Subject: Virus and Syphilis in AIDS Patients Date: Published: January 1988 CHRONIC SPIROCHETAL INFECTION AND THE PATHOGENESIS OF AIDS [From Quantum Medicine, a Journal of Comparative Therapeutics, Vol. 1, No. 1, January 1988. Footnotes are indicated but were not provided in the text from which this display was made. -- sysop] by Steven S. Caiazza, M. D. "As being is to becoming, so truth is to belief." -- Plato Physicians who treat patients with the Acquired Immune Deficiency Syndrome (AIDS) generally accept the belief that the disease is caused by a retrovirus variously called HIV, LAV, or HTLV-3.(1) This is so even though Koch's Postulates -- the gold standard which must be met before a cause and effect relationship between an infection agent and a particular disease can be validated -- have never been satisfied.(2) The truth of the matter, however, is that increasingly clinicians as well as researchers and scientists are questioning whether a simple retroviral model explains the myriad clinical and laboratory abnormalities we are coming to associate with AIDS.(3) In this paper, I wish to propose an alternative, bacterial model that better explains the pathogenesis of this disease and I intend to provide in support of this model a growing body of data derived from an ongoing clinical trial which began early in 1987. It is my contention that the primary insult to the immune system which ultimately results in the syndrome now called AIDS is repeated exposure to pathogenic spirochetes.(4) While the list of such spirochetes and the primary diseases associated with them is long and ranges from B. burgdorferi, the agent responsible for Lyme Disease,(5) to B. recurrentis, the cause of Relapsing Fever,(6), in the Western world we are speaking for all practical purposes about T. Pallidum and the disease it produces -- syphilis.(7) Assuming that the growing body of experts is correct and AIDS cannot be explained by a single viral model. then chronic disease with tertiary syphilis becomes more than just another candidate for the cause, but a likely candidate. It is extremely immune suppressive, especially in its chronic form.(8) It is a blood borne disease; it is transmitted venereally; and it is easily acquired in utero thus explaining pediatric AIDS. Syphilis in the United States is also increasing in the same manner AIDS is; that is, in logarithmic fashion. In fact, the Centers for Disease Control (CDC) has recently released statistics which indicate that the incidence of syphilis for the first three months of 1987 is an astonishingly 23% greater than for the same period in 1986. Furthermore and more strikingly, a full 75% of this log increase in syphilis is found in just three geographic areas within the United States -- the same three regions where the incidence of AIDS is also highest.(9) Finally, chronic syphilis has for decades been endemic in precisely the same populations most at risk for the Acquired Immune Deficiency Syndrome: gay and bisexual men, those who use parenteral drugs, the repeatedly transfused, the sexual partners of those at risk whether male or female and the unfortunate children born to those infected. But a key question associated with an entirely legitimate objection now arises. Theory and epidemiology aside, do we not have simple, readily accessible and easily performed blood tests that are perfectly able to diagnose syphilis in any of its stages? Unfortunately, the answer is no. We do not have access to such diagnostic procedures. With first encounter primary syphilis the standard screening serologic tests cannot approach 95% sensitivity. Even when dealing with secondary syphilis, an entity in which serologic markers have always been thought to be 100% accurate, we are coming to realize that it is possible to have simultaneous seronegativity and yet florid, progressive disease.