit]
Micrograph showing full-thickness epidermal necrosis with a basket weave-like stratum corneum and separation of the dermis and epidermis, skin biopsy, H&E stain
SJS, like TEN and erythema multiforme, is characterized by confluent epidermal necrosis with minimal associated inflammation. The acuity is apparent from the (normal) basket weave-like pattern of the stratum corneum.
Classification[edit]
Stevens–Johnson syndrome (SJS) is a milder form of toxic epidermal necrolysis (TEN).[48] These conditions were first recognised in 1922.[25] A classification first published in 1993, that has been adopted as a consensus definition, identifies Stevens–Johnson syndrome, toxic epidermal necrolysis, and SJS/TEN overlap. All three are part of a spectrum of severe cutaneous reactions (SCAR) which affect skin and mucous membranes.[13] The distinction between SJS, SJS/TEN overlap, and TEN is based on the type of lesions and the amount of the body surface area with blisters and erosions.[13] It is agreed that the most reliable method to classify EM, SJS, and TEN is based on lesion morphology and extent of epidermal detachment.[8] Blisters and erosions cover between 3% and 10% of the body in SJS, 11–30% in SJS/TEN overlap, and over 30% in TEN.[13] The skin pattern most commonly associated with SJS is widespread, often joined or touching (confluent), papuric spots (macules) or flat small blisters or large blisters which may also join together.[13] These occur primarily on the torso.[13]
SJS, TEN, and SJS/TEN overlap can be mistaken for erythema multiforme.[49] Erythema multiforme, which is also within the SCAR spectrum, differs in clinical pattern and etiology.[13] Although both SJS and TEN can also be caused by infections, they are most often adverse effects of medications.[13]
Prevention[edit]
Screening individuals for certain predisposing gene variants before initiating treatment with particular SJS-, TEN/SJS-, or TEN-inducing drugs is recommended or under study. These recommendations are typically limited to specific populations that show a significant chance of having the indicated gene variant since screening of populations with extremely low incidences of expressing the variant is considered cost-ineffective.[50] Individuals expressing the HLA allele associated with sensitivity to an indicated drug should not be treated with the drug. These recommendations include the following.[6][51] Before treatment with carbamazepine, the Taiwan and USA Food and Drug Administrations recommend screening for HLA-B*15:02 in certain Asian groups. This has been implemented in Taiwan, Hong Kong, Singapore, and many medical centers in Thailand and Mainland China. Before treatment with allopurinol, the American College of Rheumatology guidelines for managing gout recommend HLA-B*58:01 screening. This is provided in many medical centers in Taiwan, Hong Kong, Thailand, and Mainland China. Before treatment with abacavir, the USA Food and Drug Administration recommends screening for HLA-B*57:01 in Caucasian populations. This screening is widely implemented. It has also been suggested that all individuals found to express this HLA serotype avoid treatment with abacovir. Current trials are underway in Taiwan to define the cost-effectiveness of avoiding phenytoin in SJS, SJS/TEN, and TEN for individuals expressing the CYP2C9*3 allele of CYP2C9.[51]
Treatment[edit]
SJS constitutes a dermatological emergency. Patients with documented Mycoplasma infections can be treated with oral macrolide or oral doxycycline.[10]
Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous fluids and nasogastric or parenteral feeding) and symptomatic (e.g., analgesic mouth rinse for mouth ulcer). Dermatologists and surgeons tend to disagree about whether the skin should be debrided.[10]
Beyond this kind of supportive care, no treatment for SJS is accepted. Treatment with corticosteroids is controversial. Early retrospective studies suggested corticosteroids increased hospital stays and complication rates. No randomized trials of corticosteroids were conducted for SJS, and it can be managed successfully without them.[10]
Other agents have been used, including cyclophosphamide and ciclosporin, but none has exhibited much therapeutic success. Intravenous immunoglobulin treatment has shown some promise in reducing the length of the reaction and improving symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm environment, and intravenous analgesics.
An ophthalmologist should be consulted immediately, as SJS frequently causes the formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision, and a host of other ocular problems. Those with chronic ocular surface disease caused by SJS may find some improvement with PROSE treatment (prosthetic replacement of the ocular surface ecosystem treatment).[52]
Prognosis[edit]
SJS (with less than 10% of body surface area involved) has a mortality rate of around 5%. The mortality for toxic epidermal necrolysis (TEN) is 30–40%. The risk for death can be estimated using the SCORTEN scale, which takes a number of prognostic indicators into account.[53] It is helpful to calculate a SCORTEN within the first 3 days of hospitalization.[8] Other outcomes include organ damage/failure, cornea scratching, and blindness.[citation needed]. Restrictive lung disease may develop in patients with SJS and TEN after initial acute pulmonary involvement.[8] Patients with SJS or TEN caused by a drug have a better prognosis the earlier the causative drug is withdrawn.[8]
Epidemiology[edit]
SJS is a rare condition, with a reported incidence of around 2.6[10] to 6.1[25] cases per million people per year. In the United States, about 300 new diagnoses are made each year. The condition is more common in adults than in children.
