Physical activity, muscular strength, and polypharmacy among older multimorbid persons: Results from the KORA-Age study.

The purpose of this study was to examine whether physical activity (PA) and muscular strength (MS) are related to polypharmacy. Our cross-sectional analysis was based on 711 patients with multimorbidity (MMB), aged 65-94 years, who participated in the KORA-Age study. Participants underwent a face-to-face interview and extensive physical examinations including anthropometric measurements, registration of chronic diseases, determination of health-related behaviors (smoking, alcohol intake, physical activity, etc.), collection of blood samples and measurement of hand-grip strength. PPha was defined as the use of >4 drugs and MMB as having ≥2 of 13 chronic diseases. Prevalence of PPha was 44.6% (n=317), and a significant difference was found in the number of drugs used between participants with and without PPha (7.2±2.1 vs 2.5±1.2, P<.001). Patients in the lower compared to the upper tertile of physical activity had a significantly increased odds to be on PPha (OR: 1.64, 95% CI: 1.05-2.56, P=.031) after controlling for age, gender, BMI, family status, education, alcohol intake, smoking habits, number of diseases, hs-CRP, and telomere length. On the contrary, no significant association between muscular strength and PPha was found (OR: 1.04, 95% CI: 0.66-1.63, P=.873) after multivariable adjustment. Among older persons with MMB, lower levels of physical activity, but not low muscular strength, are associated with higher odds of PPha. Increasing the levels of physical activity appears to be highly recommended in order to potentially reduce the risk of PPha among multimorbid persons aged 65 and older.

Estimating the prevalence of Parkinson's disease (PD) and proportions of patients with associated dementia and depression among the older adults based on secondary claims data.

OBJECTIVES: While the epidemiology of Parkinson's disease (PD) has been extensively studied, data on the prevalence of PD among the older adults in Germany are scarce, based on small samples, and limited to primary data designs. This study estimated the PD prevalence among the older adults in Germany in 2006 using secondary data. METHODS: We included 815,573 health insurance members aged ≥65 years from all regions in Germany. PD was identified in case of at least one inpatient or outpatient diagnosis. An outpatient diagnosis had to be confirmed by either a subsequent diagnosis or an antiparkinsonian drug within 12 months. PD was also assumed if a first prescription was confirmed by a diagnosis within 12 months. Cases were checked for a diagnosis of dementia or depression. RESULTS: The standardized prevalence of PD was 1680 (95% confidence interval (CI): 1644-1716) cases per 100,000 persons. The prevalence increased with age and peaked in the age group of ≥90 years (4633 cases; 95% CI: 4227-5068) with higher rates in men (1729; 95% CI: 1684-1776) than in women (1644; 95% CI: 1593-1697). Dementia and depression occurred in 26.6% (95% CI: 25.8-27.5) and 32.6 (95% CI: 31.7-33.5) of PD cases, respectively. CONCLUSIONS: The age-related increase of PD prevalence and the age-specific prevalence estimates are in line with other European studies, stressing the public health relevance related to PD. In addition to the minimization of biases that might occur in primary data studies, further strengths of our findings are the large underlying sample size and the coverage of Germany.

A child with localized vulval pemphigoid and IgG autoantibodies targeting the C-terminus of collagen XVII/BP180.

Localized vulval pemphigoid of childhood (LVPC) has previously been reported in six girls. Clinical features and immunopathological data have suggested it to be a morphological variant of bullous pemphigoid. Epitope targets of the autoantibodies of these patients have not been defined in detail. We describe a 9-year-old girl with possible cicatricial LVPC and circulating IgG antibodies directed against native collagen XVII/BP180, its 120-kDa soluble ectodomain and against the C-terminus of collagen XVII/BP180. No reactivity was detected towards the NC16A domain of collagen XVII/BP180. Linear IgG and C3 deposits were found along the cutaneous basement membrane zone. On 1 mol/L salt-split skin, IgG autoantibodies were shown to bind to the epidermis, and the HLA type II allele DQB1*0301, a marker with significantly increased occurrence in patients with ocular and oral cicatricial pemphigoid, was identified in this patient. Our data suggest that LVPC is a variant of bullous pemphigoid in which direct immunofluorescence microscopy combined with immunoblot analysis can deliver valuable diagnostic information for differential diagnosis. However, differentiation between the scarring and non-scarring course of the disease cannot be made with the present diagnostic markers and therefore careful follow-up of patients with LVPC is required.

[Lichenoid pseudolymphomatous tattooing reaction]. / Lichenoid-pseudolymphomatöse Tätowierungsreaktion.

A 35 year old patient developed swellings in the red colored areas of his tattoo. Histological examination revealed a lichenoid, pseudolymphomatous infiltrative pattern, that could be distinguished from frank lymphoma by means of electron microscopy, immunohistochemistry and molecular biology. The presence of dermal dendritic cells suggests a dermal-allergic pathogenesis of non-granulomatous tattoo reactions. Therapy of choice is an excision of the inflamed areas.

Expression of a glycoprotein of the carcinoembryonic antigen family in normal and neoplastic sebaceous glands. Limited role of carcinoembryonic antigen as a sweat gland marker.

