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Summary: We describe the case of a 24-year-old male with hyper-IgE syndrome (HIES) which was diagnosed at 4 years of age and died from a very rare cardiac complication. He had typical clinical and laboratory manifestations of HIES, including total serum IgE as high as > 100,000 IU/mL. Stem cell transplantation was not available. During the 20-year follow-up, he suffered numerous various infections of the skin and deep organs, partial lung resection, as well as multiple bone fractures. At age 24, he developed acute decompensated heart failure associated with elevated serum troponin I and brain natriuretic protein. Two-dimensional echocardiogram revealed global hypokinesis of the left ventricle with estimated ejection fraction 20-25%, and catheterization revealed ectasia of multiple coronary arteries. Endomyocardial biopsy showed lymphocytic myocarditis, focal necrosis, mild fibrosis, and myxoid degeneration, but cultures were negative. The patient improved on corticosteroid therapy and was discharged on heart failure therapy and external defibrillator. Six weeks later, he developed supraventricular tachycardia and persistent global hypokinesis and was treated with amiodarone. A trial of intravenous immunoglobulin was initiated and was repeated as outpatient every four weeks for four times. However, his cardiac function did not improve and he developed severe hypotension and pulseless electrical activity arrest. Resuscitation was unsuccessful. To the best of our knowledge, this is the first reported case of HIES complicated with lymphocytic myocarditis. Both immunologists and cardiologists need to be aware of such a complication and practice caution in using immunosuppressants when the patient's immune status is markedly compromised.

Food protein-induced enterocolitis (FPIES) is a non-IgE cell- mediated food allergy that can be severe and lead to shock. Despite the potential seriousness of reactions, awareness of FPIES is low; high-quality studies providing insight into the pathophysiology, diagnosis, and management are lacking; and clinical outcomes are poorly established. This consensus document is the result of work done by an international workgroup convened through the Adverse Reactions to Foods Committee of the American Academy of Allergy, Asthma & Immunology and the International FPIES Association advocacy group. These are the first international evidence-based guidelines to improve the diagnosis and management of patients with FPIES. Research on prevalence, pathophysiology, diagnostic markers, and future treatments is necessary to improve the care of patients with FPIES. These guidelines will be updated periodically as more evidence becomes available., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)

Aim: To identify patients' characteristics associated with double balloon endoscopy (DBE) outcomes in investigation of obscure gastrointestinal bleeding (OGIB)., Methods: Retrospective study performed at an academic tertiary referral center. Evaluated endpoints were clinical factors associated with no diagnostic yield or non-therapeutic intervention of DBE performed for OGIB evaluation., Results: We included fifty-five DBE between August 2010 and April 2012. The mean age of the sample was 67 with 32 males (58.2%). Twenty-four DBE had no diagnostic yield and 30 DBE did not require therapy. Non-diagnostic yield was associated with performing two or more DBE studies in one day [odds ratio (OR): 13.72, P = 0.008], absence of blood transfusions within a year of the DBE (OR: 7.16, P = 0.03) and absence of ulcers or arteriovenous malformations (AVMs) on prior esophagogastroduodenoscopy (EGD) or colonoscopy (OR: 19.30, P = 0.033). Non-therapeutic DBE was associated with performing two or more DBE per day (OR: 18.579, P = 0.007), gastrointestinal bleeding episode within a week of the DBE (OR: 11.48, P = 0.003), fewer blood transfusion requirements prior to DBE (OR: 4.55, P = 0.036) and absence of ulcers or AVMs on prior EGD or colonoscopy (OR: 8.47, P = 0.027)., Conclusion: Predictors of DBE yield and therapeutic intervention on DBE include blood transfusion requirements, previous endoscopic findings and possibly endoscopist fatigue.

