[The first days following heart transplantation].
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Biomedical subjects
Publications and source records attributed to H Høyer.
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The course of serum zinc (S-Zn), plasma albumin (P-Alb), urinary zinc, serum alkaline phosphatase, and plasma alpha 2-macroglobulin levels was monitored in 14 adult hospitalized patients receiving oral glucocorticoid therapy, about 40-50 mg prednisone daily for various skin diseases. Within 3 days S-Zn decreased slightly from 12.6 +/- 2.3 mumol/liter (mean +/- SEM) to 11.1 +/- 2.5 mumol/liter. Then the level rose to about 14-15 mumol/liter and remained elevated, but within the normal range for the next 2 weeks. The P-Alb level showed parallel fluctuations although less pronounced. The S-Zn/P-Alb ratio increased from 0.024-0.029. No consistent patterns could be seen in the fluctuations occurring in the additional parameters studied. The possible role of ACTH on the S-Zn regulation is discussed.
A detailed clinical study of 76 males with steroid sulphatase deficiency confirmed the ichthyosis of this disorder to be identical with the classical descriptions of recessive X-linked ichthyosis. The appearance of regular ichthyotic scaling seems in most instances to be heralded by a general peeling of the skin. This characteristic feature was registered between age 1 and 3 weeks in 19 of 21 young boys followed due to a placental steroid sulphatase deficiency. Later on, polygonal scales giving a 'dirty' appearance were most pronounced on the distal parts of the body and extensor aspects of the extremities. The ichthyosis aggravates through childhood into adult age.
In the present study we monitored serum zinc (Zn) and serum alkaline phosphatase (AP) levels during Zn supplementation in (A) a young zinc depletion syndrome (ZDS) patient with severe Zn deficiency, (B) three acrodermatitis enteropathica (AEP) patients with mild Zn deficiency and (C) 7 elderly and 3 younger patients without Zn deficiency. In (A) serum Zn and serum AP values were low, but following parenteral Zn the parameters rose to normal levels (r = +0.79, p less than 0.001). In (B) serum Zn and serum AP levels decreased when oral Zn was stopped, but shortly returned to normal upon reinitiation of Zn. In (C) Zn therapy caused a rise in the serum Zn concentration whereas the serum AP activity decreased (r = -0.01, p greater than 0.1). The results suggest that serial determinations of serum Zn and serum AP during Zn supplementation may be a valid tool in the diagnosis of severe and mild Zn deficiency as well as in the exclusion of the diagnosis.
Seven patients with prurigo nodularis and one with aphthous stomatitis were given 40-115 g of thalidomide for 1 to 6 years. They all developed a predominantly sensory peripheral neuropathy mainly involving the lower limbs. Five patients had an unpleasant tight feeling around the feet. Nerve conduction studies showed small sensory action potentials from the lower limbs with normal or only mild slowing of sensory conduction velocity indicating an axonal neuropathy. The dermatological disorder improved dramatically in all, but treatment had to be discontinued because of the severe side-effects. Thalidomide, if used, should be given only over a short period because of its neurotoxic effect.
Seventy-six ichthyotic male patients with a biochemically confirmed diagnosis of steroid sulphatase deficiency are reported. Ascertainment was based on either a previous diagnosis of placental steroid sulphatase deficiency (21 probands and 15 secondary cases), or ichthyosis with steroid sulphatase deficiency (29 probands and 11 secondary cases). The ichthyotic phenotype of the first group was indistinguishable from that of the other group, and completely fitting the classic description of recessive X-linked ichthyosis. A prominent skin peeling in early infancy was found to be a characteristic feature of this syndrome. Maldescent of the testis was registered in 9 patients; and testis cancer had been diagnosed in 2 males with normally descended gonads. This high proportion of patients with gonadal abnormalities strongly indicates a relation with the steroid sulphatase deficiency. Corneal opacities, not affecting visual acuity, were seen in 14 out of 28 males by slit-lamp examination.
In an open prospective half-side trial, creams containing 10% cholesterol or 10% urea were applied to lesions in 20 steroid-sulphatase-deficient male patients with recessive X-linked ichthyosis. In 18 there was a good response to the cholesterol cream. In 13 patients the response to cholesterol was better than that to urea. None showed a better response to urea than to cholesterol. A reduction in the cholesterol content of the stratum corneum may be responsible for abnormal cornification in recessive X-linked ichthyosis.
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During the 15-year period from 1965 to 1979 a total of 142 cases of chondrodermatitis nodularis chronica helicis were diagnosed. 32% were women, a higher proportion than in earlier materials. The treatment was principally curettage followed by electrocauterization. 78 patients were re-examined after an average lag of 7.1 years. The relapse rate was 31%. This simple surgical technique seems equal to the more elaborate procedures in respect of recurrence rate and more satisfactory from a cosmetic point of view.
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65Zinc absorption in patients suffering from generalized scleroderma was studied by means of whole-body counting technique following a single dose of 65Zn. In 4 untreated patients the mean 65Zn absorption was calculated to 35% (range 20-59%). Five patients receiving oral D-penicillamine had a numerically higher mean absorption value of 55% (range 37-74%). The results corroborate earlier studies on the effect of D-penicillamine on 65Zn absorption in rats.
In zinc deficiency disorders the serum zinc concentration is low and the activity of alkaline phosphatase in serum is declining. The clinical picture includes a poor general condition and a characteristic dermatitis on hands, feet, in the face, and the anogenital region. In acute zinc deficiency, the eruption is vesico-bullous, in the chronic state parakeratotic psoriasiform. Widespread exzéme craquelée is an additional feature of the clinical picture, as seen in cirrhotics with acquired zinc deficiency. Alopecia, Beau lines on the nails, and hair changes may develop. In severe cases zinc therapy usually in the form of zinc sulphate may be administered i.v. (10-20 mg Zn daily). Oral zinc therapy is initially given in high doses (145-150 mg Zn daily). Long-term high zinc doses may interfere with copper metabolism and are only indicated for acrodermatitis enteropathica.
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Acquired zinc deficiency in two patients suffering from alcoholic liver cirrhosis is reported. Skin changes included bullae and erosions on the heels, desquamating dermatitis on feet, hands and shins, and localized alopecia. Following oral zinc therapy the skin changes disappeared and Beau lines were later seen on the finger nails. Concomitantly with the rise in the depressed plasma zinc levels, serum alkaline phosphatase and prothrombin levels rose and serum bilirubin decreased. The observations are in agreement with earlier reports dealing with congenital and conditioned zinc deficiency and oral zinc therapy in alcoholic liver cirrhosis.
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Seven groups of 8 rats each were orally loaded with zinc, the daily dose varying from 1.8 to 58 mg, corresponding to about 3 to 100 times of their estimated daily intake of zinc. To record the absorption of zinc, the rats were given a single dose of 65Zn. The retention of the isotope was measured in a whole animal counter at regular intervals. The dose of 58 mg was obviously toxic, since half of the animals died within 5 days. The net absorption of zinc in the remaining experimental groups was found to vary from about 7% in the group receiving the smallest loading dose to 1.8% in the group receiving the highest dose. From the absorption values, as determined by extrapolation of semilog retention curves, the total amount of absorbed zinc was estimated. It was found to differ from about 170 micrograms to about 530 micrograms zinc daily, increasing three times as the loading dose was increased 16 times. This discrepancy suggests the existence of regulatory mechanisms of the absorption of zinc from the intestine.