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Skin diseases in alcoholics

Authors:

Abstract

Alcohol abuse is associated with many health problems, especially skin changes. As a small, water- and lipid-soluble molecule, alcohol reaches all tissues of the body and affects most vital functions. Cutaneous diseases are now emerging as useful markers of alcoholism detectable at an early and possibly reversible stage of the disease, thus being of substantial importance to dermatologists and general practitioners. The most common skin manifestations of alcoholism presented in this review article are urticarial reactions, porphyria cutanea tarda, flushing, cutaneous stigmata of cirrhosis, psoriasis, pruritus, seborrheic dermatitis, and rosacea.
Skin Diseases in Alcoholics
Krešimir Kostoviæ, Jasna Lipozenèiæ
Department of Dermatology and Venerology, Zagreb University Hospital Center, Zagreb,
Croatia
Corresponding author:
Krešimir Kostoviæ, MD
Department of Dermatology and Venerology
Zagreb University Hospital Center
Šalata 4
10000 Zagreb, Croatia
kreso.kostovic@zg.htnet.hr
Received: 15. 03. 2004.
Accepted: 20. 04. 2004.
INTRODUCTION
Alcoholism is a chronic, progressive and poten-
tially lethal disease characterized by alcohol (etha-
nol) dependence and multiorgan dysfunction, with
genetic, environmental and psychosocial factors
playing the main role in its development. The dis-
ease is characterized by the loss of control of alco-
hol intake and continuation of the habitual alcohol
intake in spite of its deleterious consequences (1).
Social concerns have brought the issue of sub-
stance abuse into the very focus of medical interest.
Dermatologists in particular regularly encounter pa-
tients seeking help for cutaneous manifestations of
alcohol or drug abuse. The lifetime prevalence of al-
cohol abuse has been estimated to 13.7% (2).
Nearly 12.5 million Americans (approximately 5-
10% of all alcohol drinkers) develop ethanol depen-
dence. In untreated alcoholics, life expectancy is re-
duced by 12-15 years (2).
In the absence of gastrointestinal diseases or
food intake, 80-90% of ingested ethanol is absor-
bed within 30-60 minutes. The absorbed ethanol is
oxidized in the liver by the aldehyde dehydroge-
nase enzyme, and excreted via renal and respira-
tory pathways and perspiration. Although rather
low, respiratory excretion proportionally reflects the
blood concentration of alcohol, which is why breath
sampling can be used to measure the level of intoxi-
cation.
Many interactions can occur when alcohol is
taken in conjunction with drugs. These interactions
can be antagonistic (effects are blocked or re-
duced), additive (sum effect), or supra-additive; hy-
persensitivity may also be present.
The skin is not spared from the detrimental ef-
fects of alcohol abuse. Alcohol can cause patho-
181
Acta Dermatovenerol Croat 2004;12(3):181-190 REVIEW
SUMMARY Alcohol abuse is associated with many health problems, espe-
cially skin changes. As a small, water- and lipid-soluble molecule, alcohol
reaches all tissues of the body and affects most vital functions. Cutaneous
diseases are now emerging as useful markers of alcoholism detectable at
an early and possibly reversible stage of the disease,thus being of substan-
tial importance to dermatologists and general practitioners. The most com-
mon skin manifestations of alcoholism presented in this review article are
urticarial reactions, porphyria cutanea tarda, flushing, cutaneous stigmata of
cirrhosis, psoriasis, pruritus, seborrheic dermatitis, and rosacea.
KEY WORDS alcohol abuse; health effects of alcohol; alcohol and the skin
logic skin changes directly or through dysfunction of
various organs. Alcohol-induced skin pathology
may be due to a direct toxic effect or consequential
to personal neglect, environmental factors, or inap-
propriate diet. However, there is no skin lesion spe-
cific for alcoholism (2). The disease imposes great
financial burden on the health care system. Alcohol
drinks, primarily beer and wine, are best described
in the literature. Beer and wine are naturally fer-
mented beverages with maximal alcohol concentra-
tion of 3% and 8-12%, respectively. The prevalence
and severity of some skin diseases are increased in
patients prone to excessive alcohol intake. Accord-
ing to Rosset and Oki (3), the prevalence of skin
diseases is 43% in male and 33% in female
alcoholics.
Alcohol use/abuse is associated with significant
health problems. Alcoholism is an important cofac-
tor in many diseases. It is often associated with ex-
posure to venereal diseases and human immuno-
deficiency virus (HIV) infection. Chronic alcohol
abuse can lead to liver cirrhosis, which ultimately
affects all body systems. Endocrine tissues and or-
gans are damaged by alcohol abuse rather than by
consequential hepatic dysfunction or chronic mal-
nutrition.
ETHYLIC FACE (FACIES AETHYLICA)
Chronic alcoholics tend to look older and have
“dull expression”. The skin of the face appears
smooth, oily and shiny, while the color of the skin
may be sallow or grayish blue. The conjunctivae
may be reddened, with thickened eyelid margins.
Poikilodermal changes on the neck and trunk are
commonly seen (2).
FLUSHING
Flushing is the most common skin manifestation
of acute alcohol intake, defined as the occurrence
of transient redness of the face and neck associ-
ated with the feeling of heat. The face, neck and up-
per trunk are the regions characteristically involved
by flushing, which occurs due to vasodilatation (4).
It appears as congestive erythema of the skin and
may be accompanied by weakness, sweating, pru-
ritus, and headache. Flushing may also be a normal
physiologic response (blushing caused by emotio-
nal reasons) or a menopausal symptom.
CUTANEOUS MANIFESTATIONS OF
ALCOHOLIC CIRRHOSIS
The cutaneous changes associated with alco-
holic cirrhosis are well documented, ranging from
spider nevus to petechiae, which are classic stig-
mata and dermatologic signs associated with alco-
holic cirrhosis.
Spider Nevus
Spider nevus (nevus araneus) is the site of dila-
tation of superficial cutaneous arterioles surround-
ed by fine branching radiations. Pressure upon the
central arteriole leads to the development of this le-
sion. Spider nevi are generally found on the face,
neck, upper trunk, shoulders, forearms and dorsal
aspect of the hands, and are the most common and
classic vascular abnormalities of liver disease and
alcohol abuse (5). They may also occur during
pregnancy and estrogen therapy.
Palmar Erythema
Palmar erythema is characterized by warm,
light-red patches on the thenar, hypothenar and fin-
ger pads. It is usually bilateral and symmetric, with
sharply delineated peripheral margins, and can oc-
cur during pregnancy and in a number of chronic
diseases (5). Palmar erythema has been attributed
to hyperestrogenism in chronic liver disease.
