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Fibromyalgia is a syndrome of musculoskeletal pain and tenderness in specific sites, fatigue, and sleep disturbance. Fibromyalgia may occur in patients with rheumatoid arthritis and other connective tissue diseases. Despite the fact that fibromyalgia patients may have alterations in the hypothalamic-pituitary-adrenal axis, no relationship had been established between fibromyalgia and diseases of the adrenal cortex. We report a case of a 46-year-old woman who presented with a new onset of a fibromyalgia-like syndrome meeting all American College of Rheumatology criteria except chronicity. Additional clinical features, including skin pigmentation, mild hypertension, and hyponatremia, as well as further laboratory testing led to a diagnosis of autoimmune Addison's disease. After steroid replacement, the symptoms of fibromyalgia disappeared. This is the first case in English-language literature of fibromyalgia secondary to Addison's disease. We suggest Addison's disease should be considered in the differential diagnosis of any patient with a fibromyalgia-like syndrome.

Interleukin-2 (IL-2) production was studied in T lymphocytes and isolated CD4+ T lymphocytes from 12 patients with primary fibromyalgia syndrome and 10 healthy volunteers. The dose and time kinetics of IL-2 production by concanavalin A-stimulated T cells and CD4+ T cells of fibromyalgia patients differed from findings in controls by 1) a need for a higher concentration of mitogen in order to achieve optimal IL-2 secretion, and 2) a delay in the peak time of optimal IL-2 secretion. Unlike normal IL-2 secretion, which was higher after removal of CD8+ T cells, the pattern and degree of IL-2 secretion by cells from fibromyalgia patients were not changed following removal of CD8+ T cells. Addition of calcium ionophore in assays using suboptimal concanavalin A concentrations did not correct the reduction in IL-2 secretion by fibromyalgia patient T cells, but addition of phorbol myristate acetate induced normal secretion of IL-2. These findings suggest that there is a defect in the IL-2 pathway, which is related to protein kinase C activation and does not involve impairment of Ca2+ elevation, in patients with fibromyalgia.

Parathyroid cysts are much less common than other cystic lesions of the neck. The great majority of parathyroid cysts are endocrine non-functioning. Parathyroid cysts may become symptomatic because of hormonal activity or due to the size and pressure effects. This is a case history of a 43 year-old woman, who presented with dyspnea. A 9 + 8 + 6cm cervical-mediastinal parathyroid cyst causing dyspnea, dysphagia, respiratory failure and jugular vein thrombosis was found.

• Multiple myeloma and congestive heart failure developed in a patient with long-standing scleredema adultorum. Staining of the myocardium, performed after her death, was positive for acid mucopolysaccharide and negative for amyloid. To the best of our knowledge, this is the first case in which acid mucopolysaccharide has been demonstrated in the myocardium, thus explaining the cardiomyopathy of scleredema adultorum. Review of the world literature enabled us to identify a statistically significant increased prevalence of plasma cell dyscrasia among patients with protracted scleredema. In all patients, plasma cell dyscrasia appeared years after the onset of scleredema. Immunofluorescent studies were negative for immunoglobulin deposition. We assume, therefore, that the plasma cell dyscrasia was secondary to scleredema. ( Arch Intern Med 1988;148:551-553)

A patient with rheumatic heart disease, mitral stenosis, and mitral insufficiency is described. The thrombosed giant left atrium paralyzed the left vocal cord and completely obstructed the bronchi to the middle and lower lobes of the right lung. The giant left atrium mimicked a mediastinal tumor on the chest x-ray film.

Osteogenesis Imperfecta is a group of genetic conditions leading to osteoporosis with varying degrees of liability to fractures. Some patients die at birth with severe deformity and numerous fractures while others have few or no fractures and survive a natural life span. Associated features in some but not all patients include blueness of the sclerae, presenile hearing loss, dentinogenesis imperfecta, hyper-extensibility of the ligaments, and cardiovascular complications. Clinical, radiological and genetic studies have permitted the separation of at least 4 distinct syndromes. O.I. type I is a dominantly inherited syndrome of liability to fractures with distinctly blue sclerae (which remain so throughout life) associated with presenile hearing loss or a family history of otosclerotic hearing loss. O.I. type II is an autosomal recessive syndrome of lethal perinatal O.I. characterized by extreme hypoplasia of the skeleton with radiographic evidence at birth of crumpled long bones and continuously beaded ribs due to multiple fractures. O.I. type III is an autosomal recessive syndrome, often with multiple fractures at birth, severe progressive deformity of the skeleton and sclerae which are progressively less blue with age. O.I. type IV is a dominantly inherited syndrome of osseous fragility with sclerae of normal hue. The frequency of presenile hearing loss in patients with O.I. type III and type IV is not known. These observations on the heterogeneity in osteogenesis imperfecta suggest that different patterns of histological, histochemical, ultrastructural and biochemical abnormalities may be found in these different O.I. types.