[Liver function assessment in oncology practice]. / Hodnocení jaterní funkce v onkologické praxi.

The overall condition and prognosis of a patient can be affected by impaired liver function. It applies to anticancer pharmacotherapy, liver surgery and radiological interventions. The liver condition is usually assessed by common laboratory tests and clinical examination in daily practice. Liver tests consist of aminotransferases - alanine transaminase, aspartate transaminase, bilirubin, alkaline phosphatase, gamma glutamyl transpeptidase, lactate dehydrogenase, albumin and prothrombin time, less frequently prealbumin and cholinesterase. The alkaline phosphatase and aspartate transaminase are markers of a liver damage, the alkaline phosphatase and gamma glutamyl transpeptidase are most useful as markers for cholestatic liver injury. Albumin, prealbumin, cholinesterase and prothrombin time are the markers of synthetic liver function. Bilirubin and bile acids are related to the liver transport and excretory capacity. The Child-Pugh score is used to assess prognosis of chronic liver disease, mainly cirrhosis. The examination of liver function using indocyanine green helps to determinate the extent of possible liver resection. A mathematical analysis of dynamic cholescintigraphy and a calculation of hepatic extraction fraction enables quantification of liver function. Other liver function tests are of little use in oncology.

[Partial regression of CNS lesions of Erdheim-Chester disease after treatment with 2-chlorodeoxadenosine and their full remission following treatment with lenalidomide]. / Parciální regrese lozisek Erdheimovy-Chesterovy nemoci v CNS po lécbe 2-chlorodeoxyadenosinem a jejich kompletní vymizení prn lécbe lenalidomidem.

INTRODUCTION: Erdheim-Chester disease is a very rare syndrome affecting adult population. It typically causes hyperostosis of long bones, retroperitoneal fibrosis and widening of the aortic wall. Patients frequently suffer from disease-associated fevers and pain in the lower limbs. No guidelines are available for the treatment of this rare ailment. Therefore, we describe our experience with lenalidomide in a patient with poor treatment response to 2-chlorodeoxyadenosine. CASE: Diabetes insipidus and neurological problems developing over 4 years were the first signs of the disease. The disease was diagnosed from histology of the bone marrow extracted from the ilium. At diagnosis, the patient had multiple infiltrates in the brain, widened wall of the thoracic and abdominal aorta, fibrotic changes to retroperitoneum and typical hyperostosis of the long bones of lower limbs with high accumulation of technetium pyrophosphate as well as fluorodeoxyglucose. First line treatment involved 2-chlorodeoxyadenosine 5 mg/m2 s.c. for 5 consecutive days every 28 days. There was no clear treatment response identifiable on the MR scan of the brain following the third cycle and thus 4th-6th cycle consisted of 2-chlorodexyadenosine 5 mg/m2 + cyclophosphamide 150 mg/m2 + dexamethasone 24 mg day 1-5 every 28 days. After the 6th cycle, MR showed partial regression of the brain lesions. PET-CT showed an increased accumulation of fluorodeoxyglucose in bone lesions. Second line treatment involved lenalidomide 25 mg/day days 1-21 every 28 days. Lenalidomide tolerance was excellent; the number of neutrophils and thrombocytes was within the physiological range throughout the treatment period. Follow-up MR showed complete remission of the brain lesions, while follow-up PET-CT showed further increase in fluorodeoxyglucose accumulation in the bones of lower limbs. CONCLUSION: Treatment with 2-chlorodeoxyadenosine-based regimen provided partial remission of Erdheim-Chester disease lesions in the brain, while treatment with lenalidomide resulted in complete remission of these lesions. Fluorodeoxyglucose continues to accumulate in the long bones of lower limbs. We are unable to elucidate the reasons for complete remission of the disease in the brain as per the MR and its progression in the long bones according to PET-CT. Further testing of lenalidomide in the treatment of this disease is required to support further use of this perspective treatment option.

