Low Dose Naltrexone (LDN) Part One by Jeffrey Dach MD
A Drug to Reverse Narcotics Overdose
Imagine a drug addict slumped over from a lethal heroin overdose. He has shallow breathing and will die unless he receives prompt medical care in the emergency room. If he is lucky enough to make the trip to the ER, the doctors will give him an IV injection of Narcan (Naloxone), the drug of choice to reverse narcotics overdose, waking the victim and snatching him from the jaws of death.
Left Image: Duane Hanson’s sculpture “Drug Addict” from 1974, Courtesy of wikipedia. The addict sitting the floor is a sculpture in a musem. The man standing is an anonymous museum visitor. (18)
A close cousin of Naloxone is Naltrexone, another opioid antagonist used as treatment for for narcotics and alcohol addiction.
Below images: Chemical Structures of Naloxone, Naltrexone and Morphine are similar (see three diagrams below).
FDA approved since 1984
Narcan is available in the hospital operating room where anesthesiologists use it to wake up the patient after the operation. (image at left: first use of anesthesia). Opiate antagonists such as Narcan reverse the sedating effect of opiates by binding to the opioid receptors in the brain.
Above Image: First operation under ether anesthesia on October 16, 1846 (21) Courtesy Library of Congress.
Naltrexone was synthesized in 1963 and FDA approved since 1984. Naltrexone is a close chemical cousin to Narcan with very similar chemical structure, and is used to treat narcotics and alcohol addiction. (see chemical structure diagrams above). It was a surprise for me to find out that Naltrexone has other very important uses at a much lower dosage as an oral capsule. Medical scientists have been carefully studying its effect of Naltrexone on the immune system, and its clinical benefits for a host of disease states for the past 20 years.
Low Dose Naltrexone, (LDN), How Does it Work?
The beneficial effect of low dose naltrexone, LDN, was discovered by Bernard Bihari, MD (1)(1A), a physician in New York City who found that a small dose (3 mg) of naltrexone taken as a capsule at bedtime blocks the opiate receptors in the brain for a few hours during sleep, which then stimulates the brain to increase production of endorphins over the next 24 hours. These endorphins then stimulate the immune system. Although Bihari did much of the early clinical work, Zagon did much of the groundwork with animal research studies at Pennsylvania State University (3-17).
A recent publication in the Jan 2007 Journal of Gasteroenterology on the use of LDN in Crohn’s Disease, was the first breakthrough publication to appear entitled, Low-Dose Naltrexone Therapy Improves Active Crohn’s Disease by Jill Smith MD.
Left Image: Typical appearance of Crohn’s disease involving terminal ilem with ulcerations noted on barium small bowel examination (red arrows) . Courtesy of Jeffrey Dach MD, private collection.
Crohn’s disease is a severe inflammatory condition of the small bowel which can be difficult to treat. Not difficult for LDN however. Jill Smith, M.D. reported that two-thirds of her 17 Crohn’s patients went into remission, and 90% of the group had some benefit. Her article showed impressive colonoscopy photos before and after LDN treatment with complete clearing of the inflammatory changes in the bowel mucosa. Dr. Smith concluded that “LDN therapy appears effective and safe in subjects with active Crohn’s disease.”(2)
Other Conditions Which Benefit from LDN
The major therapeutic action of LDN is the restoration of normal endorphin production by the brain. This is beneficial for any condition in which there is a deficiency in endorphin production, such as autoimmune disease, cancer and HIV/AIDS. Bernard Bihari, MD, who discovered the LDN protocol has used it in hundred of patients in the following categories:
LDN for Cancer
LDN is useful for cancers of the Bladder, Breast, Colon & Rectal Cancer , Glioblastoma, Lung Cancer (Non-Small Cell), Lymphocytic Leukemia (chronic), Lymphoma Hodgkin’s and Non-Hodgkin’s) Malignant Melanoma, Multiple Myeloma , Ovarian Cancer, Pancreatic Cancer, Prostate Cancer (untreated), Renal Cell Carcinoma, Uterine Cancer.(28)
Long term remission with LDN and high dose vitamin D in tongue carcinoma has been reported.(27) LDN has been used in combination with hydroxycitrate and alpha lipoic acid as a metabolic approach to treating cancer in advanced refractory cases.(29)
Beneficial Mechanisms in Cancer
LDN has been shown to down-regulate IL-6 and TNF alpha production by immune cells, and to upregulate genes which activate apoptosis in caner cells , both of which are of benefit to the cancer patient.(25-26)
Clinical trials page for LDN (30)
LDN is useful for Autoimmune and other Diseases:
Above Image: Monthly MRI Scans of Multiple Sclerosis, small bright spots come and go, courtesy wikipedia.
