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Corticosteroids are a class of chemicals that includes the steroid hormones that are produced in the adrenal cortex of vertebrates as well as the synthetic analogues of these hormones. Corticosteroids are involved in a wide range of physiological processes, including stress response, immune response, and regulation of inflammation, carbohydrate metabolism, protein catabolism, blood electrolyte levels, and behavior.
- Glucocorticoids such as cortisol control carbohydrate, fat and protein metabolism, and are anti-inflammatory by preventing phospholipid release, decreasing eosinophil action and a number of other mechanisms.[1]
- Mineralocorticoids such as aldosterone control electrolyte and water levels, mainly by promoting sodium retention in the kidney.
Some common natural hormones are corticosterone (C
21H
30O
4), cortisone (C
21H
28O
5, 17-hydroxy-11-dehydrocorticosterone) and aldosterone.
Contents
- 1 Medical uses
- 2 Side effects
- 3 Biosynthesis
- 4 Classification
- 4.1 Chemical structure
- 4.1.1 Group A — Hydrocortisone type
- 4.1.2 Group B — Acetonides (and related substances)
- 4.1.3 Group C — Betamethasone type
- 4.1.4 Group D — Esters
- 4.1.4.1 Group D1 — Halogenated (less labile)
- 4.1.4.2 Group D2 — Labile prodrug esters
- 4.2 Route of administration
- 4.2.1 Topical steroids
- 4.2.2 Inhaled steroids
- 4.2.3 Oral forms
- 4.2.4 Systemic forms
- 5 History
- 6 See also
- 7 References
Medical uses
Synthetic pharmaceutical drugs with corticosteroid-like effects are used in a variety of conditions, ranging from brain tumors to skin diseases. Dexamethasone and its derivatives are almost pure glucocorticoids, while prednisone and its derivatives have some mineralocorticoid action in addition to the glucocorticoid effect. Fludrocortisone (Florinef) is a synthetic mineralocorticoid. Hydrocortisone (cortisol) is available for replacement therapy, e.g. in adrenal insufficiency and congenital adrenal hyperplasia.
Synthetic glucocorticoids are used in the treatment of joint pain or inflammation (arthritis), temporal arteritis, dermatitis, allergic reactions, asthma, hepatitis, systemic lupus erythematosus, inflammatory bowel disease (ulcerative colitis and Crohn's disease), sarcoidosis and for glucocorticoid replacement in Addison's disease or other forms of adrenal insufficiency.[2] Topical formulations are also available for the skin, eyes (uveitis), lungs (asthma), nose (rhinitis), and bowels. Corticosteroids are also used supportively to prevent nausea, often in combination with 5-HT3 antagonists (e.g. ondansetron).
Typical undesired effects of glucocorticoids present quite uniformly as drug-induced Cushing's syndrome. Typical mineralocorticoid side-effects are hypertension (abnormally high blood pressure), hypokalemia (low potassium levels in the blood), hypernatremia (high sodium levels in the blood) without causing peripheral edema, metabolic alkalosis and connective tissue weakness.[3] There may also be impaired wound healing or ulcer formation because of the immunosuppressive effects.
Clinical and experimental evidence indicates that corticosteroids can cause permanent eye damage by inducing central serous retinopathy (CSR, also known as central serous chorioretinopathy, CSC). A variety of steroid medications, from anti-allergy nasal sprays (Nasonex, Flonase) to topical skin creams, to eye drops (Tobradex), to prednisone have been implicated in the development of CSR.[4][5]
Corticosteroids have been widely used in treating people with traumatic brain injury.[6] A systematic review identified 20 randomised controlled trials and included 12,303 participants, then compared patients who received corticosteroids with patients who received no treatment. The authors recommended people with traumatic head injury should not be routinely treated with corticosteroids.[7]
Side effects
Lower arm of a 47-year-old female showing skin damage due to topical steroid use
Use of corticosteroids has numerous side-effects, some of which may be severe:
- Neuropsychiatric: steroid psychosis,[8] and anxiety,[9] depression. Therapeutic doses may cause a feeling of artificial well-being ("steroid euphoria").[10] The neuropsychiatric effects are partly mediated by sensitization of the body to the actions of adrenaline. Therapeutically, the bulk of corticosteroid dose is given in the morning to mimic the body's diurnal rhythm; if given at night, the feeling of being energized will interfere with sleep. An extensive review is provided by Flores and Gumina.[11]
- Cardiovascular: Corticosteroids can cause sodium retention through a direct action on the kidney, in a manner analogous to the mineralocorticoid aldosterone. This can result in fluid retention and hypertension.