[Schnitzler syndrome: diagnostics and treatment]. / Schnitzler-syndrom: diagnostika a lécba.

BACKGROUNDS: The most important diagnostic criteria for Schnitzler syndrome include chronic urticaria, the presence of monoclonal IgM immunoglobulin, marked inflammation (leukocytosis, elevated CRP and erythrocyte sedimentation rate), subfebrile temperatures or fevers and bone and joint pains. It is a rare idiopathic disease that may lead to potentially life-threatening complications such as development of secondary amyloidosis or transformation into malignant lymphoproliferation. Schnitzler syndrome should be included in differential diagnostics of chronic urticaria and fevers of unknown origin. The diagnostic algorithm is based on clinical presentation and serum and urine electrophoreses to detect monoclonal components. Blockade of interleukin-1 (IL-1), key cytokine in the pathogenesis of the disease, dominates current therapeutic protocols. Anakinra (Kineret), recombinant human IL-1 receptor antagonist, is the most widely used treatment option. According to literature, disease remission was obtained in all treated patients. Therefore, anakinra represents a significant diagnostic possibility to differentiate Schnitzler syndrome from e.g. monoclonal gammopathy of unknown significance (MGUS) associated with urticaria of different aetiology. Biological therapy with rilonacept (Arcalyst) and canakinumab (Ilaris) represents a new treatment alternative for patients, allowing prolonged dosing intervals of 1 and 8 weeks, respectively (compared to 24 hours with anakinra). The review article also presents findings of various imaging methods (conventional radiography, computed tomography, traditional bone scintigraphy) and photographs of patients with Schnitzler syndrome before and after anakinra therapy. DESIGN: The aim of the review is to draw attention to the existence of this rare autoinflammatory and potentially premalignant condition, present a simple diagnostic algorithm and provide an overview of therapeutic options for the patients. CONCLUSIONS: Malign potential of Schnitzler syndrome, possible development into systemic amyloidosis and the fact that patients are frequently referred to oncology clinics for differential diagnostics of monoclonal gammopathy, are the main reasons why clinical oncologists should be aware of Schnitzler syndrome.

[Successful treatment of Erdheim-Chester disease by 2-chlorodeoxyadenosine-based chemotherapy. Two case studies and a literature review]. / Uspesná lécba Erdheimovy-Chesterovy nemoci chemoterapií obsahující 2-chlorodeoxyadenosin. Popis dvou prípadu a prehled literatury.

INTRODUCTION: Erdheim-Chester disease is an extremely rarely occuring condition and thus an optimal treatment is not known. Two new cases have been diagnosed in our centre in 2008 and 2009. Both patients had diabetes insipidus, B symptoms (subfebrile to febrile states) and pain in long bones of lower limbs. CASE STUDIES: Imaging showed high accumulation of fluorodeoxyglucose as well as Tc-pyrophosphate in long bones of lower as well as upper limbs, aortic wall thickening with periaortic fibrosis and perirenal fibrosis. In addition, one of the patients had multiple lesions in the brain. 2-chlorodeoxyadenosine 5 mg/m2 s.c. and cyclophosphamide 150 mg/m2 administered on days 1 to 5 in 28-day cycles were selected for the treatment of both patients. Dexamethasone 24 mg/day for 5 days was added to this treatment in the second patient. Six cycles of the treatment were planned. Both patients were prescribed bisphosphonates--zoledronate and clodronate, respectively. Treatment effect was assessed with PET-CT and MR. Following treatment completion, brain infiltrates were reduced to a small residuum in the first patient who did not anymore complain of leg pain. However, there was no reduction in fluorodeoxyglucose accumulation in bone lesions and thus treatment response was assessed as partial remission. This patient is currently receiving a second line treatment and treatment follow-up is 26 months from the diagnosis. Repeated PET-CTs in the second patient showed a significant reduction in accumulation of fluorodeoxyglucose in all pathological lesions. Febrile states and pain in long bones as well as pathological fatigue ceased after the treatment. Increased CPR and fibrinogen gradually returned to their normal levels. This response is assessed as complete remission. This patient's follow-up is 16 months from the diagnosis. CONCLUSION: Administration of 2-chlorodeoxyadenosine (5 mg/m2 s.c.) + cyclophosphamide (150 mg/m2 intravenously) and dexamethasone (24 mg/day) led to partial remission in one patient; nearly complete remission of CNS infiltrates but persistent elevation of fluorodeoxyglucose accumulation in bone lesions. Complete remission with a significant reduction in accumulation of fluorodeoxyglucose in all disease lesions with normalization of originally increased inflammatory markers and disappearance of all symptoms of the disease was achieved in the second patient.

