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B-cell lineage-derived high-grade malignant lymphomas are a well-recognized complication of HIV infection. However, isolated cases of unusual hematologic malignancies such as acute myeloid leukemias (AML), multiple myeloma (MM) or plasmacytomas, and chronic leukemias have been reported. This review focuses on these uncommon malignancies supervening in the setting of HIV infection. Eighteen cases of AML have been reported. Extramedullary localizations are frequently noticed. Nontreated patients have a survival of 2.7 weeks, compared with 9.8 months for patients treated with chemotherapy; being HIV-positive is not a contraindication to the treatment of AML. Based on the observed 72% incidence of AML M4 and M5 in an HIV-infected population versus 19% to 36% expected in a non-HIV-infected population, we postulate that the association of AML and HIV is not coincidental. The monocytotropism of HIV, the chronic cytokine-mediated activation of monocytes/macrophages, and the immunodeficiency may explain this association. Twenty-two cases of MM or plasmacytomas have been described, most of them in young patients. Again, extramedullary plasma cell tumors are recorded in many patients. Physiopathologic studies suggest that MM may develop because of an antigen-driven response to the circulating viral antigens. A role for Epstein-Barr virus (EBV) in the pathogenesis, as previously described in high-grade non-Hodgkin's lymphomas, is suggested by the presence of EBV genomes in plasma cell tumors. Finally, a broad spectrum of chronic leukemias derived from B- or T-cell lymphocyte lineage has been reported. These associations seem coincidental.

High-grade malignant lymphomas associated with HIV infection are usually derived from B lymphocytes. Although a broad spectrum of T-cell-derived malignancies has been described, no case of monoclonal T large granular lymphocyte leukaemia has been reported to date. We report a case of clonal T-LGL (CD3+, CD4-, CD8+, CD56-, CD57+) in an HIV-infected. HTLV1/2-negative individual. Large granular lymphocytes are thought to represent activated cytotoxic T lymphocytes. HIV infection, as previously reported for HTLV1/2, may represent a pathway of antigen activation and lead to clonal expansion of T large granular lymphocytes.

Only a few cases of varicella-zoster virus (VZV) myelitis have been described, and nearly all have been diagnosed post-mortem. There have been no reports in the literature of successful treatment of VZV myelitis with antiviral medications. We report on two patients with AIDS who had acute severe myelitis accompanied by herpes zoster. The presence of VZV DNA in cerebrospinal fluid (CSF) was documented by the polymerase chain reaction (PCR) technique. Early treatment with acyclovir was followed by a slow but complete recovery after a phase of initial aggravation. After a follow-up of > 1 year, the two patients remained asymptomatic. We conclude that (1) VZV should be considered a curable cause of myelitis in patients with AIDS, (2) PCR assay of CSF will assist in early diagnosis, and (3) early treatment with acyclovir should aid in recovery.

We report a previously unrecognized complication of totally implanted subcutaneous ports. A patient with a totally implantable central venous device developed a septic syndrome. Blood and injection-reservoir cultures grew Staphylococcus aureus. There was no evidence of endocarditis. The port was removed but acute oliguric renal failure developed. A percutaneous renal biopsy showed acute diffuse proliferative glomerulonephritis. There was no extracapillary crescent. On immunofluorescence study, capillary wall granular deposits stained brightly for IgG and C3. These findings were thought to be consistent with infection-associated immune-complex glomerulonephritis.

Systemic mastocytosis is a rare disease that shows marked heterogeneity in clinical manifestations and prognosis. It may be associated with hematologic disorders. We describe a patient with systemic mastocytosis associated with chronic myelomonocytic leukemia accompanied by ascites, pleural effusion, and development of skin lesions along a surgical scar. The disease responded well to interferon alfa therapy. This is the second report of successful treatment of mastocytosis with interferon alfa and the first associated with a hematologic malignancy.