Nail Changes
Terry’s nails characterized by opaque white nail
plate with the exception of the distal part, which re-
tains its normal, pink color, are frequently seen in
cirrhosis patients (6). These patients may also
show transverse white strips, “clubbed nails” or
koilonychia (spoon nails). White nails are also de-
scribed in patients with cirrhosis, systemic sclero-
derma, and some other conditions (5).
Hair Changes
Hair changes are quite common, mostly in men.
Axillary, pubic and chest hairiness is reduced and
development of the female type of pubic hairiness is
frequently seen.
Caput Medusae
Caput medusae are dilated umbilical veins due
to portal hypertension.
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Skin Diseases in Alcoholics 2004;12(3):181-190
Petechiae and Ecchymoses
Petechiae and ecchymoses occur due to pro-
thrombin deficiency consequential to impaired liver
function. They mainly occur on the lower limbs in
patients with end-stage alcoholic cirrhosis.
Other skin diseases associated with alcoholism
and alcoholic cirrhosis include Dupuytren’s contra-
cture, vitiligo, disseminated superficial porokerato-
sis, nutritional deficiencies, pellagra and pellagroid
dermatoses, and skin infections.
PSORIASIS VULGARIS AND ALCOHOL
INTAKE
Epidemiology
Most epidemiologic studies carried out in the
last decade have confirmed the association of pso-
riasis and excessive alcohol intake. A study of the
prevalence of psoriasis relative to alcohol and liver
diseases found psoriasis to be more common in in-
dividuals drinking more than 50 g alcohol daily irre-
spective of liver disease (7). Another study showed
a higher prevalence of alcoholism in hospitalized
psoriatics, especially men, than in patients with
other skin diseases (8). A questionnaire study con-
ducted in Norway, revealed that psoriatics drank al-
cohol more frequently and in greater amounts than
nonpsoriatic patients (9). An Italian study confirmed
the excessive alcohol intake to be more common in
psoriatics than in the general population (10). Hig-
gins and duVivier (11) found 39% of psoriatics to
habitually take excessive amounts of alcohol,
whereas the prevalence of psoriasis in the alcohol-
ics included in rehabilitation programs was 10-fold
that recorded in the general population (12). Most of
these studies did not take into consideration the
possible additive factors, such as cigarette smok-
ing, that may have influenced the results. None of
these studies explained whether alcohol abuse in-
creases the risk of the development of psoriasis, or
it is just a phenomenon associated with the chronic
course and nature of the disease (4). Indirect evi-
dence for the possible etiologic association of alco-
hol intake and psoriasis has been provided by Stern
and Lange (13), who found cirrhosis to cause more
deaths among psoriatics than among other pa-
tients. These findings could possibly be explained
by the fact that alcoholic cirrhosis is more common
and/or more severe in psoriatics than in nonpsori-
atics.
Severity, Course and Prognosis
Generally, alcohol intake is associated with a
more severe form of psoriasis and lower therapeu-
tic responsiveness. Monk and Neill (14) found that
excessive alcohol consumption was significantly
more common in men with psoriasis who had a
more severe form of disease. In their studies con-
ducted in 1990 and 1994, Poikolainen et al (15,16)
found an association between alcohol abuse and
severity of the disease in both male and female
psoriatics. Exacerbation of psoriasis was consider-
ably more common in psoriatic patients with exces-
sive alcohol intake irrespective of sex than in pa-
tients with other skin diseases. According to Hig-
gins and duVivier (11,12), alcohol abuse is associ-
ated not only with a higher incidence and severity of
psoriasis but also with a different nature and distri-
bution of skin lesions. Thus, the patients could be
classified into two groups: one with severely in-
flamed skin and few scales, typically involving the
face, inguinal region, axillae and other flexures, and
the other predominated by hyperkeratotic foci, es-
pecially on the extremities. Little data are available
on the effect of alcohol consumption on therapeutic
results. In their study, Gupta et al (17) investigated
the relationship between alcohol consumption and
therapeutic success in 94 hospitalized patients with
moderate to severe psoriasis. Their results showed
an average daily intake of ³80 g ethanol to be more
frequently associated with lower therapeutic suc-
cess in men, but not in women. According to
Vincenti and Blunden (18), abstinence from alcohol
consumption can lead to remission, whereas
resumption of drinking habit results in exacerbation
of psoriasis.
Pathogenesis
The main question is whether the relationship
between alcohol intake and psoriasis is causative
or simply a phenomenon associated with the chro-
nic course of the disease and its social and psycho-
logical burden (19). There are several hypotheses
on the effect of alcohol on psoriasis, most of them
based on theoretical postulates and only a few on
the findings of psoriatic patient tissues. The major-
ity, if not all researchers, believes that alcohol influ-
ences psoriasis through the immune system. Alco-
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hol consumption has adverse effects on all immune
system components, thus rendering alcoholics sus-
ceptible to infection. As infections, especially strep-
tococcal, act as trigger factors for psoriasis, the ef-
fect of alcohol may imply an increased susceptibility
of these psoriatics to infection (19). A co-cultivation
model with keratinocytes obtained from psoriatic
patients and T-cell lymphoma (HUT-78) cell line
was developed in a study performed by Ockenfels
et al (20). In this model, HUT-78 cells were co-incu-
bated with keratinocytes from psoriatic patients and
cultivated for 24 h with or without the addition of eth-
anol. The levels of interleukin (IL)-2, IL-6, IL-8, inter-
feron-gand transforming growth factor (TGF)-a
were determined in supernatant culture. The levels
of interferon-gand TGF-awere increased by
150-175%, whereas the levels of IL-2, IL-6, and IL-8
showed no significant changes in the cultures with
the addition of ethanol in comparison with control
cultures. These findings may explain the exacerba-
tion of psoriasis associated with alcohol intake. This
study is highly relevant for research into psoriatic
keratinocytes, whereas the majority of other studies
did not tackle the direct immune impact of alcohol
on the skin.
PORPHYRIA CUTANEA TARDA AND
ALCOHOL INTAKE
Molecular Basis of Disease
Uroporphyrinogen decarboxylase (UROD) defi-
ciency is the main biochemical disturbance underly-
ing porphyria cutanea tarda (PCT). UROD cata-
lyzes uroporphyrinogen decarboxylation to copro-
porphyrinogen. In PCT, the hepatic activity of
UROD is less than 30% of normal values. The accu-
mulated porphyrinogens are readily oxidized to por-
phyrins, which cause phototoxic reaction upon be-
ing transported from the liver via plasma to the skin.
There are three types of PCT. One is the sporadic
form (type 1), accounting for 80% of patients, where
UROD deficiency is restricted to the liver. The sec-
ond one is the familial form (type 2), inherited as an
autosomal dominant trait, seen in the majority of the
rest of patients, with seminormal UROD activity in
all tissues; only 10%-20% of these patients have
clinical symptoms of PCT. The third form, type 3, is
the most infrequent form and biochemically similar
to type 1.