LDN treatment has benefited these diseases: ALS (Lou Gehrig’s Disease), Autism Spectrum Disorders, Chronic Fatigue Syndrome, Crohn’s Disease, Fibromyalgia, HIV/AIDS, Multiple Sclerosis (MS), Parkinson’s Disease, Psoriasis, Rheumatoid Arthritis, Scleroderma, Systemic Lupus (SLE), Ulcerative Colitis, Wegener’s Granulomatosis.
LDN Has Virtually No Side Effects:
Occasionally, during the first week’s use of LDN, patients may complain of some difficulty sleeping. This rarely persists after the first week. Should it do so, dosage can be reduced from 4.5mg to 3mg nightly.
Caution About Narcotics Withdrawal
Because LDN blocks opioid receptors throughout the body for three or four hours, people using narcotics pain pills such as Ultram (tramadol), morphine, Percocet, Duragesic, Oxycontin or codeine, should not take LDN until after complete withdrawal from their narcotic drugs. The use of LDN may induce narcotics withdrawal.
Although naltrexone is FDA approved, the LDN protocol is what is called “off-label use”, and it is unlikely that any company will spend the millions needed to fund studies for FDA approval of the LDN protocol. However, off-label use of an FDA approved drug such as naltrexone is commonplace and widely accepted. The naltrexone capsules are inexpensive, about 20 dollars a month. The treatment is safe, with no adverse side effects.
Pharmacies that offer compounded LDN capsules:
The Compounder Pharmacy 340 Marshall Ave Unit 100, Aurora, IL 60506-2956 Phone: 630-859-0333 Fax: 630-859-0114. (22)
Skip’s Pharmacy 21000 Boca Rio Rd Suite A-29 Boca Raton, Florida 33433, telephone 561-218-0111 800-553-7429 Fax: 561-218-8873 (24)
Thanks to Larry Frieders, the Compounder for bringing LDN to my attention, and for making low cost LDN capsules available to the public. (22)
Articles with related Content:
LDN Part Two (second part to this article)
Crohn’s Recovery with LDN Case Report
Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Florida 33314
Web site for low dose nalotrexone information.(1A) http://www.ldninfo.org/bbihari_cv.htm
Curriculum Vitae, BERNARD BIHARI, M.D. 29 West 15th Street New York, N.Y. 10011, (212) 929-4196 retired as of March 2007.
Low-dose naltrexone therapy improves active Crohn’s disease.Smith JP, Stock H, Bingaman S, Mauger D, Rogosnitzky M, Zagon IS. Am J Gastroenterol. 2007 Apr;102(4):820-8. Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.
OBJECTIVES: Endogenous opioids and opioid antagonists have been shown to play a role in healing and repair of tissues. In an open-labeled pilot prospective trial, the safety and efficacy of low-dose naltrexone (LDN), an opioid antagonist, were tested in patients with active Crohn’s disease. METHODS: Eligible subjects with histologically and endoscopically confirmed active Crohn’s disease activity index (CDAI) score of 220-450 were enrolled in a study using 4.5 mg naltrexone/day. Infliximab was not allowed for a minimum of 8 wk prior to study initiation. Other therapy for Crohn’s disease that was at a stable dose for 4 wk prior to enrollment was continued at the same doses. Patients completed the inflammatory bowel disease questionnaire (IBDQ) and the short-form (SF-36) quality of life surveys and CDAI scores were assessed pretreatment, every 4 wk on therapy and 4 wk after completion of the study drug. Drug was administered by mouth each evening for a 12-wk period. RESULTS: Seventeen patients with a mean CDAI score of 356 +/- 27 were enrolled. CDAI scores decreased significantly (P= 0.01) with LDN, and remained lower than baseline 4 wk after completing therapy. Eighty-nine percent of patients exhibited a response to therapy and 67% achieved a remission (P < 0.001). Improvement was recorded in both quality of life surveys with LDN compared with baseline. No laboratory abnormalities were noted. The most common side effect was sleep disturbances, occurring in seven patients. CONCLUSIONS: LDN therapy appears effective and safe in subjects with active Crohn’s disease. Further studies are needed to explore the use of this compound.