BACKGROUND: Carcinoembryonic antigen (CEA) is a well-known marker for sweat gland differentiation in adnexal neoplasms. OBJECTIVE: The aim of this study was to examine the expression of glycoproteins of the CEA family, that is, CEA-180, nonspecific cross-reacting antigens (NCAs), and biliary glycoprotein (BGP), in sebaceous glands and in neoplasms with sebaceous differentiation. METHODS: Normal adult and fetal skin, hyperplasias, hamartomas, and neoplasms with sebaceous or follicular differentiation were stained immunohistochemically with a panel of polyclonal and monoclonal antibodies highly specific for CEA-180, NCAs, and BGP. Double immunostaining was performed to correlate the CEA expression with that of epithelial membrane antigen (EMA), a glycoprotein consistently found in differentiating sebocytes. RESULTS: Whereas sweat glands coexpressed CEA, NCAs, BGP, and EMA, sebaceous glands were exclusively labeled with the antibodies recognizing BGP or EMA. Staining of the sebaceous glands was restricted to mature sebocytes, sparing immature cells. At the ultrastructural level immunoreactivity for BGP and EMA was demonstrable in the golgi area, in small vesicles, and along the cell membranes. During fetal development BGP was not found until the sebaceous glands matured. The expression of BGP and EMA was highly conserved in reactive, hamartomatous, and neoplastic proliferations of adnexal structures with sebaceous differentiation. CONCLUSION: The expression of BGP, a CEA glycoprotein, in differentiating sebocytes accounts for the reactivity of many anti-CEA antibodies with sebaceous glands and thus disqualifies the CEA family as a monospecific marker for sweat gland differentiation.

Neoplasms with sweat gland differentiation express various glycoproteins of the carcinoembryonic antigen (CEA) family.

Carcinoembryonic antigen (CEA) is a well-established marker for sweat gland differentiation in adnexal neoplasms. In contrast to previous assumptions, CEA does not represent a single oncofetal antigen but comprises a family of homologous glycoproteins, i.e. the classical CEA-180, biliary glycoprotein (BGP), and non-specific crossreacting antigens (NCA). The aim of the study was to evaluate the distribution of the respective glycoproteins of the CEA family in sweat gland neoplasms, as compared to normal sweat glands. A panel of mono-specific antibodies was applied to a total of 83 samples of hyperplastic and cystic alterations of sweat glands, sweat gland neoplasms, and cutaneous metastases of different origin. Within a single group of neoplasms the immunohistochemical profile was rather consistent. Staining for both CEA-180 and NCA-90 indicated ductal differentiation of both eccrine and apocrine glands. Co-expression of CEA-180, NCA-90, and BGP was consistent with differentiation towards the secretory part of eccrine glands or the transitional portion of proximal ducts. Neoplasms with signs of apocrine secretion showed a preferential immunoreactivity for NCA-90 and BGP. In conclusion, a specification of the members of the CEA family may be of some value in the differential diagnosis of adnexal neoplasms, but not in the discrimination of sweat gland carcinoma from metastatic carcinoma.

Glycoproteins of the carcinoembryonic antigen (CEA) family are expressed in sweat and sebaceous glands of human fetal and adult skin.

The carcinoembryonic antigen (CEA) family comprises a group of glycoproteins including the classical CEA, nonspecific cross-reacting antigens (NCA), and biliary glycoprotein (BGP). CEA glycoproteins have been identified in many glandular and mucosal tissues. In view of their putative role in cell adhesion, protein sorting, and signal transduction, CEA glycoproteins are thought to be involved in embryogenesis, architectual integrity, and secretory mechanisms of glandular epithelia. Since there are few data available on the expression of CEA-like proteins in human skin, the aim of this study was to immunohistochemically specify and localize the CEA glycoproteins in cutaneous adult and fetal glands using a panel of well-characterized antibodies. The secretory parts of eccrine sweat glands expressed CEA, NCA-90, and BGP, whereas apocrine glands remained unreactive for CEA glycoproteins. The ductal epithelia of both eccrine and apocrine glands contained CEA and NCA-90. Sebaceous glands were stained for BGP only. Electron microscopy of sweat glands showed CEA glycoprotein expression in cytoplasmic organelles and on microvilli lining the ductal surface. In sebaceous glands, BGP were demonstrated in small vesicles and along the cell membranes of differentiating sebocytes. Fetal development of cutaneous glands was associated with early expression of CEA glycoproteins. Additionally, mice transgenic for human CEA were shown to express CEA in sweat glands. The overall distribution of CEA glycoproteins in cutaneous glands was consistent with that in epithelia of other glandular tissues.

Effect of granulocyte/macrophage colony-stimulating factor on human monocytes infected with influenza A virus. Enhancement of virus replication, cytokine release, and cytotoxicity.

The activating properties of granulocyte/macrophage (GM)-CSF were studied in vitro with human monocytes infected by influenza A virus. When monocytes were pretreated for 8 h with GM-CSF (100 U/ml) and then exposed to influenza A virus, de novo virus protein synthesis was enhanced, more virus particles were released, and cells were killed at a higher rate. In virus-infected monocytes, GM-CSF induced a more rapid IFN-alpha release and potentiated production of TNF-alpha, IL-1 beta, and IL-6. Although GM-CSF or influenza A virus were each capable of independently activating TNF-alpha, IL-1 beta, and IL-6 gene transcription, a combination of both induced a massive cytokine mRNA accumulation which was readily translated into bioactive protein. Thus, GM-CSF may display a Janus-like action by accelerating virus infection but also by priming monocytes for elevated cytokine production. Whether the facilitated influenza A virus replication caused by GM-CSF may be counterbalanced by an improved cytokine response remains to be studied under more complex in vivo conditions.