Drug induced pigmentation may take on many different appearances, one of the most common being a change in the color, or pigmentation, of the skin. Presentation
Cause
Drug-induced pigmentation of the skin may occur as a consequence of drug administration, and the mechanism may be postinflammatory hyperpigmentation in some cases, but frequently is related to actual deposition of the offending drug in the skin. : 125–6 The incidence of this change varies, and depends on the type of medication involved. Some of the most common drugs involved are NSAIDs, antimalarials, psychotropic drugs, Amiodarone, cytotoxic drugs, tetracyclines, and heavy metals such as silver and gold (which must be ingested, not just worn). Pathophysiology
There are 4 possible mechanisms to how this change may occur:
Accumulation of melanin, the skin pigment
Accumulation of drug or one of its products under any layer of the skin (usually the dermis or epidermis)
Accumulation of iron throughout the dermis from drug-induced post-inflammatory changes
The synthesis of special pigments, under direct influence of the drug

See also
Skin lesion

References


== External links ==
A congenital disorder of glycosylation (previously called carbohydrate-deficient glycoprotein syndrome) is one of several rare inborn errors of metabolism in which glycosylation of a variety of tissue proteins and/or lipids is deficient or defective. Congenital disorders of glycosylation are sometimes known as CDG syndromes. They often cause serious, sometimes fatal, malfunction of several different organ systems (especially the nervous system, muscles, and intestines) in affected infants. The most common sub-type is PMM2-CDG (formally known as CDG-Ia) where the genetic defect leads to the loss of phosphomannomutase 2 (PMM2), the enzyme responsible for the conversion of mannose-6-phosphate into mannose-1-phosphate. Presentation
The specific problems produced differ according to the particular abnormal synthesis involved. Common manifestations include ataxia; seizures; retinopathy; liver disease; coagulopathies; failure to thrive (FTT); dysmorphic features (e.g., inverted nipples and subcutaneous fat pads), pericardial effusion, and hypotonia. If an MRI is obtained; cerebellar hypoplasia is a common finding.Ocular abnormalities of CDG-Ia include: myopia, infantile esotropia, delayed visual maturation, peripheral neuropathy (PN), strabismus, nystagmus, optic disc pallor, and reduced rod function on electroretinography.Three subtypes PMM2-CDG, PMI-CDG, ALG6-CDG can cause congenital hyperinsulinism with hyperinsulinemic hypoglycemia in infancy. N-Glycosylation and known defects
A biologically very important group of carbohydrates is the asparagine (Asn)-linked, or N-linked, oligosaccharides. Their biosynthetic pathway is very complex and involves a hundred or more glycosyltransferases, glycosidases, transporters and synthases. This plethora allows for the formation of a multitude of different final oligosaccharide structures, involved in protein folding, intracellular transport/localization, protein activity, and degradation/half-life.