Background: Food allergy has been gaining increasing attention, mostly as causing gastrointestinal and cutaneous reactions. Its role in asthma seems to be under-recognised., Objectives: This study's aim is to explore the frequency of involvement of a common food, namely cow's milk, in childhood asthma., Methods: 32 children (5 months to 11 years; median 24 months; mean 34 months) with asthma and a suspected history of cow's milk allergy were studied. They underwent skin prick testing (SPT) and specific IgE (sIgE) testing to whole cow's milk (WCM), casein, α-lactalbumin, and β-lactoglobulin, followed by single-blind oral milk challenge., Results: Reactions to milk challenge occurred in 12 (37.5%) including wheezing in 5 (41.7%, or 15.6% of the whole group). Children who developed wheezing at the time of challenge were younger than those who had negative challenge (23.0 months vs. 34.8 months). Challenge was positive in 33.3% of subjects who had a positive SPT, and SPT was positive in 50% of challenge-positive subjects. Regarding sIgE, challenge was positive in 26.7% of sIgE-positive subjects, and sIgE was positive in 33.3% of challenge positive subjects. Skin or serum testing with individual protein fractions did not seem to add significant advantage over testing with WCM alone., Conclusion: This study shows that cow's milk can cause wheezing in children with asthma. Although SPT seemed to be more reliable than sIgE testing, both had suboptimal reliability. It is worth considering possible milk allergy in children with asthma, particularly when poorly controlled in spite of proper routine management., (Copyright © 2012 SEICAP. Published by Elsevier Espana. All rights reserved.)

We have reported that clinically relevant concentrations of valproic acid (VPA) up-regulate the G-protein-coupled melatonin MT1 receptor in rat C6 glioma cells. To determine whether this effect occurs in vivo, the effects of chronic VPA treatment on the expression of both melatonin receptor subtypes, MT1 and MT2, were examined in the rat brain. Reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR analyses revealed significant increases in MT1 and MT2 mRNA expression in the hippocampus, following VPA (4 mg/ml drinking water) treatment for 17 d. Increases in the mRNA and protein expression of the novel neurotrophic factors, conserved dopamine neurotrophic factor and mesencephalic astrocyte-derived neurotrophic factor, were detected in the hippocampus and/or striatum. In addition, significant changes in persephin, glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor mRNA expression were observed. The robust multi-fold induction of MT1 and MT2 receptors in the hippocampus suggests a role for the melatonergic system in the psychotropic effects of VPA.

Histone deacetylase (HDAC) inhibitors represent a novel class of drugs that selectively induce cell cycle arrest and apoptosis in transformed cells. This study examined, for the first time, the effects of the relatively new HDAC inhibitor, M344 [4-dimethylamino-N-(6-hydroxycarbamoylhexyl)-benzamide], on the proliferation of MCF-7 breast cancer cells. MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assays revealed significant concentration- and time-dependent decreases in MCF-7 cell proliferation following treatment with M344 (1-100μM). In contrast to the significant induction of p21(waf1/cip1) mRNA expression following treatment with M344 (10μM) for 1 or 3 days, there was a significant decrease in p53 mRNA expression, although p53 protein levels were unchanged. Similar treatment with M344 also induced expression of the pro-apoptotic genes, Puma and Bax, together with the morphological features of apoptosis, in MCF-7 cells. The results of this study reinforce previous findings indicating that HDAC inhibitors are an important group of oncostatic drugs, and show that M344 is a potent suppressor of breast cancer cell proliferation., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

Allergist/clinical immunologist maintenance of certification and training program reaccreditation are mandatory in some countries. The World Allergy Organization conducted surveys in 2009 and 2011 to assess where such programs were available and to promote the establishment of such programs on a global level. This was done with the presumption that after such an "inventory," World Allergy Organization could offer guidance to its Member Societies on the promotion of such programs to assure the highest standards of practice in the field of allergy and clinical immunology. This review draws on the experience of countries where successful programs are in place and makes recommendations for those wishing to implement such programs for the specialty.

