[Acute disseminated encephalomyelitis in children]. / Encefalomielitis aguda diseminada en la niñez.

AIM: Acute disseminated encephalomyelitis (ADEM) is an immune-mediated inflammatory-demyelinating disease, which usually follows an infection or vaccination. It is more frequent in children. In this paper, I will review clinical, diagnosis, treatment, and prognosis data, based on last 10 years papers, including our experience with 42 patients studied at Calvo Mackenna Hospital and German Clinic of Santiago de Chile, Chile. DEVELOPMENT: ADEM symptoms present 2 to 30 days after viral or bacterial infection. There is a slight male predominance (1,3:1). The clinical picture is characterized by multiple symptoms. Prominent findings are altered level of consciousness in 50-60% of patients, and motor system dysfunction in 80-90%. Spinal cord dysfunction occurs in 20-25% of children. Optic neuritis (10-20%) is usually bilateral. Magnetic resonance imaging is the gold standard to detect typical white matter lesions, which suggest ADEM diagnosis, but a clinico-neuroimaging gap may occurs. Steroids are the first choice for treatment. In practice, they seem to be useful in up to 90% of patients. Recurrences occur in 10-30% of cases, and raise a differential diagnosis with multiple sclerosis. Mortality is as low as 0-7%. Sequelae are seen in 10-20% of patients. CONCLUSIONS: ADEM is a demyelinating condition, usually with a monophasic course and good outcome. The only way to confirm a definite diagnosis is long-term follow-up.

Encefalomielitis aguda diseminada en la niñez / Acute disseminated encephalomyelitis in children

Objetivo. La encefalomielitis aguda diseminada (EMAD)es una enfermedad inflamatorio-desmielinizante, mediada inmunológicamente,que se presenta usualmente después de una infeccióno vacunación. Es más frecuente en el niño. Se revisan aspectos clínicos,diagnósticos, terapéuticos y pronósticos de la EMAD infantilpublicado en los últimos 10 años, y se incluye además nuestraserie de 42 niños del Hospital Luis Calvo Mackenna y de la ClínicaAlemana de Santiago de Chile. Desarrollo. La EMAD se presentade 2 a 30 días después de infección viral o bacteriana. Predominalevemente en niños (1,3:1). La clínica es polisintomática. Destacanla afectación de la conciencia en el 50-60% y los trastornos motoresen el 80-90% de los pacientes. La afectación medular se observaen el 20-25%, mientras que la neuritis óptica (generalmentebilateral) aparece en el 10-20% de los niños. La resonancia magnéticaes la mejor prueba para lograr el diagnóstico de EMAD, yaque detecta lesiones multifocales de la sustancia blanca, aunqueéstas pueden aparecer más tardíamente, con un desfase clinicoimagenológicode 5 a 22 días. El tratamiento de elección son los corticoides.En la práctica, parecen tener un efecto beneficioso en hastael 90% de los pacientes. Las recidivas se presentan en el 10-30%de los casos, y plantean diagnóstico diferencial con esclerosis múltiple.La mortalidad es baja, del 0 al 7%. Las secuelas alcanzan el10-20%. Conclusiones. La EMAD es una enfermedad desmielinizantedel sistema nervioso, cuyo curso habitual es monofásico y suevolución favorable. El diagnóstico definitivo sólo se logra medianteel seguimiento prolongado

Aim. Acute disseminated encephalomyelitis (ADEM) is an immune-mediated inflammatory-demyelinating disease,which usually follows an infection or vaccination. It is more frequent in children. In this paper, I will review clinical, diagnosis,treatment, and prognosis data, based on last 10 years papers, including our experience with 42 patients studied at CalvoMackenna Hospital and German Clinic of Santiago de Chile, Chile. Development. ADEM symptoms present 2 to 30 days afterviral or bacterial infection. There is a slight male predominance (1,3:1). The clinical picture is characterized by multiplesymptoms. Prominent findings are altered level of consciousness in 50-60% of patients, and motor system dysfunction in 80-90%.Spinal cord dysfunction occurs in 20-25% of children. Optic neuritis (10-20%) is usually bilateral. Magnetic resonance imagingis the gold standard to detect typical white matter lesions, which suggest ADEM diagnosis, but a clinico-neuroimaging gap mayoccurs. Steroids are the first choice for treatment. In practice, they seem to be useful in up to 90% of patients. Recurrences occurin 10-30% of cases, and raise a differential diagnosis with multiple sclerosis. Mortality is as low as 0-7%. Sequelae are seen in10-20% of patients. Conclusions. ADEM is a demyelinating condition, usually with a monophasic course and good outcome.The only way to confirm a definite diagnosis is long-term follow-up

