Patients with rheumatic diseases who become pregnant are justifiably categorized as having high-risk pregnancies. Utilizing a multidisciplinary approach, including perinatologists, rheumatologists and anaesthetists, successful pregnancies have become the rule rather than the exception. However, women with rheumatic disease are particularly prone to develop serious obstetric problems which often result in early hospitalization and delivery. Although vigilant obstetric care improves perinatal outcome, prematurity will continue to be a major problem complicating pregnancies in women with rheumatic disease.

Sex hormones have physiological and pathological (autoimmune conditions) effects on the immune system. Studies in experimental animal models of human autoimmune diseases have clearly shown that sex hormones regulate the expression, severity and course of autoimmune diseases. Sex hormones affect the function of T, B and NK cells, and macrophages. Precisely how sex hormones affect lymphocytes is a highly complex question. Sex hormones can modulate the immune system, perhaps directly (e.g. thymic reticular tissue), or indirectly via host and many oestrogen target tissues, including the central nervous system hypothalamic-pituitary axis (the neuroendocrine tissues). The effects of sex hormones on the immune system (immunosuppression or immunopotentiation) may vary, even with the same hormone. For example, oestrogen can increase IgA levels in the uterus, but decrease IgA levels in the vagina or have no effect in lacrimal tissues (Sullivan, 1989). Therefore the effects of sex hormones on the immune system cannot be generalized but must be evaluated independently. Some of the reasons for variability in results have been reviewed in detail elsewhere (Steinberg et al, 1979; Ansar Ahmed et al, 1985b). These include, dose of hormones, age and sex-hormonal status of animals, route and time of administration, the immunocompetence of the host, stress, the metabolism of hormones (e.g. metabolism of testosterone to oestrogen) resulting in alteration of biological activity, and differential response to various antigens. The initial encounter of sex hormones with the type of target cells, the variability of secondary messengers and gene activation events are other important considerations. The effects of sex hormones on the immune system to modulate immune responses are unequivocal. The burgeoning advances in cellular immunology, endocrinology and molecular biology, should provide a better understanding of: (1) the interactions of hormones with the immune system; (2) how hormones activate specific genes; and (3) how hormones influence intracellular communication. In a clinical situation, it is hoped that androgenic compounds which lack virilizing effects, but possessing the desired immunomodulatory effects, will eventually be synthesized. These hormone analogues, in combination with specific (non-toxic) oestrogen antagonists, may offer new therapeutic avenues.

The onset of pregnancy appears to result in the amelioration of rheumatoid disease activity. This is most likely to be related to the change in hormonal, and thus immunological, status of the mother. Spontaneous abortion appears to be increased in mothers with rheumatoid disease. Whether this is due to disease status or to drug therapy is not entirely clear for all cases, but there is a suggestion that it could be the disease state. If at all possible, drugs should be avoided during pregnancy but simple anti-inflammatory drugs in low dosage probably do not produce any major problems. Immunosuppressant drugs should be avoided at all times except when the mother's health is at serious risk. The continued use of disease remitting agents throughout pregnancy is probably not necessary and there is still sufficient question as to whether these drugs could be potentially toxic to the infant. Primum non nocere.

Despite the considerable interest in antiphospholipid antibodies during the last 10 years, the clinical disorders with which they are associated are still not well understood (Love and Santoro, 1990). The concept of the antiphospholipid syndrome (APS) and a means by which this can be defined (Harris, 1987) may aid us in better classifying these patients, evaluating their clinical features, and in conducting prospective studies. Standard methods for measurement of anticardiolipin antibodies (Harris et al, 1987b; Harris and the Kingston Anticardiolipin Standardization Group, 1990) and more attention to measurement of the lupus anticoagulant (Triplett and Brandt, 1988) will ultimately play an important role in improving the diagnosis of these patients. The initiation of the Kingston AntiPhospholipid Study (KAPS) group in January 1988 paves the way for future multicentre treatment trials of these patients (Harris, 1988; Triplett, 1989; Recker and Leff, 1989). For the practising physician managing a pregnant woman with the APS, there are few clear guidelines for treatment. An appropriate approach would be to assemble a multidisciplinary team for pregnancy management, exclude other causes of pregnancy loss and select the drug regimen which will cause the least harm and has some reported efficacy. Most importantly, the patient should be followed carefully throughout her pregnancy.

Much strain is placed on the shoulder joint in all sports. Sports injuries may be caused by a single, violent incident. Fractures of the clavicle, acromioclavicular and sternoclavicular traumas, isolated fractures of the greater tuberosity and shoulder dislocations are frequent clinical pictures which today can be managed by well established procedures. Other sports injuries, however, involve over-use of the shoulder which, through repetitive harmful movements, can bring about microtraumatic lesions of the rotator cuff, glenoid labrum, acromioclavicular joint and certain peripheral nerves around the suprascapularis. In all cases, a programmed, comparative, clinical examination and complementary, sequential examinations will indicate suitable curative and preventive treatment.

Rotator cuff problems present with shoulder pain on repetitive overhead activity. Chronic irritation may develop into impingement tendonitis, with weakness of abduction and external rotation and night pain. Conservative management with rest, anti-inflammatory medicine and physiotherapy resolves the majority of symptoms. If these persist, surgical decompression affords good relief of pain.

