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Results for “Pigmentation Disorders”

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At least 271 records · Page 15Linked to original sources
PubMed1971

Ceroid pigment formation and irreversible sterility in vitamin E deficiency.

Female rats maintained on a diet deficient in vitamin E for a prolonged period of 100 to 135 days, starting from birth, failed to conceive in spite of repeated matings. Dietary vitamin E supplementation for a period of 60 days following prolonged deficiency was ineffective in reversing the sterility, although a definite growth response was observed. These observations suggest that the tissue damage caused by lipid peroxidation, as evidenced by distinct brown ceroid pigment in the uterus and fallopian tubes, may be responsible for the irreversible loss of fertility observed in the vitamin E-deficient female rats.

Animals↗
PubMed1989

Brown bowel syndrome: an unusual cause of massive dilatation of the colon.

We report a case of the brown bowel syndrome presenting as major dilatation of the colon which resembled 'toxic dilatation' and necessitated subtotal colectomy. We confirm the reported association between the brown bowel syndrome, malabsorption, and hypovitaminosis E. Furthermore we document failure of the brown pigmentation to resolve after six months in spite of vitamin E supplements and correction of the malabsorption. Finally we suggest that, although the brown bowel syndrome is rare, it should be considered in cases of major colonic dilatation where the patient is or may be suffering from a malabsorption syndrome, and where the sigmoidoscopic appearances do not suggest severe inflammatory bowel disease.

Adult↗
PubMed1981

Intra-neural ceroid-like pigment following the treatment of lepromatous leprosy with clofazimine (B663; Lamprene).

A 33 year old male Nigerian presented with widespread involvement of peripheral nerves, several of which were tender and painful. Nerve biopsies confirmed the presence of Mycobacterium leprae in both endoneurial and perineurial areas, mainly in foamy macrophages (Virchow cells), but there were also large accumulations of an amorphous, acid-fast and alcohol-fast material which was not obviously of bacterial origin. Appropriate stains indicated that this had many characteristics of lipofuscin. Although not previously known, it was at this stage discovered that the patient had received treatment with anti-leprosy drugs nearly three years before presentation in this country. One of these was clofazimine, an aniline aposafranine derivative known to produce a ceroid-like pigment in the tissues of patients treated with this drug or lepromatous leprosy.

Adult↗
PubMed1985

Drug eruptions.

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Alopecia↗
PubMed1985

Cutaneous abnormalities in uremic patients.

94 uremic patients, 68 on regular hemodialysis treatment (RHT) and 26 on chronic ambulatory peritoneal dialysis (CAPD), were followed for up to 20 months in search of dermatological manifestations. 79% of RHT and 76% of CAPD patients had some kind of cutaneous lesion. The most characteristic features of cutaneous involvement in RHT and CAPD patients were: cutaneous xerosis, pruritus, infectious manifestations and disorders of pigmentation. In 4 RHT patients, precancerous and cancerous manifestations were also observed.

Adolescent↗
PubMed1980

Neuronal ceroid-lipofuscinosis in older dachshunds.

A lysosomal storage disease with accumulation of periodic acid-Schiff- and Sudan black-positive autofluorescent granules in neurons occurred in one 5 1/2- and one 7-year-old dachshund. Ultrastructurally, the storage material consisted of membranous material arranged in stacks and fingerprint patterns. The disease was defined as ceroid-lipofuscinosis, and resembled a previously reported case in an adult dachshund.

Animals↗
PubMed1981

Type 2 GM1 gangliosidosis with long survival and neuronal ceroid lipofuscinosis.

Neurologic deterioration began in a girl before age 2 years. By 4 she was spastic and decerebrate. GM1 gangliosidosis was diagnosed by absence of beta-galactosidase activity in leukocytes and fibroblasts. She died at 17 years. Her small brain contained only 2.61 mumole glycolipid N-acetylneuraminic acid per gram, and was filled with autofluorescent material. GM1 gangliosidosis was confirmed by the presence of membranous cytoplasmic bodies, by the absence of beta-galactosidase, and by failure of complementation when the patient's fibroblasts were fused with cells from other forms of GM1 gangliosidosis. The autofluorescent material probably accumulated because of the long survival rather than the primary enzyme defect.

Brain↗
PubMed2001

Histologic, immunohistochemical, and ultrastructural findings in a case of minocycline-associated "black thyroid".

We report on a 37-yr-old woman with known antemortem ingestion of minocyclin who died suddenly from a ruptured cerebral aneurysm. At autopsy, her thyroid gland, although not enlarged, was diffusely black, caused by the deposition of a melanin-like pigment that stained positive with Schmorl's reagent. The pigment could be bleached with permanganate, and on examination by electron microscopy, it appeared to be deposited within the thyrocyte lysosomes. Additional immunostaining with many antibodies revealed an increase in vimentin staining in the follicular epithelium compared with normal control thyroid glands. Staining for cytoplasmic thyroglobulin was markedly reduced, despite normal thyroid indices performed on stored antemortem blood. Stainable ubiquitin in the follicular epithelium appeared reduced compared with control thyroid tissues. These immunohistochemical findings may reflect disruptions of lysosomal transport and function associated with the abnormal accumulation of pigment. This appears to be the only case of minocyclin-associated "black thyroid" in which extensive immunohistochemical investigations have been performed.

Adult↗
PubMed1977

Ceroidosis.

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Ceroid↗
PubMedDate not supplied

Is an imbalanced calcium-homeostasis responsible for the experimentally induced endolymphatic hydrops?

The target of the investigations were the presumably ion-transporting cells of the vestibular organ, i.e. the area of 'dark cells' of the semicircular canal and utriculus. Those cells have been assayed for structural changes by LM and EM and for alterations of the ionic content (LAMMA) in coloured guinea pigs with unilaterally induced endolymphatic hydrops. Characteristically changed structures of the secretory epithelium and disordered pigmentation in the vestibular organ were noted. Those cellular alterations were accompanied by intracellular ionic changes, especially an increased level of Ca2+ in the light cells and melanocytes. Our investigations show that, at least for experimental hydrops, an imbalanced homeostasis of Ca exists that may be responsible for the enlargement of the endolymphatic space.

Animals↗
PubMed1990

Brown-bowel syndrome. Review of the literature and presentation of cases.

Four cases of brown-bowel syndrome (BBS) are presented. BBS is found in malabsorptive conditions secondary to diseases involving the liver, pancreas, and gastrointestinal tract. Morphologically, BBS is characterized by deposition of lipofuscin in the tunica muscularis, and electron microscopy shows degradation of smooth-muscle cell mitochondria. It is probable that BBS is a manifestation of vitamin E deficiency causing smooth-muscle cell 'mitochondrial myopathy'. Normal bowel function is retained, causing bowel hypotonia, and an aggravation of the underlying disease occurs. On suspicion of BBS, diagnosis is obtained in full-wall biopsy specimens of the intestine.

Aged↗