(10)(11) Finally, we must remember that the form of syphilis we are dealing with when discussing AIDS is chronic tertiary disease. It is well known that the longer an individual has syphilis, that is the more chronic the disease, the less dependable the serologic tests become. It is simply not known how accurate -- or inaccurate -- the tests we use to attempt the diagnosis of syphilis are if the disease is in its late, chronic or tertiary stages. It could well be that by the time chronicity is reached, we could be dealing with at best a 20-30% sensitivity using any of the standard screening serologic markers. This, however, should not be surprising as the technology on which tests tests are based, while of course updated over time, nonetheless dates back to Dr. Wassermann in 1909. We are using today technology devised 80 years ago to diagnose a disease which the father of modern American medicine, Dr. William Osler, pointed out is the Great Masquerader because it can do, quite simply, anything it wants. This is a vitally important point. For Dr. Osler's remark was not meant to be a mere quit designed to impress his students. He wished to make clear that syphilis, the Great Masquerader, can present clinically in a variety of ways and can mimic virtually any other disease so that the chance of confusion is great. In fact, every sign or symptom we have come to associate with AIDS can also be found somewhere in the medical literature likewise associated with syphilis. Even the dreaded Kaposi's Sarcoma was described by Dr. Kaposi himself in a group of syphilitic men! There is a final element in the theoretical equation that must be discussed before we can move on to the clinical material. One could still object to all of the above on the basis that we do have and have had for over forty years an effective cure for syphilis, penicillin. If this is so, if penicillin does eradicate T. Pallidum, how could it possibly be linked to AIDS. The answer is deceptively simple: Yes, penicillin can cure syphilis. But since the introduction in the United States of penicillin for the treatment of syphilis just after World War II, we have consistently used the wrong preparation of the antibiotic. The treatment of choice for syphilis as determined by the Public Health Service and subsequently by the CDC is benzathine penicillin.(2) This particular preparation was chosen over several other candidates because the benzathine moiety attached to the penicillin molecule permits blood levels of the blood to remain present for upwards of several weeks. Prolonged blood levels of penicillin are neessary because T. Pallidum in order to be killed must be actively dividing, not just in a dormant, resting condition and its dividing time can be extremely prolonged. There is a major problem here, however. Because of the benzathine moiety, this form of penicillin -- the penicillin that the Centers for Disease Control recommends as THE ultimate treatment for syphilis -- does not cross the blood-brain barrier (the BBB). This barrier between the central nervous system and the rest of the body has evolved because the central nervous system does not participate in the body's immune system. The brain does not have its own protective immune function. Thus, nature has devised the blood-brain barrier. So what? So benzathine penicillin must therefore destroy the spirochete before it can get into the brain. This would be convenient fantasy if it were not for the work of Dr. Ovcinnikov in Moscow who prior to his death studied syphilis for over thirty years and produced electronmicrographs which clearly show that within hours of infection, the organism has already insinuated itself into nervous tissue. The point here is that because of our choice of the wrong form of penicillin, we physicians create, whenever we treat syphilis, a protected reservoir of infection within the body that cannot be reached by the very medicine designed to eradicate that infection. This also explains why one of the very earliest signs of AIDS/ARC is often subtle central nervous system disease.(13) For what the clinician is actually witnessing is not retroviral infection of the CNS, but very early neuro-psychiatric syphilis. To summarize at this point: 1. A viral model, especially a retroviral model, cannot by itself explain the clinical entity we have come to know as AIDS. 2. A far more tenable hypothesis is that AIDS is the end result of chronic and reactivated bacterial infection, perhaps with one of a variety of synergistic co-factors. 3. The most likely pathogens in this regard are endemic spirochetes the most important of which is the agent which causes syphilis. 