Background: Studies on serum IgE levels during pregnancy are limited., Objective: To investigate the course of serum total IgE levels during pregnancy and postpartum., Methods: 159 pregnant subjects provided 218 serum samples during various stages of pregnancy and the postpartum period. Serum total IgE geometric means were compared at various trimesters and postpartum. In addition, the postpartum IgE data were analysed according to the method of delivery. Analysis was also done according to history of allergy., Results: The geometric mean serum total IgE was 20.5 IU/ml in the first trimester, 20.8 IU/ml in the second and 22.2 IU/ml in the third. Postpartum serum IgE level showed a lower mean, 14.9 IU/ml during the early postpartum period (less than 30 days) compared to 30.3 IU/ml during the late postpartum period (30 days-25 weeks). However this was not statistically significant. Serum IgE in the postpartum period also did not differ according to method of delivery. A history of allergy was positive in 98 samples, negative in 61 and unclear in 59. Using analysis of variance, none of these three groups showed significant change in serum total IgE level during pregnancy or postpartum., Conclusion: In this cross-sectional study, serum total IgE levels showed no statistically significant changes during pregnancy or postpartum. This finding would be of greater weight if reproduced in a larger number of subjects with multiple serial samples at fixed regular time intervals during pregnancy and postpartum., (Copyright © 2010 SEICAP. Published by Elsevier Espana. All rights reserved.)

Background: The role of genetics in allergy development is well accepted. However, studies could not delineate the mode of inheritance or what is specifically being inherited. The purpose of this study was to determine the effect of genetics on the development of allergy manifestation, serum IgE level, and sensitization to specific allergens., Methods: Fifty-eight twin sets (age 7 months to 11 years) were evaluated for allergy by medical history, family history, physical examination, serum total IgE level, and percutaneous testing to selected common allergens., Results: In 25 monozygotic (MZ) sets, concordance of atopy was significantly higher than in 33 dizygotic (DZ) sets (84.6% vs 62.5%). The age at onset tended to be earlier when the mother was allergic than when the father was (23.5 months vs 30.5 months). When both twins were allergic, the intra-pair difference in age at onset was within <6 months in 50% of MZ sets versus 31.8% in DZ sets. Total IgE level in twins showed a very strong correlation in MZ sets (r 0.92), but only a moderate correlation among DZ sets (r 0.57). Skin test positivity to specific allergens did not show a significant concordance between twins in either group., Conclusion: Our study indicates that the genetic influence was strongest on the inheritance of IgE phenotype, the development of the atopic tendency, the age of onset, and to some extent on the specific allergy manifestation. The effect seemed less on determining the specific offending allergen(s), suggesting possible roles of epigenetic and environmental factors., (Copyright 2009 SEICAP. Published by Elsevier Espana. All rights reserved.)

Objective: To make recommendations based on a critical review of the evidence for the timing of the introduction of solid foods and its possible role in the development of food allergy., Data Sources: MEDLINE searches using the following search algorithm: [weaning AND infant AND allergy]/[food allergy AND sensitization]/[dietary prevention AND food allergy OR allergens]/[Jan 1980-Feb 2006]., Study Selection: Using the authors' clinical experience and research expertise, 52 studies were retrieved that satisfied the following conditions: English language, journal impact factor above 1 or scientific society, expert, or institutional publication, and appraisable using the World Health Organization categories of evidence., Results: Available information suggests that early introduction can increase the risk of food allergy, that avoidance of solids can prevent the development of specific food allergies, that some foods are more allergenic than others, and that some food allergies are more persistent than others., Conclusions: Pediatricians and allergists should cautiously individualize the introduction of solids into the infants' diet. With assessed risk of allergy, the optimal age for the introduction of selected supplemental foods should be 6 months, dairy products 12 months, hen's egg 24 months, and peanut, tree nuts, fish, and seafood at least 36 months. For all infants, complementary feeding can be introduced from the sixth month, and egg, peanut, tree nuts, fish, and seafood introduction require caution. Foods should be introduced one at a time in small amounts. Mixed foods containing various food allergens should not be given unless tolerance to every ingredient has been assessed.

Objective: This review is intended to provide an outline for the evaluation of patients suspected of having immunodeficiency, a problem that is frequently encountered in clinical practice., Data Sources: Information was obtained through a MEDLINE literature search as well as from standard textbooks in immunology. Also included is information that reflects the authors' clinical experience in the field., Results: In general clinical practice, many physicians feel inadequate to evaluate patients with suspected immune deficiencies. They also think that the process of evaluation is time-consuming, which results in misdiagnosis of a substantial percentage of such disorders. Hence, the prevalence of immunodeficiency disorders is much higher than generally thought. At present, there are >80 unique primary immunodeficiency conditions and >50 syndromes that are associated with various immunologic defects. The prevalence of secondary immunodeficiency has also been increasing because of the tragic epidemic of HIV infection, more usage of immunosuppressive medications and bone marrow stem cell transplantation, and the severe degree of malnutrition in underdeveloped countries. It is necessary for clinicians, particularly the specialists in allergy and immunology, to be able to evaluate the status of the immune system., Conclusions: Very valuable information can be gathered from the medical history and physical examination that may exclude or increase the suspicion of immunologic defect. Laboratory tests can then be appropriately selected to define the specific defect. Once the diagnosis has been settled, proper medical management can be instituted with subsequent improvement in morbidity and mortality of such disorders.

