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Conventional coronary angiography (Panel D ) confirms the stenoses of the left anterior descending artery and diagonal branch (arrows) seen on the iodine- density image (Panel B) (With permission from M generic super avana 160 mg with mastercard impotence at 35. J Cardiovasc ated discussion and scientifc debate with representatives from the Comput Tomogr 2:71–80 four main vendors buy super avana with american express impotence of organic origin icd 9. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. The contents of this work are intended to further general scientifc research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specifc method, diagnosis, or treatment by health science practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifcally disclaim all warranties, including without limitation any implied warranties of ftness for a particular purpose. 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Neither the publisher nor the author shall be liable for any damages arising herefrom. Library of Congress Cataloging-in-Publication Data is available A catalogue record for this book is available from the British Library. My aim has and includes more guidance on the further tests that been to provide a guide for use in the diagnostic hae- should be performed for any given provisional diag- matology laboratory, covering methods of collection of nosis. However, microscopy and the automated full blood specimens, blood flm preparation and staining, blood count remain the core of the book. My over- the principles of manual and automated blood counts riding purpose has been to show that microscopy not and the assessment of the morphological features of only provides the essential basis of our haematological blood cells. My objective has been that the practising practice, but can also lead to the excitement of discov- haematologist should fnd this book suffciently com- ery. The decline in the number of blood flms made prehensive to be a reference source while, at the same and the increasingly heavy clinical commitments time, the trainee haematologist and biomedical scien- of any haematologist who is not purely a laboratory tist should fnd it a straightforward and practical bench haematologist make this book more than ever neces- manual. I thought that the fourth edition, published eight gist will gain a fuller understanding of the scientifc years ago, would be the last, but it seemed a pity to basis of an important segment of laboratory haema- stop when there are still new things to be learnt about tology, while the laboratory scientist will understand the circulating blood cells. If I succeed in sending the more of the purpose and clinical relevance of labora- reader back to the microscope with renewed interest tory tests. I trust it is not too ambitious to hope to be and enthusiasm I shall be well satisfed. I should like to acknowledge parts of this and previous editions of this book, includ- Dr Helen Dodsworth without whose suggestion to an ing Carol Briggs who reviewed Chapter 2 of this edi- editor this book might not have happened. I should also like to thank the many colleagues should like to remember and acknowledge those who who provided blood flms for photography, or provided taught me to examine blood flms, particularly but not other images; they are individually acknowledged in only the late Professor Sir John Dacie, the late Professor the fgure legends. I am grateful also to those others, David Galton, the late Professor Sunitha Wickramasin- numbering many hundreds, with whom I have dis- ghe and the fortunately still surviving Professor Daniel cussed interesting and diffcult diagnostic problems Catovsky. Such seizures may not be true epilepsy, preting a blood flm require that an appropriate sam- but consequent on hypoxia following brief vagal‐induced ple from the patient, mixed with the correct amount of cessation of heart beat [1]. If venepunctures are being a suitable anticoagulant, is delivered to the laboratory performed on children or on patients unable to cooper- without undue delay. No artefacts should be introduced ate fully, then the arm for venepuncture should be gently during these procedures. Gloves should be The identity of the patient requiring blood sampling worn during venepuncture, for the protection of the per- should be carefully checked before performing a venepunc- son carrying out the procedure. This is usually done by requesting the patient to state available if either the phlebotomist or the patient is aller- surname, given name and date of birth and, for hospital gic to latex. The needle to enter the patient must not be inpatients, by checking a wristband to verify these details touched, so that it remains sterile. To reduce the chance In some circumstances, the patient should rest prior to of human error, bottles should not be labelled in advance. In endurance athletes being tested for a ‘bio- The person performing the phlebotomy must conform to logical passport’, 10 