[Updates in muscular dystrophies]. / Actualización en distrofias musculares.

INTRODUCTION: Advances in molecular genetics on lasts 15 years had modified profoundly our knowledge about muscular dystrophies. The pathogenia, caused by defectives proteins which disrupt dystrophin-associated-protein complex in most of the dystrophies, has generate a new classification based in protein and genomic defects. DEVELOPMENT: In this review, clinical, genetic, diagnostic and therapeutic aspects of the main muscular dystrophies are described. Limb girdle muscular dystrophies with Duchenne-like phenotype (sarcoglycanopathies), are identified by immunohistochemistry, as X-linked Emery-Dreifuss muscular dystrophy (emerin deficit), and classical congenital muscular dystrophy (merosine depletion). The others limb girdle muscular dystrophies, an heterogeneous phenotypical group, are detected by Western blot (mainly calpainopathies), or inmunohistochemistry in muscle (caveolinopathies) and blood (dysferlinopathies). Congenital muscular dystrophies with brain malformations: Fukuyama, muscle-eye-brain, and Walker-Warburg syndrome; and fukutin-related protein dystrophy, only may be differentiated by genetic analysis. All them shows alpha-dystroglican depletion. Autosomal dominant Emery-Dreifuss muscular dystrophy and facioscapulohumeral dystrophy are exclusively identified by DNA study. Finally, Duchenne/Becker muscular dystrophies are diagnosed by immunohistochemistry, Western blot and/or DNA analysis. Treatment of muscular dystrophies is based in physiotherapy, ventilatory support, surgery and drugs (mainly steroids, effective in Duchenne/Becker muscular dystrophies). CONCLUSION: Genic and cellular therapy are yet on experimental field, and are matter of the future. Now, accurate diagnosis is important for therapeutic management, prognosis and genetic counseling.

Actualización en distrofias musculares / Updates in muscular dystrophies

Introducción. Los avances en genética molecular de los últimos quince años han modificado profundamente nuestros conocimientos con relación a las distrofias musculares. La clarificación de la patogenia, debida a déficit de una proteína específica que altera el complejo de proteínas asociadas a la distrofina en la mayoría de las distrofias, ha generado una nueva clasificación basada en el defecto proteico y genómico. Desarrollo. En esta revisión se describe la clínica, la genética, el diagnóstico y el tratamiento de las principales distrofias musculares. Las distrofias de cinturas con fenotipo similar a Duchenne (sarcoglicanopatías) se detectan por inmunohistoquímica, igual que la distrofia muscular de Emery-Dreifuss ligada al cromosoma X (déficit de emerina) y la distrofia muscular congénita clásica (déficit de merosina). Las demás distrofias de cinturas, de fenotipo heterogéneo, se confirman por inmunotinción en el músculo (disferlinopatías, caveolinopatías) y por Western blot (especialmente calpainopatías). Las distrofias musculares congénitas con malformaciones cerebrales (Fukuyama, músculo-ojo-cerebro y síndrome Walker-Warburg), y la distrofia por defecto de FKRP (del inglés fukutin related protein), sólo pueden diferenciarse mediante un estudio genético. Todas ellas muestran depleción de -distroglicano en el músculo. La distrofia muscular de EmeryDreifuss autosómica dominante y la distrofia facioescapulohumeral se confirman mediante el estudio del ADN. La distrofia muscular de Duchenne/Becker, finalmente, se detecta por inmunohistoquímica, Western blot y/o análisis de ADN. El tratamiento de las distrofias musculares se basa en fisioterapia, apoyo ventilatorio, cirugía, y fármacos (especialmente corticoides, beneficiosos en la distrofia muscular de Duchenne/Becker). Conclusión. La terapia génicocelular se mantiene en un plano experimental y todavía es una posibilidad futura. Por ahora, el diagnóstico preciso de la distrofia muscular permite efectuar un plan de manejo, un pronóstico y un consejo genético adecuado (AU)

