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PubMed1964

[WHIPPLE'S DISEASE].

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Adrenal Cortex Hormones↗
PubMed1964

WHIPPLE'S DISEASE.

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Chloramphenicol↗
PubMedDate not supplied

[Neurologic disorders in Whipple's disease].

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.

Central Nervous System Diseases↗
PubMed1979

Quantitative and qualitative changes in phospholipid in the intestine of the gerbil and the development of lipodystrophy.

Female gerbils fed a diet containing 20% coconut oil develop an intestinal lipodystrophy that is not seen in animals fed a diet containing 20% safflower oil or a diet of 20% coconut oil supplemented with 0.1% inositol. The coconut oil diets contained 1.5% safflower oil to prevent essential fatty acid deficiency. The level of inositol in the intestinal tissue of animals fed the coconut oil diet not supplemented with inositol has been shown to be decreased. Phospholipid analyses of the intestinal tissue were undertaken to determine if this decrease in total inositol was reflected in a decrease in phosphatidylinositol or resulted in an altered phospholipid pattern. No difference in the phosphatidylinositol level was seen between animals fed 20% coconut oil with and without inositol supplementation (microgram P/gut section), although animals fed coconut oil diets had lower levels of phosphatidylinositol than animals fed safflower oil diets. Fatty acid analyses of total phospholipid and phosphatidylinositol in gut tissue revealed that animals which deveoped the lesion had an ultered phosphatidylinositol fraction with a depressed level of arachidonic acid and an elevated level of oleic acid. This suggests that the development of the intestinal lipodystrophy may be correlated with qualitative rather than quantitative changes in phosphatidylinositol.

Animals↗