minutes’ rest in a seated position has local guidelines, including those for patient identifcation. More secure identifcation of using a needle and either a syringe or an evacuated tube. Other forearm veins can be used, but they be reassured that the procedure causes only minimal dis- are frequently more mobile and therefore more diffcult comfort; they should not be told that venepuncture is pain- to penetrate. It is preferable for apprehensive often have a poorer fow and performing venepuncture patients to lie down. Chairs used for venepuncture should at these sites is more likely to lead to bruising. This is also preferably have adjustable armrests so that the arm can be true of the anterior surface of the wrist where, in addi- carefully positioned. Armrests also help to ensure patient tion, venepuncture tends to be more painful and where safety, since they make it harder for a fainting patient to there is more risk of damaging vital structures. I have personally observed one patient are not an ideal site for venepuncture and it is rarely nec- who sustained a skull fracture when he fainted at the essary to use them. Injuries that have been associated end of a venepuncture and fell forward onto a hard foor, with obtaining a blood sample from the antecubital fossa Blood Cells A Practical Guide, Fifth Edition. Alternatively, a sphyg- momanometer cuff can be applied and infated to diastolic pressure, but the use of a tourniquet is usually quicker and simpler. If it is particularly important to obtain a specimen without causing haemoconcentration, e. Otherwise it can be left applied while blood is being obtained, to ensure a continuing adequate fow of blood. It is preferable that the tourniquet is applied for no more than a minute, but the degree of haemoconcentra- tion may not be great, even after 10 minutes’ application. A winged cannula may reduce the chance of include damage to the lateral antebrachial cutaneous injury to nerves [7] and is certainly preferable for small nerve [3] and inadvertent arterial puncture. A 19 or 20 gauge needle is suit- tions are more likely with the less accessible basilic vein able for an adult and a 21 or 23 gauge for a child or an than with the median antecubital or the cephalic vein. When using a syringe, the plunger If anterior wrist veins have to be used, there is a risk of should frst be moved within the barrel of the syringe damage to the radial or ulnar nerve or artery. A thrombosed vein feels cord‐like and is not a single movement or in two separate movements for the compressible. An artery has a thicker wall and is pul- skin and the vein, depending on personal preference and satile. With one hand steadying overweight people) it is identifed by palpation after the barrel of the syringe so that the needle is not acciden- applying a tourniquet to achieve venous distension.

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In cases of chronic chest pain buy cheap super avana 160mg line erectile dysfunction medicine in ayurveda, an exercise tolerance test with thallium scan should be done to rule out coronary insufficiency or myocardial infarction buy super avana 160 mg otc erectile dysfunction and diabetes. It may be wise to do immediate coronary angiography if the condition deteriorates so that balloon angiography, bypass surgery, or reperfusion therapy may be initiated. Therapeutic trial of antacids or proton pump inhibitors (reflux esophagitis, peptic ulcer) 16. Utilizing the methods outlined above, what is your list of possible diagnoses at this point? Additional history reveals that the patient has had several previous attacks of a similar nature over the past 10 years, but never lasting this long. The pain does not radiate to the neck or down the arm, and is not accompanied by diaphoresis. The discussion that follows will also concentrate on the most significant of 209 these. The significant lesions of the skin and subcutaneous tissues include sebaceous cysts, cellulitis, neurofibromas, lipomas, and contusions. In the ribs, look for fractures, contusions, multiple myeloma, and primary and metastatic tumors. In the cartilage, there may be a protruding xiphoid process or a lump at the costochondral junctions in Tietze syndrome. Years ago it was common for empyema, lung abscesses, pleural and pulmonary tuberculosis, and fungi (actinomycosis especially) to work their way out to the skin and form a mass or fistula: This is now unusual. Carcinoma of the lung and mesothelioma, however, may form a mass on the chest wall by direct extension. In the mediastinal structures, aortic aneurysms used to be a common cause of a pulsating chest wall mass, but they are now rarely seen. Cardiomegaly and pericardial effusions occasionally cause a noticeable protuberance of the precardium but not as frequently as in the past. Approach to the Diagnosis The approach to this diagnosis is again a good clinical history and physical examination along with correlation of signs and symptoms. Furthermore, the infection is usually bacterial, and