We report four cases of varicella-zoster pancreatitis in immunocompromised hosts. All 4 patients presented a severe immunodeficiency because of chronic lymphoproliferative disorders (mainly lymphoma and Hodgkin disease) and long-term immunosuppressive therapy. Varicella zoster pancreatitis is a very unusual presentation of varicella-zoster infection. Few cases of pancreatitis occurring after bone marrow transplantation have been reported. All 4 patients presented with acute epigastric pain associated with transient elevation of serum amylase. The vesicular rash followed the presenting symptoms of severe abdominal pain by 8 days. This clinical presentation, occurring in immunocompromised patients, defines a set of symptoms which should lead the physician to suspect varicella-zoster pancreatitis, even in the initial absence of the characteristic skin vesicular eruption. Early institution of antiviral therapy seems mandatory.

Agranulocytosis is the most serious problem, potentially fatal, that can occur during antithyroid drug therapy. The use of hematopoietic growth factors is an attractive approach to reduce the period of this drug-induced neutropenia. We report two cases of severe antithyroid drug-related agranulocytosis (granulocyte count < 0.1 x 10(9)/L) treated with Granulocyte Colony-Stimulating Factor (G-CSF) or Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF). The delay to observe a granulocyte count superior to 1 x 10(9)/L was respectively 1 and 5 days. Our results, with others, clearly show that hematopoietic growth factors are effective in severe antithyroid drug-induced agranulocytosis.

The present article describes the clinical and pathological findings in 5 human immunodeficiency virus (HIV)-infected patients with muscle toxoplasmosis. The patients had marked lymphopenia (5/5), with less than five CD4+ cells/mm3 (3/3), when they developed fever (5/5), and multiorgan failure (5/5), including diffuse encephalitis, pneumonia, pancytopenia, and myopathy. Muscle involvement included weakness and wasting (4/5), myalgias (3/5), and high serum creatine kinase levels (3/3). Serology for toxoplasmosis showed high IgG titers in 3 patients (3/4). Anti-Toxoplasma therapy resulted in complete recovery in 2 patients. Muscle toxoplasmosis was detected by biopsy (3/5) or postmortem evaluation (2/5), and was identified using immunocytochemistry and electron microscopy. Toxoplasma cysts were detected in 0.5 to 4% of muscle fibers close to or remote from necrotic fibers and inflammatory infiltrates. Muscle fibers strongly expressed the major histocompatibility complex class I antigen (2/2) as in polymyositis. We suggest that Toxoplasma gondii should be sought by muscle biopsy in patients who have acquired immunodeficiency syndrome with fever, encephalitis, multiorgan dysfunction, and elevated serum creatine kinase levels of obscure origin.

A 41-year-old male homosexual with AIDS was hospitalized for temperature elevation to 40 degrees C with confusion. Neurologic evaluation found psychomotor slowing and temporospatial disorientation with no focal signs. The CD4 count was 100/mm3. CSF analysis and the CT scan were normal. Despite antiviral treatment the patient died fifteen days after admission. Gross appearance of the brain was normal. Histologic examination disclosed multiple, small foci of demyelination characteristic of progressive multifocal leukoencephalopathy. These foci were disseminated among the U fibers. In situ hybridization and immunocytochemical studies demonstrated papovavirus particles in oligodendrocytes and a few astrocytes. This case shows that papovavirus infection in AIDS patients may be responsible for a diffuse febrile encephalopathy with normal CT scan findings and a rapidly progressive course.

A 19-year-old male intravenous drug abuser, was admitted to hospital with a one-week history of lower limb weakness and urinary retention. He was known to have been HIV-seropositive for 3 years and had been treated for cerebral toxoplasmosis. Neurological examination confirmed flaccid paraparesis with weak ankle jerks and bilateral extensor plantar responses. There was no obvious sensory deficit. Neurological examination was otherwise normal. CSF contained 63 mg/dl protein and 10 leucocytes/mm3. Myelography was normal. He died 1 month later from septic peritonitis. Neuropathological examination showed chronic lesions of toxoplasmosis in brain. Small necrotic foci with myelin loss, proliferation of microglia, macrophages and multinucleated giant cells (MGC) were disseminated in the whole spinal cord, mostly in the white matter, but the brain was spared. Immunohistochemistry demonstrated p24 and p17 HIV antigens in macrophages, MGC and microglial cells. These lesions resemble those of so called 'multifocal giant cell encephalitis'. The present case demonstrates that HIV-related multifocal inflammatory changes may be restricted to the spinal cord and may be a cause of myelopathy in AIDS patients.