- Metabolic: Corticosteroids cause a movement of body fat to the face and torso, resulting respectively in "moon face" and "buffalo hump". and away from the limbs. Due to the diversion of amino-acids to glucose, they are considered anti-anabolic, and long term therapy can cause muscle wasting[12]
- Endocrine: By increasing the production of glucose from amino-acid breakdown and opposing the action of insulin, corticosteroids can cause hyperglycemia,[9] insulin resistance and diabetes mellitus.[9]
- Skeletal: Steroid-induced osteoporosis may be a side-effect of long-term corticosteroid use. Use of inhaled corticosteroids among children with asthma may result in decreased height.[13]
- Gastro-intestinal: While cases of colitis have been reported, corticosteroids are therapeutically employed when the colitis has an auto-immune nature, e.g. ulcerative colitis and Crohn's disease. While the evidence for corticosteroids causing peptic ulceration is relatively poor except for high doses taken for over a month,[14] the majority of doctors as of 2010[update] still believe this is the case, and would consider protective prophylactic measures.[15]
- Eyes: chronic use may predispose to cataract and retinopathy.
- Vulnerability to infection: By suppressing immune reactions (which is one of the main reasons for their use in allergies), steroids may cause infections to flare up, notably candidiasis.[16]
- Pregnancy: Corticosteroids have a low but significant teratogenic effect, causing a few birth defects per 1,000 pregnant women treated. Corticosteroids are therefore contraindicated in pregnancy.[17]
- Habituation: Topical steroid addiction (TSA) has been reported in long-term users of topical steroids (users who applied topical steroids to their skin over a period of weeks, months, or years).[18][19] TSA is characterised by uncontrollable, spreading dermatitis and worsening skin inflammation which requires a stronger topical steroid to get the same result as the first prescription. When topical steroid medication is lost, the skin experiences redness, burning, itching, hot skin, swelling, and/or oozing for a length of time. This is also called 'red skin syndrome' or 'topical steroid withdrawal'(TSW). After the withdrawal period is over the atopic dermatitis can cease or is less severe than it was before.[20]
Corticosteroids were voted Allergen of the Year in 2005 by the American Contact Dermatitis Society.[21]
Biosynthesis
Corticosteroid biosynthetic pathway in rat
The corticosteroids are synthesized from cholesterol within the adrenal cortex. Most steroidogenic reactions are catalysed by enzymes of the cytochrome P450 family. They are located within the mitochondria and require adrenodoxin as a cofactor (except 21-hydroxylase and 17α-hydroxylase).
Aldosterone and corticosterone share the first part of their biosynthetic pathway. The last part is mediated either by the aldosterone synthase (for aldosterone) or by the 11β-hydroxylase (for corticosterone). These enzymes are nearly identical (they share 11β-hydroxylation and 18-hydroxylation functions), but aldosterone synthase is also able to perform an 18-oxidation. Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the adrenal cortex; 11β-hydroxylase is found in the zona fasciculata and zona glomerulosa.
Classification
Chemical structure
In general, corticosteroids are grouped into four classes, based on chemical structure. Allergic reactions to one member of a class typically indicate an intolerance of all members of the class. This is known as the "Coopman classification",[22] after S. Coopman, who defined this classification in 1989.[23]
The highlighted steroids are often used in the screening of allergies to topical steroids.[24]
Group A — Hydrocortisone type
Hydrocortisone, hydrocortisone acetate, cortisone acetate, tixocortol pivalate, prednisolone, methylprednisolone, and prednisone (Short- to medium-acting glucocorticoids).
Group B — Acetonides (and related substances)
Triamcinolone acetonide, triamcinolone alcohol, mometasone, amcinonide, budesonide, desonide, fluocinonide, fluocinolone acetonide, and halcinonide.
Group C — Betamethasone type
Betamethasone, betamethasone sodium phosphate, dexamethasone, dexamethasone sodium phosphate, and fluocortolone.