Cancer Lett. 1983 Nov;21(1):89-94. Opioid antagonists inhibit the growth of metastatic murine neuroblastoma.Zagon IS, McLaughlin PJ.
Naltrexone (NTX), an opiate antagonist, had an inhibitory effect on the growth of S20 Y neuroblastoma in A/Jax mice. Daily injections of 0.1 mg/kg NTX resulted in a 69% tumor take, 70% delay in time prior to tumor appearance, and a 60% increase in median survival time. Inoculation of NB in control mice resulted in 100% tumor take within 15 days. The pattern and incidence of metastases of NTX and control mice were similar. These results show that NTX has antineoplastic activity, and suggests a role for the endogenous opioid system in neuro-oncogenic events.
Life Sci. 1983 Dec 12;33(24):2449-54.
Naltrexone modulates growth in infant rats.Zagon IS, McLaughlin PJ.
Naltrexone, a potent opiate antagonist, had both stimulatory and inhibitory effects on somatic growth in preweaning rats depending on dose. Daily injections of 50 mg/kg naltrexone, which blocked morphine-induced analgesia for 24 hr/day, resulted in increased body and organ weights, and acceleration in the appearance of physical characteristics and maturation of spontaneous motor activity. Naltrexone in a dosage of 1 mg/kg, which blocked morphine-induced analgesia for 4 hr/day, had the opposite effects. These results show that naltrexone can modulate growth, and suggest a role for the endorphins and opiate receptors in developmental events.
Brain Res. 1999 Dec 4;849(1-2):147-54. Cloning, sequencing, expression and function of a cDNA encoding a receptor for the opioid growth factor, [Met(5)]enkephalin.
Zagon IS, Verderame MF, Allen SS, McLaughlin PJ. Department of Neuroscience, The Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, PA, USA.
The native opioid growth factor (OGF), [Met(5)]enkephalin, is a tonic inhibitory peptide that modulates cell proliferation and tissue organization during development, cancer, cellular renewal, wound healing and angiogenesis. OGF action is mediated by a receptor mechanism. We have cloned and sequenced a 2.1-kilobase (kb) cDNA for a receptor to OGF (OGFr). The open reading frame was found to encode a protein of 580 amino acids, and eight imperfect repeats of nine amino acids each were a prominent feature. The protein encoded by this cDNA exhibited the pharmacological, temporal and spatial characteristics of the OGFr. Functional studies using antisense technology demonstrated an enhancement in cell growth. The molecular organization of the OGFr has no homology to classical opioid receptors. These results provide molecular validity for the interaction of OGF and OGFr in the regulation of growth processes.
Opioid growth factor regulates the cell cycle of human neoplasias.Zagon IS, Roesener CD, Verderame MF, Ohlsson-Wilhelm BM, Levin RJ, McLaughlin PJ.
Department of Neuroscience and Anatomy, H-109, The Pennsylvania State University, College of Medicine, Hershey, PA 17033, USA.