[Schnitzler syndrome: case report, the experience with glucocorticoid and anakinra (Kineret) therapies and monitoring of systemic cytokine response]. / Schnitzler-syndrom: popis prípadu, zkusenosti s lécbou glukokortikoidy a preparátem anakinra (Kineret) a sledování cytokinové odpovedi organizmu.

Schnitzler syndrome is a rare idiopathic disease characterized by chronic urtica, presence of monoclonal IgM immunoglobuline and further, less common symptoms. This case report describes another case of this disease affecting a male adult born in 1963. The first symptoms, eruptions of non-pruritic urticarial rash, appeared in this patient at the age of 43. In addition, bone pains (mainly tibias) and joint pains (mainly knees) were present. Later on however, severe attacks of fever, chills and shaking together with bone and joint pains were added to during which new urticarial eruptions appeared. Primarily, the man was followed up without any substantial therapeutic results at a department of dermatovenerology, subsequently, due to a finding of monoclonal IgM kappa immunoglobulin (serum concentration 1.9 g/l) he was referred to our department for the reason of gammopathy being a differential diagnosis. On a CT scan hyperostosis in claviculae and pelvic bones was identified. Also on the CT, an increase in cortical thickness was described in the long bones of the lower extremities, where areas of technetium pyrophosphate accumulation were identified on a bone scintigraphy. These areas were found in the chest and sacral regions as well. From the blood exams, the proinflammatory status of the organism was apparent (CRP 35.9 mg/l, erythrocyte sedimentation rate 92 mm/h, leukocytes 12.4 x 10(9)/l). After excluding other differential diagnoses, the patient was diagnosed with Schnitzler syndrome. As regards therapy, we made initial use of the effect of corticoids which abated the symptoms, however, these were causing serious adverse reactions in the form of iatrogenous Cushing's syndrome. The therapy took a turn only after biologic therapy with anakinra (interleukin-1 receptor antagonist) had started, which minimized the Schnitzler symptoms with very good drug tolerance. In the work we measured serum levels of interleukins for disease activity monitoring. The most sensitive were interleukins IL-6 and especially IL-18 the levels of which were the highest at the time of clinical exacerbation of the disease, whereas the levels of IL-1beta and TNF-alpha (tumour necrosis factor) were during all measurements below the limit of detection. Concerning the growing numbers of the reports on successful biological therapy with anakinra and our positive experience, we propose that the therapeutic response to anakinra should be included within the diagnostic criteria of Schnitzler syndrome, which is significant above all in differential diagnosis thereof.

[Diabetes insipidus followed, after 4 years, with dysarthria and mild right-sided hemiparesis--the first clinical signs of Erdheim-Chester disease. Description and depiction of a case with a review of information on the disease]. / Diabetes insipidus, následovaný po 4 letech dysartrií a lehkou pravostrannou hemiparézou--první klinické príznaky Erdheimovy-Chesterovy nemoci. Popis a zobrazení prípadu s prehledem informací o této nemoci.