Alcohol and Other Risk Factors for PCT
Alcohol. Elder (21) found excessive alcohol in-
take to be a factor commonly associated with the
development of PCT. Alcohol abuse defined as the
intake of >40 g alcohol daily is found in 30-90% of
PCT patients. However, PCT is not a common com-
plication of alcoholism, as only 2% of cirrhotic alco-
holics have PCT. Obviously, alcohol is an important
factor in the pathogenesis of PCT, but not the main
cause of the disease.
Iron. Iron metabolism abnormalities are fre-
quently seen in PCT. Total body iron store is in-
creased in 60-65% of cases (22). Alcohol may con-
tribute to the pathogenesis of PCT by increasing
iron absorption (23,24).
Other risk factors. Hepatotropic viruses (hepati-
tis B and C) and estrogens are important factors for
PCT.
Alcohol and PCT Pathogenesis
Alcohol and hepatic UROD. Excessive alcohol
intake can temporarily reduce UROD activity in red
blood cells (25). However, neither the measure-
ment of urinary excretion of porphyrin (25-27) nor
the measurement of hepatic porphyrin concentra-
tion (28) indicates the hepatic UROD activity to be
frequently decreased in alcoholics.
Alcohol and hepatic heme synthesis. Alcohol in-
creases urinary excretion of coproporphyrin III. In
nonalcoholics, this effect is short-lived and directly
dependent on alcohol dosage (27,29-31). In chro-
nic alcoholics, the excretion of coproporphyrin is
frequently increased (26,31,32). The mechanism
by which alcohol increases the excretion of copro-
porphyrin III is not clear. It is believed that an in-
creased coproporphyrin III excretion reflects its en-
hanced hepatic production (21). The increased syn-
thesis of coproporphyrin III and hemoprotein re-
quires induction of hepatic 5-aminolevulinate (ALA)-
synthase, the enzyme regulating the rhythm of
heme synthesis. Occasional high ethanol doses
lead to transient enhancement of hepatic ALA-syn-
thase in PCT patients (33,34). The activity of ALA-
synthase is less increased in chronic alcoholics
with liver cirrhosis (23). In alcoholics, changes in
the porphyrin metabolism are more common than
PCT. In the pathogenesis of PCT, these changes
184 ACTA DERMATOVENEROLOGICA CROATICA
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Skin Diseases in Alcoholics 2004;12(3):181-190
may lead to UROD inactivation in predisposed pa-
tients.
ROSACEA AND ALCOHOL INTAKE
Rosacea is a chronic cutaneous disease typi-
cally involving the middle parts of the face, charac-
terized by mild flushing, permanent erythema and
telangiectasia (35). In more severe forms, papules,
pustules and rhinophyma may occur. According to
these symptoms, rosacea is classified into four
grades: I, mild flushing; II, permanent erythema and
telangiectasia; III, papules and pustules; and IV,
rhinophyma and tissue hyperplasia.
The factors known to act as triggers of flushing
in rosacea include emotional stress, warm drinks,
spiced food, and alcohol (36). Alcohol can precipi-
tate the progression of rosacea and, like in other
skin diseases, contributes to a depressed thera-
peutic response (2,37). Psychogenic factors are
also considered to play a role in rosacea.
A relationship of skin disease and stress is pre-
sumed in 90% of patients, whereas the association
of stress and alcohol consumption has been defi-
nitely established (38). There is strong clinical and
histologic evidence for sunlight to contribute to the
development of rosacea (35,39). Also, UV light in
combination with recurrent flushing appears to lead
to rosacea grade II (40).
Less is known about the triggers leading to pro-
gression to the papulopustular form of rosacea
(grade III). Implication of immunoregulatory mecha-
nisms has been postulated (39). In alcoholics, de-
pression of the cell-mediated immunity is found,
which may account for the progression of rosacea
in chronic alcoholics (40,41). Recently, the interest
has been focused on the possible role of Helico-
bacter (H.) pylori in the pathogenesis of rosacea.
However, the available results are contradictory
(42,43). It has been definitely demonstrated that H.
pylori has a central role in the development of duo-
denal ulcer. The increased incidence of peptic ulcer
in alcoholics may explain the possible causal rela-
tionship between H. pylori and rosacea (40). In the
study by Rebora et al (43), 84% of rosacea patients
were H. pylori positive. There is a higher rate of H.
pylori association with grade II (erythematous) than
with the more advanced grade III (papulopustular)
rosacea. The patients with excessive alcohol intake
had an increased level of collagen III propeptide, a
marker of enhanced collagen metabolism (44). Am-
plified skin collagen was detected in histologic stud-
ies in the skin of alcoholics (3), and may play a role
in the mechanism of hyperplasia observed in grade
IV rosacea (40).
ACNE VULGARIS AND ALCOHOL
INTAKE
Acne may be precipitated or aggravated by alco-
hol consumption in some patients (2). Propioni-
bacterium acnes is known to be responsible for the
pustular component of the disease. Skin infections,
including folliculitis, are more common in alcohol-
ics. The bacteria and yeasts produce reactive and
toxic acetaldehyde in the presence of high amounts
of alcohol (45), which could account for the adverse
effect of alcohol in skin diseases implying an infec-
tive component (40). Furthermore, the incidence of
acne in alcoholics aged around 40 years can reach
26% (46,47). Nevertheless, any direct causal rela-
tionship between alcohol consumption and acne
has been denied. Oral retinoid therapy is the treat-
ment of choice in the most severe forms of acne.
The dosage and clinical effects of oral retinoids are
limited, and the risk of side effects is increased by
excessive alcohol intake (48).
SEBORRHEIC DERMATITIS AND
ALCOHOL INTAKE
Strong association seems to exist between
seborrheic dermatitis and alcohol consumption. Al-
though seborrheic dermatitis is also quite common
among nonalcoholics, excessive alcohol intake has
been demonstrated to potentially lead to precipita-
tion and exacerbation of the disease (49). Parish
and Fine (46) reported that 11% of alcoholics in
their study suffered from seborrheic dermatitis.
Rosset and Oki (3) found seborrheic dermatitis of
the scalp in 10%, and seborrheic changes on the
face and other body surfaces in 7% of alcoholics,
i.e. in twice more patients than expected.