the chill indicates that the bacteria have invaded the bloodstream. To start with, each organ in the body can be infected by an “itis” of the parenchyma, an “itis” of the capsule, or an abscess. Abscess: This should prompt the recall of cerebral abscess, epidural or subdural abscess, dental abscess, retropharyngeal abscess, lung abscess or empyema, liver abscess, subdiaphragmatic abscess, perinephric abscess, abscessed diverticulum, appendiceal abscess, tubo-ovarian abscess, pelvic abscess, prostatic abscess, and furuncles or carbuncles. Systemic infection: Some systemic infections are particularly likely to be associated with a chill. Malaria, relapsing fever, Weil 212 disease, rat-bite fever, yellow fever, smallpox, Rocky Mountain spotted fever, acute poliomyelitis, and pulmonary tuberculosis belong in this group. Venous thrombosis: Phlebitis in various portions of the body is often associated with chills. Cavernous sinus thrombosis, lateral sinus thrombosis, pylephlebitis, and, less frequently, thrombophlebitis of the extremities may be associated with a chill. Miscellaneous: Chills are often associated with intravenous injection of drugs or antibiotics, transfusion, hemolytic anemia, and introduction of contaminated equipment into the body. Approach to the Diagnosis The approach to the diagnosis of a patient with chills is similar to that of a patient with fever. However, when fever and chills are the only symptoms, a workup similar to that found below may be necessary. Careful charting of the temperature while the patient remains off aspirin or other antipyretics will be rewarding, especially in the diagnosis of malaria. V—Vascular suggests an infarction of the subthalamic nucleus, which produces hemiballism. I—Intoxication suggests Wilson disease, phenothiazine, lead or manganese toxicity, and carbon monoxide poisoning. T—Trauma suggests chorea from concussion, basilar skull fracture, or intracerebral hematoma. E—Endocrine and epilepsy suggest the possibility that the chorea is related to an epileptic focus. When presented with a case of clubbing, one might simply use anatomy and think of all the major internal organs (except the kidney); one would then be closer to an accurate and reliable differential diagnosis. To be more scientific, apply basic physiology to provide an extensive and organized differential diagnosis. The important basic science, then, is 1 physiology; according to Mauer, the principle common denominator is anoxia. Anoxic anoxia or poor intake of oxygen would suggest the first category of disease, pulmonary; most significant among these are chronic diseases of the lung, including chronic bronchitis and emphysema, empyema, pulmonary tuberculosis, carcinoma of the lung, pneumoconiosis, bronchiectasis, and pulmonary fibrosis. Acute pneumonia, pneumothorax, and bronchial asthma (where there may be many short episodes of anoxia) do not usually lead to clubbing. Table 16 Clubbing and Pulmonary Osteoarthropathy In the next group of disorders, the lungs may be normal but a significant amount of blood never reaches the alveoli; I call this shunt anoxia. Here are classified the tetralogy of Fallot and other congenital anomalies of the heart, recurrent pulmonary emboli, cirrhosis of the liver (associated with 216 small pulmonary arteriovenous shunts), and pulmonary hemangiomas. Thus, anemic anoxia may be a factor in portal cirrhosis, biliary cirrhosis, Banti disease, chronic malaria, and subacute bacterial endocarditis. It may also be a factor in disorders of the gastrointestinal tract, such as regional ileitis, ulcerative colitis, and carcinoma of the colon. Histotoxic anoxia is Mauer’s another explanation for clubbing in patients without low arterial oxygen saturation. This group includes subacute bacterial endocarditis, myxedema, ulcerative colitis, intestinal tuberculosis, and amebic dysentery. Of course, this is a regular occurrence in chronic methemoglobinemia or sulfhemoglobinemia. Approach to the Diagnosis The clinical approach to clubbing involves being certain that clubbing is present. A curved fingernail is not good evidence, and the “drumstick” appearance (which makes the finger look like a true club) does not occur until late. Early clubbing is determined by the angle between the nail- covered portion and the skin-covered portion of the dorsal surface of the terminal phalanx. When the angle becomes 180 degrees and disappears, that is, when the terminal phalanx becomes flat, clubbing exists. Careful examination for cyanosis and a thorough evaluation of the heart and lungs will determine the cause in most cases. Pulmonary function 218 studies, and arterial blood gases before and after exercise and before and after 100% oxygen, will help confirm the diagnosis in many cases. Blood cultures, stool culture and examination, and thorough radiologic studies of the gastrointestinal tract will be necessary in obscure cases. Because somnolence may be simply an early stage of coma, its etiologies are almost all identical to the etiologies of coma.

