Acquired C1 inhibitor deficiency associated with systemic lupus erythematosus affecting the central nervous system

Article Abstract:

The complement system is a group of proteins in blood that, when sensitized, destroy bacteria and other cells. Complement proteins are among the molecules found in blood that may be deficient or abnormal in systemic lupus erythematosus. Complement deficiencies are also associated with angioedema (a condition characterized by hives and fluid accumulation in skin, mucous membranes, or organs), and with disorders involving lymphocytes (immune cells important in fighting infection). The case report of a 22-year-old woman is the first known association between a deficiency of complement protein 1 (C1) inhibitor and systemic lupus erythematosus. The patient had been treated with steroids seven years previously for lupus, but had no history of angioedema. She was hospitalized for fever and had other symptoms of active lupus. Within six months, she was rehospitalized for fever recurrence, and laboratory tests indicated worsening of inflammation. After steroid therapy was tapered, she developed mania (mental disturbance characterized by excitement or overactivity), which coincided with recurrence of fever and abnormal blood tests, and was referred for further treatment. Electroencephalography (recording of brain waves) and cerebrospinal fluid (which bathes the brain and spinal cord) also indicated nervous system involvement. She had no signs of angioedema, but was found to have low blood levels of the complement proteins C4, C2, C1 inhibitor, and C1q. (Levels of C3 were normal.) Three days of treatment with steroids led to improvement in the patient's mental status and improvements in cerebrospinal fluid analysis, the electroencephalogram reading, and the complement levels. It is possible that the C1 inhibitor deficiency may have been related to the activation of lymphocytes that occurs in lupus, but further study is needed to explore this theory. The great reduction in C4 levels likely contributed to the mental disturbance, and did not appear to be related to underlying angioedema. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Complement deficiency (Immunology), Complement deficiencies, Mania

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Serum soluble interleukin 2 receptor in systemic lupus erythematosus: effects of disease activity and infection

Article Abstract:

Systemic lupus erythematosus (SLE) is one of the autoimmune diseases in which antibodies are inappropriately made against the body's own molecules. The mechanisms underlying the development of these antibodies are unclear. Lymphocytes, immune cells important in fighting infection, may be activated in autoimmune diseases. Upon activation, T lymphocytes, or T cells, shed one of their surface proteins; this protein is known as interleukin 2 receptor. Blood levels of the soluble interleukin 2 receptor (sIL2R) are measurable. It was hypothesized that levels of this protein may correlate with disease activity in SLE. The usefulness of these measurements was evaluated in a study of 100 patients with SLE during active and inactive phases of the disease, and when 24 of the patients developed infections. Twenty-three control subjects without inflammation were also studied. Blood levels of sIL2R were higher in patients with inactive SLE than in controls, and higher in patients with active SLE than in those with inactive SLE. Levels of the protein fell as active SLE was controlled by medication, but did not correlate with severity of disease activity (classified as mild, moderate, or severe). SLE patients who developed infections had three-fold or higher increases in blood levels of sIL2R than those without infection. Patients with chronic yeast infections or tuberculosis had the highest sIL2R levels among those with infections. The findings indicate that although blood levels of sIL2R help to distinguish active from inactive SLE, they are not sensitive to disease severity. The sIL2R levels are a useful indicator of infection in SLE patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Interleukin-2, Drug receptors

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A new model of diabetic pregnancy with genetic hypertension: pregnancy in spontaneous hypertensive rats with neonatal streptozocin-induced diabetes

Article Abstract:

Diabetes can be induced in a strain of rats that naturally has high blood pressure. This creates an animal model that will enable researchers to study the combined effects of hypertension and diabetes in pregnancy. Female 2-day-old rats from this strain were injected with an agent that induces diabetes. They were mated when adult to male rats from the same strain, and blood pressure, plasma glucose values, and urinary albumin excretion were monitored during pregnancy. Rats with both complications had more adverse symptoms and poorer outcomes among the pups compared with control rats with hypertension alone. Inducing diabetes in the immature rat offers advantages over other time periods. Inducing it in the virgin adult rat causes severely abnormal blood sugar levels, and many become are infertile. Inducing it after pregnancy raises the question of whether the drug directly affects the fetus.

Models, Evaluation, Preeclampsia, Diabetic nephropathies, Diabetes in pregnancy, Gestational diabetes, Animal models in research, Animal research models

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