NUMMULAR ECZEMATOUS
DERMATITIS AND ALCOHOL INTAKE
Nummular eczematous dermatitis is more com-
mon in patients prone to alcohol abuse. More so,
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Skin Diseases in Alcoholics 2004;12(3):181-190
nummular eczematous dermatitis has been consid-
ered a significant indicator of the possible exces-
sive alcohol consumption. In one study, excessive
alcohol intake was recorded in more than 90% of
patients with nummular eczematous dermatitis
(11). As differentiated from patients with other in-
flammatory dermatoses, hepatic functional tests
are frequently elevated in these patients (50). Also,
abstinence is associated with clinical improvement
of nummular eczematous dermatitis, whereas con-
tinuation of habitual drinking may lead to therapeu-
tic difficulties and frequent disease relapses (40).
ALCOHOL AND INTOLERANCE
SYNDROMES, URTICARIAL AND
ANAPHYLACTOID REACTIONS
Intolerance syndromes associated with alcohol
intake include flushing syndromes and urticarial re-
actions, which are characterized by different patho-
logic mechanisms and clinical manifestations
(Table 1).
There are two groups of alcohol dependent
flushing syndromes: drug-alcohol flushing syndro-
mes associated with concomitant use of particular
drugs and alcohol (51,52), and simple alcohol flush-
ing not associated with drugs. Simple alcohol flush-
ing is found in 3-29% of westerners and 47-85% of
easterners (mostly Asiatic), which is why it is
named “oriental flushing” (53,54).
In flushing syndromes, erythema develops sev-
eral minutes upon alcohol intake predominantly on
the face and trunk, whereas the symptoms resolve
within 1-2 h. On the other hand, the severity of
drug-alcohol flushing does not increase with the in-
creasing amount of alcohol consumed, the severity
of simple alcohol flushing depends on the amount
of alcohol ingested (51,52). Both groups of flushing
syndromes can be accompanied by nausea, dizzi-
ness, headache, vomiting, and somnolence. Drug-
alcohol flushing syndromes occur with concomitant
intake of alcohol and the antidiabetic chlorpropa-
mide, antibiotic cephalosporin, and antimycotic gri-
seofulvin (52,55-59). Acquired flushing syndromes
can also occur in Hodgkin’s disease and other
malignant tumors, mastocytosis and hypereosino-
philic syndrome (60).
Urticarial reactions accompany various clinical
conditions and are considerably less common.
Contact urticarias are restricted to the site of alco-
hol contact, whereas anaphylactoid reactions are
systemic and occasionally life-threatening events
that follow oral ingestion of very small amounts of
alcohol. Within several minutes, erythema and
urticarial changes involve the upper trunk, and are
followed by asthma, hypotension and loss of con-
sciousness.
Although the intolerance syndromes may occur
early in life, their initial manifestation may occur af-
ter years of asymptomatic alcohol consumption
(61).
Pathogenetic Mechanisms
Modifications in alcohol metabolism have been
well documented in flushing syndromes, both ac-
quired and genetic. In patients with oriental flush-
ing, there is a hereditary defect of the aldehyde
dehydrogenase enzyme (61-65). Prostaglandins,
endogenous morphins, and abnormal susceptibility
to mastocyte release of histamine are candidate
cofactors for its occurrence (66).
The effect of chlorpropamide in drug-alcohol
flushing has been investigated in many studies. Dif-
ferent pathogenetic mechanisms have been pro-
posed, but it seems most likely that the genetic ba-
sis is involved. In addition to an increased drug con-
centration in the circulation, particular iso-enzymes
may be sensitive to the inhibitory effect of chlorpro-
pamide (55,56,67); however, aldehyde dehydroge-
nase is not altered.
In contact urticaria, immune, nonimmune and
other forms have been identified. Immune forms are
186 ACTA DERMATOVENEROLOGICA CROATICA
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Skin Diseases in Alcoholics 2004;12(3):181-190
Table 1. Intolerance syndromes, urticarial and ana-
phylactic reactions
Flushing syndromes
acquired:
drug-alcohol flush reactions
malignant diseases
genetic:
oriental flush syndrome
Urticarial reactions:
contact urticaria
generalized urticarial reactions/anaphylaxis
contact dermatitis
characterized by positive skin tests and positive
Prausnitz-Küstner reaction (68,69). In nonimmune
forms, positive skin reactions are induced by alde-
hydes and low aliphatic alcohols (70). In alcoholic
contact dermatitis, direct irritative effects of alcohol
are considered to play a substantial role (71-73).
Alternatively, positive epicutaneous tests might
point to a delayed immune reaction (60). In alco-
hol-induced urticarial and anaphylactic reactions,
the effects of prostaglandins, endogenous morph-
ins and mastocyte degranulation are considered to
be the main pathogenetic factors (74-76). IgE medi-
ated type 1 allergic reaction has also been discus-
sed (77).
Allergologic Testing for Alcohol
Intolerance Syndromes, Urticarial and
Anaphylactoid Reactions
Comprehensive allergologic testing should be
done to differentiate the type of alcohol intolerance,
to assess the severity of disease, and to exclude
other potential causes (e.g., other alcohol drink in-
gredients, food, or food additives) (Table 2).
Therapy
Avoiding any contact with alcohol and its metab-
olites, especially alcohol ingestion, is the most im-
portant measure in therapy for alcohol intolerance.
The medications used include oral or parenteral
antihistaminics and corticosteroids.
PRURITUS AND ALCOHOL INTAKE
Some 40% of patients treated for alcohol de-
pendence complain of pruritus (78), which mostly
occurs due to impaired liver function. However, pru-
ritus may precede liver cirrhosis, and it seems that it
does not necessarily have be related to hepatic
functional impairment itself (40). A crawling sensa-
tion under the skin that may precipitate delusions of
arthropod infestation may be experienced by some
cocaine abusers, as well.
SKIN INFECTIONS AND ALCOHOL
INTAKE
Alcohol abuse predominantly inhibits T-lympho-
cytes and reduces cell immunity, at the same time
reducing the function of neutrophils and killer cells.
That is why skin infections are more common in al-
coholics. According to literature reports, aspergillo-
sis, disseminated candidiasis, human papilloma-
virus infection, sporotrichosis, erysipelas and other
streptococcal cutaneous infections are more fre-
quently observed in alcoholics (2). The prevalence
of tinea pedis, onychomycosis and other forms of
dermatomycoses is higher in alcoholics because of
their suppressed immunity, poor hygiene, and unfa-
vorable socioeconomic conditions (46).
CONCLUSION
Comprehensive research and numerous stud-
ies have demonstrated that the effects of alcohol
are implicated in many skin diseases. Therefore,
physicians should take alcohol abuse as the possi-
ble causative factor for skin diseases in consider-
ation in their daily practice. Dermatologists should
appraise the effect of alcohol and drug abuse on the
etiology of their patients’ skin diseases and compli-
ance with treatments. Also, dermatological tests
should be part of medical examination in patients
suspected to take excessive amounts of alcohol.