In 2004, diabetes insipidus was the first clinical sign of Erdheim-Chester disease in our patient. Following introduction of substitution therapy with adiuretin, the patient had no further health complaints for four years until 2008 when he gradually developed dysarthria and, consequently, movement disorder in the form of mild right hemiparesis. The first CNS CT scan (2004) did not reveal any pathology. The first pathological MRI of the brain in 2006 - thickening of pituitary stalk by pathological infiltration to 4-5 mm. During the following year, further infiltrates were detected in the CNS. The number and size of CNS infiltrates increased gradually on MRIs performed repeatedly up to 2008. Erdheim-Chester disease has become suspected based on PET-CT examination at the end of 2008. CT showed irregular structure of the skeleton with noticeable sclerotic foci in otherwise osteoporotic bone structure; changes were the most evident in the long bones of lower limbs, in the pelvic bones, skull and arms, while only one vertebra was affected from within the entire spine. Finding ofthickened aortic wall (up to 8 mm) as another pathological circumstance was consistent with the Erdheim-Chester disease-associated changes described as coated aorta. CT scan revealed clear fibrotic changes in the area of retroperitoneum. Applied fluorodeoxyglucose has accumulated in the bone foci described on CTscans as well as in the thickened wall ofthe thoracic and abdominal aorta (SUV 3.6). Tc-pyrophosphonate skeleton scintigraphy showed the same bone foci as PET-CT. Full body MRI showed pathological signal from the bone marrow of the above mentioned locations, particularly during STIR imagining, where there was clear abnormal signal corresponding to accumulated histiocytes, the higher signal of which was well-differentiated from the normal bone marrow. Measurement of bone mineral density with DEXA confirmed reduced density in lumbar vertebrae to the average value of - 2.7 SD (the lowest value was -3.1SD). The disease is associated with elevated inflammatory parameters: leucocytosis, thrombocytosis, elevated CRP and fibrinogen levels. Diagnosis was verified following histological assessment ofiliac bone marrow, where focal infiltrations with foamy histiocytes of typical immunophenotype (CD68+, CD1a-, S100-) were confirmed. Treatment was initiated with chemotherapy consisting of 2g/m2 of cyclophosphamide on day 1 and 200 mg/m2 of etoposide IV infusion on days 1-3, and followed by administration of 5 microg/kg of G-CSF and collection of haematopoietic peripheral blood stem cells (PBSC). PBSC collection was followed by 5-day administration of 5 mg/m2/day of 2-chlorodeoxyadenosine (Litac) administered to the patient at monthly intervals.

[Schnitzler syndrome--report on a fourteen-year course of the disease and an overview of information on the disease]. / Schnitzleruv syndrom--popis ctrnáctiletého prubehu nemoci a prehled informací o této nemoci.