The native opioid growth factor (OGF), [Met5]-enkephalin, is a tonic inhibitory peptide that modulates cell proliferation and migration, as well as tissue organization, during development, cancer, homeostatic cellular renewal, wound healing, and angiogenesis. OGF action is mediated by the OGF receptor (OGFr). To investigate the target of OGF as to cell proliferation, the effects of excess OGF, and a deprivation of OGF-OGFr interaction by an opioid antagonist, naltrexone (NTX), were examined in 3 human cancer cell lines: pancreatic (BxPC-3), colon (HT-29), and head and neck (CAL-27). OGF exposure decreased growth, DNA synthesis, and mitosis, and increased the doubling time from control levels. FACS analysis revealed a marked increase in cells in the G0/G1 phase and compensatory reduction in cells in S and G2/M phases. Consistent with this observation, the percentage of labeled mitosis (PLM) analysis showed a notable increase in the time of the G0/G1 phase. Receptor blockade with NTX increased the rate of growth, length of DNA synthesis and mitotic phases, and decreased doubling time from control values. FACS analysis indicated an increase in the proportion of cells in S and G2/M phases, and a decrease in the number of cells in the G0/G1 phase. PLM evaluation demonstrated a shortening of the length of the S and G2 phases in the 3 cell lines, and decreases in the M and G0/G1 phases in some cancers. These results indicate that OGF action is directed at the G0/G1 phase, but interruption of OGF-OGFr interfacing has widespread repercussions on the cell cycle. The data on blockade of OGF-OGFr during log phase growth suggest a requisite escorting of the growth peptide and its receptor through the cell cycle.
Cancer Lett. 1996 Mar 29;101(2):159-64.
Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone.Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS.
Nude mice inoculated with human colon cancer (HT-29) and receiving 0.1 mg/kg naltrexone (NTX) beginning immediately after tumor cell injection exhibited a marked retardation in tumorigenicity. This dosage of NTX, which blocked opioid receptors for 6-8 h/day, resulted in a delay of 2.4-fold in tumor appearance compared to control subjects. At the time (10 days) when all control mice had tumors, 80% of the mice in the 0.1 mg/kg NTX group had no signs of neoplasia. Binding capacity, but not affinity, of [3H][Met5]-enkephalin was reduced 85% of control levels in tumor tissue from mice of the 0.1 NTX group. Plasma, but not tumor tissue levels of [Met5]-enkephalin were elevated (2.5-fold) in contrast to control values. These results suggest that daily intermittent opioid receptor blockade with NTX provokes the interaction of opioids and receptors in the interval following drug availability, with opioids serving to inhibit tumorigenicity of human colon cancer.
Cancer Lett. 1997 Jan 30;112(2):167-75. Opioid growth factor (OGF) inhibits human pancreatic cancer transplanted into nude mice.Zagon IS, Hytrek SD, Smith JP, McLaughlin PJ.
Nude mice inoculated with human pancreatic cancer (BxPC-3) cells and receiving 5 mg/kg of opioid growth factor ([Met5]enkephalin; OGF) three times daily exhibited a marked retardation in tumorigenicity compared to animals injected with sterile water (controls). OGF-treated animals had a delay of 43% in initial tumor appearance compared to control subjects (10.6 days). At the time when all of the control mice had tumors, 62% of the mice in the OGF group had no signs of neoplasia. Tumor tissue excised from mice after 30 days was assayed for levels of [Met5]enkephalin and zeta opioid receptors. Tumor tissue levels of [Met5]enkephalin were 24-fold greater in OGF-treated mice than controls, but plasma levels of OGF were 8.6-fold lower in animals receiving OGF. Specific and saturable binding of radiolabeled [Met5]enkephalin to nuclear homogenates of pancreatic tumor tissue was recorded, with a binding affinity (Kd) of 10 nM and a binding capacity (Bmax) of 46.8 fmol/mg protein. Binding capacity, but not affinity, of [3H-Met5]enkephalin was reduced by 58% of control levels in tumor tissue from mice of the OGF group. OGF and the zeta (zeta) opioid receptor were detected in human pancreatic tumor cells by immuno-cytochemistry. These results demonstrate that an endogenous opioid and its receptor are present in human pancreatic cancer, and act as a negative regulator of tumorigenesis in vivo.
Science. 1983 Aug 12;221(4611):671-3. Naltrexone modulates tumor response in mice with neuroblastoma.Zagon IS, McLaughlin PJ.
Matthew, PM, Froelich CJ, Sibbitt WL, Jr., Bankhurst AD, Enhancement of natural cytotoxicity by beta-endorphin, J Immunol 130, pp.1658-1662, Apr 1983.
Zagon IS, McLaughlin PJ, Naltrexone modulates tumor response in mice with neuroblastoma, Science 221, pp.671-3, Aug 12, 1983.
Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS, Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone, Cancer Lett 101(2), pp. 159-64, Mar 29, 1996.