References
1 Morse RM, Flavin DK. The definition of alcoholism.
JAMA 1992;268:1012-4.
2 Sanchez MR. Alcohol, social behavior disorders, and
their cutaneous manifestations. Clin Dermatol 1999;
17:479-89.
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Kostoviæ and Lipozenèiæ: Acta Dermatovenerol Croat
Skin Diseases in Alcoholics 2004;12(3):181-190
Table 2. Allergologic testing for alcohol intolerance
syndromes
In vitro tests:
total/specific IgE
in vitro histamine release
Prick tests and scratch tests:
ethanol (96%)
acetaldehyde
acetic acid (0.96%-9.6%)
citric acid (0.1%)
Oral challenge:
food additives
ethyl alcohol (10-20 L/0.01-10%) (v/v)
pure ethanol in water
3 Rosset M, Oki G. Skin diseases in alcoholics. Q J Stud
Alcohol 1971;32:1017-22.
4 Wolf R, Tüzün B, Tüzün Y. Alcohol ingestion and the cu-
taneous vasculature. Clin Dermatol 1999;17:395-403.
5 Ruocco V, Psilogenis M, Schiavo A, Wolf R. Dermato-
logical manifestations of alcoholic cirrhosis. Clin
Dermatol 1999;17:463-8.
6 Greer KE. Cutaneous hepatology. In: Callen JP, Jorizzo
JL, Greer KE, editors. Dermatological signs of internal
disease. Philadelphia: W.B. Saunders, 1995. p. 233-9.
7 Chaput JC, Poynard T, Naveau S, Penso D, Durrmeyer
O, Suplisson D. Psoriasis, alcohol and liver disease. Br
Med J (Clin Res Ed) 1985;291:25.
8 Morse RM, Perry HO, Hurt RD. Alcoholism and psoria-
sis. Alcohol Clin Exp Res 1985;9:396-9.
9 Braathen LR, Botten G, Bjerkedal T. Psoriatics in Nor-
way. A questionnaire study on health status, contact
with paramedical professions, and alcohol and toba-
cco consumption. Acta Derm Venereol Suppl (Stockh)
1989;142:9-12.
10 Zamboni S, Zanetti G, Grosso G, Ambrosio GB,
Gozzetti S, Peserico A. Dietary behavior in psoriatic
patients. Acta Derm Venereol Suppl (Stockh) 1989;
146:182-3.
11 Higgins EM, duVivier AW. Cutaneous disease and al-
cohol misuse. Br Med Bull 1994;50:85-98.
12 Higgins EM, duVivier AW. Alcohol and the skin. Alco-
hol 1992;27:595-602.
13 Stern RS, Lange R. Cardiovascular disease, cancer, and
cause of death in patients with psoriasis: 10-year pro-
spective experience in a cohort of 1380 patients. J In-
vest Dermatol 1988;91:197-201.
14 Monk BE, Neill SM. Alcohol consumption and psoria-
sis. Dermatologica 1986;173:57-60.
15 Poikolainen K, Reunala T, Karvonen J, Lauharanta J,
Karkkainen P. Alcohol intake: a risk factor for psoriasis
in young and middle-aged men? BMJ 1990;300:780-3.
16 Poikolainen K, Reunala T, Karvonen J. Smoking, alco-
hol and life events related to psoriasis among women.
Br J Dermatol 1994;130:473-7.
17 Gupta MA, Schork NJ, Gupta AK, Ellis CN. Alcohol in-
take and treatment responsiveness of psoriasis: a pro-
spective study. J Am Acad Dermatol 1993;28:730-2.
18 Vincenti GE, Blunden SM. Psoriasis and alcohol abuse.
J R Army Med Corps 1987;133:77-8.
19 Wolf R, Wolf D, Ruocco V. Alcohol intake and psoria-
sis. Clin Dermatol 1999;17:423-30.
20 Ockenfels HM, Keim-Maas C, Funk R, Nussbaum G,
Goos M. Ethanol enhances the INF-g, TGF-aand IL-6
secretion in psoriatic co-cultures. Br J Dermatol
1996;135:746-51.
21 Elder GH. Alcohol intake and porphyria cutanea tarda.
Clin Dermatol 1999;17:431-6.
22 Halten J, Krook H. Follow-up studies on an unselected
ten-year material of 360 patients with liver cirrhosis in
one community. Acta Med Scand 1963;173:479-87.
23 Bonkovsky HL, Banner BF, Lambrecht RW, Rubin RB.
Iron in liver disease other than hemochromatosis.
Semin Liver Dis 1996;16:65-82.
24 Felsher BJ, Kushner JP. Hepatic siderosis and porphyria
cutanea tarda: relation of iron excess to the metabolic
defect. Semin Hematol 1977;14:243-52.
25 McColl KE, Moore MR, Thompson GG, Goldberg A.
Abnormal haem biosynthesis in chronic alcoholics. Eur
J Clin Invest 1981;11:461-8.
26 Watson CJ, Sutherland D, Hawkinson V. Studies of
coproporphyrin: the isomer distribution and per diem
excretion of urinary coproporphyrin in cases of cirrho-
sis of the liver. J Lab Clin Med 1954,37:8-28.
27 Aziz MA, Schwartz S, Watson CJ. Studies of copro-
porphyrin III: re-investigation of isomer distribution in
jaundice and liver disease. J Lab Clin Med 1964;
63:596-604.
28 Elder GH. Porphyrin metabolism in porphyria cutanea
tarda. Semin Hematol 1977;14:227-42.
29 Elder GH, Roberts AG. Uroporphyrinogen decarboxyl-
ase. J Biomembr Bioenerg 1995;27:207-14.
30 Sinclair PR, Gorman N, Shedlofsky SI, Honsinger CP,
Sinclair JF, Karagas MR, et al. Ascorbic acid deficiency
in porphyria cutanea tarda. J Lab Clin Med 1997;
130:197-201.
31 McColl KEL, Thompson GG, Moore MR, Goldberg A.
Acute ethanol ingestion and haem biosynthesis in
healthy subjects. Eur J Clin Invest 1980;10:107-12.
32 Schoenfeld N, Mamet R, Leibovici L, Lanir A. Alco-
hol-induced changes in urinary aminolevulinic acid
and porphyrins: unrelated to liver disease. Alcohol
1996;13:59-63.
33 Shanley BC, Zail SS, Joubert SM. Effect of ethanol on
liver d-aminolevulinate synthetase in rats. Lancet 1968;
1:70-7.
34 Shanley BC, Zail SS, Joubert SM. Effect of ethanol on
liver d-aminolevulinate synthetase and urinary
porphyrin excretion in symptomatic porphyria. Br J
Hematol 1969;17:389-96.