4. Syphilis is transmitted in precisely the ways it would have to be transmitted in order to explain the epidemiology of this disease and is highly endemic in all the traditional AIDS risk groups. 5. All signs and symptoms of AIDS have their counterparts in syphilis and/or other spirochetal diseases. 6. There is no "Gold Standard" for the serologic diagnosis of syphilis and the sensitivity of the diagnostic procedures presently used is at best poor and when dealing with chronic disease terrible. 7. We have been inadequately treating syphilis with the wrong preparation of penicillyn for over 40 years thus creating an entire population of chronically diseased. Upon reactivation and/or re-exposure, this chronic state evolved into the entity known as AIDS. II "Cease to be ruled by dogmas and authorities; look at the world." -- Roger Bacon Theory and hypothesis must be grounded in fact, in the real world, or else they are idle and worthless speculation. How do we build a foundation for all I have just said that can be reproducibly grounded in fact, in reality? I have already pointed out that there is at present no Gold Standard for the serologic diagnosis of syphilis. To make matters worse, T. Pallidum has never been and cannot be grown in any culture medium.(14) And if that were not enough to make matters difficult, remember that we are dealing with a chronic infection and, as with so many other chronically established infectious diseases, it can be impossible to directly visualize the organism in fixed tissue. Clearly, there is only one way out of this dilemma. One must go to the patients themselves. One must create a trial of AIDS and ARC (AIDS Related Complex) individuals, treat them properly and aggressively for chronic tertiary syphilis while withholding all antiviral agents and, as Roger BAcon would urge, observe what happens. This is precisely what I have been in the process of doing during 1987. But for the purposes of this paper, I am intentionally leaving out all of the less ill ARC patients and restricting myself only to those patients who easily meet CDC criteria for full-blown AIDS and who, therefore, are among the most sick in my practice. Thus, by orthodox criteria most of these patients ought already to be dead. By orthodox criteria nothing I am doing can possibly be of any benefit to these unfortunate individuals. Table One represents clinical and laboratory parameters of ten of my most seriously ill AIDS patients. All are anti-HIV positive. All have either had Pneumocystis carinii pneumonia and/or Kaposi's Sarcoma, along with a wide multiple variety of other AIDS related health problems. All have been hospitalized at least once. One patient has both Kaposi's Sarcoma along with P. Carinii pneumonia. All are ART non-reactive. None of the ten demonstrates by traditional criteria any serologic evidence of active syphilis. Five of the ten are repeatedly FTA-ABS reactive. Four of the ten give histories of past diagnosis and treatment for syphilis. Thus, two individuals out of ten have a repeatedly positive FTA-ABS without a history of ever having had or been treated for syphilis. Out of three cases of Kaposi's Sarcoma represented, there is remission in all and regression of lesions in two. Ten of ten patients have responded to treatment and are presently clinically improved. All have outlived their initial prognoses. All are employed holding down full time jobs and living ostensibly normal lives. But all remain gravely ill and still carry a guarded to poor prognosis. All were treated with doxycycline alone or a combination of intramusucular benzathine penicillin and doxycycline. None had any important side effects from the antibiotics used. All continue on medicine. No antiviral agent were used except topical and oral acyclovir. Central Nervous System symptoms (depression, poor short-term memory, irritability, difficulty in concentrating, and loss of libido) rarely respond to Benzathine, but would always promptly respond to 400 mg of doxycycline a day in divided doses. If aqueous penicillin were used, the central nervous system would be the first to respond. Nine of ten patients experienced an increase in their