Zagon IS, Hytrek SD, Lang CM, Smith JP, McGarrity TJ, Wu Y, McLaughlin PJ, Opioid growth factor ([Met5]enkephalin) prevents the incidence and retards the growth of human colon cancer, Am J Physiol 271(3 Pt 2), pp.R780-R786, Sep 1996
Zagon IS, McLaughlin PJ, Duration of opiate receptor blockade determines tumorigenic response in mice with neuroblastoma: a role for endogenous opioid systems in cancer, Life Sci 35, pp. 409-416, 1984.
Zagon IS, McLaughlin PJ, Opioid antagonist modulation of murine neuroblastoma: A profile of cell proliferation and opioid peptides and receptors, Brain Res 480, pp. 16-28, 1989.
Duane Hanson’s sculpture “Drug Addict” from 1974 (together with an unidentified museum guest). Picture taken at an exhibition at the Louisiana Museum of Modern Art, Denmark. Source Own work Date Spring 1975 Public domain.
Re-enactment of the first operation under anesthesia (ether). The actual operation took place on October 16, 1846; Daguerrotype TITLE: Operating room of the Massachusetts General Hospital, Boston. Mr. Holman with surgeons: John Mason Warren, George Hayward, Solomon D. Townsend, John Collins Warren and James Johnson around man on operating table. Daguerreotype by Southworth & Hawes, ca. 1850. No known restrictions on publication.
The Compounder Pharmacy 340 Marshall Ave Unit 100 ~ Aurora, IL 60506-2956
Phone: 630-859-0333 Fax: 630-859-0114
Drug Addiction Medication May Treat Other Diseases Dr. Max Gomez NEW YORK (CBS)
(24) Skip’s Pharmacy LDN PAGE 21000 Boca Rio Rd Suite A-29 Boca Raton, Florida 33433 561-218-0111 800-553-7429 Fax: 561-218-8873
(25) Front Immunol. 2017 Jul 11;8:809.Naltrexone Inhibits IL-6 and TNFα Production in Human Immune Cell Subsets following Stimulation with Ligands for Intracellular Toll-Like Receptors.Cant R1, Dalgleish AG1, Allen RL1.
The opioid antagonist naltrexone hydrochloride has been suggested to be a potential therapy at low dosage for multiple inflammatory conditions and cancers. Little is known about the immune-modulating effects of naltrexone, but an effect on the activity of toll-like receptor 4 (TLR4) has been reported. We analyzed the effects of naltrexone hydrochloride on IL-6 secretion by peripheral blood mononuclear cells (PBMC) in vitro following stimulation with ligands for TLR4 and for the intracellular receptors TLR7, TLR8, and TLR9. Naltrexone did not affect cell viability or induce apoptosis of PBMC. Intracellular staining demonstrated that naltrexone inhibited production of IL-6 and TNFα by monocyte and plasmacytoid dendritic cell subsets within the PBMC population following treatment with ligands for TLR7/8 and TLR9, respectively. No effect of cytokine production by PBMC following stimulation of TLR4 was observed. Additionally, naltrexone inhibited IL-6 production in isolated monocytes and B cells after TLR7/8 and TLR9 stimulation, respectively, but no effect on IL-6 production in isolated monocytes after TLR4 stimulation was observed. These findings indicate that naltrexone has the potential to modulate the secretion of inflammatory cytokines in response to intracellular TLR activity, supporting the hypothesis that it may have potential for use as an immunomodulatory drug
26) Int J Oncol. 2016 Aug;49(2):793-802. doi: 10.3892/ijo.2016.3567. Epub 2016 Jun 7. Naltrexone at low doses upregulates a unique gene expression not seen with normal doses: Implications for its use in cancer therapy. Liu WM1, Scott KA1, Dennis JL1, Kaminska E1, Levett AJ1, Dalgleish AG1.