35 Jansen T, Plewig G. Rosacea: classification and treat-
ment. J R Soc Med 1997;90:144-50.
36 Rebora A. Rosacea. J Invest Dermatol 1987;88 (Suppl
3):56s-60s.
37 Higgins EM, duVivier A. Alcohol abuse and treatment
resistance in skin diesease. J Am Acad Dermatol
1994;30:1048.
38 Puchalski Z. Psychosomatic Aspekte bei Patienten mit
Alopecia areata, Rosacea und Lichen ruber planus. Z
Hautkr 1983;58:1648-54.
39 Rebora A. The red face: rosacea. Clin Dermatol
1993;11:225-34.
188 ACTA DERMATOVENEROLOGICA CROATICA
Kostoviæ and Lipozenèiæ: Acta Dermatovenerol Croat
Skin Diseases in Alcoholics 2004;12(3):181-190
40 Higgins E, duVivier A. Alcohol intake and other skin
disorders. Clin Dermatol 1999;17:437-41.
41 Tonnensen H. Reversibility of alcohol-induced im-
mune depression. Br J Addict 1992;87:1025-8.
42 Sharma VK, Lynn A, Kaminski M, Vasudeva R, How-
den CW. A study of the prevalence of Helicobacter
pylori infection and other markers of upper gastrointes-
tinal tract disease in patients with rosacea. Am J
Gastroenterol 1998;93:220-2.
43 Rebora A, Drago F, Parodi A. May Helicobacter pylori
be important for dermatologists? Dermatology 1995;
191:6-8.
44 Autio P, Risteli J, Kiistala U, Risteli L, Karvonen J,
Oikarinen A. Serum markers of collagen synthesis and
degradation in skin diseases. Altered levels in diseases
with systemic manifestation and during systemic gluco-
corticoid treatment. Arch Dermatol Res 1993;285:
322-7.
45 Hook-Nikanne J, Kariniemi AL, Renkonen OV,
Mustakallio K, Salaspuro M. Could bacterial acetal-
dehyde production explain the deleterious effect of al-
cohol on skin diseases? [letter]. Acta Derm Venereol
1995;75:330.
46 Parish LC, Fine E. Alcoholism and skin disease. Int J
Dermatol 1985;24:300-1.
47 Shellow WV. The skin in alcoholism. Int J Dermatol
1983;22:506-10.
48 Soria C, Allegue F, Galiana J, Ledo A. Decreased
isotretinoin efficacy during acute alcohol intake.
Dermatologica 1991;182:203.
49 Holzegel K. How do I treat seborrheic eczema? [in Ger-
man]. Z Hautkr 1986;61:479-81.
50 Higgins EM, duVivier AWP, Peters TJ. Drinking habits
of patients with psoriasis. Clin Sci 1993;84:33.
51 Vasiliou V, Malamas M, Marselos M. The mechanism
of alcohol intolerance produced by various therapeutic
agents. Acta Pharmacol Toxicol Copenh 1986;58:
305-10.
52 Waldhäusl W. To flush or not to flush? Comments in
the chlorpropamide-alcohol flush. Diabetologia 1984;
26:12-4.
53 Yokoyama A, Muramatsu T, Ohmori T, Kumagai Y,
Higuchi S, Ishii H. Reliability of a flushing question-
naire and the ethanol patch test in screening for inac-
tive aldehyde dehydrogenase-2 and alcohol-related
cancer risk. Cancer Epidemiol Biomarkers Prev 1997;
6:1105-7.
54 Tsuritani I, Ikai E, Date T, Suzuki Y, Ishizaki M, Yamada
Y. Polymorphisms in ALDH2-genotype in Japanese
men and the alcohol – blood pressure relationship. Am
J Hypertens 1995;8:1053-9.
55 Illson RM, Hockaday TD. Chlorpropamide-alcohol
flush: a critical reappraisal. Diabetologia 1984;26:
6-11.
56 Bonisolli L, Pontiroli AE, De Pasqua A, Calderara A,
Maffi P, Gallus G, et al. Association between chlorpro-
pamide-alcohol flushing and fast acetylator phenotype
in type I and type II diabetes. Acta Diabetol 1985;22:
305-15.
57 Fraser AG. Pharmacokinetic interactions between alco-
hol and other drugs. Clin Pharmacokinet 1997;18:
123-32.
58 Fett DL, Vukow LF. An unusual case of severe griseo-
fulvin-alcohol interaction. Ann Emerg Med 1994;24:
95-7.
59 Saxe TG. Drug-alcohol interactions. Am J Fam Physi-
cian 1986;33:159-62.
60 Sticherling M, Brasch J. Alcohol: intolerance syn-
dromes, urticarial and anaphylactoid reactions. Clin
Dermatol 1999;17:471-92.
61 Sticherling M, Brasch J, Brüning H, Christophers E.
Urticarial and anaphylactoid reactions following etha-
nol intake. Br J Dermatol 1995;132:464-7.
62 Nagoshi CT, Dixon LK, Johnson RC, Yuen SH. Familial
transmission of alcohol consumption and the flushing
response to alcohol in three Oriental groups. J Stud Al-
cohol 1988;49:261-7.
63 Ward RJ, McPherson AJ, Chow C, Ealing J, Sherman DI,
Yoshida A, et al. Identification and characterization of
alcohol-induced flushing in Caucasian subjects. Alco-
hol Alcohol 1994;29:433-8.
64 Takeshita T, Morimoto K, Mao X, Hashimoto T,
Furuyama J. Characterization of the three genotypes of
low Km aldehyde dehydrogenase in a Japanese popu-
lation. Hum Genet 1994;94:217-23.
65 Itoh T, Matsumoto M, Nakamura M, Okada A,
Shirahashi N, Hougaku H, et al. Effects of daily alcohol
intake on the blood pressure differ depending on an in-
dividual’s sensitivity to alcohol: Oriental flushing as a
sign to stop drinking for health reasons. J Hypertens
1997;15:1211-7.
66 Miller NS, Goodwin DW, Jones FC, Pardo MP, Anand
MM, Gabrielli WF, et al. Histamine receptor antago-
nism of intolerance to alcohol in Oriental population. J
Nerv Ment Dis 1987;175:661-7.
67 Agarwal DP, Goedde HW. Human aldehyde dehydro-
genase isoenzymes and alcohol sensitivity. Isoenzy-
mes Curr Top Biol Med Res 1987;16:21-48.
68 Maibach HI, Johnson HL. Contact urticaria syndrome.
Contact urticaria to diethyltoluamide. Arch Dermatol
1975;111:726-30.
69 Odom RB, Maibach HI. Contact urticaria: a different
contact dermatitis. Cutis 1976;18:672-6.
