O-p′DDD therapy in Cushing's syndrome and in obesity with Cushingoid changes

Danowski, T. S.; Sarver, Margaret E.; Moses, Campbell; Bonessi, James V.

doi:10.1016/0002-9343(64)90008-7

Cited by 32 publications

(3 citation statements)

References 20 publications

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“…This was achieved, however, at the expense of troublesome side-effects even with the relatively low dosage used. Whilst anorexia, nausea, vomiting and diarrheoa are common, skin rashes and alopecia are also well documented (Lubitz et al, 1973) whilst encephalopathy is unusual (Danowski et al, 1964). In patients demonstrating a hormonal response the need for glucocorticoid replacement therapy should be anticipated (Schein, 1972) and, indeed, replacement doses of a mineralocorticoid are also frequently required (Hogan et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

HEPATIC MICROSOMAL ENZYME INDUCTION AND ADRENAL CRISIS DUE TO o,p’DDD THERAPY FOR METASTATIC ADRENOCORTICAL CARCINOMA

Hague

May

Cullen

1989

Clinical Endocrinology

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Two cases are described in which metastatic adrenocortical carcinoma associated with Cushing's syndrome was treated with mitotane (o,p'DDD). The first patient had initially been treated by bilateral adrenalectomy and, whilst responding to mitotane biochemically and by remission of metastases, experienced repeated episodes of adrenal crisis requiring a substantial increase in steroid therapy. The second patient failed to respond to the drug, but evidence of hepatic enzyme induction was noted during its administration. It is suggested that hepatic microsomal enzyme induction can occur in association with treatment with mitotane and that this can lead to an increased destruction of exogenous steroid with clinical consequences.

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Section: Discussionmentioning

confidence: 99%

HEPATIC MICROSOMAL ENZYME INDUCTION AND ADRENAL CRISIS DUE TO o,p’DDD THERAPY FOR METASTATIC ADRENOCORTICAL CARCINOMA

Hague

May

Cullen

1989

Clinical Endocrinology

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“…Among workers in a plant manufacturing polybrominated biphenyls (PBBs), a high prevalence of primary hypothyroidism was encountered (Bahn et al 1980). Although non-occupational, treatment of patients with the organochlorine pesticide o,p'-DDD decreased serum protein-bound iodine (Danowski et al 1964). Long term toxic effects of consumed grain treated with hexachlorobenzene included reduced plasma thyroid hormone levels accompanied by thyromegaly (Peters et al 1982).…”

Section: Introductionmentioning

confidence: 99%

Interactions of halogenated industrial chemicals with transthyretin and effects on thyroid hormone levels in vivo

Berg¹,

Raaij²,

Bragt³

et al. 1991

Arch Toxicol

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Previous results in experimental systems have suggested that hydroxylated PCBs may decrease thyroid hormone levels through associative interaction with transthyretin. In the present paper it was investigated whether this property was also shared by various industrial chemicals, mainly pesticides. In total, 65 compounds from 12 chemical groups were analyzed for direct interference with the T4 binding site of transthyretin using a competitive binding assay. Sixty per cent of the compounds were competitive at a concentration level of 100 microM. Relatively strong interactions were observed by several chlorophenols, chlorophenoxy acids and nitrophenols, as well as by individual compounds such as hexachlorobenzene, dicofol, bromoxynil and tetrachlorohydroquinone. Examples from these chemical groups, e.g. pentachlorophenol, 2,4-dichlorophenoxybutyric acid, dinoseb and bromoxynil, also reduced plasma TT4 levels in rats. In addition, bromoxynil decreased plasma TT3 levels. The results suggest the existence of a number of halogenated industrial chemicals with a potential for lowering plasma thyroid hormone levels through interference with hormone transport carriers.

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“…Fortunately, no obvious toxic sign except for temporary nausea and vomiting was recognized in this case. However, decreased PBI and hypercholesterolemia were seen during the course of treatment, as reported by Donowski et al(1964).…”

mentioning

confidence: 58%

A Case of Adrenocortical Cancer Treated with O, P'-DDD

et al. 1969

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SynopsisO,P'-DDD was given to a 41-year-old Japanese woman with metastatic adrenocortical carcinoma with dosage of 8g a day orally. The treatment resulted in objective regression of all metastases for 237 days. Significant decrease was seen in 17-ketosteroid, 17-hydroxycorticosteroid, 17-ketogenic steroids, estrogen in the urine, and 17-hydroxycorticosteroid, cortisol in plasma during the course of treatment.

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O-p′DDD therapy in Cushing's syndrome and in obesity with Cushingoid changes

Cited by 32 publications

References 20 publications

HEPATIC MICROSOMAL ENZYME INDUCTION AND ADRENAL CRISIS DUE TO o,p’DDD THERAPY FOR METASTATIC ADRENOCORTICAL CARCINOMA

HEPATIC MICROSOMAL ENZYME INDUCTION AND ADRENAL CRISIS DUE TO o,p’DDD THERAPY FOR METASTATIC ADRENOCORTICAL CARCINOMA

Interactions of halogenated industrial chemicals with transthyretin and effects on thyroid hormone levels in vivo

A Case of Adrenocortical Cancer Treated with O, P'-DDD

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