It has been reported that lower doses of the opioid antagonist naltrexone are able to reduce tumour growth by interfering with cell signalling as well as by modifying the immune system. We have evaluated the gene expression profile of a cancer cell line after treatment with low-dose naltrexone (LDN), and assessed the effect that adapting treatment schedules with LDN may have on enhancing efficacy. LDN had a selective impact on genes involved with cell cycle regulation and immune modulation. Similarly, the pro-apoptotic genes BAD and BIK1 were increased only after LDN. Continuous treatment with LDN had little effect on growth in different cell lines; however, altering the treatment schedule to include a phase of culture in the absence of drug following an initial round of LDN treatment, resulted in enhanced cell killing. Furthermore, cells pre-treated with LDN were more sensitive to the cytotoxic effects of a number of common chemotherapy agents. For example, priming HCT116 with LDN before treatment with oxaliplatin significantly increased cell killing to 49±7.0 vs. 14±2.4% in cultures where priming was not used. Interestingly, priming with NTX before oxaliplatin resulted in just 32±1.8% cell killing. Our data support further the idea that LDN possesses anticancer activity, which can be improved by modifying the treatment schedule.
27) Khan, Akbar. “Long-Term Remission of Adenoid Cystic Tongue Carcinoma with Low Dose Naltrexone and Vitamin D3–A Case Report.” Oral Health Dent Manag 13.3 (2014): 721-724. Remission of Tongue Carcinoma with Low Dose Naltrexone and Vitamin D3 Khan Akbar 2014
28) Low Dose Naltrexone Akbar Khan 2016 Presentation Orlando.pdf Low Dose Naltrexone LDN for Cancer Akbar Khan 2016 Presentation Orlando
29) Anticancer Res. 2014 Feb;34(2):973-80.
Metabolic treatment of cancer: intermediate results of a prospective case series. Schwartz L1, Buhler L, Icard P, Lincet H, Steyaert JM. Ecole Polytechnique Laboratoire LIX, 91128 Palaiseau, France.
The combination of hydroxycitrate and lipoic acid has been demonstrated by several laboratories to be effective in reducing murine cancer growth.PATIENTS AND METHODS:All patients had failed standard chemotherapy and were offered only palliative care by their referring oncologist. Karnofsky status was between 50 and 80. Life expectancy was estimated to be between 2 and 6 months. Ten consecutive patients with chemoresistant advanced metastatic cancer were offered compassionate metabolic treatment. They were treated with a combination of lipoic acid at 600 mg i.v. (Thioctacid), hydroxycitrate at 500 mg t.i.d. (Solgar) and low-dose naltrexone at 5 mg (Revia) at bedtime. Primary sites were lung carcinoma (n=2), colonic carcinoma (n=2), ovarian carcinoma (n=1), esophageal carcinoma (n=1), uterine sarcoma (n=1), cholangiocarcinoma (n=1), parotid carcinoma (n=1) and unknown primary (n=1). The patients had been heavily pre-treated. One patient had received four lines of chemotherapy, four patients three lines, four patients two lines and one patient had received radiation therapy and chemotherapy. An eleventh patient with advanced prostate cancer resistant to hormonotherapy treated with hydroxycitrate, lipoic acid and anti-androgen is also reported.
RESULTS:One patient was unable to receive i.v. lipoic acid and was switched to oral lipoic acid (Tiobec). Toxicity was limited to transient nausea and vomiting. Two patients died of progressive disease within two months. Two other patients had to be switched to conventional chemotherapy combined with metabolic treatment, one of when had a subsequent dramatic tumor response. Disease in the other patients was either stable or very slowly progressive. The patient with hormone-resistant prostate cancer had a dramatic fall in Prostate-Specific Antigen (90%), which is still decreasing.
CONCLUSION:These very primary results suggest the lack of toxicity and the probable efficacy of metabolic treatment in chemoresistant advanced carcinoma. It is also probable that metabolic treatment enhances the efficacy of cytotoxic chemotherapy. These results are in line with published animal data. A randomized clinical trial is warranted.
30) Listing of all clinical trials and medical literature on LDN.
Link to this article: http://wp.me/P3gFbV-z5
Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Florida 33314
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Thank you for creating awareness about the positive effects Low dose Naltrexone on numerous diseases. I have Sheehan’s Syndrome and Relapsing Polychondritis. LDN has provided me with a bit more energy and my RP flares have diminished.
I have been using LDN for a couple of months. I purchase my LDN through a compound ding pharmacy. Best Lisa aka #HypoGal
# LDN #SheehansSyndrome #RelapsingPolychondritis #Inflammation #HypoGalBlog
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