Ichthyosis

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Related to xeroderma: ichthyosis

ichthyosis

[‚ik·thē′ō·səs]
(medicine)
A congenital skin disease characterized by dryness and scales, especially on the extensor surfaces of the extremities.

Ichthyosis

 

fish skin disease, xeroderma, a skin disease characterized by sharply increased keratogenesis and retarded keratolysis.

Incidence of ichthyosis is a familial condition in half the cases and hereditary in 25 percent. It appears in early childhood (most often around age three), intensifies at puberty, and lasts throughout life. It is expressed in dryness of the skin and the accumulation of horny masses on the skin’s surface, in the form of scales or of massive horny plates that resemble fish scales. The excretion of oil and perspiration decreases sharply. The affection spreads over the entire skin surface, except at joint folds, axillae, and inguinal folds. On the face and scalp, ichthyosis appears in the form of furfuraceous desquamation. The condition of the skin improves in the summertime as a result of increased excretion of oil and sweat. Ichthyosis is treated with hot baths containing soda or table salt, followed by lubrication of the skin with emollient creams. Cod-liver oil and vitamins may be taken internally (in particular vitamin A). In the summer, prolonged sojourns in the south can be helpful (sea bathing).

I. N. VEDROVA

References in periodicals archive ?
Caption: Figure 1: Representative agarose gel image showing nucleotide polymorphism by polymerase chain reaction (PCR) restriction fragment length polymorphism of (a) xeroderma pigmentosum complementation group D (XPD) C22541A at codon 156 of the exon 6 (lane 1: 100bp DNA ladder, lane 2: Uncut PCR product, lane 3: Wild-type allele, lane 4: Heterozygote, and lane 5: Variant allele), (b) XPD G23592A at codon 312 in the exon 10 (Lane 1: 100bp DNA ladder, lane 2: Uncut PCR product, lane 3: Asp/Asp genotype lane 4: Asp/Asn genotype, and lane 5: Cys/Cys genotype), and (c) XPD A35931C at codon 751 in the exon 23 (lane 1: 100bp DNA ladder, lane 2: Uncut PCR product, lane 3: Lys/Lys genotype lane 4: Lys/Gln genotype, and lane 5: Gln/Gln genotype)
Xeroderma pigmentosum-Cockayne syndrome complex, De Sanctis Cacchione variant (dSCS) and Rothmund Thomson syndrome (RTS) were among the differential diagnosis until further investigations were carried out.
Xeroderma, which was found in 373 subjects (3.68%), was most commonly observed in girls in the 6-11-year age group.
A 64-year-old man with a medical history of micropapillary thyroid cancer and stage IIIb lung adenocarcinoma with no evidence of active disease for 3 years after chemotherapy and radiation presented with subjective complaints of new onset fatigue, nausea, scalp tenderness, and xeroderma. His medications included gabapentin 300 mg four times a day for chemotherapy-induced neuropathy, erlotinib 150 mg once daily for epidermal growth factor receptor- (EGFR-) positive lung adenocarcinoma, and omeprazole 40 mg once daily for subjective gastroesophageal reflux disease.
The consequences of NER defects can be explained by three autosomal recessive syndromes: xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy [76].
A study examining light sources in the environment of a child with xeroderma pigmentosum suggested that indoor lights emit unexpected amounts of UV light as measured by a spectral radiometer.
This outcome occurred, at least in part, because an enzyme that repairs UV-damaged skin - xeroderma pigmentosum group A (XPA) - shifted its daily cycle to be less active in the day.
Stomach pain, muscle and bone pain, fever, headaches, tachycardia, edema, prolonged Q-T interval on electrocardiography (ECG), chest pain, hypotension, fatigue, headache, insomnia, rigors, paresthesia, anxiety, dizziness, depression, pain, dermatitis, pruritus, xeroderma, diaphoresis, erythema, hypokalemia, hyperglycemia, nausea, sore throat, hypomagnesemia, hyperkalemia, weight gain, abdominal pain, vomiting, diarrhea, anorexia, constipation, and decreased appetite.
The importance of NER is evidenced by the severe human diseases that result from in-born genetic mutations of NER proteins such as xeroderma pigmentosum and Cockayne's syndrome [18, 19].
Xeroderma Pigmentosum (XP) is a rare autosomal recessive disorder, first described by Hebra and Kaposi in 1874, which is caused by a defective nucleotide excision repair (NER) system, which produces mainly skin, ocular, and neurologic alterations [1, 2].
Its association with sun-exposed areas of the skin and its increased prevalence in patients with xeroderma pigmentosum have supported theories that exposure to UV light plays a role in the development of KA [2,16].
demonstrated that transgenic expression of the human xeroderma pigmentosum groupC(XPC) gene throughalentiviralvectorcould mitigate this age-related decline in pluripotency markers expression by DPSCs.