Pseudocyanosis

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Histology of a skin biopsy in pseudocyanosis: deposits of iron-containing pigment in the dermis and basal epidermis layers (Prussian blue reaction).

Under a pseudocyanosis refers to a bluish or gray-bluish discoloration of the skin and / or mucous membranes, in contrast to the cyanosis not to a reduced oxygen content of the blood ( hypoxemia back) or a decreased blood flow, but usually pigment deposits. The possible causes are drug side effects or the ingestion of certain metals and metal compounds. In addition, some diseases can lead to the appearance of pseudocyanosis. Pseudocyanosis is always probable if cardiovascular disease can be ruled out as the cause and the change does not fade with finger pressure.

The dark reddish skin changes in polycythemia vera are sometimes referred to as pseudocyanosis .

Drug-induced pseudocyanosis

Amiodarone

After long-term use of the drug amiodarone , which is used to treat cardiac arrhythmias, photosensitization of the skin and rarely blue-gray pigmentation is observed. According to current doctrine, this is due to the light-induced formation of lipofuscin in dermal macrophages , which slowly regresses after the medication is discontinued. In a more recent study, however, no lipofuscin could be detected, but intradermal deposits of the drug itself.

Minocycline

The antibiotic minocycline from the tetracycline group, which is often used in acne therapy, can also lead to abnormal pigmentation if used over a long period of time. In the area of ​​the skin, three forms are distinguished. In type I there is a bluish black or gray pigmentation of the face, especially in areas where acne-related scarring or inflammation is present. Type II manifests itself on the skin of the shins or forearms as blue-gray pigmentation. A diffuse dirty brown discoloration in sun-exposed areas is observed in type III . The pigment of types I and II deposited extracellularly in the dermis and in dermal macrophages shows positivity in the histochemical detection of iron ( Berlin blue color), but also proves to be immunohistochemically positive for melanin . Type III shows melanin-positive pigmentation in basal keratinocytes and in dermal macrophages. The pathobiochemical causes of pigmentation are unknown; polymerized metabolites or insoluble chelation products of the drug may play a role. The pigmentation in types I and II are reversible, in type III irreversible.

Chlorpromazine and thioridazine

The neuroleptic and phenothiazine derivative chlorpromazine used in the treatment of schizophrenia and bipolar affective disorders can apparently lead to abnormal pigmentation symptoms in the sense of pseudocyanosis even after short-term use. In chronic therapy, this affects 1–3% of hospitalized patients and manifests itself in sun-exposed skin areas. The literature provides contradicting information on the reversibility of the changes. The pigmentation is probably based on a binding of the drug to pheomelanin and a prolonged retention in pigmented cells of the skin. The side effect of localized increased skin pigmentation has also been described for the phenothiazine derivative thioridazine .

Imipramine and clomipramine

An undesirable side effect of the tricyclic antidepressant imipramine is hyperpigmentation of sun-exposed skin areas due to deposits of a golden-brown, granular pigment in the superficial dermis. The etiology is probably based on the deposition of a complex of an imipramine metabolite with melanin. Correspondingly, the pigment shows a strong positivity in the Fontana-Masson color, while the iron detection is negative. Similar changes are also reported as a side effect of taking the tricyclic antidepressant clomipramine .

Chloroquine and hydroxychloroquine

Abnormal blue-black pigmentation of the skin is seen in connection with therapy with the antimalarial drug chloroquine . The chemical composition of the pigment distributed within the dermis has not been fully clarified. Histochemically, there is a positivity in the iron staining, the silvering and the Mallory staining. Long-term use of the derivative hydroxychloroquine can also lead to the deposition of a coarse-grained yellow-brown pigment in the superficial dermis, some of which can be displayed in the Fontana-Masson color, but not in the iron color (according to Perl). For both chloroquine and hydroxychloroquine, it is assumed that the substances combine with melanin.

Clofazimine

Clofazimin is a red phenazine dye that is used in the treatment of rhinoscleroma , lupus erythematosus , leprosy and other mycobacterial infections. The treated patients regularly develop a reddish discoloration of the skin and conjunctiva, which turns into a purple-brownish tinge with chronic use. Histologically, there are deposits of the drug in macrophages and, in the long term, increased epidermal melanin pigmentation and lipofuscin deposits. The changes are reversible after discontinuation of the drug.