Introduction. Advances in molecular genetics on lasts 15 years had modified profoundly our knowledge about muscular dystrophies. The pathogenia, caused by defectives proteins which disrupt dystrophin-associated-protein complex in most of the dystrophies, has generate a new classification based in protein and genomic defects. Development. In this review, clinical, genetic, diagnostic and therapeutic aspects of the main muscular dystrophies are described. Limb girdle muscular dystrophies with Duchenne-like phenotipe (sarcoglycanopathies), are identified by immunohistochemistry, as X-linked EmeryDreifuss muscular distrophy (emerin deficit), and classical congenital muscular dystrophy (merosine depletion). The others limb girdle muscular dystrophies, an heterogeneous phenotypical group, are detected by Western blot (mainly calpainopathies), or inmunohistochemistry in muscle (caveolinopathíes) and blood (dysferlinopathies). Congenital muscular dystrophies with brain malformations: Fukuyama, muscle-eye-brain, and Walker-Warburg syndrome; and fukutin-related protein dystrophy, only may be differentiated by genetic analysis. All them shows alpha-dystroglican depletion. Autosomal dominant Emery-Dreifuss muscular distrophy and facioscapulohumeral dystrophy are exclusively identified by DNA study. Finally, Duchenne/Becker muscular dystrophies are diagnosed by immunohistochemistry, Western blot and/or DNA analysis. Treatment of muscular dystrophies is based in physiotherapy, ventilatory support, surgery and drugs (mainly esteroids, effective in Duchenne/Becker muscular dystrophies). Conclusion. Genic and cellular therapy are yet on experimental field, and are matter of the future. Now, accurate diagnosis is important for therapeutic management, prognosis and genetic counseling (AU)

Fabricated hyalS micropatterns and surface guidance of NCTC 2544 continuous cell line: an in vitro study.

Surface topography is important in establishing tissue organisation adjacent to implants, smooth surfaces generally being associated with fibrous encapsulation. By virtue of its large hydrated molecular volume and its capacity to form molecular matrix, hyaluronic acid can expand the interfibrillar collagen spaces to allow the movement of cells, although it can also hamper their locomotion. Low molecular-weight hyaluronan can also stimulate cell proliferation, especially at low concentrations. The aim of the present work was to evaluate in vitro the growth and migratory behaviour of NCTC 2544 keratinocytes cultured on different materials microstructured with hyaluronic acid or sulfated hyaluronic acid to assess the possibility of using these devices in the repair process of soft tissues. Ultrastructural morphological analyses, morphometric evaluations and detection of cytoskeletal elements were performed. Our observations provide evidence that micrometer-size parallel grooves of hyaluronic acid can influence cell growth behaviour since cells seeded onto the microstructured substrate arranged themselves according to a shape and an orientation that clearly reflected the chemotropism exerted on them by the two forms of acid. These data also highlight the importance of accurate microtexture fabrication. We intend to follow up these in vitro studies with in vivo experimental applications using PET and gelatin substrates structured with HyalS to evaluate wound healing responses, and to extend our investigations of the cytoskeletal modifications induced by different microstructures.

Genomic relationships between Medicago murex Willd. and Medicago lesinsii E. Small. investigated by in situ hybridization.