The central nervous system was examined in 135 adult AIDS patients who died between August 1982 and December 1990. Twenty two brains showed non-diagnostic changes including microglial nodules, discrete myelin pallor with reactive astrocytosis, mineralization of blood vessels and granular ependymitis. In 105 brains with specific changes, toxoplasmosis was the most frequent finding (55 cases) manifested by multifocal necrotic lesions or diffuse pseudo-encephalitic process. Other opportunists included cytomegalovirus (21 case), progressive multifocal leukoencephalopathy (1 cases), cryptococcosis (6 cases), mycobacterium avium intracellulaire (2 cases), varicella-zoster virus (2 cases), aspergillosis (1 case) and multiple bacterial microabscesses (1 case). Multinucleated giant cells were found in 52 cases. In 40 cases, they were widely disseminated throughout the brain and in 39 cases, they were associated with diffuse or multifocal white matter changes. Fifteen cases had a cerebral lymphoma, 9 hepatic encephalopathy, 1 centropontine myelinolysis and 1 focal pontine leukoencephalopathy. Three cases had a cerebral haemorrhage due to disseminated intravascular coagulation, antithrombin therapy and amyloid angiopathy. Spinal changes in 13 cases included vacuolar myelopathy (7 cases), HIV myelitis (1 case) and ganglio-radiculitis (1 cases), cytomegalovirus myelo-radiculitis (1 case) secondary spread from a lymphoma (1 case) and spinal infarcts due to disseminated intravascular coagulation (1 case). These lesions were frequently atypical and various combinations of all these pathologies were encountered in the same brain, sometimes in the same area and occasionally in the same cell. Chronological variations in the incidence of some complications could be related to changes in treatment.

Antacid characteristics of three drugs containing aluminium and magnesium salts (combination of clay with aluminium and magnesium hydroxides, aluminium and magnesium hydroxide mixture and hydrotalcite) have been studied in a dynamic situation simulated by the "artificial stomach" model, simultaneously taking into account both gastric fluxes, a constant secretory flux and variable emptying fluxes. Therapeutic doses of the drugs were added 1. to 100 ml of 0.1 N HCl, without or with 1% or 5% meat extract, and 2. 100 ml of pooled human gastric juice (96 mmol/l, pH 1.1). In addition, antacid activity of 0.5 g aluminium and magnesium hydroxides, taken alone or in combination, were evaluated when added to 100 ml of 0.1 N HCl. In aqueous HCl solution or in human gastric juice, the three antacid drugs exhibited 1. a neutralising activity characterised by pH-rise and 2. a buffering capacity close to pH 3.8. In addition, hydrotalcite exhibited also buffering capacity at pH 1.2. The antacid-induced capacity, expressed as H+ mmol, to recover initial pH were very similar, indicating that antacid physiochemical properties are similar in HCl solution or in gastric juice. H+ consumption depended upon emptying fluxes. The same antacid characteristics were observed when antacids were mixed with 1% meat extract while 5% meat extract resulted in a modification of antacid characteristics. Therefore the antacid capacities of respective mixtures were of smaller magnitude (50-60%) than the sum of the activities of antacids plus meat extracts.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been proven since 1986 that in myocardial infarction the sooner thrombolysis is performed the better. Forty-four patients were selected to enter a double-blind randomized trial in which they received either an acylated plasminogen streptokinase activator complex or a placebo. The injections were given intravenously at home within the first 3 hours (within the first 2 hours in 26 of them), by doctors from Mobile care units. This home treatment in the acute phase made it possible to gain 75 minutes on average, and up to 90 minutes when it was performed by an anaesthetist trained in emergency management. No serious complication, such as haemorrhagic or allergic reaction, occurred, and arrhythmia was no more frequent in the treated group than in the placebo group. Home thrombolysis did not delay admission to a cardiology Intensive Care unit (66 min. versus 64 min). Mean coronary patency was 75 per cent, and up to 82 per cent, in patients treated within 2 hours of the first symptoms. There was no significant difference between areas of reperfused or not reperfused patients in relation to time (P less than 0.08). Diagnosis sensitivity was 100 per cent. Thus, home thrombolysis is feasible and safe when performed by trained emergency medical teams and when criteria for inclusion and exclusion are fulfilled.

