Table 18-3. Drugs and endocrine disease

Drug*	Effect
Drugs inducing endocrine disease
Chlorpromazine	Increase prolactin, causing galactorrhoea
Metoclopramide (and all dopamine antagonists)
Oestrogens
Iodine	Hyperthyroidism
Amiodarone
Lithium	Hypothyroidism
Amiodarone
Chlorpropamide	Inappropriate ADH secretion
Ketoconazole	Hypoadrenalism
Metyrapone, aminoglutethimide
Chemotherapy	Ovarian and testicular failure
Drugs simulating endocrine disease
Sympathomimetics	Mimic thyrotoxicosis or phaeochromocytoma
Amfetamines
Liquorice	Increase mineralocorticoid activity; mimic aldosteronism
Carbenoxolone
Purgatives	Hypokalaemia
Diuretics	Secondary aldosteronism
ACE inhibitors	Hypoaldosteronism
Drugs affecting hormone-binding proteins
Anticonvulsants	Bind to TBG – decrease total T4
Oestrogens	Raise TBG and CBG – increase total T4/cortisol
Exogenous hormones or stimulating agents
Use, abuse or misuse, by patient or doctor, of the following:
Steroids	Cushing’s syndrome
	Diabetes
Thyroxine	Thyrotoxicosis factitia
Vitamin D preparations	Hypercalcaemia
Milk and alkali preparations
Insulin	Hypoglycaemia
Sulphonylureas

A detailed history including the past, family and social history is essential for making the diagnosis, planning appropriate management and interpreting results of borderline hormonal blood tests. The past history should include previous surgery or radiation involving endocrine glands, menstrual history, pregnancy and growth in childhood. A full drug history is mandatory as endocrine problems are quite often iatrogenic (Table 18.3). Family history of autoimmune disease, endocrine disease including tumours, diabetes and cardiovascular disease is frequently relevant, and knowledge of family members’ height, weight, body habitus, hair growth and age of sexual development may aid interpretation of the patient’s own symptoms.

Physical signs are listed under the relevant systems.

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