Glenohumeral instability is an important cause of shoulder pain and disability in an active population. An awareness of the prevalence of recurrent instability, either in the form of dislocation or subluxation, is particularly useful in the assessment of the young athlete presenting with shoulder pain. Young adults presenting with rotator cuff tendinitis may have an underlying instability as the primary cause of their problem. A careful clinical examination should determine whether the instability is voluntary or involuntary, of traumatic or atraumatic onset, and the primary direction of the instability, as these factors have important implications with regard to treatment. Anterior glenohumeral instability is most common and the incidence of recurrent instability following on from an initial dislocation is high in the young active patient. An intensive rehabilitation programme is indicated for all initial dislocations or subluxations but surgery may become necessary after failure of conservative treatment. Care must be taken to determine accurately those patients with voluntary or multi-directional instability and a longer trial of conservative treatment is indicated here, as results of operative treatment in those cases are less favourable. Conservative treatment should be directed at strengthening the dynamic stabilizers of the shoulder joint, notably the rotator cuff muscles. Additional X-ray views are needed to demonstrate all the radiological changes associated with recurrent instability and further evaluation with examination under anaesthesia and arthroscopy is beneficial in the assessment of these patients. Arthroscopic surgery also has a role in the treatment of patients with symptomatic labral pathology and is now being used to perform stabilization procedures in selected cases. Many operative procedures have been described for stabilization of the shoulder and these should be directed at correcting the pathology present. Restoration of the patient's flexibility and strength postoperatively is essential, especially in the athlete in order to allow a full return to sporting activity.

Sjögren's syndrome is the result of lymphocyte-mediated destruction of exocrine glands that leads to diminished or absent glandular secretions and mucosal dryness. The manifestations from the alimentary system in patients with Sjögren's syndrome include, within the mouth, mucosal dryness, atrophy, accelerated dental decay and enlargement of the major salivary glands. Dysphagia is a common complaint and is probably secondary to oesophageal dysfunction. The symptoms from gastric involvement are nausea, epigastric pain and dyspepsia which might be attributable to chronic atrophic gastritis. Whether the small bowel is affected in Sjögren's syndrome patients is not clear. However, nutritional deficiencies have been noted in these patients. Pancreatic involvement is perhaps expressed as subclinical, acute or chronic pancreatitis, and finally there have been a large number of studies dealing with liver involvement in Sjögren's syndrome. From these reports it is clear that many patients with Sjögren's syndrome have abnormal biochemical liver function tests and some of them may also have abnormal liver biopsy. The pathogenic process responsible for the hepatic damage and for the salivary gland destruction could be similar.

Although intestinal bypass procedures are no longer performed, important lessons have been learned concerning clinical arthritides resulting from bacterial overgrowth and immune complex deposition. This information is of considerable value in patients who present with the clinical picture of intestinal bypass arthritis on the basis of other bowel abnormalities. Furthermore, the pathogenetic mechanisms involving bacterial overgrowth, release of bacterial antigens, and immune complex deposition may be pertinent to many types of inflammatory arthritis.

Ankylosing spondylitis (AS) is probably produced by repeated episodes of Klebsiella-reactive arthritis, usually in HLA-B27-positive individuals. This concept is based on immunological, microbiological and serological considerations. Immunological studies based on anti-B27 tissue typing sera and anti-B27 monoclonal antibodies indicate that HLA-B27 cross-reacts with antigens found in Klebsiella, Salmonella, Shigella and Yersinia micro-organisms. Salmonella, Shigella and Yersinia gut infections are associated with a reactive arthritis that occurs predominantly in HLA-B27-positive individuals. However, microbiological studies indicate that only Klebsiella, but not Salmonella, Shigella or Yersinia, can be isolated in faecal cultures obtained from AS patients. Furthermore, serological studies involving a number of different techniques demonstrate that only antibodies against Klebsiella, but not against Salmonella, Shigella or Yersinia, can be identified in active AS patients. The evidence is sufficiently extensive to warrant long-term studies involving Klebsiella reduction in the bowel flora of AS patients, in an attempt to reduce the severity and modify the development of the disease. It would appear that Klebsiella-reactive arthritis is the precursor stage occurring in the early and active phases of AS. Only future studies can determine whether this disease will remain a taxonomic curiosity or provide guidelines for therapeutic sequelae which will be of benefit to AS patients.

Postenteric reactive arthritis is one of several syndromes in which arthritis appears to be secondary to gastrointestinal tract pathology. A wide range of microbes may trigger this type of arthritis. On the other hand, there are differences between strains in their arthritogenic potential. Two possible mechanisms, not mutually exclusive, can be forwarded to explain these findings: first, particular characteristics of the infective organisms are necessary to initiate events leading to reactive arthritis and, second, particular anatomical locations and a certain degree of mucosal involvement are needed to initiate the process. Studies on humoral and cellular immune responses have not revealed any unifying feature that could explain the pathogenesis of reactive arthritis. The HLA allele B27 plays some kind of key role. Yet the elucidation of the fine structure of B27 specificity has not led to any immediate breakthrough in the understanding of the pathogenetic pathways. Experience of reactive arthritis associated with acquired immunodeficiency syndrome suggests that helper T cells are not involved. Antigen persistence may be connected with continuation of the inflammation. Recent developments in the serology of enteric bacterial infections will provide additional tools for uncovering the triggering agents in reactive arthritis. 'Idiopathic reactive arthritis' associated with clinically silent terminal ileitis is an interesting disease entity requiring further characterization.