[Chronic obstructive pulmonary disease in the light of new guidelines -  brief summary of phenotypically oriented guidelines for nonpulmonary physicians]. / Chronická obstrukcní plicní nemoc pohledem nových doporucení -  souhrn aktuálního fenotypove zamereného standardu Ceské pneumologické a ftizeologické spolecnosti pro internisty.

INTRODUCTION: COPD is a global health and social problem. Morbidity and mortality increases in the Czech Republic. There are currently several global statements and strategies. METHODS: The Czech Pneumological and Phthisiological Society (CPFS) at the end of 2011 mandated the Section of bronchial obstruction in drafting national guidelines concerning the stable COPD. Subsequently, this document was discussed during the National Consensus Conference (COPD forum) in November 2012 and presented at series of local workshops and national conferences. National guidelines has been subject to a review and eventually posted on the website for another round of comments. DIAGNOSIS: A modern approach to COPD is a view of the patient through the pulmonary function, symptoms, exacerbation rates and the presence of specific phenotypes. CPFS identified six clinically relevant phenotypes: frequent exacerbators, COPD and asthma overlap, COPD and bronchiectasis overlap, emphysematic phenotype, bronchitic phenotype and phenotype of pulmonary cachexia. TREATMENT: TREATMENT recommendations can be divided into four elementary steps: the first step is the Elimination of all risks factors. The second one is the Standard therapy including in particular inhaled bronchodilators, pulmonary rehabilitation, and treatment of severe comorbidities. The third step is the Targeted therapy centered on clinical phenotypes of COPD. The final fourth step is the treatment of respiratory insufficiency and palliative care of the terminal COPD. CONCLUSION: The optimal treatment of COPD requires a personalized approach to the patient.

[Treatment of Crohn's disease]. / Lécba Crohnovy choroby.

Dietetic treatment of Crohn's disease has the objective to calm down the gut either by a polymeric or elemental diet. In superacute conditions also total parenteral nutrition can be used. In the quiescent stage the patient must have an adequate energy intake and a low-residue (low-fibre) diet. As to medication, sulfasalazine which has some side-effects is abandoned and 5-ASA (5-aminosalicylic acid) preparations are used, either by the oral route or in enemas, while 4-ASA is little used in this country and is known as PAS. The administration of corticoids which also have side-effects will be abandoned in favour of so-called rapidly metabolized corticoids (Tixocortol pivalate, beclomethasone, budenoside and fluticasone) by the oral route and in enemas and foams. As antimicrobial treatment ciprofloxacine is used combined with metronidazole. As to immunosuppressive drugs azathioprine, 6-mercaptopurine, cyclosporin A, cyclophosphamide and methotrexate are tested. A hope for the future is so-called biological treatment (anticytokines, monoclonal antibodies against cytokines, against CD4+ TNF, interleukines IL-10 and 11, immunoglobulin; plasmapheresis is also tested). Treatment must be individual and surgery as late as possible, only in case of complications, and should be very sparing, stenoses should be treated by plastic operations of strictures.

[Current views on the development and course of Crohn's disease]. / Soucasné názory na vznik a prubeh Crohnovy choroby.

Among etiological factors suspected of causing Crohn's disease a number of bacteria was listed (Yersinia, Mycobacterium kansasi, Mycobacterium pseudotuberculosis) as well as viruses (measles). None of them however can be considered as the only agent. As to external influences, we know the adverse effect of smoking, the toxic effect Al and oral contraceptives. The listed causes may enhance the development of mesenteric thromboses or immunocomplex vasculitis with ischaemization of a certain portion of the small or large intestine with subsequent inflammation. So far we do not know what starts the immunological reaction, but subsequently the process takes place via cytokines, prostaglandin PGE2, leukotriene LTB4 and liberation of free oxygen radicals (this knowledge is applied in therapy). The authors discuss the problem whether Crohn's disease is one clinical entity with a different course or whether a single diagnosis comprises two or more pathological units.

[Bone demineralization in Crohn's disease, its diagnosis, therapy and prevention]. / Demineralizace kostí u m. Crohn, její diagnostika, lécba a prevence.

In 20-60% of patients with Crohn's disease bone demineralization is found, usually osteoporosis, but also osteoporosis with malatic features. The cause is the reduced calcium intake (loss of appetite, lactose intolerance and malabsorption), reduced vitamin D intake and corticoid therapy. Nowadays the diagnosis is facilitated by the use of densitometers (ultrasonic and DEXA) and markers of osteoresorption and new bone formation. In treatment in addition to calcium and vitamin D used for a long time, fluorides are administered (only as monofluorophosphate), nasal thyrocalcitonin and bisphosphonates of the third series (alendronate). In postmenopausal women also hormonal treatment can be used unless contraindicated. However, burdening of the bones with regular exercise is a necessity. For prevention adequate calcium and vitamin D intake is important, non-smoking, and exercise.