Medicago murex Willd. is an annual species (2n = 14) widespread in the wild and of remarkable interest for pastures in regions with a mediterranean climate. It is considered closely related to Medicago lesinsii E. Small (2n = 16) but, up to now, there is no evidence demonstrating their genetic affinity. This research was undertaken to investigate the genomic relationships between M. murex and M. lesinsii by using genomic in situ hybridization (GISH). In this study GISH experiments were performed using both species as sources of chromosomes and genomic probes. To better evaluate the results of the hybridization, the labelled DNA of each species was hybridized to chromosomes of the same species and to chromosomes of the diploid Medicago littoralis (2n = 16). Strong hybridization signals were found on chromosomes of M. murex and M. lesinsii after GISH. Differences in the hybridization strength were not observed when slides from interspecific hybridization were compared with the control preparations. These results suggest that consistent divergences of the DNA sequences did not occur after the separation of the two species. Instead very reduced cross hybridization was found on chromosome spreads of M. littoralis hybridized with the DNA of M. lesinsii or M. murex. The distribution of the ribosomal genes (rDNA) investigated by fluorescent in situ hybridization (FISH) appeared similar in both M. murex and M. lesinsii. The GISH technique may be a valuable approach to obtain information on evolution of the 2n = 14 species and on the origin of the polyploids Medicago rugosa (2n = 30) and Medicago scutellata (2n = 30). The first attempt to investigate the genomic composition of M. scutellata using a genomic probe is reported in this paper.

The Triticeae genetic resources of central Italy: collection, evaluation and conservation.

One hundred and six landraces belonging to 7 species of the Triticeae tribe were collected in central Italy by DBVBA (Perugia University), DIBIAGA (Ancona University) and ARSSA (Abruzzo Region Agricultural Development Agency) in different individual and joint missions. A few accessions were supplied by private and other public organisations. Triticum dicoccum Schubler is the most widespread species, followed by T. aestivum L., T. monococcum L., T. spelta L., T. turgidum var. durum Desf., Secale cereale L. and Hordeum vulgare L. Besides the presence of landraces reproduced by farmers over generations, information related to on-farm management and to qualitative/organoleptic traits as well as information related to their local names, uses, traditions and social context was gathered during the missions. The majority of the accessions was characterised by morphological and phenological traits and molecular markers. This work shows the presence of morpho-phenologic and genetic differences among landraces and the importance of some species in the agricultural systems and food customs of the investigated area. Particularly for emmer three well distinct landraces are present, "Farro Italia Centrale", "Farro della Garfagnana" and "Farro Italia Meridionale". Other interesting and traditional landraces are the "Solina" common wheat in Abruzzo and the "Orzo mondo" naked barley in Marche. Most of the populations are still cultivated in marginal lands and under low input or organic agronomic conditions; nevertheless, in many cases, they are found near modern varieties in conventional agriculture systems. Moreover, the in situ (on-farm) conservation of Triticeae landraces in central Italy is strictly linked to elderly farmers.

[Neonatal hypotonia]. / Hipotonía neonatal.

INTRODUCTION: Neonatal hypotonia is a condition which appears to expand continually. Since the 1980s new clinical disorders, such as mitochondriopathies, peroxisomal diseases, disorders of the beta-oxidation of fatty acids, congenital myasthenic syndromes and botulism in infants have been described. At the same time, considerable progress has been made in the understanding of congenital myopathies, congenital muscular dystrophy and neonatal myotonic dystrophy. In this review we describe the most relevant conditions in which hypotonia is seen, and give guidelines for orientation in the study of newborn babies with this condition. We emphasize the importance of a clinical approach based on the family history (myotonic dystrophy, transitory neonatal myasthenia), the prenatal history (fetal movements, polyhydramnios) and neurological examination (facial diplegia, lingual fasciculations, arthrogryposis, respiratory difficulty) which permits early completion of studies, including muscle biopsy--very useful in the neonatal period--and genetic analysis. This allows the prognosis of the condition to be established early so that timely and effective genetic counselling may be given to the parents, avoiding recurrence of the serious morbi-mortality of many of these conditions.