Group D — Esters
Group D1 — Halogenated (less labile)
Hydrocortisone-17-valerate, halometasone, alclometasone dipropionate, betamethasone valerate, betamethasone dipropionate, prednicarbate, clobetasone-17-butyrate, clobetasol-17-propionate, fluocortolone caproate, fluocortolone pivalate, and fluprednidene acetate.
Group D2 — Labile prodrug esters
Hydrocortisone-17-butyrate, hydrocortisone-17-aceponate, hydrocortisone-17-buteprate, ciclesonide and prednicarbate.
Route of administration
Topical steroids
Main article: Topical steroid
For use topically on the skin, eye, and mucous membranes.
Topical corticosteroids are divided in potency classes I to IV,
Inhaled steroids
for use to treat the nasal mucosa, sinuses, bronchii, and lungs.[25] This group includes:
- Flunisolide[26]
- Fluticasone furoate
- Fluticasone propionate[26]
- Triamcinolone acetonide[26]
- Beclomethasone dipropionate[26]
- Budesonide[26]
There is also a combination preparation containing fluticasone propionate and salmeterol xinafoate (a long-acting bronchodilator).[26] It is approved for children over 12 years old.
Oral forms
Such as prednisone and prednisolone.[27]
Systemic forms
Available in injectables for intravenous and parenteral routes.[27]
History
First known use was in 1944.[28] Tadeusz Reichstein together with Edward Calvin Kendall and Philip Showalter Hench were awarded the Nobel Prize for Physiology and Medicine in 1950 for their work on hormones of the adrenal cortex, which culminated in the isolation of cortisone.[29]
Corticosteroids have been used as drug treatment for some time. Lewis Sarett of Merck & Co. was the first to synthesize cortisone, using a complicated 36-step process that started with deoxycholic acid, which was extracted from ox bile.[30] The low efficiency of converting deoxycholic acid into cortisone led to a cost of US $200 per gram. Russell Marker, at Syntex, discovered a much cheaper and more convenient starting material, diosgenin from wild Mexican yams. His conversion of diosgenin into progesterone by a four-step process now known as Marker degradation was an important step in mass production of all steroidal hormones, including cortisone and chemicals used in hormonal contraception.[31] In 1952, D.H. Peterson and H.C. Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone.[32] The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $0.46 per gram by 1980. Percy Julian's research also aided progress in the field.[33] The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.
See also
- Vitiligo
- Steroids (general term)
- Fluorometholone
- List of steroid abbreviations
References
- ^ Joseph P. Edardes. "Steroids and Warfarin Therapy". Coumarin Anticoagulant Research Progress. Nova Publishers, 2008. p. 18.
- ^ Higashi AS, Zhu S, Stafford RS, Alexander GC (Dec 2011). "National trends in outpatient asthma treatment, 1997-2009". Journal of General Internal Medicine 26 (12): 1465–1470. doi:10.1007/s11606-011-1796-4. PMID 21769507.
- ^ Werner R (2005). A massage therapist's guide to Pathology (3rd ed.). Pennsylvania: Lippincott Williams & Wilkins.
- ^ Carvalho-Recchia, CA; Yannuzzi, LA; Negrão, S; Spaide, RF; Freund, KB; Rodriguez-Coleman, H; Lenharo, M; Iida, T (2002). "Corticosteroids and central serous chorioretinopathy". Ophthalmology 109 (10): 1834–7. doi:10.1016/S0161-6420(02)01117-X. PMID 12359603.
- ^ "The New York Times :: A Breathing Technique Offers Help for People With Asthma". buteykola.com. Retrieved 2012-11-30.
- ^ Alderson P, Roberts I. "Plain Language Summary". Corticosteroids for acute traumatic brain injury. The Cochrane Collaboration. p. 2.
- ^ Alderson, P.; Roberts, I. (2005). Alderson, Phil, ed. "Corticosteroids for acute traumatic brain injury". Cochrane Database Syst Rev (1): CD000196. doi:10.1002/14651858.CD000196.pub2. PMID 15674869. edit
- ^ Hall, Richard. "Psychiatric Adverse Drug Reactions: Steroid Psychosis". Director of Research Monarch Health Corporation Marblehead, Massachusetts.