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Arterial blood gas analysis will distinguish those cases associated with anoxia such as pulmonary emphysema and cyanotic heart disease buy super avana australia impotence natural supplements. Determining the blood erythropoietin will help to differentiate cases where the erythropoietin is the stimulus such as renal carcinoma and pulmonary emphysema order super avana american express impotence is a horrifying thing. Bone marrow examination (myeloproliferative disorder) 665 666 Periorbital and facial edema. Increased desire for water may be due to a decreased intake, as in prolonged abstinence, vomiting of pyloric stenosis and intestinal obstruction, and diarrhea of any cause. Anything that decreases the effective circulatory volume, such as hypoalbuminemia, may cause retention of salt and consequent thirst through the rennin– angiotensin–aldosterone mechanism. The increased output may result from a solute diuresis in diabetes mellitus and hypercalcemic states (e. Increased output of salt and water in excessive sweating of work or fever will lead to thirst. This mechanism is an additional factor in hyperthyroidism and diabetes mellitus where diaphoresis is common. Drugs such as lithium and demeclocycline hydrochloride (Declomycin) can damage the distal tubule and cause renal diabetes insipidus. Drugs such as belladonna alkaloids, amitriptyline hydrochloride, parasympatholytic drugs, and gallic acid may cause a dry mouth and an excessive thirst. Approach to the Diagnosis The approach to the diagnosis of polydipsia involves establishing the presence or absence of other symptoms such as polyuria, polyphagia, weakness, and weight loss. Polydipsia with polyuria and excessive appetite (polyphagia) should suggest diabetes mellitus or hyperthyroidism, whereas polydipsia with polyuria alone should suggest a form of diabetes insipidus (pituitary, renal, or psychogenic). The laboratory workup involves checking intake and output, blood sugars, electrolytes, and a thyroid profile. Utilizing your knowledge of physiology, what would be on your list of possible causes? The appetite may be based on a psychic desire for food, a lack of food or a particular vitamin, impaired intake of food, an increased metabolism of the body (and consequently an increased need for food), increased uptake of food by the cell, and inability of the cell to absorb food, causing “cell starvation. Psychic desire for food: This occurs in many chronic anxiety and depressed states and is frequently associated with obesity. Lack of food or a particular ingredient in food: Starvation and avitaminosis can cause polyphagia. Impaired uptake of food: Rapid mobility of food in gastric hypersecretion and intestinal bypass as well as preempting of food by intestinal worms may cause polyphagia on this basis. Increased body metabolism: Hyperthyroidism, rapid growth of adolescence, and gigantism are included in this category. Increased uptake of food by the cell: Any condition associated with hyperinsulinism (functional hypoglycemia and insulinomas) is recalled in this category. Approach to the Diagnosis Association with other symptoms is the key to a definitive diagnosis of polyphagia. Polyphagia with polyuria, polydipsia, weakness, and weight loss suggest hyperthyroidism or diabetes mellitus. The laboratory workup should include thyroid function studies, a skull x-ray for pituitary size, glucose tolerance tests, and, possibly, a 48-hour fast with frequent blood sugar determinations. Case Presentation #74 A 28-year-old white man complained of a ravenous appetite for several months. Utilizing your knowledge of physiology, what would be your differential diagnosis? Further history reveals that the patient had experienced episodes of weakness, palpitations, and sweating during the same period of time. Many physiologic conditions increase the output of urine (stress, exercise, and warm weather associated with copious drinking). From a pathophysiologic standpoint, polyuria results from one of four mechanisms: (a) increased intake of fluids, (b) increased glomerular filtration rate, (c) increased output of solutes such as sodium chloride and glucose, and (d) inability of the kidney to reabsorb water in the distal tubule. Increased intake of fluid: As already mentioned, increased intake can occur under stress and nervous tension. It becomes pathologic in psychogenic diabetes insipidus when 6 to 10 L of fluid may be ingested each day. Increased glomerular filtration rate: This is a factor in the polyuria of hyperthyroidism and fever of any