Primary hypogammaglobulinaemia: a survey of clinical manifestations and complications

The records of 240 patients with common variable immunodeficiency,seven with thymoma-associated hypogammaglobulinaemia and 44patients with X-linked agammaglobulinaemia seen at this centreover the past 20 years, were reviewed. Although substantialadvances have been made in treatment there continues to be adelay in diagnosis, as well as high mortality and morbidityrates. Hypogammaglobulinaemia is associated with a high incidenceof chronic sinopulmonary infection, chronic diarrhoea, malignancy,joint disease and hepatitis. There is particular concern thatinfection with mycoplasmas and enteroviruses can be resistantto treatment. The high incidence of lymphoma and gastric carcinomain patients with common variable immunodeficiency is highlighted.     

Fluorimetric Studies of the Formation of Riboflavin-β-Cyclodextrin Inclusion Complex: Determination of the Stability Constant by use of a Non-linear Least-squares Model

The non-linear least-squares model for calculation of the stability constant (K_st) of a drug-cyclodextrin complex has been used in fluorimetry studies. Complexation of riboflavin with β-cyclodextrin (β-CyD) was monitored fluorimetrically by measuring changes in the fluorescence intensity of the vitamin in the presence of various amounts of β-CyD. Formation of an inclusion complex was confirmed in the solid state by differential scanning calorimetry (DSC) and in aqueous solution by proton nuclear magnetic resonance spectroscopy (¹H NMR). The experimental K_st value (2112 M^?1) derived from the fluorimetry studies appeared to fit well to a 1:1 drug-to-cyclodextrin molar ratio according to the non-linear mathematical model. The model is particularly suitable for fluorescent compounds of which fluorescence intensity is influenced by the presence of cyclodextrins.     

Aetiology of Acute Pharyngitis and Clinical Response to Empirical Therapy with Erythromycin Versus Amoxicillin

Guthrie R M, Ruoff G E, Rofman BA, Ginsberg D, Karp R R, BrownS M and Schulz GA. Aetiology of acute pharyngitis and clinicalresponse to empirical therapy with erythromycin versus amoxicillin.Family Practice 1988; 5: 29–35. One hundred and eighty-nine adults with acute pharyngitis hadculture and serological evaluation for groupA beta haemolyticstreptococci (GABHS), Mycoplasma pneumoniae, and Branhamellacatarrhalis. Sixteen patients had evidence for infection withGABHS, none for M. pneumoniae, and one for B. catarrhalis. Forthose with GABHS, there was no significant difference betweenempirical treatment by erythromycin or amoxicillin. For thosewithout GABHS, empirical treatment with erythromycin appearedto result in a statistically significant reduction in coughand a noticeable but less than significant reduction of othersymptoms when compared to empirical treatment with amoxicillin.The new formula tion of erythromycin utilized in this study(PCE) may be associated with a reduction in gastrointestinalintolerance from that reported with other erythromycin products.     

Subchronic Toxicity of Cupric Sulfate Administered in Drinking Water and Feed to Rats and Mice

Subchronic Toxicity of Cupric Sulfate Administered in DrinkingWater and Feed to Rats and Mice. HÉBERT, C. D., ELWELL,M. R., TRAVLOS, G. S., FITZ, C. J., AND BUCHER, J. R. (1993).Fundam. Appl. Toxicol. 21, 461–475. The effects of acute poisoning by cupric sulfate in a numberof species are well known; however, the effects of chronic low-levelingestion of cupric sulfate are less well characterized. Becauseexposure of humans to cupric sulfate may occur through drinkingwater, food, soil, or ambient air, subchronic toxicity studieswere conducted in male and female F344/N rats and B6C3F₁ miceby the drinking water (2-week exposure) and dosed feed (2-and13-week exposure) routes. Animals were evaluated for histopathology,clinical pathology, reproductive toxicity, and tissue metalaccumulation, and target organs were examined by a variety ofspecial stains and by electron microscopy to characterize theobserved lesions. In drinking water, cupric sulfate concentrationsof 300 to 100 ppm produced no ill effects, whereas concentrationsof 3000 to 30,000 ppm were lethal to rats and mice within 2weeks. In feed, cupric sulfate concentrations of 4000 to 16,000ppm caused significant reductions in body weight gain in bothspecies in the 2- and 13-week studies. Hyperplasia and hyperkeratosisof the limiting ridge of the forestomach were present in bothspecies in the 2- and 13-week studies. Rats in the dosed feedstudies had a dose-related increase in inflammation in the liverand changes in clinical chemistry parameters which were indicativeof hepatocellular damage and cholestasis. Histologic changesin the kidneys of rats consisted of a dose-related increasein the number and size of eosinophilic protein droplets in theepithelial cytoplasm and the lumina of the proximal convolutedtubules. Droplets were larger and more numerous in males thanin females. Urinalysis results were suggestive of renal tubularepithelial damage. Iron staining of spleens from treated animalsindicated a marked depletion of iron stores in both male andfemale rats, but not in mice, while hematologic and clinicalchemistry alterations in rats in the 13-week study, along withhistologic changes in bone in the 2-week dosed feed study, wereindicative of a microcytic anemia. Cupric sulfate produced noadverse effects on any of the reproductive parameters measuredin rats or mice of either sex. These results indicate that cupricsulfate at high exposure levels is a hepatic and renal toxicant,as well as an inducer of anemia in rodents, with rats more sensitivethan mice following subchronic exposure.