Hipotonía neonatal / Neonatal hypotonia

Introducción. La hipotonía neonatal es un cuadro en permanente expansión. A partir de la década de los 80, se han agregado nuevas entidades clínicas, como mitocondriopatías, enfermedades peroxisomales, trastornos de la betaoxidación de los ácidos grasos, síndromes miasténicos congénitos y botulismo del lactante. A la vez, se ha avanzado mucho en el conocimiento de las miopatías congénitas, distrofia muscular congénita y distrofia miotónica neonatal. Desarrollo y conclusiones. En esta revisión se describen los cuadros más relevantes que producen hipotonía, y se dan pautas para orientar el estudio de los recién nacidos afectados. Se enfatiza la importancia de la orientación clínica basada en antecedentes familiares (distrofia miotónica, miastenia neonatal transitoria), prenatales (movimientos fetales, polihidroamnios) y examen neurológico (diplejía facial, fasciculaciones linguales, artrogriposis, dificultad respiratoria), que permite completar tempranamente los estudios, incluidos la biopsia muscular -de gran valor en el período neonatal- y el análisis genético. Ello hace posible establecer precozmente el pronóstico de la enfermedad y dar consejo genético oportuno y eficaz a los padres, evitando la recurrencia de la grave morbimortalidad que muchas de estas enfermedades conllevan (AU)

Enhancement of micronuclei frequency in the Tradescantia/micronuclei test using a long recovery time.

The Tradescantia/micronuclei test (TRAD/MCN) is a well-validated test for monitoring environmental genotoxicants. These pollutants induce at the early meiotic stage of pollen mother cells chromosome fragments which become micronuclei at the tetrad stage. The standard test protocol requires some hours of exposure of the inflorescences and a recovery time of about 24 hours to reach the early tetrad stage. Since the recovery period represents a critical step of the TRAD/MCN, experiments were performed to establish its length in plants of clone #4430 of the hybrid T. hirsutiflora x T. subacaulis which is widely used in environmental monitoring. The aim of the present research was to ascertain the exact duration of recovery time in order to improve the sensitivity of the TRAD/MCN test. First, studies were performed to select the flowers at the beginning of the meiosis, and then anthers were sampled and studied for a period of 48-86 hours. The complete meiosis in the plants examined required about 80 hours. Second, exposure to genotoxic substances followed by different recovery times was carried out to demonstrate that effectiveness of the TRAD/MCN test is closely related to the duration of the recovery time. The test was carried out by exposing inflorescences to known mutagens (sodium azide and maleic hydrazide) for six hours followed by different recovery times (24-72 hours). The results showed that the frequency of micronuclei in the pollen mother cells increased with the length of the recovery time.

First Report of Lentil Ascochyta Blight Caused by Ascochyta lentis in Italy.

In May 1997, ascochyta blight incited by Ascochyta lentis Vassiljevsky was observed at an incidence of less than 5% in lentil (Lens culinaris Medik.) fields in Umbria (Central Italy). Symptoms appeared on leaves and stems as tan spots surrounded by a dark margin. Small black pycnidia that produced a pink exudate containing hyaline, 1 septate, 14.2 to 15.8 × 3.5 µm conidia under high humidity were visible in the center of the spots. The fungus was consistently isolated on potato dextrose agar from diseased leaves or stems. To satisfy Koch's postulates, a conidial suspension (106 conidia per ml) of the fungus was sprayed on leaves of 20-day-old lentil plants (landrace Castelluccio) that were maintained in a humidity chamber for 96 h after inoculation. Lesions resembling symptoms that occurred in the field were observed on plants 3 weeks after inoculation. Symptoms were not observed on control plants sprayed with water. The fungus reisolated from the diseased plants was identical to the original isolates. Based on morphological characteristics of pycnidia and conidia as well as pathogenicity, the fungus was identified as A. lentis. A deep-freeze blotter method (2) was used to detect A. lentis in lentil seeds of 20 local landraces used by Umbrian farmers and two accessions from Canada and Turkey, as well as in seed collected from infected fields. The fungus was present only in the two lentil accessions with an incidence of about 5%. Although the fungus had been isolated from Italian seed germplasm in 1986 (1), this is the first report of ascochyta blight occurring in lentil crops in Italy. The heavy rainfalls that characterize the first stage of lentil cultivation in Umbria are favorable for disease development while hot and dry conditions that usually occur during flowering and maturation prevent the dissemination of inoculum and the infection of the seeds. For these reasons, some Umbrian areas could be more suitable for production of ascochyta-free lentil seeds. References: (1) W. J. Kaiser and R. M. Hannan. Phytopathology 76:355, 1986. (2) T. Limonard. Proc. Int. Seed Test. Assoc. 33:343, 1968.