Background: Ingestion is the principal route for food allergens, yet some highly sensitive patients may develop severe symptoms upon skin contact., Case Report: We describe five cases of severe food allergic reactions through skin contact, including inhalation in one., Methods: The cases were referred to a university allergy clinic, and evaluation comprised detailed medical history, physical examination, skin testing, serum total and specific IgE, and selected challenges., Results: These cases were found to have a strong family history of allergy, early age of onset, very high total serum IgE level, and strong reactivity to foods by skin prick testing or RAST. Interestingly, reactions occurred while all five children were being breast-fed (exclusively in four and mixed in one)., Conclusions: Severe food allergic reactions can occur from exposure to minute quantities of allergen by skin contact or inhalation. Food allergy by a noningestant route should be considered in patients with the above characteristics.

Objective: This presentation is designed to critically review information on presentations of food hypersensitivity reactions that may be considered unusual regarding the source or nature of allergen, route of exposure, or clinical manifestation., Data Sources: Information has been gathered primarily through a thorough search of the English literature relevant to human subjects. Some clinical cases were also included from the author's own clinical experience., Study Selection: Information summarized here was critically selected on the basis of proven or acceptable scientific validity., Results: The findings indicate that food allergy presentation can be unusual in three main aspects. First, the offending allergen may not be the obvious food that was ingested or be a food protein incorporated in a nonfood product. Second, systemic reactions can be provoked by very minute quantities of food allergens that may even get access through noningestant routes, eg, inhalation, odor, skin contact, or mucous membrane contact. Third, the clinical manifestations are not limited to the few gastrointestinal, cutaneous, and respiratory symptoms with which we are generally familiar., Conclusions: The extent of food allergy presentation is more than has been generally realized. Our awareness of such unusual presentations adds new knowledge and should prompt our interest in carefully evaluating patients with obscure allergic reactions for possible food allergy.

Objective: This review is intended to be an authoritative summary of the pathogenesis of osteoporosis, a problem that may be encountered in allergy practice. It also provides an outline for identification of subjects at high risk and directions for their appropriate evaluation, management, and prevention of the disease., Data Sources: References were obtained through a MEDLINE literature search as well as from previous reviews. Relevant articles were critically reviewed and their conclusions were included., Results: Osteoporosis is a relatively common disease that is associated with significant morbidity and mortality. The management and prevention of osteoporosis have been improved by an increased awareness of the magnitude of the problem, a better understanding of the pathogenesis, development of a better technique for assessment of bone mineral density, and the availability of specific medications. With the increase in human life-span and the increasing use of glucocorticosteroids for a wide variety of diseases, the incidence of osteoporosis has been on the rise., Conclusion: Glucocorticosteroids are the most common medications that cause or contribute to the pathogenesis of osteoporosis and have been widely used in allergy practice. It is important for physicians to appreciate the current basic understanding of osteoporosis and to be able to identify patients at high risk for this serious disorder, and to initiate appropriate intervention at a sufficiently early time to be effective. Medications for treatment and prevention of osteoporosis include: calcium, vitamin D, estrogen, bisphosphonates, calcitonin, and others are reviewed in this article.