- ^ a b c Korte SM (2001). "Corticosteroids in relation to fear, anxiety and psychopathology". Neurosci Biobehav Rev 25 (2): 117–42. doi:10.1016/S0149-7634(01)00002-1. PMID 11323078.
- ^ C R Swinburn, J M Wakefield, S P Newman, and P W Jones Evidence of prednisolone induced mood change ('steroid euphoria') in patients with chronic obstructive airways disease" Br J Clin Pharmacol 1988 December; 26(6) 709–713. URL:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1386585/
- ^ Benjamin H. Flores and Heather Kenna Gumina. The Neuropsychiatric Sequelae of Steroid Treatment. URL:http://www.dianafoundation.com/articles/df_04_article_01_steroids_pg01.html
- ^ Per-Olof Hasselgren, Nima Alamdari, Zaira Aversa, Patricia Gonnella, Ira J Smith, and Steven Tizio. CORTICOSTEROIDS AND MUSCLE WASTING ROLE OF TRANSCRIPTION FACTORS, NUCLEAR COFACTORS, AND HYPERACETYLATION. Curr Opin Clin Nutr Metab Care. 2010 July; 13(4): 423–428. URL:http://ncbi.nlm.nih.gov/pmc/PMC2911625
- ^ Zhang, L; Prietsch, SO; Ducharme, FM (Jul 17, 2014). "Inhaled corticosteroids in children with persistent asthma: effects on growth.". The Cochrane database of systematic reviews 7: CD009471. doi:10.1002/14651858.CD009471.pub2. PMID 25030198.
- ^ Pecora PG, Kaplan B (1996). "Corticosteroids and ulcers: is there an association?". Ann Pharmacother 30 (7–8): 870–2. doi:10.1177/106002809603000729. PMID 8826575.
- ^ Martínek J, Hlavova K, Zavada F et al. (June 2010). ""A surviving myth" —corticosteroids are still considered ulcerogenic by a majority of physicians". Scand J Gastroenterol 45 (10): 1156–61. doi:10.3109/00365521.2010.497935. PMID 20569095.
- ^ Fukushima, C.; Matsuse, H.; Tomari, S.; Obase, Y.; Miyazaki, Y.; Shimoda, T.; Kohno, S. (2003). "Oral candidiasis associated with inhaled corticosteroid use: Comparison of fluticasone and beclomethasone". Annals of Allergy, Asthma & Immunology 90 (6): 646–651. doi:10.1016/S1081-1206(10)61870-4. PMID 12839324. edit
- ^ Shepard, TH.; Brent, RL.; Friedman, JM.; Jones, KL.; Miller, RK.; Moore, CA.; Polifka, JE. (April 2002). "Update on new developments in the study of human teratogens". Teratology 65 (4): 153–61. doi:10.1002/tera.10032. PMID 11948561.
- ^ Nnoruka, Edith; Daramola, Olaniyi; Ike, Samuel (2007). "Misuse and abuse of topical steroids: implications.". Expert Review of Dermatology 2 (1): 31–40. doi:10.1586/17469872.2.1.31. Retrieved 2014-12-18.
- ^ Sanjay, Rathi; D'Souza, Paschal (2012). "Rational and ethical use of topical corticosteroids based on safety and efficacy.". Indian Journal of Dermatology 57 (4): 251–259. doi:10.4103/0019-5154.97655.
- ^ Fukaya, M; Sato, K; Sato, M; Kimata, H; Fujisawa, S; Dozono, H; Yoshizawa, J; Minaguchi, S (2014). "Topical steroid addiction in atopic dermatitis.". Drug, healthcare and patient safety 6: 131–8. doi:10.2147/dhps.s69201. PMID 25378953.
- ^ "Contact Allergen of the Year: Corticosteroids: Introduction". Medscape.com. 2005-06-13. Retrieved 2012-11-30.
- ^ Rietschel, Robert L. (2007). Fisher's Contact Dermatitis, 6/e. Hamilton, Ont: BC Decker Inc. p. 256. ISBN 1-55009-378-9.