Schnitzler syndrome is a rare disease characterised by chronic urticaria and the presence of monoclonal IgM immunoglobulin, and by other symptoms. We report ourexperience with 14-year treatment of a patient. The first medical examination in our workplace was at the beginning of 1995 and the patient was diagnosed with the disease in 1996 (at the age of 52). Antihistaminics, the first medication used to relieve the symptoms of urticaria, had no subjective or objective effect. After the detection of osteolytic-osteosclerotic changes in the pelvic region, in areas with intense pain, we started treatment with pamidronate (90 mg at 28-day intervals), and the pain disappeared completely within 3 months of application of the drug. When the bisphosphonate therapy was interrupted, the pain recurred and receded completely after renewal of bisphosphonate administration. After the diagnosis, we gave the patient high doses of dexametazone (40 mg day 1-4, 10-13 and 20-23, at 28-day cycles). However, the therapy suppressed urticaria only on the days dexametasone was administered and the effect did not last when the drug was discontinued. Therefore we moved to continuous daily doses of prednisone (10-30 mg, depending on the intensity of problems), which was the only therapy with a long-term effect which was relatively well tolerated at the same time. Based on the excellent effect of 2-chlordeoxyadenosine in Waldenström's macroglobulinaemia, three cycles of this therapy were administered to the patient in 1996 (0.1 mg/kg/day, 7 days, at 28-day intervals). After the first infusion, urticarious lesions disappeared, but the positive effect on skin eruptions was limited in time and lasted only 14 days after the last infusion, i.e. the medication proved ineffective from a long-term point of view. The first improvement lasting for a longer period of time (partial remission) was achieved by regular application of interferon alpha (3 QU 3 times a week). However, adverse effects of interferon alpha prevailed after two years and the therapy was discontinued. Similarly phototherapy using the PUVA method resulted in partial regression of urticarious symptoms. Subsequently tested cyclosporine A (5 mg/kg/day) brought no benefit. Thalidomide (100 mg in the evening) administered on a continuous basis relieved pruritus and improved sleep disturbed by pruritus. However, adverse effects prevailed after 4 months and the therapy had to be discontinued, too. In 2005, we were hoping to achieve positive results with the most effective treatment for multiple myeloma of the time, a combination of bortezomib (1.3 mg/m2 i.v. on day 1, 4, 8 and 11, thalidomide 100 mg daily and dexametazon 20 mg p.o. on days 1-4 and 8-11 in 21-day cycles --VTD). A total of 4 complete cycles and 4 cycles with bortezomib reduced by 50% were applied. Urticarious eruptions were reduced by at least 50% in the course of the therapy, and also the concentration of monoclonal immunoglobin decreased temporarily by more than 50%. However, after the therapy was discontinued, the symptoms returned with their original intensity, which means that VTD regime did not provide a long-term therapeutic response. In 2007, we started the anakinra (Kineret) therapy. Skin symptoms disappeared after the first injection and a dose of 100 mg/ day has kept the patient free of skin symptoms for 12 months by now. Also the CRP value which had been constantly high returned to normal, and haemoglobin values increased to achieve physiological range. In the course of 14 years, we confirmed partial therapeutic effect of glucocorticoids administered on a continuous basis, as well as a partial therapeutic effect of interferon alpha, thalidomide and PUVA, but all the therapies had to be discontinued due to adverse effects. A major turn, i.e. the complete disappearance of skin symptoms and normalisation of CRP and haemoglobin values, only came with anakinra which has become the drug of the first choice for the above syndrome.

Fluorodeoxyglucose positron emission tomography in multiple myeloma, solitary plasmocytoma and monoclonal gammapathy of unknown significance.

The aim of our study was to evaluate the role of fluorine-18 fluorodeoxyglucose positron emission tomography (FDGPET) in 49 patients with plasma cell malignancies. FDG-PET results were verified by conventional imaging methods, including plain radiographs, magnetic resonance imaging (MRI) and computer tomography (CT). Focally increased FDG uptake was observed in three (23 %) of 11 newly diagnosed myeloma patients with negative bone radiographs. Focally increased tracer uptake was found in five of 26 patients with MM in remission but with suspected relapse. Of the 20 patients who had negative FDG-PET scans, only one relapsed 12 months after FDG-PET examination.. FDG-PET was positive in two of six patients with MGUS and with suspected progression to MM or with suspected other malignancy. In one case a thyroid carcinoma was later detected, in the other an intestinal tumor was found. We conclude that FDG PET might contribute to initial staging of MM patients with negative bone radiographs and is useful for the follow-up of patients in remission especially in non-secretory MM and in patients with large plasmocytoma (>5 cm) after radiochemotherapy.

[The value of fluorodeoxyglucose positron emission tomography in multiple myeloma]. / Prínos fluorodeoxyglukózové pozitronové emisní tomografie (FDG-PET) u mnohocetného myelomu.

