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The Morris syndrome is a X-linked recessive condition due to a complete or partial insensitivity to androgens, resulting in a failure of normal masculinization of the external genitalia in chromosomally male individuals. This failure of virilization can be either complete or partial depending on the amount of residual androgen receptor function. The phenotype of individuals with partial androgen insensitivity syndrome may range from mildly virilized female external genitalia to mildly undervirilized male external genitalia. We describe a case of Partial Androgen Insensitivity Syndrome in a 21-year-old patient with a 46, XY karyotype, bilateral inguinal masses, clitoral enlargement and partial posterior labial fusion. Surgical care consisted of bilateral orchiectomy and plastic surgery of external genitalia. The patient underwent estrogen replacement therapy.

The concept of risk in the field of avitaminoses is very important and useful for the practitioner, who should consider two aspects: a) risk factors, which could be individual (physiological, pathological and psychological) and extra-individual (alimentary, environmental, etc.); b) subjects with an elevated risk of avitaminosis (childhood, old age, pregnancy, etc.). In these subjects the risk can be a generical one, when there is an elevated requirement for all vitamins (nursing women, sportmen, etc.) or a specific one, when there is a high requirement only for a single vitamin (osteomalacia, some professional diseases, use of oral contraceptives) or a vew of them (alcoholism, diabetes, etc.). On the basis of this kind of knowledge it is easy for the practitioner to estimate which vitamins are necessary for each subject or for a group of subjects in physiological or in pathological conditions. For example, there is an elevated risk of apyridoxinosis in old age (acalciferolosis in aged women), of athiaminosis and apyridoxinosis in diabetes, of apyridoxinosis in oral contraceptives users, of axeroftolosis in hyperthyroidism, of athiaminosis, apyridoxinosis, aniacinosis and anascorbosis in alcoholics. In the second chapter the concept of the latency period in avitaminosis is illustrated. This period corresponds to the interval between the moment when deficiency stimulus starts operating and the moment when its effect, that is the picture of avitaminosis, appears. The latency time is not measurable, on account of the difficulties in establishing the onset of the deficiency stimulus; generally it is very long and is followed by the period of biochemical symptomatology and subsequently by the one of clinical symptomatology. Each of these three phases can be further divided in several steps, which have summarized in a Table. The last chapter is dedicated to the classification of avitaminoses. From the etiopathogenetic point of view avitaminoses can be due to: a) deficiency of introduction (alimentary level)); b) deficiency of absorption (enteric level); c) deficiency of utilization (tissue level). From the clinical point of view avitaminoses can be distinguished in deficiency with: a) a complete clinical symptomatology (scurvy, beriberi, pellagra, rickets, osteomalacia, xerophthalmia, hemeralopia); b) an incomplete clinical symptomatology (mono- or oligo-symptomatic or partial clinical picture); c) a biochemical symptomatology only (subclinic or clinically asymptomatic picture).

The concept of "drug induced avitaminoses" originates from the observation that drugs may cause vitamin deficiencies. These avitaminoses belong to the "iatrogenic disvitaminoses" and can be subdivided into two groups since they may either represent unwanted side effects of a drug or may be utilized for therapeutical purpose. In the latter case they can be considered as "planned avitaminoses". All drugs are generally able to produce a deficiency of one or more vitamins and therefore have a "devitaminizing power". It would be desirable to quantify this property of drugs in terms of a "devitaminization index". Knowledge of this index, which should be acquired for new drugs during clinical research, is of primary importance since it allows to adapt the dosage and use of the drug to the vitaminic status of the patient and enables to foresee and prevent damages due to vitamin deficiency. Drug induced avitaminioses are produced more easily and are more severe if the devitaminizing power of the drug and its dosage are high, the therapy is long and the vitaminic status of the patient is optimal. Many subjects (old people, children, etc.) have an elevated risk of avitaminoses. Drug induced avitaminoses are produced by mechanisms acting both at the intestinal level (absorption, endogenous production, etc.) and at the tissue level (metabolism, utilization, etc.). Some of the mechanisms have not been completely clarified. These avitaminoses are numerous and frequent, but their prevention is relatively easy and always achievable. They constitute a new disease and cause an additional damage with respect to the primary illness. The social and economic aspects of this damage are evident considering that many pharmacological profilactic and therapeutic treatments of social illnesses, such as diabetes, tuberculosis, epilepsy, rheumatic diseases, etc. have a devitaminizing power. It is clear therefore that this pathology is particularly important in preventive medicine and that it must be known not only by practitioners and biologists but also outside the medical field.

The incorrect use of the terms vitamin overdosage and overload, hypervitaminosis and dysvitaminosis gives rise to errors in the classification and evaluation of their etiology and pathogenesis. Vitamin overdosage and overload are observed with every vitamin and produce high blood and tissue levels of the vitamin itself; however, the overdosage can be obtained only upon administration of high doses of a vitamin, while vitamin overload may originate from a variety of factors. Hypervitaminoses are known for vitamin A and D; they are accompanied by high blood levels, but are characterized by a specific symptomatology. The term dysvitaminosis comprises "every alteration of the physiological status of the vitamin, in terms of both its deficiency and its surplus". These considerations provide a unitary view of vitamin pathology and lead to the following proposal of an etiopathogenetic classification of dysvitaminoses: class A) dysvitaminoses due to overload, class B) dysvitaminoses due to deficiency. Each class in turn may be divided into congenital and acquired syndromes. In class A) the congenital syndromes are still not well known, the acquired syndromes comprise those with hypervitaminosis (hypervitaminosis A and D) and those without hypervitaminosis (for the other vitamins). In class B) the congenital syndromes comprise diseases produced by inborn enzymatic errors and by other etiologies, the acquired syndromes can be distinguished in physiological (age, pregnancy, etc.) and pathological (nutritional, iatrogenic, etc.) ones. On this basis hypervitaminoses A and D can be considered as non obligatory dysvitaminoses due to overload; their origin has a complex etiology, since the liposolubility of the vitamins and the prolonged use of high dosages are not the only factors responsible for the hypervitaminosis.

A loading dose of tryptophan induces a marked increase of tryptophan-pyrrolase (substrate induction) and a decrease of 3-OH-anthranilic-oxidase values in rat liver; in the kidneys of the same experimental animals the 3-OH-anthranilic-oxydase is instead unchanged. In other experimental conditions (surrenectomized or pyridoxine depleted rats, with or without tryptophan loading; with prednisolone loading) a more or less important substrate induction is always reported, whereas no variation occurs in the values of 3-OH-anthranilic-oxydase. These data are not sufficient to state whether there is a connection between the opposite responses of the two enzymatic activities obtained after tryptophan loading in rat liver homogenate. On the other hand, it should be kept in mind that they do not represent the overall effect induced by the aminoacid loading, but refer only to one moment of the action exerted by the loading itself. In order to acquire a thorough knowledge of the observations made so far and to formulate some assumptions which may be helpful for the interpretation of the relevant mechanisms, it is necessary to investigate the kinetics of both enzymes, and to study their regulatory mechanisms in particular after tryptophan loading.

The problem of the relationship between the thiamine and autonomic system drugs was studied about 30 years ago. To the vitamin was attributed an excitatory effect upon the peripheric section of parasympathetic nervous system and a synergic action with acetylcholine. Both an acetylcholine-like substance and thiamine are liberated at the nerve terminals after a stimulation. A similar synergic action of thiamine with adrenaline was also demonstrated. The study of the relationship between these drugs and the vitamin B1 is also now interesting. We want to stimulate a new series of experiments on this subject with the reprint of this review.