cause. Increased output of solutes: Uncontrolled diabetes mellitus (where the solute is glucose) and hyperthyroidism (where the solute may be glucose or urea) are examples of this type of polyuria. Diuretics are a significant cause of this type of polyuria because they increase the amount of solute arriving at the distal tubule and hold onto the water that would otherwise be absorbed. Approach to the Diagnosis The diagnosis of polyuria depends largely on the association of other symptoms. Polyuria, polyphagia, and polydipsia suggest diabetes mellitus and hyperthyroidism. Polyuria with only polydipsia suggests psychogenic or idiopathic diabetes insipidus; the Hickey–Hare test will differentiate the two. Polyuria with polydipsia and weakness but with no significant weight loss suggests hypercalcemia and possible hyperparathyroidism. Chronic nephritis will be diagnosed by examination of the urine sediment and a specific gravity that remains at 1. Nephrogenic diabetes insipidus can be differentiated from neurogenic diabetes insipidus by the inability of the kidney to respond to a pitressin injection. Serum and urine osmolality (pituitary diabetes insipidus, nephrogenic diabetes insipidus) 7. Endocrine consult Case Presentation #75 A 38-year-old white woman presents to your office with a history of weakness, fatigue, depression, and frequency of urination over the past year. Further history reveals that she had an episode of right flank pain and hematuria 6 months ago. Each structure in the popliteal space may be involved by one or two conditions that cause a mass or swelling. In visualizing the anatomy, one encounters the skin, subcutaneous tissues, muscles, bursae, veins, arteries, lymphatics, nerves, and bones. Skin: The skin may be involved by urticaria, sebaceous cysts, carbuncles, lipomas, hemangiomas, and various other skin masses. Subcutaneous tissue: Lipomas, sarcomas, and cellulitis are the main lesions encountered. Muscle: Contusions of the gastrocnemius and semimembranosus muscles may cause a mass in the popliteal fossa. Bursae: Popliteal cysts (Baker cysts) may result from filling of the bursa between the gastrocnemius and semimembranosus muscles with a gelatinous or serous substance. Artery: An aneurysm of the popliteal artery may result from atherosclerosis or a gunshot wound. When there is a loud bruit over the artery and distention of the veins, an arteriovenous fistula should be considered. Lymphatics: Enlarged popliteal nodes may result from infections in the distal portion of the extremity, tuberculous adenopathy, or metastatic malignancy.

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Depending on the cause purchase super avana toronto impotence kidney disease, it can be classifed into primary or secondary intestinal lymphangiectasia cheap 160mg super avana overnight delivery erectile dysfunction doctor in mumbai. The edema is pitting because the oncotic pressure is low due to hypoalbuminemia resulting from exudative enteropathy. Malabsorption may cause fat-soluble vitamin def- ciencies and hypocalcaemia leading to convulsions. Macroscopic abnormalities are usually obvious with the creamy yellow of jeju- nal villi corresponding to marked dilatation of the lymphatics within the intestinal mucosa. Histological examination of duodenal, jejunal, and ileal biopsies confrms the presence of lacteal juice, dilated mucosal and submucosal lymphatic vessels with polyclonal normal plasma cells. Elevated IgE levels without underlying allergic diathesis or disease has also been reported. The B-cell defects are characterized by low immunoglobulin levels (IgA, IgG, IgM) and poor antibody responses. However, severe and recurrent infections have been reported in case reports and case series. The absence of long-chain triglyceride in the diet may decrease the engorgement of the intestinal lymphatics with chyle, thereby preventing their rupture with ensuing protein and T-cell loss. After a few weeks, this treatment may lead to reversal of clinical and labora- tory measures such as hypoalbuminemia and lymphocytopenia. The disruption of the gastrointestinal tract by infammation and the associated symptoms of pain, nausea, and diarrhea lead to reduced food intake, reduced nutrient use, and ultimately to impaired nutrition status in these patients (Figure 11. Several studies have documented weight loss in 70%–80% of hospitalized patients and 20%–40% of outpatients with Crohn’s disease. Active disease within the small bowel can also lead to both macronutrient and micronutrient malab- sorption. Although nutrition intervention can ameliorate