History[edit]
SJS is named for Albert Mason Stevens and Frank Chambliss Johnson, American pediatricians who jointly published a description of the disorder in the American Journal of Diseases of Children in 1922.[54][55]
Notable cases[edit]
Ab-Soul, American hip hop recording artist and member of Black Hippy[56]
Padma Lakshmi, actress, model, television personality, and cookbook writer[57]
Manute Bol, former NBA player. Bol died from complications of Stevens–Johnson syndrome as well as kidney failure.[58]
Gene Sauers, three-time PGA Tour winner[59]
Samantha Reckis, a seven-year-old Plymouth, Massachusetts girl who lost the skin covering 95% of her body after taking children's Motrin in 2003. In 2013, a jury awarded her $63M in a lawsuit against Johnson & Johnson, one of the largest lawsuits of its kind.[60] The decision was upheld in 2015.[61]
Karen Elaine Morton, she appeared in Tommy Tutone's "867-5309/Jenny" video and was Playmate of the Month in the July 1978 issue of "Playboy."[62]
Research[edit]
In 2015, the NIH and the Food and Drug Administration (FDA) organized a workshop entitled “Research Directions in Genetically-Mediated Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis”.[8]
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^ Jump up to: a b Su SC, Hung SI, Fan WL, Dao RL, Chung WH (2016). "Severe Cutaneous Adverse Reactions: The Pharmacogenomics from Research to Clinical Implementation". International Journal of Molecular Sciences. 17 (11). doi:10.3390/ijms17111890. PMC 5133889. PMID 27854302.
Jump up ^ Ciralsky, JB; Sippel, KC; Gregory, DG (July 2013). "Current ophthalmologic treatment strategies for acute and chronic Stevens-Johnson syndrome and toxic epidermal necrolysis". Current Opinion in Ophthalmology. 24 (4): 321–8. doi:10.1097/icu.0b013e3283622718. PMID 23680755.
Jump up ^ Foster et al. 2013, Prognosis.
Jump up ^ Enerson, Ole Daniel (ed.), "Stevens-Johnson syndrome", Whonamedit?, archived from the original on 3 December 2013.
Jump up ^ Stevens, A.M.; Johnson, F.C. (1922). "A new eruptive fever associated with stomatitis and ophthalmia; Report of two cases in children". American Journal of Diseases of Children. 24 (6): 526–33. doi:10.1001/archpedi.1922.04120120077005. Archived from the original on 3 January 2014.
Jump up ^ Ramirez, Erika (8 August 2012). "Ab-Soul's timeline: The rapper's life from 5 years old to now". billboard.com. Billboard. Archived from the original on 17 February 2013. Retrieved 7 December 2012.
Jump up ^ Cartner-Morley, Jess (8 April 2006). "Beautiful and Damned". The Guardian.
Jump up ^ "Manute Bol dies at age 47". FanHouse. AOL. 19 June 2010. Archived from the original on 2010-06-21.
Jump up ^ Graff, Chad (31 July 2013). "3M golf: Gene Sauers thriving after torturous battle with skin disease". St. Paul Pioneer Press. Archived from the original on 3 October 2014.
Jump up ^ "Family awarded $63 million in Motrin case". Boston Globe. 13 February 2013. Archived from the original on 5 September 2017.
Jump up ^ "$63 million verdict in Children's Motrin case upheld". Boston Globe. 17 April 2015. Archived from the original on 31 October 2016.
Jump up ^ Morton, Karen. "Karen Morton Biography". imdb.com. Archived from the original on 2 October 2016.
External links[edit]
Classification
D
ICD-10: L51.1
ICD-9-CM: 695.13
OMIM: 608579
MeSH: D013262
DiseasesDB: 4450
External resources
MedlinePlus: 000851
eMedicine: emerg/555 derm/405
Patient UK: Stevens–Johnson syndrome
Orphanet: 36426
Boyer, Woodrow Allen (May 2008). Understanding Stevens–Johnson Syndrome & Toxic Epidermal Necrolysis (New Expanded ed.). Raleigh, North Carolina: Lulu Press.
Bentley, John; Sie, David (2014-10-08). "Stevens-Johnson syndrome and toxic epidermal necrolysis". The Pharmaceutical Journal. 293 (7832). Retrieved 2014-10-08.
hide
v
t
e
Urticaria and erythema (L50–L54, 695, 708)
Urticaria
(acute/chronic)
Allergic urticaria
Urticarial allergic eruption
Physical urticaria
Cold urticaria
Familial
Primary cold contact urticaria
Secondary cold contact urticaria
Reflex cold urticaria
Heat urticaria
Localized heat contact urticaria
Solar urticaria
Dermatographic urticaria
Vibratory angioedema
Pressure urticaria
Cholinergic urticaria
Aquagenic urticaria
Other urticaria
Acquired C1 esterase inhibitor deficiency
Adrenergic urticaria
Exercise urticaria
Galvanic urticaria
Schnitzler syndrome
Urticaria-like follicular mucinosis
Angioedema
Episodic angioedema with eosinophilia
Hereditary angioedema
Erythema
Erythema multiforme/
drug eruption
Erythema multiforme minor
Erythema multiforme major
Stevens–Johnson syndrome, Toxic epidermal necrolysis
panniculitis (Erythema nodosum)
Acute generalized exanthematous pustulosis
Figurate erythema
Erythema annulare centrifugum
Erythema marginatum
Erythema migrans
Erythema gyratum repens
Other erythema
Necrolytic migratory erythema
Erythema toxicum
Erythroderma
Palmar erythema
Generalized erythema
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