GASTROINTESTINAL MANIFESTATIONS.

The gastrointestinal tract may be involved in 50% of patients. Up to 25% of patients have esophageal complaints, including difficulty swallowing. The lack of

radiographic abnormalities suggests stress, whereas if positive, scleroderma-overlap syndrome should be considered. In addition, dysphagia may result from hiatal hernia and gastric reflux. Dyspepsia is common, especially with stress and with NSAID and steroid use. Abdominal pain, nausea, and vomiting are also common. In the absence of peptic ulcers and adverse medication effect, a cause is rarely determined. On the other hand, one should always consider mesenteric vasculitis, which is characterized by intermittent lower abdominal pain eventually progressing to an acute abdomen. The diagnosis is usually confirmed by angiography. Pancreatitis (8% of patients) should also be considered in the presence of upper abdominal pain, nausea, and vomiting. Pancreatitis may reflect vasculitis and/or the use of steroids. Hepatomegaly is uncommon, but liver chemistry abnormalities (lactic dehydrogenase, serum glutamate pyruvate transferase) are common, especially in patients with active disease or those taking NSAIDs. Persistent liver chemistry abnormalities may suggest cirrhosis; chronic, active, or persistent hepatitis; granulomatous hepatitis; cholestasis; infection (e.g., hepatitis); or drug toxicity--and may warrant a liver biopsy.

NEUROPSYCHIATRIC MANIFESTATIONS.

These symptoms occur in virtually all patients(Table 289-5). Many patients manifest anxiety and/or depression, often in response to their illness and the threat of loss of health, family, and job, disfigurement, disability, dependency, and death. Symptoms may include psychosomatic complaints such as insomnia, anorexia, constipation, myalgia, arthralgia, fatigue, palpitations, diarrhea, dizzy spells, hyperventilation, memory loss, emotional lability, confusion, decreased concentration, headaches, and cognitive defects. Frank psychosis may develop and be manifested as compulsive-obsessive behavīor, phobias, and even suicide. These symptoms may also precede a diagnosis of SLE by

years and leading to frustration by the patient and physician regarding the correct diagnosis. These psychological responses to illness should be differentiated from organic brain disease, which may cause the same symptoms. Most useful in discriminating functional from organic disease are tests of cognitive function and psychological tests (e.g., the Minnesota Multiphasic Personality Inventory); other tests such as MRI, electroencephalography (EEG) with evoked potentials, and antiribosomal P-protein antibody determinations may also be useful. Cerebrospinal fluid (CSF) analysis is most useful to exclude infection, although some physicians note a correlation of IL-6, elevated protein levels, and antineuronal antibodies with CNS activity.

Psychosis is said to occur in about 24% of patients. Psychosis can also be caused by renal failure (uremic encephalopathy), hypertension (with multiple cerebral infarcts), metabolic abnormalities, infection, or drugs (tranquilizers, antidepressants, narcotics, beta-blockers, NSAIDs, cimetidine, antimalarials, alcohol, caffeine, benzodiazepine, and others). Steroids may cause or help clear a psychosis; clearing of a psychosis after steroid therapy suggests that the psychosis had an organic etiology. Medications may cause other problems: aseptic meningitis from azathioprine, ibuprofen, and other NSAIDs and, rarely, headaches, hallucinations, mental confusion, psychosis, seizures, and neuromyopathy from antimalarials.

Headaches are a frequent complaint and are usually due to stress and tension; migraine has been noted in 10 to 37% of patients. Other causes of headache include cold food, hangover, nitrites, monosodium glutamate, hunger, sinusitis, dental or eye disease, and malignancies.

Seizures are said to occur in 15 to 20% of patients and include grand mal, petit mal, temporal lobe, focal, and jacksonian seizures. Seizures may reflect an old scar or an acute inflammatory episode or may be due to metabolic imbalances, uremia, hypertension, infections, tumors, head trauma, or vasculopathy. When associated with other aspects of a lupus exacerbation, a CNS etiology should be suspected. CNS vasculitis is rare.

Cranial or peripheral neuropathies develop in 10 to 15% of patients. They usually occur coincident with lupus exacerbation. Cranial neuropathies include those affecting eye muscles, trigeminal neuralgia, facial weakness, and vertigo. Peripheral neuropathy is usually asymmetrical and mild and affects more than one nerve (mononeuritis multiplex).

Stroke has been noted in up to 15% of patients secondary to hemorrhage or thrombosis, antiphospholipid antibodies, hypertension, ITP, and thrombocytopenia. Less common are movement disorders (e.g., ataxia, choreoathetosis, hemiballismus) and transverse myelitis. Meningitis is not uncommon and may be due to either microorganisms or medication.

The eye is frequently involved by rash involving the eyelid, conjunctivitis, or keratoconjunctivitis. A characteristic finding is retinal "cotton wool" exudates (cytoid bodies), usually near the disk. They reflect a microangiopathy of retinal capillaries and localized microinfarction of the superficial nerve fiber layers of the retina. Whereas old textbooks cited a frequency of 10 to 25%, they are now seen only rarely.