Pseudocyanosis due to metals and metal compounds

silver

Progressive blue-gray discolouration of the skin is observed after chronic ingestion of silver compounds (e.g. silver nitrate , silver iodide ) or colloidal silver . A distinction is made between generalized ( argyria ) and localized ( argyrosis ) forms. Here, too, skin areas exposed to light are preferably affected. Light microscopy shows small, rounded, brown-black granular deposits in the area of ​​the basement membrane of the hair follicle epithelium .

gold

Gold compounds are used, among other things, in the therapy of rheumatoid arthritis ( chrysotherapy ). Chronic consumption can lead to deposits of gold in the form of brown-black pigment in dermal macrophages.

Pseudocyanosis as a symptom of the disease

Hemochromatosis

When hemochromatosis is a common genetic disorder that can associated with a pathologically high intestinal absorption of iron and lead to deposition of iron in parenchymal organs and in the skin.

Addison's disease

Primary adrenal insufficiency ( Addison's disease ) can lead to slow onset, progressive generalized hyperpigmentation of the skin due to increased secretion of the pituitary hormones MSH (melanocyte-stimulating hormone) and ACTH (adrenocorticotropic hormone).

Malignant melanoma

In rare cases, a clinically undetected malignant melanoma can lead to a diffuse slate-gray pigmentation ( melanosis ) of the skin, which can be misinterpreted as cyanosis. The pigmentation is a secondary phenomenon that is due to the presence of melanin metabolites in the circulation and in dermal macrophages or is based on a diffuse single cell metastasis.

Neonatal pseudocyanosis

A blue-gray discoloration of the skin can rarely be seen in newborns, which is likely to be associated with prenatal contusions , for example with a disproportionate relationship between the body size of the fetus and the maternal pelvis. This is based on hemosiderin deposits within the skin that occur after bleeding .

Unusual forms of pseudocyanosis

Food coloring

A case report describes the occurrence of pseudocyanosis after excessive consumption of blue food coloring ( brilliant blue FCF ). The synthetic dye was absorbed in the context of artificial nutrition, the substance being added to the tube feeding in order to be able to better recognize possible aspiration of stomach contents.

Textile paint

Sudden bluish discoloration of the skin due to textile dye has been documented in a number of case reports. Clinically, the changes are often initially misinterpreted as true cyanosis. Anamnestic information and the often possible washing off of the color ultimately lead to the correct diagnosis.

Hair dyes

An individual report describes a pseudo-cyanotic discoloration of the hands after applying a hair dye. The patient was an elderly woman who habitually scratched her head.

Infectious pseudochromhidrosis

This is a rare disease in which the skin changes color due to the secretion of sweat containing pigments. The cause is an increase in pigment-producing bacteria such as Bacillus spp. (blue color) or Pseudomonas aeruginosa (blue-green color).