[Lichen planopilaris simulating postmenopausal frontal fibrosing alopecia (Kossard)]. / Lichen planopilaris unter dem Bild einer postmenopausalen frontalen fibrosierenden Alopezie (Kossard).

A 68-year old woman presented with a frontal fibrosing alopecia and lesions of the buccal mucous membranes typical for lichen planus. Postmenopausal frontal fibrosing alopecia (PFFA) has recently been described by Kossard as a distinct entity characterized by progressive recession of the frontotemporal and parietal hair margins leading to permanent alopecia in the form of a symmetrical band-like area of scanning in postmenopausal women. The histology (perifollicular lymphocytic infiltration and fibrosis, increase of apoptosis of hair follicle keratinocytes) is indistinguishable from that of lichen planopilaris. The localization and age- and sex-related characteristics of PFFA are not sufficient to delineate it as a discrete entity from lichen planopilaris. Our observation of oral lichen planus in a postmenopausal woman with frontal fibrosing alopecia points to the possibility that PFFA actually may represent a variant of lichen planopilaris with a predilection for the frontotemporal hairline. Other variants of lichen planopilaris include multifocal lichen planopilaris, disseminated lichen planopilaris (Lassueur-Graham-Little syndrome), lichenoid pseudopelade, and any combination of these ("mixed type"). An effective therapy of PFFA is not known. Also, treatment of lichen planopilaris forms in which fibrosis predominates over inflammation is similarly problematic, but the natural course of these diseases seems to be self-limited.

Ingestive and inhalative allergy to the mushroom Boletus edulis.

This is the first report on inhalative and ingestive allergy to the common edible mushroom Boletus edulis (Be) (English, edible boletus; German, Steinpilz; French, bolet; Italian, porcino or boleto) belonging to the class Basidiomycetes. Four cases observed in our allergy unit are presented, showing different clinical manifestations of this rare allergy: as an occupational problem or life-threatening anaphylactic reactions after eating Be. In all cases, skin prick-to-prick tests with raw Be were strongly positive: in three cases, specific IgE against Be could be found. The symptoms were reproducible after an inhalation challenge test. It is noteworthy that not only can Basidiomycetes cause airborne allergy but also that edible mushrooms from this class can cause inhalative and intestinal allergy. The two patients with strong anaphylactic reactions demonstrate that Be may have great allergenic potential.

[Dapsone in granulomatous rosacea]. / Dapson bei granulomatöser Rosazea.

We report on two patients with granulomatous rosacea and another patient with granulomatous perioral dermatitis who responded well to dapsone. Dapsone has a pharmacological double function as both an antibiotic and an antiphlogistic drug. Before the introduction of isotretinoin, dapsone had its place in the treatment of severe acne. To date, its use in granulomatous rosacea has not been described. When hematologic parameters are monitored, dapsone is considered a safe and cost-effective drug, especially in countries where isotretinoin is not readily available. However, the definite value of dapsone in granulomatous rosacea should be established by a controlled study.

Eosinophilic myositis with eosinophilic cellulitislike skin lesions. Association with increased serum levels of eosinophil cationic protein and interleukin-5.