- ^ Coopman S, Degreef H, Dooms-Goossens A (July 1989). "Identification of cross-reaction patterns in allergic contact dermatitis from topical corticosteroids". Br. J. Dermatol. 121 (1): 27–34. doi:10.1111/j.1365-2133.1989.tb01396.x. PMID 2757954.
- ^ Wolverton, SE (2001). Comprehensive Dermatologic Drug Therapy. WB Saunders. p. 562.
- ^ "Asthma Steroids: Inhaled Steroids, Side Effects, Benefits, and More". Webmd.com. Retrieved 2012-11-30.
- ^ a b c d e f Frieden, Thomas R. (March 2004). "Inhaled Corticosteroids — Long-Term Control Asthma medicine" (PDF). New York City Asthma Initiative.
- ^ a b "Systemic steroids (corticosteroids). DermNet NZ". . DermNet NZ. 2012-05-19. Retrieved 2012-11-30.
- ^ Webster. "First therapeutic use of Corticosteroid". Retrieved 30 July 2012.
- ^ http://nobelprize.org/nobel_prizes/medicine/laureates/1950/kendall-lecture.pdf
- ^ Sarett, Lewis H. (1947). "Process of Treating Pregnene Compounds", U. S. Patent 2,462,133
- ^ Marker, Russell E.; Wagner, R. B.; Ulshafer, Paul R.; Wittbecker, Emerson L.; Goldsmith, Dale P. J.; Ruof, Clarence H. (1947). "Steroidal Sapogenins". J. Am. Chem. Soc. 69 (9): 2167–2230. doi:10.1021/ja01201a032. PMID 20262743.
- ^ Peterson D.H., Murray, H.C. (1952). "Microbiological Oxygenation of Steroids at Carbon 11". J. Am. Chem. Soc. 74 (7): 1871–2. doi:10.1021/ja01127a531.
- ^ Julian, Percy L., Cole, John Wayne, Meyer, Edwin W., and Karpel, William J. (1956) "Preparation of Cortisone". U. S. Patent 2,752,339
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Steroid hormones (and metabolic intermediates)
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| Precursors |
- Cholesterol
- 22R-Hydroxycholesterol
- 20α,22R-Dihydroxycholesterol
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| Corticosteroids |
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Glucocorticoids
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- Corticosterone
- Cortisol
- Cortisone
- DHC
- Deoxycortisol
- Deoxycorticosterone
- 17-Hydroxypregnenolone
- 17-Hydroxyprogesterone
- Pregnenolone
- Progesterone
- THB
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Mineralocorticoids
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- Aldosterone
- Corticosterone
- Cortisol
- Deoxycortisol
- Deoxycorticosterone
- 5α-Dihydroaldosterone
- 16α,18-Dihydroxy-11-deoxycorticosterone
- 18-Hydroxy-11-deoxycorticosterone
- 18-Hydroxycorticosterone
- 18-Hydroxydeoxycorticosterone
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| Sex steroids |
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Androgens
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- 3α-Androstanediol
- Androstenediol
- Androstenedione
- Androsterone
- DHEA
- DHEA sulfate
- Dihydrotestosterone
- Epiandrosterone
- Epitestosterone
- 16-Hydroxyandrostenedione
- 16-Hydroxy-DHEA
- 16-Hydroxy-DHEA sulfate
- Testosterone
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Estrogens
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- 3β-Androstanediol
- DHEA
- Estetrol
- Estradiol
- Estrone
- Estriol
- 2-Hydroxyestrone
- 16-Hydroxyestrone
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Progestogens
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- Deoxycorticosterone
- DHDOC
- 5α-Dihydroprogesterone
- 17-Hydroxyprogesterone
- Progesterone
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| Neurosteroids |
- Allopregnanolone
- 3α-Androstanediol
- Androsterone
- Cholesterol
- Corticosterone
- DHC
- DHDOC
- DHEA
- DHEA sulfate
- DHP
- Deoxycorticosterone
- Estradiol
- Etiocholanolone
- 17-Hydroxypregnenolone
- 17-Hydroxyprogesterone
- Isopregnanolone
- Pregnanolone
- Pregnenolone
- Pregnenolone sulfate
- Progesterone
- THB
- THDOC
- Pheromones: Androstadienol
- Androstadienone
- Androstenol
- Androstenone
- Estratetraenol
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| Others |
- Vitamin D: 7-Dehydrocholesterol
- Calcidiol/Calcifediol
- Calcitriol
- Cholecalciferol
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Corticosteroid signaling
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Glucocorticoid signaling
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Receptor
(ligands) |
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GR
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Agonists
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Mixed (SEGRAs)