Gelox antacid activity has been evaluated in a dynamic procedure by using the "artificial stomach" model that mimics both gastric fluxes, gastric secretion and gastric emptying. At time 0, the gastric reservoir has been filled by 100 ml of 0.1 N hydrochloric acid solution without or with protein, or by 100 ml of human gastric juice (pH 1.1). Gastric secretion was simulated by a constant 3 ml/min flux of HCl solution or of human gastric juice. Gastric emptying fluxes varied from 1.5 to 4.5 ml/min. Gelox addition to 100 ml of 0.1 N HCl or of human gastric juice induced 1) a pH-rise from 1.0 to 4.5-5.8, 2) a buffering capacity close to pH 3.6-4.0 and 3) the consumption of an acid amount between 25 and 50 mmol according to emptying fluxes, for recovering initial pH. In a mixture of HCl 0.1 N and protein extract 1 or 5%, Gelox induced 1) a pH-rise related to the protein concentrations, 2) a buffering capacity close to pH 3.2-3.9 when 1% protein extract has been used, and close to pH 5.0-5.9 with 5% protein extract and 3) a greater acid consumption with 1% than with 5% protein extract. For both protein concentrations, the resistance for recovering the initial pH, expressed as the amount of consumed mmol H+, was therefore less than the sum of individual capacities of proteins and Gelox.(ABSTRACT TRUNCATED AT 250 WORDS)

Antacid capacity of two aluminium containing-antacid drugs was evaluated in vitro; the first drug contained aluminium hydroxide (Alternagel), the second, aluminium phosphate (Phosphalugel). The antacid evaluation was performed 1) in a closed system by measuring antacid activity by down titration, 2) by a dynamic evaluation simulating acid secretion and gastric emptying. The results were reported both to the recommended therapeutical dose and to 100 mg aluminium. In static conditions, without gastric emptying, it was shown that aluminium hydroxide and phosphate acted by their buffer capacity in pH range less than or equal to pH 1.5. The therapeutical dose of aluminium phosphate displayed greater antacid activity than aluminium hydroxide, this fact being due to the empiric choice of the doses. With regard to aluminium content, aluminium phosphate activity remained greater than that of aluminium hydroxide although the difference decreased with decreasing pH values. The antacid capacities were related to the emptying outputs. Antacid activity corresponding to 100 mg aluminium was similar in both antacids less than pH 1.5. This effect was dependent on emptying rates. It can be suggested that Al was responsible for antacid activity in both preparations, and that the buffering capacity was supported by the change of aluminium cation in hydrolysis intermediary compounds.

Torsade de pointes represents a potential complication of chronic amiodarone therapy. Several reports have emphasized the need for a loading dose in order to achieve therapeutic blood levels rapidly. We report a case of torsade de pointes following a single oral dose of amiodarone (1400 mg or 30 mg kg-1) administered after short intravenous loading for prevention of paroxysmal atrial flutter. Torsades de pointes were preceded and associated with marked QT prolongation and bradycardia. This report suggests that careful monitoring of patients undergoing oral amiodarone loading is necessary.

A model of an 'artificial stomach' has been constructed in order to take into account some of the parameters lacking in conventional in vitro antacid evaluation, namely the interaction between secretory flux and variation in emptying fluxes, the presence of proteins, and the use of human gastric juice instead of an aqueous solution of hydrochloric acid. The 'artificial stomach' has two elements, the 'stomach' and the pH recording system. The 'stomach' includes a 'gastric' reservoir receiving secretory flux and is emptied by variable fluxes. Aluminium phosphate gel has been studied in 100 ml of 0.1 N HCl, without and with 1 or 5% meat extracts and also in 100 ml of human gastric juice. The antacid effect of 1 or 5% meat extracts has also been assessed. The antacid effect of aluminium phosphate was characterized by the pH rise of the 'gastric' contents, the buffering capacity, and the dilution of gastric contents. These factors were modulated by emptying fluxes. The same characteristics were found when antacid was studied in gastric juice. Proteins exerted a neutralizing effect and modified aluminium phosphate's antacid capacity. A mechanism for buffering capacity by cation aluminium is suggested.