BACKGROUND: Peripheral and tissue eosinophilia are associated with a group of idiopathic inflammatory syndromes. The idiopathic hypereosinophilic syndrome represents a spectrum of disorders characterized by prolonged eosinophilia of an undetectable cause and significant organ dysfunction. The pathogenic role of the eosinophil in these conditions is attested to by evidence of eosinophil activation and degranulation at sites of tissue injury. Recently, an overlapping range of idiopathic eosinophilic muscle disease with an overall good prognosis has been described. RESULTS: We describe a patient with a syndrome of idiopathic myositis with eosinophilia and eosinophilic cellulitislike cutaneous manifestations. Histopathological studies of the skin and muscle revealed eosinophilic infiltration. Elevated serum levels of eosinophilic cationic protein and interleukin-5 paralleling disease activity were detected. CONCLUSIONS: This patient demonstrates clinical and laboratory features of eosinophilic myositis with eosinophilic cellulitislike skin lesions. The elevated serum levels of interleukin-5 and eosinophilic cationic protein may be responsible for the eosinophilia and tissue injury, respectively. With the advances in our understanding of cytokine-dependent regulatory mechanisms governing the eosinophil reaction, more targeted ways of manipulating eosinophilia as well as the entry and activation of eosinophils within specific tissues can be expected.

[Delayed allergic reaction to Chlorambucil (Leukeran). Case report and literature review]. / Allergie vom Spättyp auf Chlorambucil (Leukeran). Fallbeschreibung und Literaturübersicht.

A 63-year-old man developed a mild hemorrhagic diathesis which led to the diagnosis of chronic lymphatic leukemia. Treatment with prednisone and chlorambucil was initiated. During the first 10 day-cycle (10 mg chlorambucil and 100 mg prednisone) no side effects were noted. On the 8th day of second cycle (10 mg chlorambucil and 25 mg prednisone) the patient noticed fever, tiredness, myalgia, pruritus and erythema on the skin. The third cycle (10 mg chlorambucil alone) hat to be stopped on the second day due to the development of myalgia, generalized erythroderma with exfoliation and edema of the face and arms. In the patch-test with chlorambucil, a strongly positive (histologically verified) allergic reaction was noted. A lymphocyte stimulation test (detecting in vitro lymphocytes sensitized to chlorambucil) was also positive. These findings, together with the marked clinical reaction to chlorambucil alone, led to the diagnosis of a delayed hypersensitivity reaction to chlorambucil. Such well documented allergic reactions to chlorambucil are very rarely described in the literature. Up to now only 1 case of immune hemolytic anemia, 1 case of Lyell-syndrome, 2 cases of delayed hypersensitivity reactions and a few cases of less well documented type I reactions have been described. In all these cases no crossreactivity with other alkylating agents occurred, and hence all patients could be successfully treated with cyclophosphamide.

[Pollinosis in Canton Ticino. A prospective study in Locarno]. / Pollinose im Kanton Tessin. Eine prospektive Studie in Locarno 1990-1993.

A study was carried out in the southern part of Switzerland (Canton Ticino) in 1990-1993 to determine the spectrum of cutaneous sensitivity to a large amount of pollens and several perennial allergens (50), using skin prick tests in a sample of 503 consecutive patients suffering from hay fever. The Canton Ticino is a very specific geographical and botanical area which includes several plants of the alpine and Mediterranean flora as well as representatives of the tropical flora, forming a unique pattern from a botanical and allergological point of view. The results of the study indicate that in this region the patients have symptoms of hay fever almost 10 months a year (from December until October) with a peak in May and June (88% and 73% of the patients respectively have symptoms in these months). The symptoms are mainly localized in the upper respiratory tract and eyes. Asthmatic symptoms were found in about 23% of the patients. At the top of the allergen list were grass-pollens (72% of the patients had sensitivity); rye (69%); olive tree (54%); birch (46%); chestnut (37%); ash tree (36%); alder tree (33%); ragweed (17%); parietaria (18%). Of real interest in this study area are, besides the classical allergy-inducing pollens, those of chestnut, parietaria, olive tree, ash tree and cupressaceae (for example cypress). Chestnut pollens represent about 30% of the airborne pollens in this region. 30% of the patients had sensitivity against dust mites (Dermatophagoides pteronissimus und D. farinae), and 20% against cats. Sensitivity against 8 mould spores was 2-9%.