A Few More H. pylori & cea Articles

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Helicobacter Pylori and its Eradication in cea

Szlachcic A, Sliwowski Z, Karczewska E, Bielans

J Physiol Pharmacol. 1999;50:777-786

cea is a common condition of unknown etiology usually accompanied

by gastrointestinal symptoms and favorably responding to the

treatment with antibiotics. This study was designed to examine the

prevalence of gastric Helicobacter pylori (Hp) infection verified by

13C-UTB-test, CLO, Hp culture and serology (IgG) in patients with

rosacea. Gastroduodenoscopy was combined with pentagastrin secretory

test and antral and fundic biopsy samples were taken for histological

evaluation (the Sydney system). Blood samples were also taken for the

determination of plasma gastrin using RIA and plasma interleukin (IL)-

8 and tumor necrosis factor alpha (TNF alpha) using ELISA. This study

was performed in 60 patients, 31-72 years old, with visible papules

and pustules associated with erythema and flushing on the face and on

60 age- and gender-matched patients without any skin diseases but

with similar as in rosacea gastrointestinal symptoms but without

endoscopic changes in gastroduodenal mucosa (non-ulcer dyspepsia -

NUD). The Hp prevalence in rosacea patients was about 88 % as

compared to 65% in control NUD patients. Among rosacea patients, 67%

were cytotoxin associated gene A (CagA) positive, while in NUD

patients only 32% were CagA positive. cea patients showed

gastritis with activity of about 2.1 in antrum and 0.9 in the corpus

of the stomach while those with NUD only mild gastritis with activity

of approximately 1.0 confined to the antrum only. Following initial

examination, typical 1 wk anti-Hp therapy including omeprazole (20 mg

bd.), clarithromycin (500 mg bd.) and metronidazole (500 mg bd.) was

carried out. After eradication, 51 out of 53 treated rosacea patients

became Hp negative. Within 2-4 weeks, the symptoms of rosacea

disappeared in 51 patients, markedly declined in 1 and remained

unchanged in 1 other subject. A dramatic reduction in activity of

gastritis (to 0.3 in antrum and to 0.1 in corpus) was observed. Basal

plasma gastrin decreased from 48 +/- 5 pM before to 17+/-3 pM after

eradication, while pentagastrin-induced maximal (MAO) declined,

respectively, from about 16.6 +/- 4.2 to 8.5 +/- 1.8 mmol/h. Plasma

TNF alpha and IL-8 were reduced after the therapy by 72% and 65%,

respectively. We conclude that: 1) cea is a disorder with various

gastrointestinal symptoms closely related to gastritis, especially

involving the antrum mucosa, with Hp expressing cagA in the majority

of cases and elevated plasma levels of TNF alpha and IL-8; 2) The

eradication of Hp leads to a dramatic improvement of symptoms of

rosacea and reduction in related gastrointestinal symptoms,

gastritis, hypergastrinemia and gastric acid secretion; and 3)

cea could be considered as one of the major extragastric symptoms

of Hp infection probably mediated by Hp-related cytotoxins and

cytokines.

Helicobacter pylori Infection and Skin Diseases

Wedi B, Kapp A

J Physiol Pharmacol. 1999;50:753-776

There is increasing evidence for systemic effects of gastric H.

pylori infection which may result in extragastrointestinal disorders.

This review summarizes the available medical literature up to

September 1999, identified through a MEDLINE research including own

studies, regarding H. pylori and skin diseases. Due to current

knowledge best evidence for a potential link of H. pylori infection

exists for chronic urticaria although the data are still conflicting.

Thus, the search for H. pylori should be included in the diagnostic

management of chronic urticaria. With regard to other skin diseases

such as rosacea, hereditary or acquired angioedema due to C1-esterase

inhibitor deficiency, systemic sclerosis, Schonlein-Henoch purpura,

Sjogren's syndrome, sweet's syndrome, and atopic dermatitis only

single of few cases have been reported so far. Thus, we clearly need

further randomized, double-blind and placebo-controlled studies

including adequate diagnostic schedules, sufficient eradication

treatment protocols, confirmation of eradication, and adequate

control groups to establish a role of H. pylori in skin diseases.

Caution must be taken not to accuse H. pylori as the infectious agent

responsible for every disease, particularly since H. pylori infection

is very common. Although from an epidemiological and morphological

view the skin diseases to which H. pylori has been linked seem to be

completely different it is striking that in most of them an

autoimmune pathogenesis is suspected or considerable vascular

impairment can be found.