T4/T8 ratios. Six of ten patients showed increases in total B cells. Eight of ten demonstrated increases in total Helper(T4)cells. Of paramount and overriding importance, however, all patients -- ten out of ten -- experienced, by clinical parameters, dramatic improvement. Whether this improvement persists remains to be seen. The full role occult tertiary syphilis is playing in AIDS is yet to be fully elucidated. But that syphilis bears an intimate relationship to AIDS is no longer a debatable issue. Simply put, if there is no syphilis on board, there is no clinical AIDS. Therefor, that we must treat syphilis more aggressively and diagnose it more clinically, are no longer issue for debate. This material is preliminary. It requires follow-up and careful analysis. More work on the relationship between spirochetal infection and clinical AIDS must be funded and must be done. But the task is fundamentally a clinical one. It is up to the practitioners to do this job, not the scientists and bench people. Enough technology exists. It is up to the clinician to recognize that and use it. The only ones who can possibly prosper are the patients. [Following is a Table of statistics on ten patients.] TABLE ONE AIDS PATIENTS BEING TREATED FOR SYPHILIS ONLY (ALL PATIENTS ARE ANTI-HIV POSITIVE) PATIENT #1 06.22.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 P. CARINII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR SEVERE ADENOPATHY FTA: N/R 7.2X10E6u IM NODES RESOLVING 10KG WEIGHT LOSS DOXYCYCLINE: 7 KG WEIGHT GAIN SEVERE THRUSH 400-MG PO qD THRUSH RESOLVED AIDS ENCEPHALOPATHY SENSORIUM CLEAR LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB PRIOR TO RX DURING RX BEFORE TOT WBC = 3.0 TOT WBC = 3.1 HCT =38.3 HCT =45.8 TOT LYMPHS = 1419 TOT LYMPHS = 1457 PLATE- PLATE- TOT B CELLS = 71 TOT B CELLS = 58 LETS = 104 LETS = 192 TOT C CELLS = 1277 TOT C CELLS = 1078 CHOLES- CHOLES- TOT T4 = 213 TOT T4 = 277 TEROL = TEROL = TOT T8 = 937 TOT T8 = 830 131 MG/DL 162 MG/DL T4/T8: .23 T4T8:0.33 PATIENT #2 06.11.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 KAPOSI'S SARCOMA OF ART: N/R DOXYCYCLINE: KAPOSI'S RECEDING SKIN AND PHARYNX FTA: N/R 400 MG PO qD THRUSH RESOLVED SEVERE THRUSH FEVERS RESOLVED DAILY ENERGY NORMAL NOCTURNAL FEVERS SENSORIUM CLEAR SEVERE FATIGUE/MALAISE AIDS ENCEPHALOPATHY LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 4.9 TOT WBC = 3.7 HCT =38.3 HCT =45.8 TOT LYMPHS = 2087 TOT LYMPHS = 1280 PLATE- PLATE- TOT B CELLS = 21 TOT B CELLS = 179 LETS = 104 LETS = 192 TOT T CELLS = 1938 TOT T CELLS = 947 CHOLES- CHOLES- TOT T4 = 313 TOT T4 = 166 TEROL = TEROL = TOT T8 = 1398 TOT T8 = 666 131 MG/DL 162 MG/DL T4/T8 RATIO: .22 T4/T8 RATIO: 0.25 PATIENT #3 09.10.87 CLINICAL DATA CLINICAL STATUS SYPHILIS CLINICAL STATUS PRIOR TO THERAPY SEROLOGY THERAPY SEPTEMBER 87 P. CARINII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR SEVERE FATIGUE FTA: 3+ 7.2X10E6u IM ENERGY NORMAL MILD ENCEPHALOPATHY DOXYCYCLINE: SENSORIUM CLEAR MILD THRUSH 400-MG PO qD THRUSH RESOLVED LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB PRIOR TO RX DURING RX BEFORE TOT WBC = 3.7 TOT WBC = 3.6 HCT =31.0 HCT =45.8 TOT LYMPHS = 518 TOT LYMPHS = 702 ESR=74MM/HR ESR=35MM/HR TOT B CELLS = 26 TOT B CELLS = 77 CHOLES- 104 CHOLES- TOT C CELLS = 311 TOT C CELLS = 169 TEROL = TEROL = TOT T4 = 21 TOT T4 = 14 174 MG/DL 218 MG/DL TOT T8 = 233 TOT T8 = 119 FERRITIN=2094 FERRITIN719 T4/T8: .09 T4T8:0.12 CALCIUM=8.9 CALCIUM=9.7 PATIENT #4 07.16.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 P.CARENII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR SEVERE THRUSH FTA: N/R 7.2X10E6u IM THRUSH RESOLVED CHRONIC FURUNCULOSIS DOXYCYCLINE: SKIN NOW CLEAR SEVERE ADENOPATHY 400-MG PO qD COLITIS RESOLVED SEVERE FATIGUE NODES RESOLVING DAILY ENERGY NORMAL NOCTURNAL FEVERS FEVERS RESOLVED CHRONIC PROCTITIS RESOLVED HERPETIC LESIONS LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 5.0 TOT WBC = 5.0 URATE = 3.7 URATE = 5.2 TOT LYMPHS = 1555 TOT LYMPHS = 2290 GLOBU- GLOBU- TOT B CELLS = 342 TOT B CELLS = 298 LIN = 3.9 LIN = 4.9 TOT T CELLS = 8248 TOT T CELLS = 1787 CHOLES- CHOLES- TOT T4 = 16 TOT T4 = 46 TEROL = TEROL = TOT T8 = 482 TOT T8 = 1099 149MG/DL 169MG/DL T4/T8 RATIO: 0.03 T4/T8 