Objective: Pancreatic enzyme is essential in the treatment of cystic fibrosis (CF), but intolerance to it occasionally occurs. We encountered a child who was intolerant to multiple commercially available preparations of pancreatic enzymes and, hence, desensitization was attempted, with success., Case Presentation: A 33-month-old girl was diagnosed with CF at 6 months of age. Initially, she was started on Pancrease MT 16, which was subsequently discontinued because fecal fat studies were normal and she seemed to do well on Nutramigen and vitamin supplements. At 29 months of age, she developed diarrhea with bulky stools and weight loss. A fecal fat 72-hour study revealed a coefficient of absorption of 50%. She was treated with Pancrease MT 16, but had consistent vomiting 1 to 2 hours after administration of enzymes. The vomiting occurred on switching to different pancreatic enzymes preparations, ie, Creon 10, Viokase, and Pancrease MT 16. Vomiting occurred even with small doses of enzymes disguised in food. She had no history suggestive of gastroesophageal reflux, peptic ulcer, or pork allergy, and no vomiting on days when enzymes were not given. This was suggestive of type I hypersensitivity reaction. Pancreatic enzymes were discontinued, and she was given a low-fat, high-carbohydrate diet with satisfactory weight gain., Methods: Double-blind, placebo-controlled titrated oral challenges with pancreatic enzymes resulted in definite vomiting within 1 to 1.5 hours after challenges with Viokase and Pancrease MT 16, but not with placebo. Rush oral desensitization with Viokase solution was attempted, starting with 5 mg, and the dose was doubled every 20 minutes, aiming to reach a cumulative dose of 700 mg. However, the child vomited when a cumulative dose of 315 mg was reached. Another trial of slower desensitization was done using Pancrease MT 16 (1 capsule: 16 000 U of lipase, 48 000 U of amylase, and 48 000 U of protease), starting with 1/4 capsule per day, with increments of 1/4 capsule every 3 days, until an entire capsule was reached by day 10, then increased by approximately 1/2 capsule every 4 days until reaching the therapeutic dose of 1 capsule with each meal by day 25., Results: The patient tolerated this fairly well and has been on this treatment and regular diet for >1 year, without any adverse reaction. This illustrates a rare case of gastrointestinal adverse reaction to pancreatic enzymes that was treated successfully with desensitization., Conclusion: Pancreatic enzyme intolerance, although rare, would be a major problem in the management of patients with CF. Hence, desensitization would be essential and may be accomplished successfully using the protocol described in this report.

Because food allergy treatment is basically avoidance of the offending food(s), identification of the latter becomes the cornerstone for management. At present, the elimination-challenge test is the most definitive procedure for verification of a cause-and-effect relationship between a particular food and a certain reaction, allergic or not. The oral challenge test is most reliable when conducted in a double-blind, placebo-controlled manner. In routine clinical practice, however, single-blind testing is satisfactory in most cases. Open challenge testing might be acceptable in young children or for screening the least suspected foods. It would be prudent to avoid the test, in any of its forms, in instances where a specific food caused a life-threatening reaction. Caution needs to be practiced in planning, conducting, and interpreting the results of challenge tests. Difficulties may be encountered in disguising the test food, choosing a placebo, reproducing the natural exposure, incorporation of possible associated factors, and avoiding any bias on the patient's or observer's part.

For an infant to develop allergy (atopy), three main factors seem to be needed: genetic predisposition, allergen exposure, and contributory factors. The role of genetics seems to be mainly in transmitting a general atopic constitution and controlling the general IgE response. Together with environmental exposure, genetics possibly plays a role in determining the allergic shock organ and the specific offending allergen. Of the vast number of environmental allergens, food by far seems to be the major one in infancy, followed by indoor allergens then outdoor aeroallergens. Several intrinsic and extrinsic contributory factors can enhance the development of allergy, perpetuate its chronicity, or facilitate precipitation of symptoms. These factors can be immunologic defects, gastrointestinal diseases, infections, or nonspecific irritants such as tobacco smoke inhalation. Understanding all these factors is essential in formulating any program for allergy prevention in infants.

The role of food allergy in the respiratory tract is often underestimated. A wide variety of food-induced respiratory symptoms has been described. In some patients, a food additive rather than a food protein is the offending agent. This presentation focuses on food-induced asthma and milk-induced chronic pulmonary disease in infants.