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- Dagrocorat
- Fosdagrocorat
- Mapracorat
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Antagonists
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- 3α-Hydroxytibolone
- 3β-Hydroxytibolone
- Aglepristone
- Asoprisnil
- C108297
- C113176
- CORT-108297
- Cyproterone acetate
- Ketoconazole
- Lilopristone
- LLY-2707
- Miconazole
- Mifepristone
- Onapristone
- Org 34850
- PCN
- Telapristone
- Tibolone
- Toripristone
- Ulipristal acetate
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Enzyme
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Modulators
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- 20,22-desmolase, 17α-hydroxylase/17,20-lyase, 3β-HSD, 11β-HSD, 21-hydroxylase, 11β-hydroxylase, and 18-hydroxylase) (see also Steroid hormone metabolism modulators)
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| Others |
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Precursors/prohormones
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- Cholesterol
- 22R-Hydroxycholesterol
- 20α,22R-Dihydroxycholesterol
- Pregnenolone
- Pregnenolone sulfate
- 17-Hydroxypregnenolone
- Progesterone
- 17-Hydroxyprogesterone
- 11-Deoxycorticosterone
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Indirect
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- ACTH (corticotropin)
- CRH
- DHEA
- DHEA sulfate
- Plasma proteins (albumin, transcortin)
- Vasopressin
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See also: Androgenics • Estrogenics • Mineralocorticoids • Progestogenics
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Mineralocorticoid signaling
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Receptor
(ligands) |
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MR
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Agonists
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- 11-Deoxycorticosterone (desoxycortone)
- 11-Deoxycortisol (cortodoxone)
- 16α,18-Dihydroxy-11-deoxycorticosterone
- 17-Hydroxyaldosterone
- 18-Hydroxy-11-deoxycorticosterone
- 19-Norprogesterone
- Aldosterone
- Corticosterone
- Desoxycortone acetate
- Desoxycortone enanthate
- Desoxycortone glucoside
- Desoxycortone pivalate
- Hydrocortisone (cortisol)
- Fludrocortisone
- Fludrocortisone acetate
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Antagonists
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- 3α-Hydroxytibolone
- 3β-Hydroxytibolone
- 6β-Hydroxy-7α-thiomethylspironolactone
- 7α-Thiomethylspironolactone
- 17-Hydroxyprogesterone
- Benidipine
- Canrenoate potassium (potassium canrenoate)
- Canrenoic acid
- Canrenone
- Dicirenone
- Drospirenone
- Eplerenone
- Finerenone
- Gestodene
- Mespirenone
- Mexrenoate potassium
- Mexrenoic acid
- Mexrenone
- Oxprenoic acid
- Oxprenoate potassium (RU-28318)
- Pregnenolone
- Progesterone
- Prorenoate potassium
- Prorenoic acid (prorenoate)
- Prorenone
- RU-26752
- Spirorenone
- Spironolactone
- Spiroxasone
- Tibolone
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| Enzyme |
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Modulators
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- 20,22-desmolase, 17α-hydroxylase/17,20-lyase, 3β-HSD, 11β-HSD, 21-hydroxylase, 11β-hydroxylase, and 18-hydroxylase) (see also Steroid hormone metabolism modulators)
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|
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| Others |
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Precursors/prohormones
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- Cholesterol
- 22R-Hydroxycholesterol
- 20α,22R-Dihydroxycholesterol
- Pregnenolone
- Pregnenolone sulfate
- 17-Hydroxypregnenolone
- Progesterone
- 17-Hydroxyprogesterone
- 11-Deoxycorticosterone
- 18-Hydroxydeoxycorticosterone
- Corticosterone
- 18-Hydroxycorticosterone
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Indirect
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- ACTH (corticotropin)
- CRH
- Plasma proteins (albumin, transcortin)
- Vasopressin
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See also: Androgenics • Estrogenics • Glucocorticoids • Progestogenics
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| Authority control |
- LCCN: sh85001012
- NDL: 00563657
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