adverse effects on growth failure, permanent growth impairment can still occur in 19%–35% of children with Crohn’s disease. Dual-energy x-ray absorptiometry is widely accepted as a quantitative measurement technique for assessing skeletal status at all ages. Children should be assessed relative to age or body size and sex, with bone mineral density expressed as z-scores. Vitamin D supplementation and higher serum 25-hydroxyvitamin D levels have also been shown to be associated with quiescent disease activity. Ferric iron has been used as well with reportedly reduced side effects and good effcacy. Although a dose of 1 mg of folic acid is commonly used in pediatrics, the folic acid requirement of children with Crohn’s disease has not been determined. Stunting is usually seen in patients with long-standing uncontrolled disease or delayed diag- nosis. Well-nourished patients should try to achieve recommended caloric intakes and recommended daily allowances of vitamins and micronutrients. A more recent systematic review confrmed higher rates of remission in corticosteroid-treated patients. However, clinical studies, registries, and case reports warn of the increased risk of infections, particularly tuberculosis and fungal infections. The incidence of infections, however, increased in patients given infiximab more frequently. During the 36-month follow-up, the most prevalent adverse events were respiratory infec- tions. Intestinal atresia, gastroschisis, intestinal agangliono- sis, volvulus, and necrotizing enterocolitis are the most common causes. The immedi- ate manifestations are voluminous diarrhea, hypovolemia, hyponatremia, and Enteric Syndromes Leading to Malnutrition and Infections 273 hypokalemia. Iron, phosphorus, and water- soluble vitamins are predominantly absorbed in the proximal intestine. As most patients with short-bowel syndrome have an intact duodenum and proximal jeju- num, defciencies of these entities are rare but patients tend to develop calcium and magnesium defciencies. Loss of part or whole of the ileum can result in vitamin B12 and bile salt malabsorption. Gastrointestinal hormones, such as gastrin, cho- lecystokinin, secretin, gastric inhibitory polypeptide, and motilin, are produced by endocrine cells in the proximal intestinal tract. H2-receptor antagonists, proton pump inhibitors, antidiarrheal agents, cholestyramine, and octreotide have all been used to control the diarrhea. Inadequate zinc intake affects a third of some populations in Southeast Asia and sub-Saharan Africa, where children are most severely affected. In these countries, zinc-related growth stunt- ing affects 40% of preschool children and zinc supplementation has been shown to dramatically reduce common infant morbidities and mortalities. Without treatment, skin lesions slowly evolve into erosions and patients develop generalized alopecia and diarrhea. Patients with advanced disease will also experience growth delay, mental slowing, poor wound healing, anemia, photophobia, hypogeusia, anorexia, delayed puberty, and hypo- gonadism in boys and men. Thus, the presence of a depressed serum or plasma zinc level does not always indicate zinc defciency. In addition, the zinc level may be within normal limits in a defciency dermatitis that nevertheless responds to zinc replacement therapy. Serum or plasma zinc levels and zinc-dependent enzyme levels should be monitored every 3 to 6 months and the dose of zinc should be adjusted appropriately. Typically, clin- ical improvement is seen very rapidly, within days to weeks, before a signifcant change in serum zinc levels. In defciency dermatitis caused by low dietary zinc, replacement Enteric Syndromes Leading to Malnutrition and Infections 275 therapy should be initiated at 0. Importantly, in patients who are malnourished, a multinutrient replacement approach is warranted. The histopathology of coeliac disease: Time for a standardized report scheme for pathologists. Grains of truth: Evolutionary changes in small intestinal mucosa in response to environmental antigen challenge. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac dis- ease. Review article: The diagnosis and treatment of haematinic def- ciency in gastrointestinal disease. Folic acid concentration in the serum and erythrocytes of patients with celiac disease. A prospective study of the prevalence of undiagnosed coeliac disease in laboratory defned iron and folate defciency. Nutritional status in adolescents and young adults with screen-detected celiac disease. Gastric morphology and function in dermatitis herpetiformis and in coeliac disease.