276 ECOLOGICAL TREATMENT OF BACTERIAL
VAGINOSIS
SIR,-Bacterial vaginosis is related to a suppression of lactobacilli and the concomitant predominance of anaerobic bacteria. 13 This disturbance may be due to an alteration of the ecology of the vagina, perhaps caused by unsatisfactory conditions for the growth of lactobacilli. We have evaluated the efficacy of different procedures whose aim was to support the relation between lactobacilli and the
vaginal mucosa. In an open randomised trial we investigated four treatments in a total of 61 patients who fulfilled three of the following criteria of bacterial vaginosis: (1) subjective symptoms of foul-smelling discharge; (2) pH of the vaginal fluid above 4-5; (3) malodour evoked by the addition of potassium hydroxide to the discharge; and (4) presence of "clue cells" in the wet smear without increased numbers of leucocytes. Patients with trichomonas infestation, yeast infection, or positive cultures of Chlamydia trachomatis and Neisseria gorwrrhoeae were excluded. Treatment was two doses daily for 7 days into the vagina of: (1) 5 ml 0-92% v/v acetic acid jelly (’Aci-Jel’ Ortho Cilag); (2) 5 ml ’Dienoestrol’ cream (100 g/g, Ortho Cilag); (3) 5 ml of commercially available yoghurt based on Lactobacillus acidophilus, more than 1011/ml and pH less than 4,6 (Aria, Sweden); or (4) 500 mg metronidazole tablets. The effect of treatment was evaluated four weeks later by recording presence or absence of the bacterial vaginosis criteria. Metronidazole was effective, with a cure rate of 13/14, similar to that reported.’ The other treatments were only occasionally successful (acetic acid 3/17; dienoestrol 1/16; and yoghurt 1/14). The cause of the disturbed vaginal ecology in bacterial vaginosis may be more profound than expected. The disturbance may result from altered attachment mechanisms between lactobacilli and vaginal epithelium, followed by competition with other microorganisms. If acidity is crucial for a normal vaginal ecology, neither supplementation by yoghurt nor oestrogen support restores normality. Only eradication of amine-producing anaerobes is effective. Department of Obstetrics and Gynaecology, Karolinska Institute, Huddinge University Hospital, S-141 86 Huddinge, Sweden
BENGT FREDRICSSON KATARINA ENGLUND LEON WEINTRAUB ANDERS ÖLUND
Department of Microbiology, Karolinska Institute
CARL-ERIK NORD
1. Mardh
PA, Taylor Robinson D. Bacterial vaginosis. Scand J Urol Nephrol 1984, suppl 86. 2. Fredricsson B, Nord C-E. Influence of metronidazole treatment on the vaginal microbiological flora. Scand J Infect Dis 1983; suppl 40: 91-94. 3. Fredricsson B, Hagström B, Evaldson G, Nord C-E Gardnerella-associated vagmitis and anaerobic bactena. Gynecol Obstet Invest 1984; 17: 236-41. 4. Bistoletti P, Fredricsson B, Hagström B, Nord C-E. Comparison of oral and vaginal metronidazole therapy for nonspecific bacterial vaginosis Gynecol Obstet Invest 1986; 21: 144-49.
rlasrma
Magnesium
Urinary magnesium excretion related
to
mmol/
L
plasma magnesium
concentration.
A = magnesium depletion in seven patients with normal renal function;’ B = mean result of four normal subjects on magnesium-deficient diet;’ C = three cases of renal magnesium wasting associated with hypokalaemia;’ D normal sib of patients described in E; E two patients with renal magnesium wasting, distal renal tubular acidosis, and nephrocalcinosis;’ F four results from one patient with renal magnesium wasting in vanous states of magnesium repletion;5 G = the patient referred to us for =
=
=
investigation. Area to left of dotted line represents results with plasma magnesium below lower limit of normal (0-7 mmol/1), but above the limit of normal for 24 h urinary magnesium excretion in presence of hypomagnesaemia (0 5 mmol),
than 0-5mmol is abnormal. Any patient whose results fall to the left of the dotted line in the figure must be considered to have a renal magnesium leak. In hypomagnesaemia the differentiation of a renal versus gastrointestinal cause is achieved by considering the urinary magnesium excretion.
J. E. SCOBLE Renal Transplant Unit, Royal Free Hospital, London NW3 2QG
P. SWENY Z. VARGHESE J. MOORHEAD
1. Dirks JH, Alfrey AC Normal and abnormal magnesium metabolism. In: Shner RW, ed. Renal and electrolyte disorders. Boston: Little, Brown, 1986: 331-59 2. Shils ME. Experimental human magnesium depletion Medicine (Baltimore) 1969; 48: 61-82. 3. Gitelman HJ, Graham JB, Welt LG. A new familial disorder characterized by hypokalaemia and hypomagnesemia. Trans Ass Am Phys 1966; 79: 221-33. 4 Michelis MF, Drash AL, Linarelli LG, De Rubertis FR, Davis DB. Decreased bicarbonate threshold and renal magnesium wasting in a sibship with renal tubular acidosis Metabolism 1972; 21: 905-20. 5. Runeberg L, Collan Y, Joiken EJ, Lahdevirta J, Aro A. Hypomagnesemia due to renal disease of unknown etiology Am J Med 1975; 59: 873-81.
INVESTIGATING HYPOMAGNESAEMIA
HLA ANTIGENS AND GERM-CELL TUMOURS
SIR,-Hypomagnesaemia is becoming an increasing problem with the use of agents such as cisplatin and the aminoglycosides. The diagnosis of a renal leak versus malabsorption is important. A patient was referred to us for investigation of hypomagnesaemia. The cause was not obvious but malabsorption had been considered because urinary magnesium excretion was "within the normal range". It is recorded1 that with normal renal function magnesium depletion leading to hypomagnesaemia results in 24 h urinary magnesium excretion falling to 0-5 mmol or less. The figure summarises published values for urinary magnesium excretion and plasma magnesium. The subjects can be divided into those with normal renal function and those with renal magnesium leaks of various sorts. The patient referred to us had a renal magnesium leak since she continued to lose magnesium in her urine when she was hypomagnesaemic. A presumptive diagnosis of Bartter’s syndrome has been made as a low fractional distal chloride reabsorption has been demonstrated in the absence of evidence of diuretic ingestion. We feel that it is not widely recognised that in the investigation of a patient with hypomagnesaemia a 24 h urinary magnesium greater
SIR,-Oliver et all reported the frequency of HLA antigens in patients with germ-cell tumours of the testicle and mentioned that we2 had provided no correlation of HLA antigen distribution with histological subclassification. We have studied 132 patients referred for treatment to either the second department of medicine or the urology department of the University of Vienna between January,1979,and January, 1986.As in our prehminary report, covering 66 patients, there has been in the 132 patients a significant increase in B13 (p<0’01, corrected for number of comparisons; table I) in stage iv disease (haematogenous metastases) and of DR2 in stage I disease (p < 0 001). The increase in DR5 in stage iv disease previously reported by us is no longer significant. The only other significant change in HLA antigen frequency is an increase in DR1in seminoma (p < 0035), a change mentioned in one of our earlier reports.3 Although these results seem to differ substantially from Oliver’ss in the various, sometimes small, subgroups, a joint calculation of published data is of interest (table n). The pooled data from the three studies that provide correlations with histological subgroups