Individual evidence

  1. ^ A. Baernstein, KM Smith, JG Elmore: Singing the blues: is it really cyanosis? In: Respir Care. 53 (8), Aug 2008, pp. 1081-1084. PMID 18655745
  2. ↑ Peter Reuter: Springer Lexicon Medicine. Springer, Berlin a. a. 2004, ISBN 3-540-20412-1 .
  3. ↑ A. Ammoury, S. Michaud, C. Paul, C. Prost-Squarcioni, F. Alvarez, L. Lamant, F. Launay, J. Bazex, N. Chouini-Lalanne, MC Marguery: Photodistribution of blue-gray hyperpigmentation after amiodarone treatment: molecular characterization of amiodarone in the skin. In: Arch Dermatol. 144 (1), Jan 2008, pp. 92-96. PMID 18209173
  4. ↑ TO Geria, AL Tajirian, G. Kihiczak, RA Schwartz: Minocycline-induced skin pigmentation: an update. In: Acta Dermatovenerol Croat. 17 (2), 2009, pp. 123-126. PMID 19595269 .
  5. ↑ S. Loganathan: Chlorpromazine-induced skin pigmentation with short-term use in a patient with bipolar disorder: a case report. In: Prim Care Companion J Clin Psychiatry. 9 (4), 2007, pp. 316-317. PMID 17934561
  6. ↑ U. Mårs, BS Larsson: Pheomelanin as a binding site for drugs and chemicals. In: Pigment Cell Res. 12 (4), Aug 1999, pp. 266-274. PMID 10454295
  7. ^ H. Berger: Pigmentation after thioridazine. In: Arch Dermatol. 100 (4), 1969, p. 487. PMID 5358114
  8. ^ ME Ming, J. Bhawan, CM Stefanato, TH McCalmont, LM Cohen: Imipramine-induced hyperpigmentation: four cases and a review of the literature. In: J Am Acad Dermatol. 40 (2 Pt 1), Feb 1999, pp. 159-166. PMID 10025739
  9. ↑ ML D'Agostino, J. Risser, L. Robinson-Bostom: Imipramine-induced hyperpigmentation: a case report and review of the literature. In: J Cutan Pathol. 36 (7), Jul 2009, pp. 799-803. PMID 19519613
  10. ↑ Z. Tunca, MI Tunca, A. Dilsiz, U. Bayol, M. Hancioğlu: Clomipramine-induced pseudocyanotic pigmentation. In: Am J Psychiatry. 146 (4), Apr 1989, pp. 552-553.
  11. ^ P. Marriott, PF Borrie: Pigmentary changes following chloroquine. In: Proc R Soc Med. 68 (8), Aug 1975, pp. 535-536.
  12. ↑ PK Puri, NI Lountzis, W. Tyler, T. Ferringer: Hydroxychloroquine-induced hyperpigmentation: the staining pattern. In: J Cutan Pathol. 35 (12), Dec 2008, pp. 1134-1137. PMID 18727667
  13. ^ CK Job, L. Yoder, RR Jacobson, RC Hastings: Skin pigmentation from clofazimine therapy in leprosy patients: a reappraisal. In: J Am Acad Dermatol. Aug 23 (2 Pt 1), 1990, pp. 236-241. PMID 2145325
  14. ^ Y. Kim, HS Suh, HJ Cha, SH Kim, KS Jeong, DH Kim: A case of generalized argyria after ingestion of colloidal silver solution. In: Am J Ind Med. 52 (3), Mar 2009, pp. 246-250. PMID 15502068
  15. ^ CE Keen, K. Brady, N. Kirkham, DA Levison: Gold in the dermis following chrysotherapy: histopathology and microanalysis. In: Histopathology . 23 (4), Oct 1993, pp. 355-360. PMID 7905458
  16. ↑ JK Limdi, JR Crampton: Hereditary haemochromatosis. In: QJM . 97 (6), Jun 2004, pp. 315-324. PMID 15152104
  17. ↑ R. Kumar, S. Kumari, PK Ranabijuli: Generalized pigmentation due to Addison disease. In: Dermatol Online J. 14 (2), Feb 28, 2008, p. 13. PMID 18700116
  18. ^ MV Klaus, F. Shah: Generalized melanosis caused by melanoma of the rectum. In: J Am Acad Dermatol. 35 (2 Pt 2), Aug 1996, pp. 295-297. PMID 8698909
  19. ↑ M. Nelson: Letter: Pseudocyanosis neonatorum. In: Br Med J . 2 (5970) Jun 7, 1975, p. 561. PMID 1148716
  20. ^ AJ Zillich, RJ Kuhn, TJ Petersen: Skin discoloration with blue food coloring. In: Ann Pharmacother. 34 (7-8), Jul-Aug 2000, pp. 868-870.
  21. ↑ T. Breithardt, M. Namdar, B. Hess: The "blue" man. In: ` Switzerland Med Forum. 6, 2006, p. 612.
  22. ↑ Stenberg Åsa. Sudden blåfärgning av huden - ett oroande symtom. In: Läkartidningen. 48, 2001, p. 5521. ( Full text ( Memento from March 27, 2014 in the Internet Archive ) PDF; 50 kB)
  23. ^ NG Gold: Points from letters: Pseudocyanosis. In: Br Med J. 3, 1974, p. 119.
  24. ↑ CA Ingvaldsen, TM Leegaard, G. Kravdal, C. Mørk: Infectious Pseudochromhidrosis: A Case Report and Literature Review. In: Acta Derm Venereol. 2019 Oct 14. PMID 31612235