[Disorders of bone mineralization and their treatment in Crohn's disease]. / Poruchy mineralizace kostí u Crohnovy choroby a jejich lécba.

Frequent complications of Crohn's disease include disorders of bone mineralization. They are due to a reduced dietary calcium supply in patients with lactose intolerance and a certain degree of malabsorption of calcium as well as vitamin D. The position is made worse by corticoids used in treatment of the basic disease, because they interfere not only with vitamin D conversion into its active (and much more effective) metabolites but also with osteoid formation In the early diagnosis of demineralization a densitometer can be used; markers of bone metabolism are used so far less frequently. As to treatment either blockers of enhanced bone resorption can be used (Ca, vitamin D, bisphosphonates and thyrocalcitonin) or substances stimulating new formation of bone (F, growth factors, in postmenopausal women hormonal substitution treatment) or a combination of preparations from both groups can be used. An irreplaceable part is played also by exercise, depending, of course, on the patient's general condition.

[Prevalence of bone decalcification in the treatment of Crohn's disease]. / Prevalence odvápnení kostí pri lécbe Crohnovy nemoci.

In clinically active Crohn's disease the bone mineralization is impaired due to calcium malabsorption by the inflamed intestinal wall which is potentiated by diarrhoea and the thus accelerated transit time. To this we must add the shortening of the gut after operations, the inadequate dietary calcium supply or possibly calcium elimination in case of concurrent lactose intolerance. Corticoid treatment leads also to deterioration of bone mineralization. This is the reason why the authors assessed in 98 patients with Crohn's disease the bone mineralization, using the method of clavicular bone index (NIBA). Then treatment was started: a high protein diet, calcium forte, Ossin (sodium fluoride), vitamin D forte, anabolics and regular physical exercise. Check-up examinations after one year revealed that the index was restored in the majority of patients (60.84%) to normal. The above treatment is thus effective. It must be, however, regular and of a long-term character, in some patients it must extend over many years. We had, however, also patients who although subjected to an extensive resection of the gut and treated for prolonged periods with corticoids, had permanently an index between 100 and 120% without treatment.

Incidence of colorectal cancer in proctocolitis: a retrospective study of 959 cases over 40 years.

The incidence of colorectal cancer was studied by the actuarial method in 959 patients with idiopathic proctocolitis seen from 1942 to 1981. Forty five per cent had rectal, 23% left-sided, and 32% total involvement of the colon. Six cancers were found: one in the rectal, one in the left-sided, and four in the total form of the disease. The risk of cancer per patient year in total colitis was zero per 2151 patient years in the first decade, 1/462 in the second decade, 1/315 in the third decade, and 1/75 in the fourth decade. The cumulative risk of developing cancer was zero at 10 years of duration of the disease, approximately 5% at 20 years, 15% at 30 years, and 20% at 35 years. This increase in risk of cancer is less than reported in some other series. Geographical differences in the incidence of cancer in proctocolitis could influence the risk and therefore also the long-term management of patients with proctocolitis in different geographical areas.

Hyperplasia of Brunner's glands. Radiology, endoscopy and biopsy findings in 11 cases of diffuse, nodular and adenomatous form.

Eleven cases of hyperplasia of Brunner's glands are reported including 10 cases of diffuse and nodular type and one case of Brunnerian polyadenomatosis. Histological changes were identified in aspiration biopsy specimens and termed "biopsy indication of hyperplasia of Brunner's glands". Polypoid pattern seen roentgenologically and endoscopically in the case of the adenomatous type was constant whereas in the case of the diffuse and nodular type it was not constant; it is suggested that this is due to irregular contraction of muscularis mucosae disrupted by protruding Brunner's glands. Most patients had epigastric distress; less than half had duodenitis.

Histochemistry of the human duodenal mucosa with special reference to the gradient of activities of the brush border enzymes.

Histochemical examination of aspiration biopsy specimens of the duodenum in 8 healthy volunteers and 23 patients with various gastrointestinal disorders revealed no characteristic abnormality except for a rather frequent absence of the activity of disacharidases especially of lactase. A distinct difference of disacharidase was established between the duodenum and the jejunum in some individuals. A systematic study of different levels of the upper gastrointestinal tract established the fact that the activity of brush border enzymes of enterocytes starts to appear in individually different parts of the duodenum and sometimes even as low as in the jejunum. The distribution of lysosomal enzymes and the activity of dehydrogenases display differences as well. Consequently specimens from different parts of the duodenal and jejunal mucosa are not equivalent and cannot be used alternatively for diagnostic purposes. Biopsies of duodenal mucosa are not adequate for the diagnosis of the malabsorption syndrome.