In clinical practice at present, milk allergy may be suspected by medical history, skin testing, or RAST. None of these procedures has shown an optimal correlation with the result of challenge testing. The obvious need for better diagnostic tests has stimulated numerous attempts to improve the current tests and to develop new ones. The use of individual milk protein fractions for skin testing or RAST has not shown superiority over using whole cow's milk. Lymphoblast transformation and leukocyte inhibition factor production have shown low specificity. The few studies on neutrophil chemotactic activity have shown contradictory results. Morphometric and immunohistochemical studies of small intestinal biopsy specimens seem to be more suitable for research studies than for routine clinical practice. The reliability of in vitro tests on cultured intestinal epithelium remains to be verified and is far from being applicable in clinical practice. The diversity of immunologic mechanisms of milk allergy is largely responsible for the difficulty encountered in developing a highly reliable test in the diagnosis of various reactions to milk allergy.

Food allergy is one of several causes of adverse reactions to foods. The underlying immunologic mechanism varies from one manifestation to another, hence no current single laboratory test can be expected to be positive in every case. The diagnosis could be suggested by information gathered from the medical history or screening procedures, such as trials of elimination diets, the food/symptom diary, skin testing, and in vitro-specific IgE antibody measurement. All foods suspected by any of the aforementioned methods should be subjected to verification by appropriate elimination-challenge testing, preferably in a double-blind, placebo-controlled manner. Basically, treatment is dietary elimination, and its success requires identification and avoidance of all offending foods and control of other contributory factors.

The atopic status of patients with leprosy was assessed by medical history, physical examination, serum total IgE, and specific IgE antibodies to common allergens (by skin testing and RAST). Tests for specific IgE antibody to Mycobacterium leprae were performed by RAST and immunoblotting technique. We studied 28 patients with leprosy and 49 control subjects. The two groups did not differ significantly in the prevalence of atopic disease. The IgE level was significantly higher in the patients, however, than in the control subjects, whether there was atopy (296.1 versus 96.3 IU/ml) or not atopy (72.9 versus 18.9 IU/ml). Neither RAST nor immunoblotting technique detected significant levels of IgE antibodies to M. leprae. Our data indicate that leprosy was associated with increased total IgE level, but clinical atopy in patients with leprosy was similar to that in control subjects. The observed IgE increase in patients with leprosy appears to be generally nonspecific.

Serum IgE levels in healthy blood donors who had no history of atopy were measured by a paper-disc RIA and analyzed according to the donors' smoking habits. The IgE geometric mean for regular smokers was 41.7 IU/ml, which was significantly higher than that for nonsmokers (19.3 IU/ml) or rare smokers (22.7 IU/ml). Whereas 28% of smokers had IgE levels greater than 200 IU/ml, none of the rare smokers or nonsmokers did. IgE levels in smokers showed a moderate inverse correlation with the degree of smoking. The mean IgE level was 189.8 IU/ml in those who smoked 1-9 cigarettes/day but only 32.8 IU/ml in those who smoked 10-19 cigarettes per day and 11.1 IU/ml in those who smoked 20 or more cigarettes/day. The number of years a person smoked did not seem to significantly influence the IgE level. The mean IgE level in ex-smokers (50.5 IU/ml) was much lower than in current light smokers but was still higher than in nonsmokers. There was a moderate inverse correlation between IgE levels and duration of cessation of smoking. Our data suggest a characteristic pattern for the influence of cigarette smoking on serum IgE level, namely, a striking rise associated with light smoking and a remarkable drop in heavy smokers, and such changes seemed reversible after the habit was stopped. Smoking status, therefore, appears to be an important consideration in interpreting serum IgE levels and in revising the "norms" of IgE levels.

Interest in food allergy has increased among physicians as well as the public. The symptoms are mainly in the gastrointestinal tract, the skin, and the respiratory system. Other organs are less commonly affected. The offending food can be suspected from the medical history, by skin testing, or by serum-specific IgE antibodies (RAST). Verification, however, depends on documentation of disappearance of symptoms after avoidance of the offending food and their recurrence on reintroduction of that food. Treatment is mainly dietary avoidance. Its success, however, depends on many factors. Pharmacologic agents may be needed in some cases for symptomatic relief and possibly for prophylaxis. The awareness on the part of the primary physician of the manifestations of food allergy and its diagnosis should enhance the physician's expertise in dealing with such patients regarding further management.