70 Wilkin JK, Fortner G. Ethnic contact urticaria to alco-
hol. Contact Dermatitis 1985;12:118-20.
71 Fisher AA. Topically applied alcohol as a cause of con-
tact dermatitis. Cutis 1983;31:588-600.
72 Melli MC, Sertoli A. Sensitization from contact with
ethyl alcohol. Contact Dermatitis 1986;14:315.
ACTA DERMATOVENEROLOGICA CROATICA 189
Kostoviæ and Lipozenèiæ: Acta Dermatovenerol Croat
Skin Diseases in Alcoholics 2004;12(3):181-190
73 Ophaswongse S, Maibach HI. Alcohol dermatitis: aller-
gic contact dermatitis and contact urticaria syndrome.
A review. Contact Dermatitis 1994;30:1-6.
74 Elphinstone PE, Kobza Black A, Greaves MW. Alco-
hol-induced urticaria. J R Soc Med 1985;78:340-1.
75 Ting S. Anaphylactoid reaction to ethanol [letter]. Ann
Allergy 1992;69:463.
76 Kelso JM, Keating MU, Squillace DL, O’Connell EJ,
Yunginger JW, Sachs MI. Anaphylactoid reaction to
ethanol [letter]. Ann Allergy 1990;64:452-4.
77 Przybilla B, Ring J, Galosi A. Alcohol anaphylaxis. Al-
lergy against the ethanol metabolite acetic acid? [in
Germam]. Allergologie 1986;9:164-9.
78 Shellow WV. The skin in alcoholism. Int J Dermatol
1983;22:506-10.
190 ACTA DERMATOVENEROLOGICA CROATICA
Kostoviæ and Lipozenèiæ: Acta Dermatovenerol Croat
Skin Diseases in Alcoholics 2004;12(3):181-190
... The majority of cutaneous manifestations associated with ethanol abuse are indirectly mediated through the impairment of various organ systems. Most of them are induced by liver toxicity, by an inappropriate diet or by various organ dysfunctions (Chou et al., 1996;Higgins & du Vivier, 1994a,b;Kostovic & Lipozencic, 2004;Smith & Fenske, 2000;Vogl et al., 2005). ...
... Palmar erythema, or ''liver palms,'' is another vascular finding associated with ethanol abuse. It is characterized by warm, florid, light-red patches usually on the palms of the hands and fingertips ( Figure 3A and B) (Kostovic & Lipozencic, 2004;Vogl et al., 2005). The soles may similarly be affected. ...
... Active blood flow is required for pulsation presence since spider nevi are noted to fade after death. The classic distribution includes the face, V area of the neck, upper chest, arms, hands, and, rarely, the mucous membranes, abdomen, and legs (Kostovic & Lipozencic, 2004;Vogl et al., 2005). The etiology of the vascular changes is not clear, although decreased metabolism of estrogen (typically of the alcoholic cirrhotic patients) has been implicated. ...
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Abstract For a good performance in Clinical and Forensic Toxicology it is important to be aware of the signs and symptoms related to xenobiotic exposure since they will assist clinicians to reach a useful and rapid diagnosis. This manuscript highlights and critically analyses clinical and forensic imaging related to ethanol abuse. Here, signs that may lead to suspected ethanol abuse, but that are not necessarily related to liver disease are thoroughly discussed regarding its underlying mechanisms. This includes flushing and disulfiram reactions, urticaria, palmar erythema, spider telangiectasias, porphyria cutanea tarda, "paper money skin", psoriasis, rhinophyma, Dupuytren's contracture, multiple symmetrical lipomatosis (lipomatosis Lanois-Bensaude, Madelung's disease), pancreatitis-related signs, black hairy tongue, gout, nail changes, fetal alcohol syndrome, seborrheic dermatitis, sialosis and cancer.
... Alcohol induced skin pathology may be due to a direct toxic effect or consequential to personal neglect, environmental factors, or inappropriate diet. 4 However, though cutaneous manifestations in alcoholism has been studied earlier, literature studying the correlation of such dermatological disease to the various factors of alcohol abuse such as duration of alcohol intake, quantity consumed, severity of alcohol dependence, is lacking; especially in the Indian population, and it was with this objective that this study was undertaken. ...
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p class="abstract"> Background: Alcoholism is a potentially fatal condition damages skin directly or through organ dysfunction. Studies suggested that dermatological manifestations have also been found to be a marker of alcohol misuse. The aim of the study was to assess the various cutaneous manifestations of alcohol dependence. Methods: This study consisted of 205 cases diagnosed with alcohol dependency attending dermatology department and psychiatry wards, above 18 years of age. A detailed clinical examination and dermatological examination including hair, nails, oral and genital mucosa was performed. Alcoholic liver disease was diagnosed on clinical findings, abdominal sonogram and LFT. Results: Among the study cases 50.25% cases had alcoholic liver disease. The severity of alcohol dependence score ranged from 1-60 with Ameena score of 24.68. It was seen that 45.23% (90) of alcoholics were mildly dependent, 41.7% (83) of alcoholics were moderately dependent, and 13.07% (26) were severely dependent on alcohol. Seborrheic dermatitis, urticaria, hyperhidrosis was among the commonly encountered dermatoses. Conclusions: Cutaneous manifestations are a significant pointer to underlying, perhaps undetected problem of alcohol dependency and an awareness of these signs is imperative to alter a dermatologist to problems of alcohol abuse even in a busy clinic.</p
... Per each time of drinking alcohol body gets dehydrated which initially can deplete skin blood's capillaries flow (fluids). Consequently, chronic drinking of alcohol can have detrimental impacts on skin health in long-terms [3]. ...
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Nutrition refers the necessary foods for health and the states of being free from illnesses [1]. A healthy diet contains natural foods , plant-based nutrients, wholegrains to meet human daily requirements. A mix of proper proteins, carbohydrates, and fat and enough vitamins are the keys for optimal diet. Poor nutrition primary can result in undesired appearances in human [2]. Research shows low quality food components at the first stage exacerbate the skin integrity. Among different foods and beverages frequents drinks intakes such as alcohol dramatically affect the appearances and skin features. Per each time of drinking alcohol body gets dehydrated which initially can deplete skin blood's capil-laries flow (fluids). Consequently, chronic drinking of alcohol can have detrimental impacts on skin health in long-terms [3]. Some evidence-based studies outline consuming dairy products which combined with high levels of refined foods negatively impact skin texture. It is believed that, eliminating dairy intakes products like skimmed milk, yogurt, and cheese can protect skin features from conditions such as acne and rosacea [4].
... Per each time of drinking alcohol body gets dehydrated which initially can deplete skin blood's capillaries flow (fluids). Consequently, chronic drinking of alcohol can have detrimental impacts on skin health in long-terms [3]. ...