RATIO: 0.04 PATIENT #5 06.04.87 CLINICAL DATA CLINICAL STATUS SYPHILIS CLINICAL STATUS PRIOR TO THERAPY SEROLOGY THERAPY SEPTEMBER 87 P. CARINII PNEUMONIA ART: N/R DOXYCYCLINE: LUNGS REMAIN CLEAR SEVERE THRUSH FTA: N/R 400 MG PO qD THRUSH RESOLVED 30 KG WEIGHT LOSS DOXYCYCLINE: 12 KG WEIGHT GAIN CHRONIC COLITIS 200 MG PO qD COLITIS RESOLVED SEVERE FATIGUE ENERGY NORMAL AIDS ENCEPHALOPATHY SENSORIUM CLEAR LABORATORY DATA IMMUNE STUDIES IMMUNE STUDIES OTHER LAB PRIOR TO RX DURING RX BEFORE TOT WBC = 3.0 TOT WBC = 3.7 HCT =36.5 HCT =44.2 TOT LYMPHS = 840 TOT LYMPHS = 1664 TOT B CELLS = 59 TOT B CELLS = 183 CHOLES- 104 CHOLES- TOT C CELLS = 731 TOT T CELLS = 1082 TEROL = TEROL = TOT T4 = 160 TOT T4 = 350 154 MG/DL 197 MG/DL TOT T8 = 445 TOT T8 = 583 T4/T8 RATIO: 0.34 T4/T8 RATIO: 0.60 PATIENT #6 06.09.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 P.CARENII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR SEVERE AIDS DERMATITIS FTA: N/R 7.2X10E6u IM SKIN NOW CLEARD SEVERE THRUSH DOXYCYCLINE: THRUSH RESOLVED 15 KG WEIGHT LOSS 400-MG PO qD 7 KG WEIGHT GAIN DAILY BICILLIN: FEVERS RESOLVED NOCTURNAL FEVERS 2.4x10e6u IM ENERGY NORMAL SEVERE FATIGUE q WEEK LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 3.6 TOT WBC = 3.4 HCT = 33.0 HCT = 42.2 TOT LYMPHS = 1152 TOT LYMPHS = 748 ESR=81MM/HR ESR=40MM/HR TOT B CELLS = 23 TOT B CELLS = 7 FERRITIN FERRITIN TOT T CELLS = 910 TOT T CELLS = 554 =2428 =2028 TOT T4 = 18 TOT T4 = 30 C-REACT PRO C-REACT PRO TOT T8 = 546 TOT T8 = 389 =16 =7.1 T4/T8 RATIO: 0.03 T4/T8 RATIO: 0.04 PATIENT #7 08.11.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 P.CARENII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR MODERATE THRUSH FTA: N/R 7.2X10E6u IM THRUSH RESOLVED 10 KG WEIGHT LOSS DOXYCYCLINE: 4 KG WEIGHT GAIN SEVERE FATIGUE 400-MG PO qD ENERGY NORMAL LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 2.8 TOT WBC = 4.0 HCT = 36.3 HCT = 38.2 TOT LYMPHS = 558 TOT LYMPHS = 1560 PLATELETS PLATELETS TOT B CELLS = 47 TOT B CELLS = 172 =123 =125 TOT T CELLS = 441 TOT T CELLS = 1123 TOT T4 = 82 TOT T4 = 125 TOT T8 = 329 TOT T8 = 640 T4/T8 RATIO: 0.25 T4/T8 RATIO: 0.20 PATIENT #8 09.10.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 P.CARENII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR KAPOSI'S SARCOMA FTA: N/R 7.2X10E6u IM KAPOSIS STABLE SEVERE ADENOPATHY DOXYCYCLINE: NODES RECEEDING EXTREME FATIGUE 400-MG PO qD ENERGY NORMALIZING BICILLIN: 2.4x10E6u IM q WEEK LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 6.6 TOT WBC = 7.2 ESR=54MM/HR ESR=22MM/HR TOT LYMPHS = 1227 TOT LYMPHS = 1454 PLATELETS PLATELETS TOT B CELLS = 233 TOT B CELLS = 131 =169 =185 TOT T CELLS = 699 TOT T CELLS = 1032 TOT T4 = 147 TOT T4 = 291 TOT T8 = 368 TOT T8 = 538 T4/T8 RATIO: 0.40 T4/T8 RATIO: 0.54 PATIENT #9 08.11.87 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 P.CARENII PNEUMONIA ART: N/R BICILLIN: LUNGS REMAIN CLEAR SEVERE ADENOPATHY FTA: 3+ 7.2X10E6uIM NODES RESOLVING RECURRENT IMPETIGO DOXYCYCLINE: SKIN NOW CLEARIN DAILY LOW/GRADE FEVERS 400-MG PO qD FEVERS RESOLVING FATIGUE/MALAISE BICILLIN: ENERGY NORMAL 2.4x6u IM q WEEK LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 5.1 TOT WBC = 6.8 HCT=37 VOL% HCT=37.9 VOL% TOT LYMPHS = 1596 TOT LYMPHS = 2311 CALCIUM=8.9 CALCIUM=9.5 TOT B CELLS = 176 TOT B CELLS = 254 TOT T CELLS = 1309 TOT T CELLS = 1779 TOT T4 = 128 TOT T4 = 324 TOT T8 = 958 TOT T8 = 1202 T4/T8 RATIO: 0.13 T4/T8 RATIO: 0.27 PATIENT #10 CLINICAL DATA CLINICAL STATUS SYPHILIS THERAPY CLINICAL STATUS PRIOR TO THERAPY SEROLOGY SEPTEMBER 87 KAPOSI'S SARCINA ART: N/R BICILLIN: KAPOSI'S RECEEDING MARKED ADENOPATHY FTA: 2+ 7.2x10E6uIM NODES RESOLVING SEVERE FATIGUE DOXYCYCLINE: ENERGY NORMALIZING MILD THRUSHIGUE 400-MG PO qD THRUSH RESOLVED LABORATORY PARAMETERS IMMUNE STUDIES IMMUNE STUDIES OTHER LAB OTHER LAB PRIOR TO RX DURING RX BEFORE DURING TOT WBC = 3.8 TOT WBC = 2.8 GLOBULIN GLOBULIN TOT LYMPHS = 1178 TOT LYMPHS = 1568 =3.5 = 4.4 TOT B CELLS = 271 TOT B CELLS = 345 CHOLESTEROL CHOLESTEROL TOT T CELLS = 742 TOT T CELLS = 956 =128 MG/DL =165 MG/DL TOT T4 = 24 TOT T4 = 78 TOT T8 = 589 TOT T8 = 768 T4/T8 RATIO: 0.04 T4/T8 RATIO: 0.10 [The above was published in Quantum Medicine, Vol. 1, No. 1, January 1988]