PubMed Health⌕ Search

Biomedical subjects

Andreas Holstein

Publications and source records attributed to Andreas Holstein.

6 recordsLinked to original sources
PubMed2006

Autoantibody profiles in microscopic colitis.

OBJECTIVE: The etiology of microscopic colitis is unclear; an autoimmune response and pharmacological induction have been proposed as possible mechanisms. We conducted a multicentre cross-sectional study to compare the antibody profiles of patients with collagenous and lymphocytic colitis with those of a control group. METHODS: The medical histories and antibody profiles of 26 patients with collagenous and 16 patients with lymphocytic colitis were compared with the corresponding data of 43 controls without gastroenterological disease. Antibodies to the following structures were determined: intestinal goblet cells, antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies, anti-Saccharomyces cerevisiae antibody (ASCA), tissue transglutaminase, gliadin, pancreatic acini, glutamate decarboxylase, tyrosine phosphatase IA-2 and thyroid (microsomal anitbodies, MAB). RESULTS: Patients with collagenous and lymphocytic colitis had been treated significantly more often with H(2)-receptor antagonists and non-steroidal anti-inflammatory drugs (P = 0.026 and 0.014, respectively). Additional diseases of presumed autoimmune etiology were present in 43% (18/42) of patients. Comparison with the controls showed significantly more positive findings for ANA immunoglobulin G (IgG), gliadin immunoglobulin A (IgA) and ASCA (IgA and IgG) in patients with collagenous colitis but not in those with lymphocytic colitis. Collagenous colitis was associated with positive ASCA in 15% of patients and lymphocytic colitis in 13%. CONCLUSIONS: The autoantibodies investigated are of no diagnostic relevance to microscopic colitis. Positive ANA and strong associations with other autoimmune diseases point to an autoimmune etiology. H(2)-receptor antagonists and non-steroidal anti-inflammatory drugs might also be of pathogenetic significance.

Adult↗
PubMed2006

Rheumatoid-like nodules in the spleen: new extraintestinal manifestation of Crohn's disease?

A 26-year-old, HLA-B27 positive man with steroid dependent Crohn's disease presented with abdominal lymphadenopathy and multiple abscess-like masses in the spleen and liver 2 years after the initial diagnosis. A biopsy of one of the liver lesions showed epitheloid cell granuloma, no microorganisms were detected despite intensive investigations. The liver lesions and the lymphadenopathy repeatedly disappeared completely in response to prednisolone pulse therapy while the lesions in the spleen remained practically unchanged. One year later, on immunosuppressive therapy with azathioprine and low-dose prednisolone, the patient's condition exacerbated with development of fever, disseminated arthritides and enlargement of the splenic lesions. Following ineffective antimicrobial treatment, a splenectomy was carried out. Histology showed that the splenic parenchyma was filled with abacterial, rheumatoid granulomas. After a renewed flare-up of severe extraintestinal symptoms, the patient is now asymptomatic on immunosuppressive therapy with azathioprine and prednisolone. Abdominal lymphadenopathy is no longer present and the liver lesions are regressing. The intermittent course and the positive response to immunosuppressive therapy point to a further extraintestinal manifestation of Crohn's disease.

Adult↗
PubMed2005

The Glu23Lys polymorphism in KCNJ11 and impaired hypoglycaemia awareness in patients with type 1 diabetes.

Impaired awareness of hypoglycaemia affects approximately 25% of all patients with type 1 diabetes (T1D). Duration of diabetes and tight glycaemic control represent the main risk factors for hypoglycaemia unawareness. However, even among patients with good glycaemic control and longstanding T1D, awareness of hypoglycaemia may be intact. Genetic factors might explain some of this remaining variability, and genes involved in central glucose sensing should represent plausible candidates. Some evidence indicates that ventromedial hypothalamus glucose-responsive neurons require the potassium inward rectifier (KIR) 6.2 subunit of the K(ATP) channel to sense glucose. Therefore, the effects of the Glu23Lys polymorphism in the KCNJ11 (KIR6.2) gene (potassium inwardly rectifying channel, subfamily J, member 11) on impaired hypoglycaemia awareness in 217 patients with T1D were studied. Hypoglycaemia awareness status was determined using standardized questionnaires. Genotyping of the Glu23Lys in a cohort of T1D subjects was done using the TaqMan allelic discrimination assay (frequency of the Lys-allele = 0.35; P = 0.57 for Hardy-Weinberg equilibrium). The study confirms that diabetes duration, C-peptide, and HbA(1c) represent risk factors for impaired hypoglycaemia awareness. However, no significant effect of the Glu23Lys polymorphism on impaired hypoglycaemia awareness was observed with or without adjustment for age, diabetes duration, C-peptide, and HbA(1c). Even though the study provides a relatively large dataset, it is possible that small differences may have been missed.

Adult↗
PubMed2005

Successful photo-and phenobarbital therapy during pregnancy in a woman with Crigler-Najjar syndrome type II.

Severe hyperbilirubinemia in a pregnant mother suffering from Crigler-Najjar syndrome type II is a threat to the unborn child and may result in brain injury. We report the case of a Gly71-->Arg/Tyr486-->Asp homozygous mother of East Asian descent, who was treated with phototherapy during embryogenesis and with phenobarbital during the rest of the pregnancy. This resulted in significantly reduced bilirubin levels in the mother, who gave birth to a healthy boy. A neonatal hyperbilirubinemia resolved spontaneously.

Adult↗
PubMed2002

Clinical implications of hepatogenous diabetes in liver cirrhosis.

BACKGROUND: Hepatogenous diabetes is a common complication of liver cirrhosis. The aim of the present study was to examine the clinical and therapeutic implications and the prognostic significance of hepatogenous diabetes in patients with liver cirrhosis. METHODS: The prospective cohort study was conducted in 52 patients with histologically confirmed liver cirrhosis (44% Child A, 37% Child B, 19% Child C). The examination included a history, determination of basal C-peptide and glycosylated hemoglobin (HbA(1c)) and, in some cases, a 3 h oral glucose tolerance test with 100 g glucose. Patients were also examined for signs of diabetic retinopathy and information on the further course of illness was obtained. RESULTS: Seventy-one percent of patients with liver cirrhosis had manifest diabetes, 25% had impaired glucose tolerance and only 4% had normal glucose tolerance. In most cases, the hepatogenous diabetes was clinically asymptomatic. Sixteen percent of patients with hepatogenous diabetes had a family history of diabetes; only 8% had retinopathic complications. Within 5.6 +/- 4.5 years after diagnosis of liver cirrhosis, 52% of the diabetics had died, mainly of complications of the cirrhosis. There were no diabetes-associated or cardiovascular deaths. CONCLUSIONS: Hepatogenous diabetes differs from type 2 diabetes in that there is less often a positive family history and that the cardiovascular and retinopathic risk is low. The prognosis of cirrhotic patients with diabetes is more likely to be negatively affected by the underlying hepatic disease and its complications than by the diabetes. Antihyperglycemic treatment of hepatogenous diabetes should always be carefully weighed up in each individual case.

Adult↗