... Clinical manifestations of coagulative dysfunction in patients with liver disease range from skin hemorrhages typically on the lower limbs [74], such as bruising, petechiae (1 to 2 mm in diameter), mid-size purpura (3 to 5 mm), and larger ecchymosis (1 to 2 cm; Fig. 8), epistaxis, gingival or more life-threatening gastrointestinal bleeding [75,76]. Cullen's and Grey-Turner's signs observed in ethanol abusers are both ecchymotic and develops most commonly in conjunction with acute necrotizing pancreatitis [1]. ...
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Ethanol is the most abused psychoactive substance. Accordingly to World Health Organization ethanol ranks among the top five risk factors for disease, disability and death (3.3 million/year) throughout the world. This manuscript highlights and critically analyses clinical and forensic signs related to hepatoxicity of ethanol that may lead to suspected of abuse. Namely, steatosis, jaundice, cirrhosis, hemorrhoids, esophageal varices caput medusae, ascites, petechiae, ecchymoses, splenomegaly, hemochromatosis, xanthelasma, nutritional deficiency, testicular atrophy, gynecomastia and dilated congestive cardiomyopathy are discussed and related to the toxic mechanism of ethanol.
... Alcohol abuse is associated with many health problems, especially skin changes (33). As a small, water-and lipid-soluble molecule, alcohol reaches all tissues of the body and affects most vital functions. ...
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Alcoholism is a growing medical and public health issue both in adults and in the younger generation. It is a multietiological phenomenon influenced by genetic, psychological, cultural and other factors. Alcoholic beverages have traditionally been prepared from various ingredients such as grapes, hops, rice, honey, etc. Drinking prevalence has varied and is more pronounced in women and the youth. Alcoholism is shown to be of neurophysiological etiology and may lead to impairment of all human body systems. The most frequent cause of death in alcoholics are diseases of the cardiovascular system. The problem of alcoholism at workplace is very important since by affecting health and reducing work productivity it leads to accidents, injuries and decreased working capacity. Efficient solving of alcoholism and related problems includes early detection, so it is necessary to orient the health care services towards primary prevention and early interventions.
Chapter
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Introduction The links between major depression and dermatological diseases are more and more documented in the literature. In an opening prospect, our study would like to open a wide field, usually limited at the psychopathology, for a general women population and for a more general conception of the link between depressive feeling and sensitiveness of the skin. Subject and methods 243 women, from witch 127 depressives, 63 alcoholics and 53 healthy have answered our questionnaires (S.D.S., P.I.L.L.) to evaluate the frequency of appearance of sensations in the skin and the subjective intensity of depressive symptoms. Results Our results show a higher cutaneous sensitiveness with the depressive women and also with the alcoholics. They also underline a significant correlation between depressive feeling and the frequency of complaint tied of the skin. Conclusion The skin and the mood are not only tied in the field of the depressive disorder. The skin is an organ sensible to the mood and it can reveal a depressive mood with women suffering of major depression as well as in the general population. We advise the physicians (dermatologists, psychiatrists, generalists⋯) not to come to quickly to the conclusion that there is a major depression when a patient, whose the body speaks, expresses a depressive feeling.
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The diagnosis of anaphylactoid reactions to alcoholic beverages may be troublesome, as not only ethanol but also other ingredients, such as molds, yeasts, preservatives, and colouring or flavouring agents have to be considered. True sensitization to ethanol itself is a rare event. In man ethanol is metabolized to acetic acid via acetaldehyde. - In a 22-year-old female, who had suffered repeatedly from anaphylactic reactions after the ingestion of alcohol beverages and of vinegar containing dishes, strongly positive prick test reactions to acetic acid (9.6% and 0.96%) and vinegar were observed; control tests in other subjects with these agents were negative. Skin tests with ethanol, acetaldehyde, wine and beer yielded only negative or irritative reactions. Oral provocation with increasing amounts (0.01-0.1-1.0 ml) of ethanol (absulute, analytical grade) in tap water resulted in severe anaphylaxis after ingestion of 1.0 ml. Thus in this patient pure ethanol elicits anaphylactic reactions that seem to be caused by an immediate type allergic reaction to the ethanol metabolite acetic acid.
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In Reply ?The thoughtful letter from Drs Howard and Donovan serves to highlight some of the difficulties in communicating the concept of a revised definition of alcoholism to a widely varied audience of scientists, clinicians, and laypersons. We welcome the opportunity to respond to their critique and hope to clarify some of the confusion about denial.We disagree with their judgment that our definition is "vague." To the contrary, we have been quite specific, given the length of our article, about the nature of this defense mechanism, its clinical ubiquity, and its roots in biopsychosocial phenomena.Further, we do not think there is "inadequate empirical justification" for including this construct. In fact, the lion's share of justification is just that?empirical. The difficulties have arisen more in scientific attempts to define, delineate, describe, and measure the denial process. Virtually all experienced clinicians point to the denial mechanism as a key construct
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Aldehyde dehydrogenase with a low Michaelis constant (Km), ALDH2, is a major enzyme involved in the conversion of acetaldehyde, a toxic metabolite of ethanol, into acetic acid in the liver. Inherited deficiency of ALDH2 activity is found in half of Japanese, and is characterized by “Oriental flushing” after alcohol consumption. The aim of the present study is to evaluate the influence of the genetic polymorphism in alcohol metabolism on the sensitivity to the pressor effect of alcohol. Genotypes of ALDH2 were determined in 403 middle-aged Japanese men using genomic DNA extracted from white blood cells. Two hundred and forty-three (60%) of the subjects were shown to be homozygotes for the normal ALDH2 gene, 25 (6%) of the subjects were homozygotes for the mutant ALDH2 gene, and the remaining 135 (33%) were heterozygotes. None of the homozygotes for the mutant gene drank enough to show the pressor effect of alcohol. Elevations of blood pressure associated with increasing alcohol consumption or with elevations of serum γ-glutamyl transpeptide (GTP) level were not different between the other two ALDH2-genotypes. It can be concluded that polymorphism in the ALDH2-genotype found in Japanese men does not affect the individual sensitivity to the pressor effect of alcohol. Am J Hypertens 1995;8:1053–1059
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In this paper the clinical evidence in support of a role for iron in the pathogenesis of PCT is reviewed. In addition, the biochemical derangements that result from excess iron is considered. In the light of the described findings, it seems appropriate to discard the old concept that PCT is a purely acquired disease caused by hepatic injury from alcohol or other exogenous agents. Our present concept of the etiology of PCT is that two primary factors are essential for the full biochemical expression of the disease. Once is an inherited enzyme defect, decreased urodecarb activity, and the other an acquired factor, hepatic siderosis.