UNLABELLED: The aim of this study was investigate the appearance of multiple myeloma on flurorine--18 fluorodeoxyglucose positron emission tomography (FDG-PET). Furthermore the accuracy of FDG-PET in detecting myeloma lesions and its influence on patient's management were evaluated. METHODS: Altogether 50 patients, 13 patients with newly diagnosed multiple myeloma with negative radiographs, 4 patients with solitary plasmocytoma, 27 patients in remission with suspected relapse and 6 patients with monoclonal gammopathy of unknown significance (MGUS) with suspicion for multiple myeloma or other malignancy underwent FDG-PET examination. The results of routinely performed radiographs, and MR or CT imaging modalities as well as the clinical course were used for verification of the FDG-PET results. RESULTS: Focally increased tracer uptake was observed in 3 (23 %) of newly diagnosed myeloma patients with negative radiographs and was verified with CT or MR with followed indication for therapy. The FDG-PET was negative in two cases of newly diagnosed multiple myeloma with negative radiographs, no focal infiltration on MR imagination, but with anemia, high monoclonal imunoglobulin and bone marrow infiltration, which was indication for therapy. In all other cases FDG-PET negativity in asymptomatic myeloma had good prognostic significance; these patients are without progression after with a median follow up 14 (7-20) months. Focally increased tracer uptake was found in 5 of the 27 patients in remission. In 4 cases of them it was due to multiple myeloma relapse, in one case due to ovarial carcinoma. Only in 1 patient the PET-FDP failed to recognize extraosseal progression on the scull. 21 patients had true negative FDG-PET imagination, in 1 case disease relapsed 12 months after FDG-PET examination; the other 20 patients are still without progress of this disease with median follow up 15 (7-20) months. FDG-PET was positive in 2 from the 6 patients with MGUS. In one of them carcinoma of thyreoidea was detected, in second the FDG-PET activity was localized in gut, tumor was verified with CT and colonoscopy. CONCLUSION: In conclusion, FDG PET might contribute to initial staging of radiographs negative multiple myeloma and might be useful for follow up of patients in remission, especially in consecratory multiple myeloma, or in patients with large plasmocelular tumor (> 5 cm) after concomitant radiochemotherapy.

[Hereditary pheochromocytoma--a family affected by von Hippel-Lindau disease]. / Hereditární feochromocytom--rodina postizená von Hippel-Lindauovou chorobou.

The authors present a case of a 37 year old male (proband) with a 13 year history of progressive sight impairment leading to blindness and a 4 year history of a mild hypertension. He was incidentally found to have large adrenal tumors after an ultrasound kidney examination. The tumors were confirmed with CT scan and magnetic resonance imaging. A bilateral pheochromocytoma was biochemically demonstrated and successfully removed. The eye diagnosis of angiomatosis retinae von Hippel-Lindau was ascertained after a search of the patient files in other medical departments, which led to a family screening. Proband's brother, having hypertension and a history of a cerebellar astrocytoma operation, was also diagnosed with CT scan to have a bilateral pheochromocytoma. Unfortunately, at the same time he was found to have a large irremovable neuroendocrine pancreatic carcinoma, which caused complications and his eventual death. Both proband and his brother were affected by the same CGG(Arg167)->CAG(Gln) mutation in the exon 3 of the VHL gene. Other living and examined family members were not affected, which was confirmed by negative genetic testing. One year after the pheochromocytoma operation, proband was diagnosed to have a retroperitoneal tumor left to the aorta, clinically silent, with slightly and non-constantly elevated urine norepinephrine and normetanephrine. Metaiodobenzylguanidine scintigraphy showed that it was a paraganglioma. The old CT and magnetic resonance picture review demonstrated that the tumor had already been present at the time of the operation. It was surgically removed and histologically verified. It is a pity that proband had not been sent by his ophthalmologist for an endocrine examination when the eye diagnosis was determined. Affection of the family would have been discovered earlier, and proband's brother might have possibly been saved.

Cerebral perfusion pressure and spect in patients after craniocerebral injury with transtentorial herniation.

