A large proportion of erythrodermic patients in this study were HIV positive. Inflammatory dermatoses were the commonest cause of erythroderma in all the patients studied. Drug reactions were the commonest cause in HIV positive patients. In the young black patient, erythroderma may be a marker for HIV infection.
Drug-induced cutaneous rashes, whether confined to the skin or part of a systemic disease, are characterised by a spectrum of inflammatory disease patterns that include perivascular dermatitis, nodular and diffuse dermatitis, vesiculobullous lesions, pustular eruptions, sclerodermoid reactions, vasculitis, folliculitis/perifolliculitis and panniculitis. While a single drug can elicit a range of reaction patterns, no reaction pattern is specific for a particular drug. Although the temporal link between initiation of drug therapy and the onset of the drug rash is critical to the diagnosis, drug reactions may also occur during the course of chronic drug ingestion. Clues to the drug-induced nature of the cutaneous eruption include the presence of overlapping histological reaction patterns and incongruent clinical and histopathological features. While eosinophils are an important tell-tale sign of a drug-induced reaction, they may also be conspicuous in skin rashes devoid of a drug association. Furthermore, eosinophils may be sparse or absent in some drug exanthems. Heightened awareness of the mimicry of a wide spectrum of cutaneous pathology by an ever-increasing range of therapeutic agents is pivotal to the diagnosis of drug-induced skin pathology.
In 1934, Reis described an enzyme which lie claimed to be highly specific amid which acted only on nucleotides with the phosphate group attached to the fifth carbon of the pentose ; that is, on adenosine-5'-monophsosphoric acid and on
Hurler's disease is characterized by chondro-dystrophic skeletal changes, corneal opacities, hepatosplenomegaly and mental defect. The skeletal changes are such that the patient presents a large head, grotesque facies, deformed limbs and kyphosis.
The sites of action in the central nervous system of the rat of thiamine diphosphatase, an enzyme liberating phosphate from Vitamin B1, is described and illustrated. The optic tectum of the domestic fowl has also been examined. Some histological and cytochemical properties of the enzyme in these two species is compared. The activity of this enzyme may be involved in the pathological disturbances and tissue damage occurring in thiamine deficiency.
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