The increasing awareness by the medical profession, as well as the public, of food allergy imposes the parallel task of accurate diagnosis and proper treatment. A carefully obtained medical history and a properly conducted elimination-challenge test are the most valuable as well as the least expensive procedures for diagnosis. Other selected in vivo and in vitro tests may enhance the diagnostic ability and may verify the immunologic basis of the food-induced reaction. Treatment is basically dietary avoidance, and its success depends on several factors. Pharmacologic agents may be needed for symptomatic treatment, and in certain instances for prophylaxis. The need still exists for developing an effective procedure of hyposensitization.

Sera of 17 patients with gluten-induced celiac disease were studied. Total serum IgE and IgD, as well as specific IgE and IgD antibodies to selected food antigens, were determined. Total IgE levels were within the normal range. Specific IgE antibodies to wheat, alpha-gliadin, cows's milk, rice and buckwheat were comparable to those of normal controls. In the celiac subjects total IgD levels were also within the normal range but IgD antibodies to wheat were high whereas IgD antibodies to milk were lower than in pooled normal sera. The levels of IgE or IgD antibodies to either wheat or milk showed no relationship to the presence of precipitins to the antigens of these two foods. The study did not demonstrate a role for IgE in celiac disease. That IgD antibodies may play a role is suggested by the elevated serum IgD antibodies to wheat antigens.

The intraocular pressure - as measured by Schiötz tonometer - was studied in 378 smokers, 151 ex-smokers, and 495 non-smokers. It was found the the three groups have practically the same distribution of intraocular pressure, and that the latter has non relationship to the smoking habit.

Roles of various infections, neoplasms and granulomatous diseases in fever of unknown origin were studied in 22 patients. Bacterial infections were responsible in seven (32 percent), herpes viruses in five (23 percent), neoplasms in four (18 percent) and granulomata in two (9 percent) cases. Patients with herpes infections had initially no clinical or routine laboratory clues to viral involvement, and were given an intensive workup for 5 to 15 days. The diagnosis was made on the basis of cytomegalovirus or Epstein-Barr virus lgM antibody titers.

To date the most reliable procedure for the diagnosis of milk hypersensitivity is a properly conducted elimination-challenge test. Several in vitro tests have been developed but because of the diverse underlying mechanisms of hypersensitivity reactions to milk developing a single laboratory test that can be universally positive in every patient would be rather difficult. However, with a better categorization of milk-sensitive patients, together with the development of relevant, standardized and practical tests, the laboratory diagnosis of milk allergy should become more reliable. Milk hypersensitivity can be effectively treated and is largely preventable. Avoidance is the most effective mode of treatment and results in a good prognosis. In instances where the desired degree of avoidance cannot be attained pharmacologic agents may be of help. The need still exists for developing an effective procedure of hyposensitization. For prevention, prolonged breast feeding should be recommended, especially in infants of atopic families.

Medical registrations of births in Norway during 1967 and 1968 were utilized in a study of the course and outcome of pregnancy in 542 women with pulmonary tuberculosis. A comparison with 112,530 pregnancies in women reporting no disease was made. Tuberculous women were found to have an excess of pregnancy complications, miscarriage, and labour difficulties. Their live births, however, were comparable with respect to gestation period, birth weight, morbid conditions and mortality to those of women reporting no disease.

The water and electrolyte status was studied in 26 children with acute asthma, 8 of whom required hospital admission. Patients were evaluated before therapy, during hospital management, and at least 10 days after symptoms had subsided. Laboratory evaluation included serum electrolytes, BUN, sOsmo, urinalysis, and uOsmo. Data were analyzed for the manifestations of SI-ADH. Mild serum hyposmolarity was noted initially in only two patients and during the hospital stay in one patient for a short time, but none of the patients fulfilled the criteria of SIADH. At the time of presentation at the emergency room, none of the 26 patients had clinical signs of dehydration, yet some degree of hypertonicity seemed to be present in most patients. This study shows that children with acute asthma are ordinarily not at high risk of SIADH and fluid therapy should be included in the management. Nevertheless, because such patients may be at risk of pulmonary edema, vigorous fluid administration should be discouraged, except to correct dehydration.