We present a group of 29 consecutive head injured comatose patients with the syndrome of transtentorial herniation. All patients had urgent surgery and then continuous monitoring of ICP, CPP, blood pressure and jugular bulb oximetry was instituted. Two postoperative CT and SPECT examinations were performed in each patient. 15 patients had a normal CPP (> 70 mmHg) throughout the postoperative period, 80% of them had a favourable outcome. On the other hand 14 patients had decreased CPP lasting at least one hour and only 36% of them had a favourable outcome (p < 0.05). Similar relationships were found comparing GOS in patients with normal and increased ICP (> 20 mmHg) and normal and decreased SjO2 (< 55%). All but 3 patients had ischaemia on SPECT. Ischaemia improved on the 2nd SPECT in 11 patients and 10 (91%) of them had a favourable outcome. GOS (mean follow up 9 months) is: 12 patients good, 5 moderately disabled, 2 vegetative, 10 died. We conclude that SPECT is able to disclose even reversible ischaemic changes. In these patients all effort has to be made to keep CPP on normal levels. Improvement in cerebral perfusion is related to a better outcome.

[Traumatic intracranial hemorrhage with a clinical temporal conus syndrome]. / Traumatické nitrolební krvácení s klinickým syndromem temporálního konusu.

The authors investigated a consecutive group of 14 patients treated at the Neurosurgical Clinic on account of traumatic intracranial haemorrhage, admitted with the clinical temporal conus syndrome (GCS 3-5, ipsilateral or bilateral mydriasis, failure of vital functions). All had emergency operations and at the intensive care unit the cerebral perfusion pressure and the saturation in the jugular bulb was monitored continuously. On the first and fifth day after surgery a check-up CT and SPECT examination was made. Only two patients had ischaemia during the first CT check-up, while 11 patients had impaired perfusion on the first SPECT. Improving perfusion on the check-up SPECT was the sign of a favourable prognosis, while ischaemia on the first CT was in both instances fatal. The Glasgow Outcome Score (GOS) six months after the injury was as follows: 9 patients had a good result, 2 patients were moderately disabled 3 patients died. The authors consider the following as basic prerequisites of a favourable outcome: not only early operation but also monitoring and treatment of impaired cerebral perfusion.

[Cisapride (Prepulsid) in the prevention of postoperative gastrointestinal atony]. / Význam cisapridu (Prepulsidu) v prevenci pooperacní atonie trávicího ústrojí.

Administration of cisapride, 3 x 5 mg in a suspension one day before surgery and 30 mg 3 and 8 hours after abdominal surgery with subsequent administration of 2 x 30 mg in suppositories up to the time when oral ingestion is possible, hastens significantly the restoration of GIT motility as compared with placebo. It can be therefore recommended as effective medication in the prevention of complications caused by impaired motility of the digestive tract.

[Proton pump blockers and their significance in gastroenterology]. / Blokátory protonové pumpy a jejich význam v gastroenterologii.

Extremely effective drugs used in the therapy of diseases etiologically associated with excessive HCl secretion by the gastric mucosa include proton pump blockers. Their obvious advantage, as compared with commonly used drugs, is that they cause a marked drop of HCl production by the gastric mucosa regardless of the type of stimulus, i.e. whether parietal cell receptors are influenced. Their therapeutic action is extremely effective, while side-effects are minimal. The publication gives the basic indications of administration of proton pump blockers, compares their therapeutic efficiency with H2 blockers and draws attention to possible pitfalls of therapy.

[IgA antibodies against Epstein-Barr virus capsid antigen]. / Protilátky trídy iga proti kapsidovému antigenu viru Epsteina-Barrové.

The authors describe infection with the Epstein-Barr virus (EBV) which is associated with the formation of various types of antibodies--heterophil (HP) antibodies as well as antibodies against individual EBV antigens. They evaluate the contribution of a recently elaborated and introduced method used for detection of antibodies against the capsid antigen of the EBV class IgA (anti-VCA IgA) by indirect immunofluorescence to the diagnosis of acute and chronic EBV infections. Anti-VCA IgA are useful in the diagnosis of EBV infections if the patient has no longer HP and anti-VCA IgM, but only anti-VCA IgG. If, however, in addition to anti-VCA IgA also anti-VCA IgA are present, their presence can be the only detectable sign of a recent EBV infection and also a sign of reactivation of chronic EBV infection.